Volume I No. III April 2016 BENGAL HEART JOURNAL A PUBLICATION OF THE CSI - WEST BENGAL BRANCH
Secretariat : INDIAN HEART HOUSE P-60, C.I.T. Road, Scheme VII-M Editor : Dr. P. K. Deb Kankurgachi, Kolkata-700054 Published by : Dr. D. Roy Ph : (033) 2355-1500/6308= Tele Fax : (033) 2355-6308 E-Mail : [email protected]= Website : www.csiwb.org.in
BENGAL HEART JOURNAL Volume I No. III APRIL 2016
Contents
1.P. K. Deb, Editorial ...... 3-4 2. Case Report : Pranay Chatterjee, Pritam Kumar Chatterjee, Sukumar Ghosh Malignant melanoma of unknown primary origin presenting as cardiac metastasis ...... 5-7 3. Diabetes and Heart : Dr Subhayan Bhattacharya, Dr Soumyabrata Roy Chaudhuri, Dr Debmalya Sanyal Arrythmia in diabetics ...... 8-12 4. Case Report : Dr Suchit Majumdar A case of a dif cult posteroseptal accessory pathway - how to suspect and approach to ablate ...... 13-14 5. Original Article : Biswajit Bandyopadhyay, Amitava Chattopadhyay, Mahua Roy, Indira Banerjee Left subclavian artery stenosis treated with trans - catheter stent placement in children ...... 15-20 6. Review Article : Munna Das Novel mapping systems in cardiac electrophysiology - a perspective ...... 21-25 7. Case Report : Dr. Md. Azizul Haque Spontaneous thrombosis within coronary sinus ...... 26 8. Case Report : Amitabha Chakrabarty, Manujesh Bandyopadhyay A non cardiac etiology of atrial fibrillation : don't forget the mediastinum ...... 27-29
9. Review Article : Subhayu Das, Amitava Gupta Modeling of human heart using a systems approach - a survey of recent trends ...... 30-33
10. Image corner : Dr.Soumitra Kumar Many a times ECG holds the clue ...... 34-35
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EDITORIAL Dr. P. K. Deb
ELECTRICITY AND HEART The knowledge that electric current can have effect on heart was first demonstrated way back in 1775, by Peter Christian Abildgaard, who applied electric shock on the chest of a hen, rendered lifeless with a prior shock to the head, to bring back its pulse. It was remarkable to note that though the hen was subjected to repeated shocks it recovered well and later even laid an egg.1 Thus began the quest for the relationship between electric current and heart. In 1838,Carlo Matteucci, Professor of Physics at the University of Pisa, showed that an electric current accompanies each heart beat.2 In 1887 British physiologist Augustus D. Waller of St Mary's Medical School, London published the first human electrocardiogram. It was recorded with a capilliary electrometer from Thomas Goswell, a technician in the laboratory.3 In 1893 Dutch physiologist, Willem Einthoven introduced the term ‘electrocardiogram’ at a meeting of the Dutch Medical Association.4 Later in1906 Einthoven published the first organised presentation of normal and abnormal electrocardiograms recorded with a string galvanometer. Left and right ventricular hypertrophy, left and right atrial hypertrophy, the U wave (for the first time), notching of the QRS, ventricular premature beats, ventricular bigeminy, atrial flutter and complete heart block were all described.5 In 1951 Paul Zoll, a Boston cardiologist developed first external tabletop pacemaker that was successfully applied to the treatment of heart block , ushering in the modern era of clinical cardiac pacing.6 Late 1950’s to early 1960’s witnessed several important achievements in the field of cardiac pacing by multiple persons and their teams working in different parts of the world: they were the “golden years” of pacing. Three landmark “firsts” were : the first battery-operated wearable pacemaker (1957), the first totally implantable pacemaker (1958) and the first long-term correction of heart block with a self-contained, implantable pacemaker (1960).6 These events had far-reaching consequences and opened up the field to the future. In this issue of the journal we gave special emphasis on the application of electrical principles for the understanding as well as treatment of the heart. In the review article by Shubhayu Das et al7 the basic engineering principles on which the heart can be modeled for better understanding of its physiology and pathology, has been stressed. In the other review article, Munna Das 8, dealt with the novel electrophysiologic methods for arrhythmia treatment.Both these,we believe,will enlighten our readers.
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It is our proud privilege to inform you that the journal received encouragement and acclodes from quite a number of doyens of Indian cardiology. According to their suggestion, we introduce from this issue two new topics- Diabetes and Heart and Image Corner. We hope these will make interesting reading. Finally our apologies for being late to bring out this issue. But as you all know a toddler is bound to tumble and we express our sincere gratitude for bearing with us.
References : 1. Abildgaard, Peter Christian. Tentamina electrica in animalibus. Inst Soc Med Havn. 1775; 2:157-61. 2. Matteucci C. Sur un phenomene physiologique produit par les muscles en contraction.Ann Chim Phys 1842;6:339- 341 3. Waller AD. A demonstration on man of electromotive changes accompanying the heart's beat. J Physiol (London) 1887;8:229-234 4. Einthoven W: Nieuwe methoden voor clinisch onderzoek [New methods for clinical investigation]. Ned T Geneesk 29 II: 263-286, 1893 5. Einthoven W. Le telecardiogramme. Arch Int de Physiol 1906;4:132-164 (translated into English. Am Heart J 1957;53:602-615) 6. Aquilina O .Abrief history of cardiac pacing.Images Paediatr Cardiol. 2006Apr-Jun; 8(2): 17–81. 7. Das Shubhayu, Gupta Amitava.Modeling of Human Heart using a Systems Approach - A Survey of Recent Trends.Bengal Heart J 2016;1: 29-32 8. Das Munna .Novel Mapping Systems in Cardiac Electrophysiology -Aperspective. Bengal Heart J 2016;1: 20-24
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Case Report Malignant Melanoma of Unknown Primary Origin Presenting as Cardiac Metastasis Pranay Chatterjee123 , Pritam Kumar Chatterjee , Sukumar Ghosh . 1. Senior Resident; 2. RMO-cum-Clinical Tutor; 3.Head of the Department. Department of Cardiology. Calcutta National Medical College Corresponding Author : Pranay Chatterjee
Abstract : Malignant melanoma has a very high propensity to metastasize to the heart. However, melanoma may sometimes present as a metastatic lesion in the absence of a primary lesion, which are called melanomas of unknown primary origin. We report a case in which a patient presented with a metastatic malignant melanoma in the right atrium with pericardial effusion and without a primary origin. Key words : Melanoma; Neoplasm, unknown primary; Unknown primary; Heart neoplasm. Fig. 1. Chest computed tomography. An inhomogeneous Introduction : Malignant melanomas are tumors enhancing mass in the right atrium (arrow) and a massive with the highest rates of cardiac metastasis. amount of pericardial effusion were identi ed However, cardiac metastasis is diagnosed in less than 1% of patients with malignant melanoma because less than 10% of these patients present with cardiac symptoms.1-3 Identi cation of cardiac metastasis from melanoma usually means that the patient is suffering systemic metastasis. Unlike typical cardiac metastasized patients, we report a rst case of a patient with a metastatic malignant melanoma in the heart without an identi able primary source or additional metastasis in Korea. Fig. 2. Two-dimensional cardiac echocardiogram. In a Case : A 59-year-old woman was admitted for subcostal view of the heart, a large mass measuring 42×31 cough and pleuritic chest pain with no history of mm was visualized in the right atrium. malignancy or heart disease. Her initial blood pressure was 110/70 mm Hg, pulse rate 70 beats/min, respiratory rate 20/min, and body temperature was 36.1°C. Jugular veins were not distended. No hepatomegaly or audible cardiac murmurs were present. Laboratory studies, including a complete blood count, liver, and chemical pro les were in normal ranges. Electrocardiography revealed a normal sinus rhythm. Chest radiography showed cardiomegaly without abnormal lesions in bilateral Fig. 3. Cardiac MRI. A large mass surrounding ascending lung elds. Chest computed tomography showed a aorta spread into transverse sinus and around pulmonary large amount of pericardial effusion and a mass in trunk and right pulmonary artery the right atrium (RA) (Fig. 1). Trans-thoracic 42×31 mm in the RA, which did not obstruct echocardiography showed a large mass measuring tricuspid valve ow. Her ejection fraction was
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normal (Fig. 2). Pericardiocentesis was performed. early stages of the disease.6 A complete resection of Effusion analysis showed a red blood cell count of an intracardiac melanoma prevents potential 1.9×1053 /mm and a white blood cell count of morbidities that are associated with progressive 3300/mm3 (lymphocytes, 55%; neutrophils, 14%). intracardiac growth, such as superior vena cava No malignant cells in the pericardial uid were syndrome, right ventricular out ow and in ow noted. Cardiac MRI also revealed a large mass obstruction, dysrhythmia, cardiac tamponade, and surrounding ascending aorta spread into transverse heart failure.6 Even when total resection is not sinus and around pulmonary trunk (Fig. 3). possible, conservative surgery can relieve Instead of tumor resection, considering the risk of symptoms and prevent imminent cardiac failure. open heart surgery and poor prognosis of extensive Conservative surgery improves the quality of a cardiac metastasis, pericardial window operation patient's life, as in our patient's case. and epicardial mass biopsy were performed to Although more than 90% of melanomas have a relieve symptoms and con rm the pathological cutaneous origin,7 melanomas may sometimes diagnosis. Pathological analysis including present metastatically in the absence of a primary immunohistochemistry revealed the nal diagnosis lesion, termed melanomas of unknown primary to be malignant melanoma (Fig. 4). The primary origin. Most authors estimate that 2-6% of patients cutaneous melanoma could not be identi ed despite are diagnosed with metastatic melanoma of careful dermatological examination. The patient unknown primary site. In particular, such a had no history of halo nevus or mole removal. metastatic melanoma in the heart such as in this Positron emission tomography revealed no other patient without a known primary cutaneous origin distant organ metastasis except for heart and is a rare presentation and chie y an anecdotal mediastinal lymph nodes. nding of metastatic melanoma. Several re-ported Discussion : Malignant melanoma has aggressive cases can be found in the literature about cardiac biological behavior and the greatest tendency for involvement with cutaneous primary malignant 1 melanoma and multiple metastasis in Korea, as well metastasis to the heart. Although autopsy studies 8,9 reported an incidence of 50% to 71%, cardiac as worldwide. As far as we know, malignant metastasis is diagnosed in less than 1% of patients cardiac melanoma without a primary origin has not with malignant melanoma be-cause less than 10% yet been reported in Korea. of these patients present with cardiac symp-toms.2 The survival of patients with unknown primary Such metastases most frequently occur after melanoma was demonstrated to be similar to that of multifocal hematological dissemination and may patients with known primary tumors when develop anywhere in the heart.3 Melanotic corresponding stages were compared.10-12 Those metastases can invade the wall of any of the 4 patients with metastases to any other visceral sites cardiac chambers, and the RA is involved most are described to have a 1 year survival rate of 41% frequently.4 and a median survival of approximately 6 11,13,14 The clinical signs and symptoms of cardiac months. Accordingly, we expected that the metastasis are un-clear and non-speci c, although outcome of this patient might be very unfavorable. when present, the clinical signs and symptoms Although total resection was not possible because include fatigue, weakness, pericardial effusion, of extensive cardiac metastasis, a pericardial congestive window operation could resolve her symptoms. heart failure, cardiac arrhythmia, superior vena After surgery, chemotherapy was planned, cava syndrome, right ventricular out ow and including cisplatin, dacarbazine, casmustine, and in ow obstruction, and transient ischemic attack.5 tamoxifen. However, the patient refused further However, patients with malignant melanoma who chemotherapy after completion of two sessions. have cardiac metastases may present symptoms The patient has survived for 14 months after only caused by tumors in other organ systems. diagnosis. She is attending our hospital's outpatient Although cardiac involvement occurs during the oncology department. course of the disease, it is rare that the initial As only few reports about cardiac metastasis of manifestation is cardiac metastasis. malignant mel-noma without cutaneous origin have A tumor's anatomic location and extent of invasion been published, we are un-certain if conservative determine the feasibility of surgical intervention, surgery is associated with prolonged survival and if which should optimally be per-formed during the the role of surgery for survival is worth further investigation.
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References : 1. Ozyuncu N, Sahin M, Altin T, Karaoguz R, Guldal M, Akyurek O. Cardiac metastasis of malignant melanoma: a rare cause of complete atrioven-tricular block.Europace 2006;8:545-8. 2. MacGee W. Metastatic and invasive tumours involving the heart in a geriatric population: a necropsy study. Virchows Arch A Pathol Anat Histopathol 1991;419:183-9. 3. Savoia P,Fierro MT, ZaccagnaA, Bernengo MG. Metastatic melanoma of the heart.J Surg Oncol 2000;75:203-7. 4. Malouf JF, Thompson RC, Maples WJ, Wolfe JT. Diagnosis of right atrial metastatic melanoma by transesophageal echocardiographic-guided transvenous biopsy.Mayo Clin Proc 1996;71:1167-70. 5. Qu G, Kaur JS, Seward JB. Metastatic melanoma presenting as cardiac mass and hemobilia. Am J Med Sci 2003;325:157-9. 6. Basarici I, Demir I, Yilmaz H, Altekin RE. Obstructive metastatic malig-nant melanoma of the heart: imminent pulmonary arterial occlusion caused by right ventricular metastasis with unknown origin of the pri-mary tumor. Heart Lung 2006;35:351-4. 7. Chang AE, Karnell LH, Menck HR. The national cancer data base report on cutaneous and noncutaneous melanoma: a summary of 84,836 cases from the past decade: the American College of Surgeons Com-mission on Cancer and theAmerican Cancer Society.Cancer 1998;83: 1664-78. 8. Lee KS. Resection of cardiac metastasis of malignant melanoma.Kore-an Circ J 2000;30:1170-4. 9. Kim OG, Hong JM, Lee SJ, Hong JS. Cardiac metastasis of malignant melanoma: a case report. Korean J Thorac Cardiovasc Surg 1999;32: 840-3. 10. Baab GH, McBride CM. Malignant melanoma: the patient with an un-known site of primary origin. Arch Surg 1975;110:896-900. 11. Schlagenhauff B, Stroebel W, Ellwanger U, et al. Metastatic melanoma of unknown primary origin shows prognostic similarities to regional metastatic melanoma: recommendations for initial staging examina-tions. Cancer 1997;80:60-5. 12. Katz KA, Jonasch E, Hodi FS, et al. Melanoma of unknown primary: experience at Massachusetts General Hospital and Dana-Farber Can-cer Institute.Melanoma Res 2005;15:77-82. 13. Manola J, Atkins M, Ibrahim J, Kirkwood J. Prognostic factors in meta-static melanoma: a pooled analysis of Eastern Cooperative Oncology Group Trials.J Clin Oncol 2000;18:3782-93. 14. Balch CM, Soong SJ, Gershenwald JE, et al. Prognostic factors analysis of 17,600 melanoma patients: validation of theAmerican Joint Com-mittee on Cancer melanoma staging system.J Clin Oncol 2001;19: 3622-34.
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Diabetes and Heart Arrythmia in Diabetics Dr Subhayan Bhattacharya MBBS, DTM&H, MD(Post Graduate Trainee), School of Tropical Medicine, Dr Soumyabrata Roy Chaudhuri MBBS, MRCP, Msc (Diabetology), Consultant Physician & Diabetologist Woodlands Hospital Dr Debmalya Sanyal MD, MRCP(Dublin), DM(Endocrinology), FACE, Professor, Dept of Endocrinology, KPC Medical College, Kolkata.
Abstract : Arrhythmia is common in diabetes detection of diabetic autonomic neuropathy. Nerve mellitus. Both silent myocardial ischemia and conduction abnormalities may not be the only autonomic neuropathy associated with diabetes are component of autonomic dysfunction in diabetes. responsible for arrhythmogenesis.Atrial brillation Relationships between vascular stiffness and is the most common arrhythmia in diabetics. dysfunction of the barore ex response have also Exaggerated systemic and tissue level oxidative been noted.4,5 Furthermore, some studies have stress seems to be the key element in genesis of suggested that the primary dysfunction may be the atrial brosis that leads to atrial brillation. defective activation of central parasympathetic Ventricular arrhythmias are also common in pathways.5 Data concerning the actual prevalence diabetics and result from both atherosclerotic and of cardiovascular autonomic neuropathy and its non-atherosclerotic processes. related mortality rates are con icting. However, Key words : Diabetes mellitus, arrhythmia various studies and metaanalysis reveal that mortality rates among diabetic subjects with Diabetes and cardiovascular disease often appear to cardiovascular autonomic neuropathy are many be interchangeable term. Diabetes melli-tus has times higher than among those without.6,7 Diabetes been said to be equivalent to coronary heart disease, and depressed indexes of autonomic function had while conversely many patients with established an approximately twofold risk of mortality in the coronary heart disease suffer from diabetes or its Hoorn Study.6 Abnormalities of the autonomic prediabetes. In patients with an acute coronary nervous system, re ected by increased heart rate syndrome 20-30% have diabetes and as many as and reduced heart rate variability, are associated 1 40% have impaired glucose tolerance. with cardiovascular mortality and morbidity, and Hyperglycaemia, insulin resistance and the they have been proven to be strong predictors of consequent cellular shift to increased oxidative focal coronary atherosclerosis.7 Even patients with stress carry a high risk for the development of impaired glucose tolerance have an increased heart comorbidities and cardiovascular risk factors, rate and elevated levels of pro-in ammatory mainly hypertension, lipid disorders, pro- cytokines (interleukin-6 and tumour necrosis in ammatory state, and activation of coagulation factor-α ) in comparison to healthy controls.8 Heart 2 and thrombosis. There is evidence that, apart from rate and heart rate variability parameters were coronary artery disease, diabetic patients are also at positively associated with serum in ammation increased risk of arrhythmias. There are many markers in diabetic patients leading to underlying risk factors for an arrhythmogenic atherosclerotic process.8 Global myocardial blood substrate in patients with diabetes mellitus. ow and coronary ow reserve, studied by positron Pathogenesis : Silent Myocardial Ischaemia and emission tomography, were subnormal in diabetics Autonomic Neuropathy : The risk for with cardiovascular autonomic neuropathy. cardiovascular autonomic neuropathy depends on Cardiovascular autonomic neuropathy may the duration of the diabetes and the degree of provoke ischaemic episodes by upsetting the 4-6 glycaemic control. It is caused by injury to the balance between myocardial supply and demand. autonomic nerve bres that innervate the heart and Prolonged QT interval (a risk factor for ventricular blood vessels.3 It has been estimated that about 20% arrhythmias and sudden cardiac death) in patients of asymptomatic diabetic patients have abnormal with diabetes mellitus is associated with the extent 9 cardiovascular autonomic function.3 Heart rate of cardiovascular autonomic neuropathy. variability and barore ex testing may help in the
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Atrial Fibrillation (AF) in Diabetics : AF is the al23 analyzed the detailed three dimensional electro most common arrhythmia in clinical practice anatomic mapping of 228 patients who had DM or resulting in major cardiovascular morbidity and abnormal glucose metabolism (AGM) and mortality10 .Earlier the Framingham Study and underwent AF ablation for the rst time. Results recently a study from Movahed et al11 clearly showed that biatrial voltage measurements in DM established that DM is a powerful and independent and AGM group were signi cantly lower than risk factor for the development of AF. This close control group. Furthermore these patients also had association betweenAF and DM raises the question increased recurrence rate of AF in the follow up for pathophysiological basis for this entity. Both period. Acar et al24 has shown in their published electrical and anatomical remodelling seems to be study, that patients with DM had signi cantly important keys of these complex increased inter and intra atrial electro mechanic pathophysiological changes. Extensive brosis in delay with impaired diastolic functions comparing the atrial tissue is the anatomical hallmark of AF to controls. In streptozocin induced diabetic rat with a role in both starting and perpetuation of the model study, connexin 43 expression is upregulated arrhythmia and as the brosis expands it is more in diabetics as a gap junction protein suggesting a likely that paroxysmal AF transforms into speci c change in cell to cell integration25 . permanent or anti arrhythmic resistant type12,13 . Conversely, there are some other data suggesting Kato et al14 showed that DM related atrial brosis that uctuations in the blood glucose level rather has a potential role in starting AF in diabetic rat than the longterm hyperglycemic environment is models. Exaggerated systemic and tissue level related to increase in the incidence ofAF in diabetic oxidative stress seems to be the key element in atrial patients26 . Saito et al 27 showed that glucose brosis related to DM. Dudley et al15 compared the uctuations increase the incidence of AF in levels of superoxide in left atrial appendage streptozocin induced diabetic rat models. Huxley et between the sinus rhythm group and atrial rapid al28 failed to show any correlation between fasting pacing (ARP) groups in rat models showing that in glucose, insulin levels, HbA1c levels the ARP group left atrial superoxide anion levels measurements and AF onset in patients without were almost three times higher than the control diabetes. Another clinical study from Fatemi et al29 group. Mitochondrial oxidative stress is increased prospectively evaluated the effect of intense in diabetic human atrial tissue suggesting that there glycemic control on incidence of AF in diabetic may be a production of reactive oxygen species via patients. Interestingly, they failed to present any mitochondrial pathway specifcally at the atrial association between incident AF and intense tissue level.16 Nonenzymatic glycosylation of therapy comparing to standard therapy group. proteins and the end products of this pathway However, their choice of periodic (Advanced Glycation End products;AGEs) interact electrocardiographic testing instead of event with their receptors (RAGE) and upregulate the recorders might alter the results in terms of missing connective tissue growth factor (CGTF)17 . This the paroxysmal AF episodes occurring any time system (AGERAGE) may start or contribute to besides the of ce control. There are no randomized atrial brosis in diabetic patients via stimulation of data speci cally addressing the effect of DM in connective tissue growth factor in the atrial other supraventricular arrhythmias but there are myocardium18 . Dysfunction in the autonomic case reports discussing whether acute changes in innervation and control of cardiovascular system in metabolic pro e during ketoacidosis episodes favour of sympathetic system, might have a role in might trigger arrhythmias such as supraventricular the onset of AF.19, 20 Electrophysiological studies in tachycardia30 . Overall, DM seems to be acting a diabetic rat atrium revealed shortened atrial pivotal role in generation and maintenance of AF in effective refractory period (AERP) and increased diabetic patients. Speci c structural, electrical and dispersion of AERP. Moreover reduced heart rate electromechanical alterations in diabetic heart recovery in type 2 DM patients with preserved might create an anatomic substrate for the ejection fraction is associated with increase in the development of AF. On the other hand, acute hypo incidence of AF 21 . These clinical and laboratory or hyperglycemia, changes in electrolyte levels or studies imply that autonomic dysfunction has a role acid-base status and autonomic system distortions in the pathogenesis of AF in DM patients. Atrial may be a trigger mechanism for the arrhythmia . It is electrical structure is also affected in diabetic clear that there are still dark spots about the patients. Shortened AERP increased dispersion of relationship between AF and DM that warrants AERD and intra atrial conduction time are the key further studies. elements of atrial electrical remodeling20.22 . Chao et
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Ventricular Arrythmia and Sudden Cardiac risk of VAin patients with implantable cardioverter Death in Diabetics : Cardiovascular diseases de brillators retrospectively. A signi cant (CVD) are the leading cause of death in diabetics association between HbA1c levels of 8-10% and and DM is almost a synonym for atherosclerosis spontaneous VA incidence in diabetic patients was and coronary artery disease. High incidence and observed, rather than the diabetic condition and extent of atherosclerotic heart disease in diabetics independent from QT prolongation, stating that leads to high incidence of ventricular arrhythmias suboptimal glycemic control and persistent (VA) and sudden cardiac death (SCD) inevitably31- hyperglycemia is related with higher risk of 33. Although this close relationship between VA, spontaneous VA. In another randomized SCDs and DM is mostly based on the extent of prospective study in patients with type 2 DM and coronary artery disease among diabetics, non- documented CVD, there were high incidence of coronary atherosclerotic processes like autonomic hypoglycemia and silent VA in the insulin and/or neuropathy, microvascular disease, ventricular SU group comparing to control subjects.40 A study structural and electrical changes may partly play a from Pistrosch et al41 further analyzed effects of role in this phenomenon34 . A ventricular hypoglycemia as a trigger for VA in larger patient repolarization anomaly, which is re ected by QTc cohort with type 2 DM, revealed that hypoglycemia interval prolongation, is associated with high risk of might be able to trigger VA and interestingly a VA. There are several studies showing, marked QTc thyroid stimulating hormone level in the low prolongation in diabetic patients35 . Another strong normal range, which indicates subclinical predictor of VA, microvolt T wave alternans (TWA) hypertiroidism, is independently associated with measurement and glycemic status had been studied occurrence of VA. Although these two studies in type 2 diabetic patients without known CVD 36 . provide no casual relationship between The frequencies of atypical TWA patients were hypoglycemia and VAin diabetic patients, it may be signifcantly higher in diabetics than the control postulated that hypoglycemia may be triggering VA group and patients with atypical TWA either with sympathetic overstimulation or QT measurements had signifcantly elevated HbA1c prolongation42 . Interestingly, another study levels. Only 1% rise in HbA1c levels is linked with investigating the association between diabetes and 13 fold higher risk of having atypical TWA and VA in patients with severe heart failure revealed a suboptimal glycemic control is linked with higher negative independent relationship with diabetes risk of spontaneous VAindependent of QTc interval and VA in this patient group43 . In summary, DM duration. These results from the studies are signing might play a critical role in creating a vulnerable an electrical instability of diabetic myocardium, substrate and/or as a trigger for VA besides the which creates a potential substrate for ventricular expected risk based on the high extent and arrhythmias independent from the scarred incidence of coronary artery disease. myocardium areas from previous ischemic cardiac Unfortunately, there is not enough randomized damages.Autonomic neuropathy of diabetes results large scale data in the literature to suggest a de nite in an unbalanced sympathetic stimulation on relationship and clear pathophysiological myocardium, which may further contribute to this mechanisms for this entity. electrical instability and predispose to lethal 37 Conclusion : AF and VAare most common form of arrhythmias . Cardiac sensory neuropathy of arrhythmias, which lead to cardiovascular diabetics is another important issue that causes VA 38 complications and mortality in patients with DM. and sudden death indirectly via silent ischemia .As Inspite of evidence based risk factors for an DM creates a vulnerable myocardium for arrhythmogenic substrate that may be speci cally arrhythmias, it seems to be involved in the related to diabetes, the causal pathophysiological triggering mechanism for these arrhythmias too. A 39 and electrophysiological mechanisms of these study from ChenScarabelli et al investigated if arrhythmias still remaims to be unravelled. there is any relationship between HbA1c levels and
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3. Valensi P, Huard JP, Giroux C, Attali JR. Factors involved in cardiac autonomic neuropathy in diabetic patients. J Diabetes Complications. 1997; 11: 180-187. 4. Skrapari I, Tentolouris N, Katsilambros N. Barore ex function: determinants in healthy subjects and disturbances in diabetes, obesity and metabolic syndrome. Curr Diabetes Rev. 2006; 2: 329-338. 5. Nesto RW, Libby P. Diabetes mellitus and the cardiovascular system. In Braunwald E, Zipes DP, Libby P (eds): Heart Disease.Atextbook of cardiovascular Medicine. 6th ed. Philadelphia: WB Saunders; 2001. p 2133. 6. Gerritsen J, Dekker JM, TenVoorde BJ, et al. Impaired autonomic function is associated with increased mortality, especially in subjects with diabetes, hypertension, or a history of cardiovascular disease: the Hoorn Study. Diabetes Care. 2001; 24: 1793-1798. 7. Priori SG,Aliot E, Blomstrom-Lundqvist C, et al. Update of the guidelines on sudden cardiac death of the European Society of Cardiology. Eur Heart J. 2003; 24: 13-15. 8. Diakakis GF, Parthenakis FI, Mavrakis HE, et al. Association of impaired glucose tolerance with increased heart rate and subclinical in ammation. Hellenic J Cardiol. 2005; 46: 394-401. 9. Cardoso CR, Salles GF, Deccache W. Prognostic value of QT interval parameters in type 2 diabetes mellitus: results of a long-term follow-up prospective study. J Diabetes Complications. 2003; 17: 169-178. 10. Ball J, Carrington MJ, McMurray JJ, Stewart S. Atrial fbrillation: pro e and burden of an evolving epidemic in the 21st century.Int J Cardiol 2013; 167: 1807-1824 [PMID: 23380698 DOI: 10.1016/ j.ijcard.2012.12.093] 11. Movahed MR, Hashemzadeh M, Jamal MM. Diabetes mellitus is a strong, independent risk for atrial brillation and utter in addition to other cardiovascular disease.Int J Cardiol 2005; 105: 315-318 [PMID: 16274775]. 12. Burstein B, Nattel S.Atrial brosis: mechanisms and clinical relevance in atrial fbrillation.J Am Coll Cardiol 2008; 51: 802-809 [PMID: 18294563 DOI: 10.1016/j.jacc.2007.09.064] 13. Corradi D. Atrial fbrillation from the pathologist's perspective.Cardiovasc Pathol 2006; 23: 71-84 [PMID:24462196 DOI: 10.1016/j.carpath.2013.12.001] 14. Kato T, Yamashita T, Sekiguchi A, Sagara K, Takamura M, Takata S, Kaneko S, Aizawa T, Fu LT. What are arrhythmogenic substrates in diabetic rat atria?J Cardiovasc Electrophysiol 2006; 17: 890-894 [PMID: 16759295 DOI: 10.1111/j.1540-8167.2006.00528.x] 15. Dudley SC, Hoch NE, McCann LA, Honeycutt C, Diamandopoulos L, Fukai T, Harrison DG, Dikalov SI, Langberg J. Atrial brillation increases production of superoxide by the left atrium and left atrial appendage: role of the NADPH and xanthine oxidases.Circulation 2005; 112: 1266-1273 [PMID: 16129811 DOI: 10.1161/CIRCULATIONAHA.105.538108] 16. Anderson EJ, Kypson AP, Rodriguez E, Anderson CA, Lehr EJ, Neufer PD. Substrate-speci c derangements in mitochondrial metabolism and redox balance in the atrium of the type 2 diabetic human heart. J Am Coll Cardiol 2009; 54: 1891-1898 [PMID:19892241 DOI: 10.1016/j.jacc.2009.07.031] 17. Twigg SM, Cao Z, MCLennan SV,Burns WC, Brammar G, Forbes JM, Cooper ME. Renal connective tissue growth factor induction in experimental diabetes is prevented by aminoguanidine.Endocrinology 2002; 143: 4907-4915 [PMID: 12446618 DOI:10.1210/en.2002-220619] 18. Kato T, Yamashita T, Sekiguchi A, Tsuneda T, Sagara K, Takamura M, Kaneko S, Aizawa T, Fu LT. AGEs-RAGE system mediates atrial structural remodeling in the diabetic rat.J Cardiovasc Electrophysiol 2008; 19: 415-420 [PMID: 18298515 DOI: 10.1111/ j.1540-8167.2007.01037.x] 19. Pop-Busui R. Cardiac autonomic neuropathy in diabetes: a clinical perspective.Diabetes Care 2010; 33: 434-441 [PMID: 20103559 DOI: 10.2337/dc09-1294] 20. Otake H, Suzuki H, Honda T, Maruyama Y. In uences of autonomic nervous system on atrial arrhythmogenic substrates and the incidence of atrial fbrillation in diabetic heart.Int Heart J 2009; 50: 627-641 [PMID: 19809211 DOI: 10.1536/ihj.50.627] 21. Negishi K, Seicean S, Negishi T, Yingchoncharoen T,Aljaroudi W, Marwick TH. Relation of heart-rate recovery to new onset heart failure and atrial fbrillation in patients with diabetes mellitus and preserved ejection fraction. Am J Cardiol 2013; 111: 748-753 [PMID: 23273718 DOI: 10.1016/j.amjcard.2012.11.028] 22. Heijman J, Voigt N, Nattel S, Dobrev D. Cellular and molecular electrophysiology of atrial fbrillation initiation, maintenance, and progression.Circ Res 2014; 114:1483-1499 [PMID: 24763466 DOI:10.1161/CIRCRESAHA. 114.302226] 23. Chao TF, Suenari K, Chang SL, Lin YJ, Lo LW, Hu YF, Tuan TC, Tai CT, Tsao HM, Li CH, Ueng KC, Wu TJ, Chen SA. Atrial substrate properties and outcome of catheter ablation in patients with paroxysmal atrial fbrillation associated with diabetes mellitus or impaired fasting glucose.Am J Cardiol 2010; 106: 1615-1620 [PMID: 21094363 DOI: 10.1016/j.amjcard.2010.07.038] 24. Acar G, Akcay A, Sokmen A, Ozkaya M, Guler E, Sokmen G, Kaya H, Nacar AB, Tuncer C. Assessment of atrial electromechanical delay, diastolic functions, and left atrial mechanical functions in patients with type 1 diabetes mellitus.J Am Soc Echocardiogr 2009; 22:732-738 [PMID: 19423291 DOI: 10.1016/j.echo.2009.03.028]
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25. Watanabe M, Yokoshiki H, Mitsuyama H, Mizukami K, Ono T, Tsutsui H. Conduction and refractory disorders in the diabetic atrium.Am J Physiol Heart Circ Physiol 2012; 303: H86-H95 [PMID:22561303 DOI:10.1152/ ajpheart.00010.2012] 26. Lip GY, Varughese GI. Diabetes mellitus and atrial brillation: perspectives on epidemiological and pathophysiological links.Int J Cardiol 2005; 105: 319-321 [PMID: 16274776 DOI: 10.1016/ j.ijcard.2005.03.003] 27. Saito S, Teshima Y, Fukui A, Kondo H, Nishio S, Nakagawa M, Saikawa T, Takahashi N. Glucose uctuations increase the incidence of atrial brillation in diabetic rats.Cardiovasc Res 2014; 104: 5-14 [PMID: 25082849 DOI: 10.1093/cvr/cvu176] 28. Huxley RR, Alonso A, Lopez FL, Filion KB, Agarwal SK, Loehr LR, Soliman EZ, Pankow JS, Selvin E. Type 2 diabetes, glucose homeostasis and incident atrial fbrillation: theAtherosclerosis Risk in Communities study. Heart 2012; 98: 133-138 [PMID: 21930722 DOI: 10.1136/heartjnl-2011-300503] 29. Fatemi O, Yuriditsky E, Tsiou s C, Tsachris D, Morgan T, Basile J, Bigger T, Cushman W, Goff D, Soliman EZ, Thomas A, Papademetriou V. Impact of intensive glycemic control on the incidence of atrial brillation and associated cardiovascular outcomes in patients with type 2 diabetes mellitus (from the Action to Control Cardiovascular Risk in Diabetes Study).Am J Cardiol 2014; 114: 1217-1222 [PMID: 25159234 DOI:10.1016/ j.amjcard.2014.07.045] 30. Thomas N, Scanlon J, Ahmed M. Supraventricular tachycardia in association with diabetic ketoacidosis. BJ Diabetes VascDis 2007; 7: 244-245 [DOI: 10.1177/14746514070070050901] 31. Fox CS, Coady S, Sorlie PD, Levy D, Meigs JB, D'Agostino RB, Wilson PW, Savage PJ. Trends in cardiovascular complications of diabetes.JAMA 2004; 292: 2495-2499 [PMID: 15562129 DOI: 10.1001/jama.292.20.2495] 32. Cho E, Rimm EB, Stampfer MJ, Willett WC, Hu FB. The impact of diabetes mellitus and prior myocardial infarction on mortality from all causes and from coronary heart disease in men.J Am Coll Cardiol 2002; 40: 954- 960 [PMID: 12225722 DOI: 10.1016/ S0735-1097(02)02044-2] 33. Balkau B, Jouven X, Ducimetière P, Eschwège E. Diabetes as a risk factor for sudden death.Lancet 1999; 354: 1968-1969 [PMID: 10622302 DOI: 10.1016/S0140-6736(99)04383-4] 34. Wheeler SG, Ahroni JH, Boyko EJ. Prospective study of autonomic neuropathy as a predictor of mortality in patients with diabetes.Diabetes Res Clin Pract 2002; 58: 131-138 [PMID: 12213355 DOI: 10.1016/S0168-8227 (02)00128-6]. 35. Cardoso CR, Salles GF, Deccache W. Prognostic value of QT interval parameters in type 2 diabetes mellitus: results of a long-term follow-up prospective study.J Diabetes Complications 2003; 17: 169-178 [PMID: 12810239 DOI: 10.1016/S1056-8727(02)00206-4] 36. Molon G, Costa A, Bertolini L, Zenari L, Arcaro G, Barbieri E, Targher G. Relationship between abnormal microvolt T-wave alternans and poor glycemic control in type 2 diabetic patients.Pacing Clin Electrophysiol 2007; 30: 1267-1272 [PMID: 17897130 DOI: 10.1111/j.1540-8159.2006.00298.x] 37. Vinik AI, Ziegler D. Diabetic cardiovascular autonomic neuropathy.Circulation 2007; 115: 387-397 [PMID: 17242296 DOI: 10.1161/CIRCULATIONAHA.106.634949] 38. Faerman I, Faccio E, Milei J, Nuñez R, Jadzinsky M, Fox D, Rapaport M. Autonomic neuropathy and painless myocardial infarction in diabetic patients. Histologic evidence of their relationship.Diabetes 1977; 26: 1147-1158 [PMID: 590638 DOI:10.2337/diab.26.12.1147] 39. Chen-Scarabelli C, Scarabelli TM. Suboptimal glycemic control, independently of QT interval duration, is associated with increased risk of ventricular arrhythmias in a high-risk population. Pacing Clin Electrophysiol 2006; 29: 9-14 [PMID: 16441711] 40. Stahn A, Pistrosch F, Ganz X, Teige M, Koehler C, Bornstein S, Hanefeld M. Relationship between hypoglycemic episodes and ventricular arrhythmias in patients with type 2 diabetes and cardiovascular diseases: silent hypoglycemias and silent arrhythmias.Diabetes Care 2014; 37: 516-520 [PMID: 24041680 DOI: 10.2337/dc13- 0600] 41. Pistrosch F, Ganz X, Bornstein SR, Birkenfeld AL, Henkel E, Hanefeld M. Risk of and risk factors for hypoglycemia and associated arrhythmias in patients with type 2 diabetes and cardiovascular disease: a cohort study under real-world conditions.Acta Diabetol 2015; 52: 889-895 [PMID: 25749806 DOI: 10.1007/ s00592- 015-0727-y] 42. Laitinen T, Lyyra-Laitinen T, Huopio H, Vauhkonen I, Halonen T, Hartikainen J, Niskanen L, Laakso M. Electrocardiographic alterations during hyperinsulinemic hypoglycemia in healthy subjects. Ann Noninvasive Electrocardiol 2008; 13: 97-105 [PMID: 18426434 DOI: 10.1111/j.1542-474X.2008.00208.x] 43. Aronson D, Burger AJ. Diabetes and the occurrence of ventricular arrhythmic events in patients with severe left ventricular dysfunction.Diabetologia 2002; 45: 1440-1445 [PMID: 12378386 DOI: 10.1007/s00125-002-0915-5]
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Case Report A Case of a Difficult Posteroseptal Accessory pathway - how to suspect and approach to ablate Dr Suchit Majumdar, MD. DM. Postdoctoral fellowship in cardiac electrophysiology Consultant, Apollo Gleneagles Hospital Kolkata
Abstract : Posteroseptal accessory pathways are Figure 1 : Maximal preexcited ECG on atrial the second most common location for such pacing pathways.They are dif cult to ablate because of anatomical complexity and procedural hazards.A thorough analysis of the baseline ECG can help in accurate localization of the pathway and facilitate successful ablation. Key words : Posteroseptal accessory pathway, ablation, ECG Introduction : Posteroseptal accessory pathways are the second most common location for accessory connections and account for 25 to 30% of accessory pathways of most series1,2 . In the electrophysiology laboratory, ablation of these connections is associated with longer procedure times, greater uoroscopic exposure, and more radiofrequency The patient also had documented AF with preexcitation which put her at increased risk of sudden cardiac death. (RF) lesions than any other location. Sources of Hence the patient was taken up for EP study. While dif culty include complex anatomy, possibly cannulating the coronary sinus with the decapolar catheter, requiring right- and left-sided mapping, epicardial it was not advancing beyond a certain point. In view of connections involving the coronary venous system possibility of CS related accessory pathway, coronary angiogram was done in the left coronary system to acquire and diverticula, and injury to the right coronary the levophase for coronary venous abnormalities. The artery or AV nodal artery from ablation. coronary sinus venogram showed a diverticulum in the Nevertheless, these pathways are ablated with coronary sinus at its junction to the middle cardiac vein catheter-based techniques, with a very high degree which was preventing the catheter to go in. of success despite the potential complexity of Figure2 : MCV ostial diverticulum mapping in this area. CaseR eport : We report a case of ablation of posteroseptal accessory pathway where a thorough analysis starting from ECG helped us to clinch the location accurately and ablate it successfully. A 30 year old lady presented with recurrent palpitations, ECG at baseline showed preexcitation suggestive of Right Posteroseptal accessory pathway (? Epicardial CS related) based on Arruda algorithm ( delta isoelectric in V1, transition at V2, Negative delta in II, III,AVF). While interpreting ECG for localisation of accessory pathway location, it is always better to have a full preexcited ECG which can often be Often the CS abnormalities ( diverticulum, more commonly venous dilatation seen in middle cardiac vein ) indicate the obtained by burst atrial pacing at the EPlab. location of insertion of accessory pathways from LV which is mostly epicardial connections.
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The EPstudy showed HV interval of 18ms. Incremental algorithms however by EP study to differentiate ventricular pacing showed VA dissociation at 280ms. The right from left posteroseptal. earliest retrograde A was at CS 3,4 which corresponded to the neck of the diverticulum. Incremental atrial pacing Right Posteroseptal Left Posteroseptal showed lead II negative in the maximal preexcited ECG Difference between VA at His Difference between VA at His suggestive of CS related posteroseptal accessory pathway. and earliest VAin CS <25 msec and earliest VAin CS >25 msec Tachycardia was induced by atrial and ventricular protocols which was narrow QRS with cycle length 338ms, VA interval Long RP tachycardia Earliest retrograde atrial 104ms. Entrainment from RV apex could not be done as the activation in ORT at middle CS tachycardia was getting terminated. Negative Delta in V1 R/S>1 in V1 In view of presence of CS diverticulum, it was decided to go Earliest VA<15 mm from CS os Earliest VA>15 mm from CS os for ablation inside it as the pathway is most likely located there. Mapping was done with a bard F curve catheter with Sharp/blunt CS EGM at earliest Blunt/sharp CS EGM at earliest ventricular pacing. Fused signals with earliest A was retrograde site retrograde site mapped to the neck of the diverticulum. 3. CS related accessory pathway at insertion point Figure3 : Signal at successful ablation site often is associated with a dilatation of the vein or a diverticulum of the tributary or CS. In 21% of patients with CS muscular extensions to the left ventricle, the connection occurs in association with a CS diverticulum. These venous anomalies arise within the proximal 1.5 cm of the CS and before the middle cardiac vein in most cases; however, they can arise from the middle or posterior cardiac veins themselves. The body of the diverticulum is typically within the epicardial layers of the posterior-superior process of the left ventricle .The walls of a CS diverticulum contain ventricular musculature and are often seen to contract on angiography. This musculature is in continuity with the 40W RF energy delivered with temperature setting of 60 epicardial left ventricle and with the CS degree Celsius given for 60 seconds resulted in local VA separation and VA wenkebaching which was documented musculature at the mouth of the diverticulum to also 30min after the ablation. form the reentry circuit. CS diverticula are reported in up to 9% of all patients presenting for Discussion : The importance of presenting this case ablation; if present in patients with evidence of a lies in the following facts which must be known to posteroseptal AP, they are usually the site of an electrophysiologist while planning and ablating connection,. So, CS angiogram is must for such cases of posteroseptal accessory pathway. delineating these in order to search for pathway 1. Posteroseptal space is very complex and insertions there. CS angiogram is easily done by pathways can be at different locations here, so capturing the levophase of left coronary proper planning is needed to ablate them. angiogram. The dif culty to advance a decapolar catheter into CS if often a clue to the 2. Fully preexcited ECG gives idea of the location presence of CS structural abnormalities. of the pathway as per arruda algorithm and this can be usually achieved by burst atrial pacing in 4. The ablation inside CS also has a higher chance EP lab. If lead II is negative in the background of of recurrence of the pathway as lesion formation septal accessory pathway, a CS related is impeded by inadequate power and epicardial pathway should be thought of. If delta temperature delivery. Hence low threshold in V1 is positive , a left sided posteroseptal should be kept to use an irrigated catheter in pathway should be thought of with early switch order to give adequate lesion delivery. over to transeptal puncture. There are different References : 1. Calkins H., Yong P., Miller J., et al.: Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: nal results of a prospective, multicenter clinical trial.Circulation. 99:262-270 1999 2. Jackman W.M., Wang X., Friday K.J., et al.: Catheter ablation of accessory atrioventricular pathways (Wolff-Parkinson-White syndrome) by radiofrequency current.N Engl J Med. 324:1605-1611 1991 3. Sun Y., Arruda M., Otomo K., et al.: Coronary sinus-ventricular accessory connections producing posteroseptal and left posterior accessory pathways.Circulation 106:1362-1367 2002 4. Weiss C., Cappato R., Schluter M., et al.:Anomalies of the coronary venous system in patients with and without accessory pathways [abstract].J Am Coll Cardiol . 25:18A1995 5. Chiang C.E., Chen S.A., Yang C.R., et al.: Major coronary sinus abnormalities: identi cation of occurrence and signi cance in radiofrequency ablation of supraventricular tachycardia.Am Heart J. 127:1279-1289 1994
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Original Article Left Subclavian Artery Stenosis Treated with Trans - Catheter Stent Placement in Children Biswajit Bandyopadhyay 1234, Amitava Chattopadhyay , Mahua Roy , Indira Banerjee 1. Senior Consultant and Head; Department of Paediatric Cardiology, NH-RTIICS 2. Senior Consultant and Head; Department of Paediatric Cardiology, NSH 3. Associate Consultat; Department of Paediatric Cardiology, NH-RTIICS 4. Junior Consultant; Department of Paediatric Cardiology; NSH
Abstract : Left subclavian artery (LSA) stenosis previous sibling died few days after birth due to causing limb length discrepancy, vascular undiagnosed disease who had external stigmata of compromise or signi cant blood pressure (BP) multiple congenital anomalies. differences between both upper limbs are rarely The baby looked non - sick, non - syndromic with described in literature. Here, we are presenting no obvious external skeletal deformity. Her skin three patients with LSA stenosis, two of them colour was pink and her cry, activity, re ex were congenital and the other being acquired in origin, good. She weighed 3.6 kg and her length was who were successfully treated with trans-catheter 53cm.Her Pulse rate was 130/min, equally implantation of stents in the LSA. palpable in all other limbs, except the left hand, Key words : Left subclavian artery stenosis; limb where it was decreased in volume. The Spo2 in length discrepancy; vascular compromise; left room air was 100% both upper and lower limbs. subclavian artery stenting. There was a faint systolic murmur (2/6) at left infra - Introduction : Ischemia and gangrenous changes clavicular region. Baseline blood investigations involving limbs in newborn and infants are reported alongwith a 12 lead ECG and CXR were within in literature. Described aetiologies are thrombosis normal limits. Trans-thoracic echocardiography after arterial cannulation, purpura fulminance, (TTE) detected a structurally normal heart with compound fracture and disseminated bacterial normal sized chambers, normal estimated sepsis. In these cases limb length shortening can be pulmonary artery pressure and good biventricular appreciated in the later part of life. function. The aortic arch was right sided and LSA course appeared to be much lower down. On colour We present a 3 months old infant and a 4 yrs old Doppler study mosaic pattern of signal was child with obvious left upper limb shortening due to appreciated along the LSA. However due to poor severe LSA stenosis, congenital in origin. The alignment, continuous (CW) and pulse wave (PW) infant had early ischemic changes in the left upper doppler gradients were unsatisfactory across the limb, characterized by temperature discrepancy concerned vessel. Stenosis of LSA in a case of between the two upper limbs. Another 3years 6 otherwise structurally normal heart with Right months old child presented with BP differences AorticArch ( RAA) was considered as a provisional between the two upper limbs due to severe LSA diagnosis. A multi slice computerized tomographic stenosis as a result of a post operative complication. (MSCT) angiography was advised for the proper Case reports : delineation of her vascular abnormality. Due to presence of RAA, possibility of 22q11micro Case - 1 : A 28 days old female newborn was deletion was considered and genetic study was also referred to our hospital for evaluation of incidental planned. However, the family denied any further detection of murmur she was born of non- investigation at that point of time. consanguineous marriage, at term, delivered by normal vaginal route with an uneventful birth Two months later, the baby represented with limb history and weighed 2.8 Kg at birth, which was length discrepancy, which was recognized by her appropriate for gestational age (AGA). Her mother mother, as a visibly distressing sight. On clinical was 36 years old, second gravida, non-diabetic, examination she was an apparently healthy baby non- hypertensive, with euthyroid status without with adequate weight gain (5 Kg at 3 months). On any history of chronic illness or chronic medication measurement of the upper limb length (Tip of and exposure to any infectious diseases during this acromion to tip of middle nger), it revealed left pregnancy. Only relevant family history was upper limb (21.4 cm) was 8 mm shorter than the
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right upper limb (22.2 cm) and mid upper arm pressure (ATM). The post procedure angiography circumference of left arm (11.5 cm) was 10 mm showed the stent was perfectly placed spanning lesser than the right upper arm mid circumference across the stenotic segment, with good ow seen in (12.5 cm). distal LSA and left axillary artery. The whole There were no obvious colour changes, mottling, procedure was done aseptically and was uneventful. swelling or de nitive line of demarcation or The baby was extubated after shifting to pediatric gangrenous change in left upper limb. Spo2 intensive care unit (PICU) and was kept on heparin differences in both upper limbs were not very infusion (10U/kg/hr) overnight. She was signi cant. However, on touch there was mild discharged 48 hr post procedure observation with temperature difference between two upper limbs, stable hemodynamics. The most encouraging sign the left upper limb appeared cold on touch. Left was loss of temperature discrepancy in both upper radial artery pulse volume was decreased compared limbs, almost the same temperature was recorded in to the right radial pulse with a difference in mean both upper limbs at the time of discharge. Radial blood pressure of 10 mmHg. pulse volume was the same on both limbs; blood pressure difference was also reduced to 3mm Hg. Urgent MSCT was done which revealed RAA, rst Baby was put on tablet Aspirin @ 5mg/kg , single branch being left common carotid artery (LCCA), dose , daily for 6months. second one right common carotid artery (RCCA), third one right subclavian artery (RSA) and the last Follow-up after 3 months revealed temperature, one was LSAwith its origin much lower down from pulse volume and blood pressure measurements the descending thoracic aorta. No obvious collateral were almost equalized between two upper limbs. supply to the left arm was noted. There was no Limb lengths measurements revealed left upper external bony compression on the LSA. There was limb(22.9 cm) was 6 mm shorter ( pre procedure normal right kidney with normal single right renal was 8 mm shorter) than the right upper limb (23.5 artery, and an ectopic left kidney situated in the right cm) and mid upper arm circumference of left arm iliac fossa. (12.7 cm ) is 5 mm (pre procedure was 10 mm lesser) lesser than the right mid upper arm As there were subtle signs of early ischemic circumference (13.2 cm). changes and visible shortening of left upper limb caused by severe focal stenosis of LSA with Follow up duplex sonography (USG) con rmed a absence of collateral formation, LSA stenting as laminar ow pattern in the left subclavian and limb salvage strategy was decided. axillary arteries. The baby is being followed up for last one year. Presently there is no remaining limb After taking a proper written consent from the length discrepancy between two upper limbs. Till parents, the baby was taken to catheterization date, no further therapeutic procedure was needed. laboratory. She was intubated and ventilated and left femoral artery (LFA) access was obtained with Case - 2 : A4 years old male child was send to us for 4 (F) short sheath (Terumo medical corporation, evaluation of incidental detection of murmur. Somerset, New Jersey). Full heparinization was Clinical examination revealed an apparently done and arch angiograms were obtained in PA and healthy boy weighing 16 kg, with a height of 100 cm shallow LAO - cranial views which detected RAA with upper limb length discrepancy. Limb length with aberrant LSA and signi cant narrowing of measurement revealed left upper limb was 10 mm LSA. The most stenotic segment was 2 mm in width shorter than the right upper limb. Differences in and it was 5 mm distal to the origin of LSA. 4F pulse volume and BP (15mmHg) between the two femoral artery sheath was exchanged with a 5F upper limbs were also documented. Skin colour, sheath. LSA was threaded after repetitive attempts capillary return time, temperature, saturation were with a 0.014 x 180 cm Stabiliser super soft wire same in both upper limbs. Except grade 2/4 (Lake Region Medical, 340 lake Hazeltine Drive, ejection systolic murmur in the left infra-clavicular chaska, USA) and a 4F right Judkin's catheter. A 5F region, cardiac examination was within normal Guiding right Judkin's catheter (Cordis de Mexico limits. S.Ade C.V) was negotiated over the wire.A3.5 x 16 Relevant blood investigations, chest X- ray, EKG mm (3V Krome) stent was introduced over the wire, were within normal limits. TTE revealed a which was placed in the LSA in such a way that it structurally normal heart with RAA and aberrant fully covered the stenotic segment. The position of origin of LSA with ow acceleration across it. On wire - stent assembly was con rmed by uoroscopy PW and CW doppler interrogation, a proper and angiograms. After con rmation of satisfactory gradient across the vessel could not be obtained stent position it was in ated at 6 atmospheric even after repetitive attempts. CT angiogram of the
16 BENGAL HEART JOURNAL chest con rmed RAA with aberrant LSA. The rst and she was discharged after seven days in a stable branch was LCCA, followed by RCCA, RSA, and condition on aspirin (3mg/Kg) and was kept on LSA. There was 70-80% stenosis just beyond the regular follow up. On follow up, she had origin of LSA. Presence of limb length discrepancy satisfactory weight gain and mild cyanosis. TTE justi ed treatment and after discussion with family showed a well functioning modi ed BT shunt with members trans-catheter placement of stent across good ow in con uent branch pulmonary arteries the stenosed segment was decided. and mild left pulmonary artery origin narrowing , After obtaining a written consent from the parents no signi cant valve regurgitation with good single the patient was electively intubated and ventilated. ventricular contractility. At the age of 8 months, a Right femoral artery access was obtained by 5F diagnostic cardiac catheterization was done, for a short sheath and arch angiograms were obtained in contemplated Bidirectional Glenn shunt - that AP and shallow RAO views to delineate the detected a well functioning modi ed BT shunt, anatomy , which detected RAA and an aberrant pulmonary atresia, con uent branch pulmonary LSA with severe origin stenosis. The stenosed arteries with LPA origin narrowing, hypoplastic segment measured 13 mm in length and 2mm in right ventricle (RV), no LV out ow obstruction width. The stenosed segment was crossed with 5(F) (LVOTO) and a normal pulmonary venous wedge Judkins right catheter and 0.025 x 260 mm pressure (mean of 9 mmHg). Bidirectional Glenn angulated glide wire (Terumo medical corporation, shunt (BDG) and LPA plasty with take down of Somerset, New Jersey). The 5(F) short sheath was modi ed BT shunt was done at the age of 9 months. upgraded to a 6(F) short sheath and the 5(F) JR The post operative period was uneventful and she catheter was exchanged with 6(F) guiding JR was discharged after 5 days in a stable condition. (Cordis de Mexico S.A de C.V) . A 0.014 x 180 Immediate follow up visits showed a satisfactory stabilizer coronary wire was parked in the distal part progress but follow up at the age of 3.5 years of LSA over which a Racer 5 x 18 mm stent was detected an otherwise well grown child with mild positioned across the defect. The position of the cyanosis (saturation 85%) with a difference in pulse stent was con rmed by check angiography before volume and BP between the two upper limbs (right deploying it at 8 ATM pressure under uoroscopic upper limb BPwas 94/44/65 and left upper limb BP guidance. Post procedure angiogram showed the was 72/38/53). Length, width, colour, saturation, stent in position with good ow in LSA and left temperature and CRT were same in both upper axillary artery. The procedure was uneventful and limbs. the child was kept on 10U/kg of heparin overnight. TTE showed a well functioning BDG, good ow in He was discharged on 5mg/kg/day of oral aspirin con uent branch pulmonary arteries, mild left atrio- for the next 6 months. There was no procedure ventricular valve regurgitation, and unobstructed related complications. ow across atrial septal defect (ASD) and no Immediately after the stent was placed in the LSA, LVOTO. The aortic arch was left sided with normal pulse volume and BP differences were reduced. branching pattern and ow acceleration in LSA. Follow up visit on 3 and 6 months showed Diagnostic catheterization was decided for signi cant improvement of limb length. USG of left evaluation of the Glenn circuit and a suspected LSA upper limb was done which con rmed a laminar stenosis. ow pattern in the LSA and axillary arteries. The After an informed consent was obtained, the child boy is being followed up for last one year. Presently was intubated and ventilated. Right internal jugular there is no remaining limb length discrepancy venous (RIJV) (5F), RFA (5F) and RFV(5F) between the two upper limbs. accesses were obtained. Diagnostic catheterization Case - 3 : A 3.5 years old post cardiac surgery demonstrated a well functioning BDG, good sized patient was detected to have a discrepancy in pulse branch pulmonary arteries, non restrictive ASD, volume and BP in the upper limbs on a routine normal Glenn and PA pressures with normal follow up visit. She had undergone two cardiac indexed pulmonary vascular resistance (PVRI). surgeries, for complex congenital heart disease Arch angiogram done in shallow LAO and AP (tricuspid atresia (IA), pulmonary atresia, normally views showed severe LSA origin stenosis, where related great arteries, and small sized con uent the width of the stenosed segment was 3 mm and the branch pulmonary arteries). length was 18 mm. Multiple moderate sized collaterals were detected from RSAwith signi cant Amodi ed Blalock Taussig (BT) shunt was done at supply to the right upper lobe of lung. the age of one month to optimise the pulmonary blood ow. Post operative period was uneventful The case was discussed in a multidisciplinary board
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meeting where LSA stenting and embolisation of of nearby structures characterized by stridor, collaterals was decided that was discussed with feeding dif culties, or any chocking episodes. The parents and an informed consent was obtained . only symptoms were early ischemic changes and The child was taken up on a second sitting for LSA limb length discrepancy in one patient and only stenting and embolisation of collaterals. She was limb length shortening and BP discrepancy in the intubated and ventilated and RFA access with a 5 other one due to severe narrowing of proximal part (F) short sheath was obtained, full heparinization of aberrant LSA. was done with 100U/kg. Arch angiogram was done Tschirch E , et al reported similar type of cases of in LAO view and the LSA was crossed with a 0.014 RAA with stenosis of aberrant LSA, which was coronary wire and a 5(F) JR catheter. The coronary diagnosed antenatally by foetal echocardiography. wire was positioned distally in the LSA and an The baby was treated with 2 multi-link pixel stent Abbot vascular RX Herculink Elite 5 x 18 mm Stent (8×2.5 mm) on the 18th day of life. They had was positioned across the defect. An angiogram electively deployed the stent in the stenosed LSA con rmed the stent position which covered the before the appearance of any clinical symptoms. entire stenosed segment. The stent was deployed at Follow up study by duplex ultra sonography 8 ATM pressure under uoroscopic guidance. Post revealed signi cant residual stenosis and that baby deployment angiogram demonstrated the stent in needed repeat therapeutic intervention in the form situ with good ow in LSA up to the axillary artery. of balloon dilatation of stent with success.10 Moderate sized arteriovenous collaterals from RSA were embolized with embolization coils. In our series of patients, there were no major complications such as thrombosis, rupture, stent Discussion : Ischemic changes and limb length migration, fracture, or stent block. Blood pressure shortening are described in newborns and in early discrepancies were reduced immediately after the infancy that are mostly complications of arterial stents were deployed in the LSA. Follow up on 3, 6 cannulation induced thrombosis, with reduced and 12 months showed almost equalization of both pulses and temperature. It is reported in 2% to 33% 1,2 upper limb lengths and width (mid arm of children after arterial cannulation. Impaired circumference) and there were no features of re- growth of the limb has been recognised for 3,4 stenosis clinically which was con rmed by USG 30 years. Other described aetiologies of limb scan in all the cases. There were other alternative length shortening includes compound fracture, management options like surgical correction or disseminated sepsis and purpura fulminance. balloon dilatation of the stenotic segment. Compound fractures can directly damage epiphysis However, there is a high chance of re-stenosis with of the growth plate and may hamper limb growth in balloon dilatation alone.We have implanted non later part of life. Like our series of patients , early bio-absorbable stents, even in an infant which chances of vascular compromise and limb length might not be suf cient for her limb growth till shortening due LSA stenosis which is congenital in adolescent period. However, percutaneous stent origin is rarely described in literature. implantation into the stenotic subclavian artery A RAA represents a variant of the thoracic vascular represents a less invasive therapeutic option than anatomy and is found in approximately 0.1% of surgical intervention and a more rewarding option population.5,6 About half of these have an aberrant than only balloon dilatation of the stenotic artery.11 LSA which may arise either directly from the aorta Post operative complications like absence of pulse or from Kommerell's diverticulum. Although an is described in case of classical BT shunts or post aberrant LSA may be an isolated nding , it is aortic coarctation repair where the subclavian commonly associated with RAA. Symptoms , if artery has been used. However, severe LSAstenosis any, are due to compression of the oesophagus or after take down of modi ed BT shunt which the trachea, characterized by dysphagia or airway required stenting is exceptional in world literature. compression which can occur in infancy or adulthood.7,8,9 But such obstructive complications In summary, our case series is the rst of such a kind are rare in the neonatal period. Management of LSA in paediatric population with limb hypoplasia, with features of compression of oesophagus or vascular compromise or BP differences which were trachea mostly requires surgical reconstruction. treated successfully with trans-catheter placement However, the presenting features of our cases were of stents in the LSA. unique as there were no features of any obstruction
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Fig. 1. Left upper limb shortening in neonate (Pre procedure) Fig. 2. CT angiogram revealed critical narrowing of left subclavian artery just distal to its origin
Fig. 3. Arch angiogram revealed critical narrowing of left Fig. 4. Therapeutic stenting done in critical narrowing of left subclavian artery just distal to its origin subclavian artery
Fig. 4. & 5. Left upper limb almost equal in length 3 months after the procedure.
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References : 1. Vlad P, Hohn A, Lambert EC. Retrograde arterial catheterization of the left heart: experience with 500 infants and children.Circulation 1964;29:787-93. 2. Desilets DT, Ruttenberg HD, Hoffman RB. Percutaneous catheterisation in children.Radiology 1966;87:119-22. 3. White JJ, Talbert JL, HallerAJ. Peripheral arterial injuries in infants and children.Ann Surg 1968;167:757-66. 4. RudolphAM. Complications occurring in infants and children.Circulation 1968;37:Suppl III:59-62. 5. Victorica BE, Van Mierop LH, Elliott LP.Right aortic arch associated with contralateral congenital subclavian steal syndrome.Am J Roentgenol Radium Ther Nucl Med 1970; 108: 582–590. 6. McElhinney DB, Hoydu AK, Gaynor JW, Spray TL, Goldmuntz E, Weinberg PM. Patterns of right aortic arch and mirror-image branching of the brachiocephalic vessels without associated anomalies. Pediatr Cardiol 2001;22 : 285–291. 7. Cina CS,Arena GO, Bruin G, Clase CM. Kommerell's diverticulum and aneurysmal right-sided aortic arch: a case report and review of the literature. J VascSurg 2000;3 : 1208–1214. 8. Donnelly LF, Fleck RJ, Pacharn P, Ziegler MA, Fricke BL, Cotton RT. Aberrant subclavian arteries: cross- sectional imaging ndings in infants and children referred for evaluation of extrinsic airway compression.AJRAm J Roentgenol 2002; 178: 1269–1274. 9. Bove T, Demanet H, Casimir G, Viart G, Goldstein JP, Deuvaert FE. Tracheobronchial compression of vascular origin. Review of experience in infants and children. J CardiovascSurg 2001;42 : 663–666. 10. Tschirch E,,Chaoui R, Wauer R.R , Schneider M and Rugider M.Perinatal Management of right aortic arch with aberrant left subclavian artery associated with critical stenosis of the subclavian artery in a newborn. Ultrasound Obstet Gynecol 2005;25 : 296–298. 11. Queral LA, Criado FJ. The treatment of focal aortic arch branch lesions with Palmaz stents. J VascSurg 1996;23 : 368–375.
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Review Article Novel Mapping Systems in Cardiac Electrophysiology - A perspective Munna Das Department of Cardiology, Narayana Superspeciality Hospital, Howrah
Abstract : Cardiac electrophysiology has moved a Beyond conventional mapping strategies, the long way forward during recent decades in the identi cation and modi cation of the underlying comprehension and treatment of complex cardiac arrhythmogenic substrate has emerged as a strategy arrhythmias. Conventional radiofrequency (RF) that leads to improved outcomes. Arrhythmogenic ablation has revolutionized the treatment of many substrate modi cation also has a major role in supraventricular tachycardias (SVTs) as well as ventricular tachycardia ablation procedures. ventricular tachycardias (VTs). Success in stable Optimisation of contact between tissue and catheter arrhythmias with predictable anatomical locations and image integration are a further step forward to or characteristics identifying endocardial augment our precision and effectiveness. electrograms, such as idiopathic VT, Hybridisation of existing technologies with a atrioventricular nodal reentrant tachycardia reasonable cost should be our goal over the next few (AVNRT), atrioventricular reentrant tachycardia years. (AVRT), or typical atrial utter (AFL), has Key words : Electroanatomical mapping systems, approached 90% to 99%. However, as interest has mapping techniques, atrial brillation, ventricular turned to a broad array of more complex tachycardia, arrhythmogenic substrate, contact arrhythmias, including some atrial tachycardias force, image integration (ATs), many forms of intraatrial reentry, most Ventricular Tachycardias(VT), and atrial Correspondence : Munna Das DM(Cardiology). brillation (AF), ablation of such arrhythmias Department of Cardiology, Narayana continues to pose a major challenge. This stems in Superspeciality Hospital, Howrah-711103, part from the limitations of uoroscopy and [email protected] conventional catheter-based mapping techniques to Introduction : Since the introduction of localize arrhythmogenic substrates that are electroanatomical mapping (EAM) into clinical removed from uoroscopic landmarks and the lack practice in 1997, remarkable progress has been of characteristic electrographic patterns. made in catheter infrastructure, signal recording Newer mapping systems have transformed the and processing, catheter guidance and visualisation clinical electrophysiology (EP) laboratory, have and simultaneous real-time depiction and enabled physicians to overcome some of the processing of different types of critical information 1 limitations of conventional mapping, and have during an ablation procedure. Contemporary three- offered new insights into arrhythmia mechanisms. dimensional (3D) EAM systems (EAMS) have These newer systems are aimed at improving the signi cantly reduced the need for uoroscopic 2,3 resolution, three-dimensional (3-D) spatial visualisation of catheters. They have also created localization, and rapidity of acquisition of cardiac a precise and trustworthy 'virtual environment' activation maps. These systems use novel capable of guiding complex mapping and ablation approaches to determine the 3-D location of the procedures. The latter is enhanced by integrating mapping catheter accurately, and local data from other imaging modalities, such as electrograms are acquired using conventional, computed tomography (CT) and cardiac magnetic well-established methods. Recorded data of the resonance (CMR). Contact-based EAM remains catheter location and associated intracardiac the standard of care in most cases, while non- electrogram at that location are used to reconstruct contact and/or multipolar catheters enable high- in real time a representation of the 3-D geometry of density mapping of arrhythmias in as few as a single the chamber, color-coded with relevant EP beat. In contact-based EAMS, manual point-by- information. point mapping is required to build a proper
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activation map of the arrhythmia of interest, i.e. Ensite NavX technology in its latest version running tachycardia or extra-systoles. On the other (Velocity) uses six skin electrodes to create a high- hand, if the arrhythmia is not sustained or not frequency electric eld (8.0 kHz) in three mutually haemodynamically tolerated, point-by-point orthogonal planes on the patient's thorax, creating a mapping may be insuf cient or even not feasible. coordination system in three X/Y/Z axes. The 3D- Non-contact mapping can address this concern as it localisation of conventional electrophysiology can create a full map even from a single tachycardia catheters is based on an impedance gradient- beat Recently, the matter of optimal catheter–tissue calculation system in relation to a reference contact and its effect on obtained data and ablation electrode placed on the patient's body, too.8 Field ef cacy has been addressed by a number of scaling is a process by which through complex studies.4,5 Modern EAM techniques have also been calculations the body's non-linear impedance can enriched with high-density body surface be overcome and a more representative model of the electrocardiogram (ECG) maps projected onto mapped 3D anatomy can be built.7,8 NavX Velocity reconstructed images of cardiac chambers created is an architecturally open system within which by CT and CMR, in an attempt to map arrhythmias multiple catheters from different manufacturers can in a non-invasive way. In this review, the authors be visualised.9 An additional advantage of the NavX aim to sum up state-of-the-art EAM techniques and Velocity technology during ablation procedures is their impact on the acute- and long-term results of that it is partially insensitive to potential patient ablation of complex arrhythmias. movements, as the reference electrodes and Contact-based Electroanatomical Mapping catheters are placed either on the patient's skin or in System(EAMS) : The two most widely used the patient's cardiac chambers, respectively, and contact-based EAMS worldwide are CARTO therefore they move simultaneously with the (Biosense Webster Inc., Diamond Bar, CA, USA) patient, preventing map shifts. and EnSite NavX Velocity (St Jude Medical, St. Recently, a novel EAMS (Rhythmia Mapping, Paul, MN, US). The primary inherent feature of Rhythmia Medical, Boston Scienti c Inc., every EAMS is the non- uoroscopical and precise Marlborough, MA, US) received regulatory spatiotemporal depiction of various diagnostic and approval.Amajor advantage of the new system is its therapeutic catheters and devices into a 3D shell ability to simultaneously record large numbers of that reenacts the cardiac chamber of interest. This electrograms (EGMs) with a very high spatial 3D shell consists of 'electrical points' sampled by resolution. This is achieved through a specially the mapping catheter through contact with the designed mini basket bidirectional de ectable anatomical structure. Modern EAMS incorporate catheter (64-electrode IntellaMap OrionR High utilities enabling computer-automated multi-point Resolution Mapping Catheter, Boston Scienti c model creation while the mapping catheter is roved Inc.) The mapping catheter incorporates a basket around the anatomical structure (CARTO3 Fast electrode array (usual mapping diameter 18 mm) Map Module and EnSite NavX VelocityR One- with eight splines. Each spline incorporates eight Model Module).The CARTO system is based on small, low impedance electrodes (64 electrodes in three active weak magnetic elds(5x10-6 to 5x10-5 total). Electrode localisation is carried out by a Tesla), produced by a three-coil location pad placed magnetic sensor in the distal region of the catheter underneath the patient's thorax. Dedicated catheter combined with impedance sensing on each of the 64 tips incorporate a magnetic mini-sensor that basket electrodes. Mapping in auto mode enables continually measures the strength of the magnetic automatic annotation of activation times in sites of eld and calculates the catheter's exact position in interest without manual interventions. The features space. and capabilities of this novel EAMS have been Contemporary CARTO versions(CARTO3) can evaluated in canines by Nakagawa et al.10 A concurrently portray multiple catheters, due to a median of 4,227 EGMs with a median resolution of 2.6 mm in 6.1 minutes were obtained, enabling the sophisticated current-based catheter location 10 technology. Six electrode patches positioned at the rapid creation of a credible activation map. patient's back and chest monitor the current emitted Non-Contact Mapping System : The most widely at a unique frequency by various catheter applied non-contact mapping system uses the electrodes.6,7 Visualisation of catheters is con ned Ensite ArrayR (St. Jude Medical Inc., St Paul, MN, into a 3D virtual area called the 'matrix', which can US) basket catheter and requires a 3D Ensite NavX be built only by a magnetic sensor-equipped reconstruction created with a roving mapping manufacturer-speci c catheter. catheter to project data on. The multipolar non- contact catheter uses 64 unipolar electrodes, which
22 BENGAL HEART JOURNAL record virtual unipolar far eld EGMs using a spectrum and fractionation.17-19 However, the mathematical inverse solution of the Laplace law distance and the orientation of the mapping catheter and then project them (n=3,360) on an already bipole to the underlying tissue plays a signi cant reconstructed 3D model shell. The precision of the role in the qualitative and quantitative recorded EGMs depends on the distance from the characteristics of the acquired signal, which, in centre of the array to the endocardial surface (R- turn, in uence the results of voltage-based substrate value, displayed continuously during mapping) mapping.20 Adequate contact between catheter and with distances <40 mm giving the most accurate tissue is considered determinant to credible data.11,12 Unipolar recording analysis is used after characterisation of the underlying arrhythmogenic collection of data to build maps of interest.13 The substrate.21 Furthermore, even though lesion speci c shape of the basket catheter enables formation during ablation is evaluated through simultaneous recording of several potential sites of ful lment of certain criteria, including EGM interest without actual catheter manipulation. amplitude reduction, initial impedance and During ectopic activity, virtual unipolar EGMs impedance drop during ablation and electrode obtained at the earliest site of activation have a QS temperature, the proper contact between tissue and or rS morphology, with the intrinsic de ection catheter can be guaranteed only through its direct inscribing earlier compared with every adjacent measurement. The contact force (CF) is used to sites.13 The variable distance and orientation of the evaluate the contact between the tissue and the centre of the EnSite balloon electrode to the catheter tip. Numerous studies have demonstrated recording sites can result in differing dV/dt of the that adequate CF is crucial for radiofrequency virtual unipolar EGMs at different recording sites.13 lesion size.16–20 At the other side of the CF spectrum, Non-invasive cardiac mapping : Non-invasive it has been found that lesions placed using high power settings (45 W) and high pressures (>40 g) cardiac mapping provides information on the 21 topography of arrhythmogenic foci pre- are correlated to char and crater formation. Of procedurally, in order to reduce time consuming note, CF <100 g during ablation procedures is associated with complications, i.e. cardiac mapping times. Body surface unipolar recordings 5 are projected onto 3D reconstructed images of the perforation. Three available technologies enable heart derived from CT or CMR scans. Using direct measurement of CF during ablation complex mathematical equations, the torso procedures. The TactiCath catheter (Endosense, potentials are related to the epicardial surface of the Geneva, Switzerland) incorporates a force sensor heart.31 Using body surface potential maps between the second and third electrode, consisting (BSPM) Lai et al. demonstrated the feasibility of of a deformable body and three optical bres (0.125 this technique for approximating the site of origin of mm diameter) to measure micro-deformations that cardiac ectopic activity, propagation properties of correlate with the force applied to the catheter tip. ectopic beats and, most recently, for reporting on Infrared laser light is emitted through the proximal the value of BSMP-derived ventricular endocardial end of the three optical bres. The change of wavelength during application of CF to the tip of the reconstruction for localisation of ventricular 4 ectopic beats.14,15 catheter is proportional to the CF applied to the tip. The technology used in the ThermoCool Non-invasive mapping has strengthened efforts to SmartTouchR ablation catheter (Biosense Webster explain the mechanisms involved to the initiation Inc., Diamond Bar, CA, US) is based on the and perpetuation of AF. Haissaguerre et al. applied electromagnetic location technology used in the non-invasive electrocardiographic mapping in CARTO System .The catheter tip electrode is patients with AF and suggested a co-existence of mounted on a precision spring that permits a small multiple AF mechanisms, including wave genesis amount of electrode de ection. A transmitter coil from focal sources or rotors, as well as wave that is coupled to the tip electrode, distal to the propagation. Regarding rotors, their presence was spring, emits a location reference signal. Location not con ned to a certain small area as they shifted to sensor coils placed at the proximal end of the spring different areas of the atrium, recurring and ring detect micro-movement of the transmitter coil, 16 occasionally. representing movement of the tip electrode on the Contact Force : During an electrophysiological spring. The system senses the location information study, bipolar EGMs are the most commonly of the sensor and calculates the associated force 22 analysed waveforms. EGM properties that are based on the known spring characteristics. The usually used to draw conclusions on cardiac tissue third system, IntelliSenseR (Hansen Medical Inc., characteristics include signal amplitude, power Mount View, CA, US), can be used in conjunction
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with the use of a dedicated robot system for catheter operator and in applying of effective therapeutic ablation.23,24 solutions even for the most complex Perspectives : The exciting journey of invasive arrhythmogenic substrates. In fact, what we were electrophysiology continues with signi cant imagining 20 years ago is now becoming true. Our innovations entering and shaping the clinical primary future goal should be to improve practice. EAMS have come a long way in effectiveness of mapping with the help of EAMS improving our understanding of diverse through hybridisation of technologies available, pathophysiological mechanisms that initiate and along with implementing state-of-the-art perpetuate arrhythmias, enabling real time technology in as many electrophysiology labs visualisation of data that are essential to the worldwide as possible with rational cost.
References : 1. Gepstein L, Hayam G, Ben-Haim SA. A novel method for non uoroscopic catheter-based electroanatomical mapping of the heart: In vitro and in vivo accuracy results. Circulation 1997;95:1611–22. 2. Rotter M, Takahashi Y,Sanders P, et al. Reduction of uoroscopy exposure and procedure duration during ablation of atrial brillation using a novel anatomical navigation system. Eur Heart J 2005;26:1415–21. 3. Estner HL, Deisenhofer I, Luik A, et al. Electrical isolation of pulmonary veins in patients with atrial brillation: reduction of uoroscopy exposure and procedure duration by the use of a non- uoroscopic navigation system (NavX). Europace 2006;8:583–7. 4. Yokoyama K, Nakagawa H, Shah DC, et al. Novel contact force sensor incorporated in irrigated radiofrequency ablation catheter predicts lesion size and incidence of steam pop and thrombus. Circ Arrhythm Electrophysiol 2008;1:354–62.
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5. Shah D, Lambert H, LangenkampA, et al. Catheter tip force required for mechanical perforation of porcine cardiac chambers. Europace 2011;13:277–83. 6. Scaglione M, Biasco L, Caponi D, et al. Visualization of multiple catheters with electroanatomical mapping reduces X-ray exposure during atrial brillation ablation. Europace 2011;13:955–62. 7. Jiang Y, Farina D, Bar-Tal M, et al. An impedance based catheter positioning system for cardiac mapping and navigation. IEEE Trans Biomed Eng 2009;56:1963–70. 8. Wittkampf FH, Wever EF, Derksen R, et al. Localisa: New technique for real-time 3-dimensional localization of regular intracardiac electrodes. Circulation 1999;99:1312–7. 9. Eitel C, Hindricks G, Dagres N, et al. Ensite VelocityTM.Expert Rev Med Devices 2010;7:185–92. 10. Nakagawa H, Ikeda A, Sharma T, et al. Rapid high resolution electroanatomical mapping: Evaluation of a new system in a canine atrial linear lesion model. CircArrhythm Electrophysiol 2012;5:417–24. 11. Thiagalingam A, Wallace EM, Boyd AC, et al. Noncontact mapping of the left ventricle: insights from validation with transmural contact mapping. Pacing Clin Electrophysiol 2004;27:570–8. 12. Kumagai K, Nakashima H. Noncontact mapping-guided catheter ablation of atrial brillation. Circ J 2009;73:233–41. 13. Hindricks G, Kottkamp H. Simultaneous noncontact mapping of left atrium in patients with paroxysmal atrial brillation. Circulation 2001;104:297–303. 14. Lai D, Liu C, Eggen MD, et al. Localization of endocardial ectopic activity by means of noninvasive endocardial surface current density reconstruction. Phys Med Biol 2011;56:4161–76. 15. Lai D, Sun J, Li Y, et al. Usefulness of ventricular endocardial electric reconstruction from body surface potential maps to noninvasively localize ventricular ectopic activity in patients. Phys Med Biol 2013;58:3897–909. 16. Haissaguerre M, Hocini M, Shah AJ, et al. Noninvasive panoramic mapping of human atrial brillation mechanisms: a feasibility report. J Cardiovasc Electrophysiol 2013;24:711–7. 17. Marchlinski FE, Callans DJ, Gottlieb CD, et al. Linear ablation lesions for control of unmappable ventricular tachycardia in patients with ischemic and nonischemic cardiomyopathy. Circulation 2000;101:1288–96. 18. Nademanee K, McKenzie J, Kosar E, et al. Anew approach for catheter ablation of atrial brillation: Mapping of the electrophysiologic substrate. JAm Coll Cardiol 2004;43:2044–53. 19. Sanders P, Berenfeld O, Hocini M, et al. Spectral analysis identi es sites of high frequency activity maintaining atrial brillation in humans. Circulation 2005;112:789–797. 20. VenkatachalamKL, Herbrandson JE,Asirvatham SJ. Signals and signal processing for the electrophysiologist: part II: signal processing and artifact. CircArrhythm Electrophysiol 2011;4:974–81. 21. Mizuno H, Vergara P,Maccabelli G, et al. Contact force monitoring for cardiac mapping in patients with ventricular tachycardia. J Cardiovasc Electrophysiol 2013;24:519–24. 22. Perna F, Heist EK, Danik SB, et al.Assessment of catheter tip contact force resulting in cardiac perforation in swine atria using force sensing technology. CircArrhythm Electrophysiol 2011;4:218–24. 23. Duncan ER, Finlay M, Page SP, et al. Improved electrogram attenuation during ablation of paroxysmal atrial brillation with the Hansen robotic system. Pacing Clin Electrophysiol 2012;35:730–8. 24. Emmanuel Koutalas, Sascha Rolf, Borislav Dinov, et al. Contemporary Mapping Techniques of Complex Cardiac Arrhythmias:Identifying and Modifying the Arrhythmogenic Substrate. Arrhythmia & Electrophysiology Review, 2015;4(1):19–27
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Case Report Spontaneous Thrombosis within Coronary Sinus Dr. Md. Azizul Haque Associate Professor, Dept. of Cardiology National Medical College, Kolkata, India
Abstract : Spontaneous thrombosis within guide wire without any dif culty. LV lead was coronary sinus is very rare. Secondary thrombosis, positioned there with acceptable parameters. The now-a-days, usually occur after injury during CS patient was not symptomatic of the thrombus; hence cannulation with guide wires or catheters during we did not extract the thrombus. Atrial lead was biventricular pacing or during central venous positioned then. Patient subsequently recovered cannulation. We report a case of Spontaneous without any complications. Patient was under thrombosis within CS incidentally detected during follow-up for last 16 months without having any biventricular pacing. problem. Key words : Coronary sinus thrombosis, Spontaneous thrombus within coronary sinus is biventricular pacing very rare[1] , though secondary thrombus was Case Report : A 56 years old male with dilated common. In our patient, prior to any type of trauma cardiomyopathy with LBBB, ejection fraction of 28 to the vein, negative shadowing was present and % in NYHA class III, was posted for biventricular there was no prior central venous cannulation, pacing. He was nondiabetic; nonhypertensive with therefore, it may be presumed that the thrombus no known thrombotic disorders. He did not have was already in-situ before the procedure. Patient did any history of central venous cannulation for any not have any known thrombotic disease, so it may reason in the past. During the procedure, rst we be the procoagulant milieu in a patient with dilated had put the RV lead in position and atrial lead was cardiomyopathy which may be responsible for the kept in lower part of RA – not positioned. With the thrombus. In this era of biventricular pacing when help of a de ectable decapolar catheter, CS was CS cannulation is becoming common, the cannulated and a long sheath was positioned within possibility of venous thrombosis should always be it. Coronary venogram was performed with Swan- kept in mind in case of nonvisualisation of a ganz catheter. It showed the coronary sinus, its tributary within coronary venous system. tributaries, alongwith terminal portion of posterior cardiac vein, but not its proximal portion. To nd a suitable vein , we performed another venogram with Amplatz catheter positioned well within coronary sinus. It showed the proximal part of the posterior cardiac vein, but not the terminal portion adequately. During all these manipulations, wire or sheath were always within the coronary sinus or within the great cardiac vein. It did never enter into the posterior cardiac vein. Thereafter we took a right-angled preshaped sheath and posterior cardiac vein was selectively engaged. A selective angiogram was done which adequately visualized the proximal and terminal part of the vein with a lling defect in the middle portion. A diagnosis of spontaneous thrombosis within posterior cardiac vein was made.A0.014'' guide wire was introduced which crossed the middle part easily [ g.1] and LV Fig. 1. Selective venogram within coronary sinus [ LAO lead was put past the thrombotic portion over the view] showing lling defect in posterior cardiac vein through which guidewire was being passed.
References : 1. J Ramsaran EK, Sadigh M, Miller D. Sudden cardiac death due to primary coronary sinus thrombosis. South Med 1996; 89: 531-3.
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Case Report A non Cardiac Etiology of Atrial Fibrillation : Don't Forget the Mediastinum Amitabha Chakrabarty 12, Manujesh Bandyopadhyay 1.Consultant Thoracic Surgeon; 2. Junior Consultant ; Department of Thoracic Surgery Narayana Hrudyalaya Rabindranath Tagore International Institute of Cardiac Sciences
Abstract : Atrial brillation is a common Scan of Chest revealed a cystic lesion in the arrhythmia.Several non-cardiac diseases can posterior mediastinum located just below the contribute to it.External compression of the heart by Carina compressing the left atrium and displacing a mediastinal tumor is an extremely rare cause of the esophagus to the right hemi thorax.(Fig.2) A atrial brillation.The present case report describes a bronchogenic cyst was suspected among other case of mediastinal bronchogenic cyst causing differentials. Patient was admitted in the Critical compression of the heart thereby precipitating atrial Care Unit, managed on vasopressor and inotropes. brillation. After she was stabilized in the critical care unit, Key words : Atrial brillation,mediastinal mass, decision to operate upon was taken. Under General bronchogenic cyst. anaesthesia and Standard Monitoring, after Introduction : Abnormal budding of the primitive reviewing CT thorax, right thoracotomy was done, trachea bronchial tree gives rise to the Mediastinal the posterior mediastinum exposed and the cyst was bronchogenic cysts.Most commonly they are excised and marsupialised. The cyst wall was sent located in the mediastinum at the level of the for histopathology and found to be benign cystic tracheal bifurcation. In adults they are most lesion; also the cyst uid shows no growth on commonly asymptomatic and are discovered culture. In the immediate post operative period she incidentally on the chest radiograph.As these cysts recovered well in the intensive care unit and her enlarge they usually cause symptoms due to subsequent stay in the post-operative ward was tracheal, bronchial, or oesophageal compression. uneventful without any cardiac ailments. She could Extrinsic compression of the heart or great vessels be discharged home on her 6th post operative day appears to be a very rare occurrence. with much functional improvement (NYHA Class I/II) dyspnea with no evidence of Atrial brillation Case Report : A 42 year old non diabetic, and stable hemodyanmics. She is stable without any normotensive female presented with chest pain and cardiac or respiratory symptoms in the 6th month worsening respiratory distress for the last few years. follow up. At her arrival at the emergency department she was found to be tachycardic and hypotensive with a Discussion : Atrial brillation is the most common MAP of ~50 mmHg. A 12 lead Electrocardiogram peri operative rhythm disturbance in cardio thoracic con rmed the diagnosis of a rate controlled Atrial surgery with an incidence of 0.5% in those between 50-59 years of age to 9% in those between 80-89 Fibrillation, without any other interval changes 1 suggesting acute nature of the disease. The patient years of age. Cardiac causes of atrial brillation was not taking any rate or rhythm control include any mechanism resulting in structural and medication during this period. There was no past functional changes to the heart. The underlying history of hypertension, coronary artery disease or pathogenesis of AF involves changes in the any other signi cant co morbidity. electrophysiology of the atrial myocardium: generally premature atrial beats, which can An Echocardiogram done which failed to establish predispose the heart to a self-perpetuating cycle of any cardiac valvular anomaly, nor was there any AF.2 evidence of any clot in any cardiac chamber. There was no regional wall motion abnormality and she However, there are a number of non-cardiac cause had good systolic function. To investigate her of atrial brillation which include electrolyte worsening dyspnea on exertion (NYHA III) a imbalance, thyrotoxicosis, fever associated with Computed Tomography of the Chest was done. CT pneumonia, pharmacological and recreational drug use, and alcohol use. In this case these causes could
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be ruled out by history and physical and simple an increased incidence of AF in men with heavy blood tests (thyroid function tests, serum alcohol consumption.13,14 The "holiday heart electrolytes, and urine and serum toxicology).3 syndrome" is aptly named forAF that develops after 6,7 Hyperthyroidism increases the risk of developing heavy drinking during weekends and holidays. Atrial Fibrillation although the exact mechanism All of these conditions may precipitate AF through remains unclear, increased automaticity via an mechanisms involving increased beta-adrenergic increased beta adrenergic tone is thought to be the tone. Though it is often dif cult to predict which cause. 4 conditions lead to paroxysmal versus sustained AF, Chronic kidney disease is also linked to AF. In the it is important to recognize that in the absence of ARIC study, an evaluation of 10,328 people who structural heart disease as a substrate, the early had no history of AF found that, compared to management of these risk factors may be important participants with an estimated glomerular ltration in suppressing the onset ofAF. rate (eGFR) >90 mL/min/m2 , the hazard ratios for But in literature we have found sporadic case the development of AF were 1.3, 1.6, and 3.2 in reports with patient presenting with atrial those with eGFRs of 60 to 89, 30 to 59, and <30 brillation and symptoms of hemodynamic mL/min/m2, respectively, at a median follow-up of compromise with etiology lying in the mediastinum 10.1 years.5 such as – schwannoma, lipoma, pleural Alcohol has also been linked to AF, with up to 60% mesothelioma etc., making these a rare occurrence of binge drinkers, with or without underlying of atrial brillation. (Table 1) cardiomyopathy, developingAF. Two studies found Table 1. Review of literature on mediastinal masses associated with atrial brillation Number Author of Patient Presenting Investigations Management/ Comment Patients Characteristics Complaints for Diagnosis Therapy Kato et al 8 1 72 years, FemaleCardiogenic Shock, CT Scan Thorax, Surgical Resection HPE diagnosed the posterior Atrial Fibrillation Pericardial Fluid via Left mediastinal mass as benign Cytology, Thoracotomy schwannoma Histopathology Minematsuet al 9 1 83 years, MaleSymptoms of CT Scan-Thorax, Surgical Resection Diagnosed as a case of Congestive Heart TTE showed 70% Mediastinal Lipoma Failure EF with Gr III MR compressing the heart to cause (due to altered LA CHF like symptoms. Pre geometry by operatively was given a tumour) EuroScore of 8 Kuwabara et al 10 1 66 years, MaleRight Pleural CT Chest and Conservative Had occupational history of Effusion and Abdomen, Pleural Management as per exposure to Asbestos. Was Spontaneous Biopsy patient's decision diagnosed as a case of Pleural Pneumothorax Mesothelioma with metastasis. Tamura et al 11 1 59 years, MaleFollow up case of CT Chest, Conservative No AF in 2 month follow up CA Lung with drug Pulmonary Treatment period while on medication. refractory AF Venography, TTE, Initial episode had to be Chest X Ray terminated with DC shock. Bayraktar et al 12 1 58 years, MaleAtrial Fibrillation CT Chest, Biopsy of the lesion taken and Ventricular Echocardiography during sopagogastrocscopy achycardia in the and Esophago- diagnosed it as squamous cell ER while being gastroscopy Carcinoma of esophagus. evaluated for dysphagia. Volpi et al 13 1 36 years, MaleSudden onset CT ( Chest), TTE, Surgical Excision Cyst lined by respiratory palpitation and Chest X Ray ( PA epithelium. Symptoms were due dizziness and Lateral view) to LA compression by the subcarinal cyst. Asteriou et al 14 1 30years, FemaleSudden onset Chest X Ray, CT Surgical Excision 983 gm tumour with 15cm in palpitation and Chest and ECG. largest dimension. Post dizziness operative patient was discharged on Oral Amiodarone although he had no arrhythmia. Shlobin et al 15 1 Female Intermittent Fever CT Chest, ECG, Surgical Excision A case of mediastinal and New onset AF Chest X Ray aspergilloma which was put on long term voriconazole and capsofungin. **Reference of the articles cited are given in superscript between 8 to 15
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Fig. 1. Preoperative chest X-ray of the patient Fig. 2. CECT scan thorax of the patient
References : 1. Clinical Guideline for the Management of Pot OperativeAtrial Fibrillation: Cornwall Hospital NHS 2. Estes NAIII, et al.American HeartAssociationAtrial Fibrillation Research Summit:AConference Report From the American HeartAssocation.Circulation. 2011;124:363-372. 3. Atrial Fibrillation Outpatient Presentation and Management Michael D. Ezekowitz et al , Circulation , 2011 4. ChenYC, et al. Effects of Thyroid Hormone on theArrhythmogenicActivity of Pulmonary VeinCardiomyocytes. J Am CollCardiol. 2002;39:366-372 5. AlonsoA, et al. Chronic Kidney Disease isAssociated With the Incidence ofAtrial Fibrillation: TheAtherosclerosis Risk in Communities (ARIC) Study.Circulation . 2011;123:2946-2953. 6. Frost L, et al. Alcohol and Risk of Atrial Fibrillation or Flutter: A Cohort Study.Arch Intern Med. 2004;164:1993- 1998. 7. Mukamal KJ, et al.Alcohol Consumption and Risk ofAtrial Fibrillation in Men and Women: The Copenhagen City Heart Study.Circulation. 2005;112:1736-1742. 8. Kato M, Shiota S, Shiga K, et al. Benign giant mediastinal schwannoma presenting as cardiac tamponade in a woman: a case report.Journal of Medical Case Reports. 2011;5:61. doi:10.1186/1752-1947-5-61. 9. Minematsu N, Minato N, Kamohara K, Hakuba T. Complete removal of heart-compressing large mediastinal lipoma: a case report.Journal of Cardiothoracic Surgery. 2010;5:48. doi:10.1186/1749-8090-5-48. 10. Kuwabara H et al , Malignant pleural mesothelioma forming a huge mediastinal mass and causing atrial brillation. Indian J Pathol Microbiol 2012;55:513-5 11. Tamura M et al , A case of atrial tachycardia originating from pulmonary vein invaded by lung cancer (2012) Journal of Cardiology Cases, 5 (2) , pp. e118-e121. 12. Bayraktar UD et al , Esophageal cancer presenting with atrial brillation: A case report. Journal of Medical Case Reports. 2008;2:292. doi:10.1186/1752-1947-2-292. 13. Volpi A et al , Left atrial compression by a mediastinal bronchogenic cyst presenting with paroxysmal atrial brillation, Thorax 1988;43:216-217 14. Christos Asteriou et al , Giant mediastinal teratoma presenting with paroxysmal atrial brillation , Interactive CardioVascularand Thoracic Surgery 12 (2011) 308–310 15. Shlobin OA et al , Mediastinal mass due to Aspergillus fumigatus after lung transplantation: a case report, The Journal of Heart and Lung Transplantation : the Of cial Publication of the International Society for Heart Transplantation[2005, 24(11):1991-1994]
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Review Article Modeling of Human Heart Using a Systems Approach - a Survey of Recent Trends Subhayu Das 12, Amitava Gupta 1. Department of Appl. Electronics & Instru. Engg., Heritage Institute of Technology, Kolkata 2. Department of Power Engineering, Jadavpur University, Kolkata
Abstract : Dynamic electric modeling of the Amore fundamental approach has been synthesis of human heart have been tried since long. The era the heart model using models of the phenomena started with simple electrical models to generate associated with polarization-depolarization and ECG like signals. Next genera used combined corresponding contraction-relaxation and also Hydro-electromechanical modeling to incorporate using the visco-elasticity approach6 .Fractional the physiological properties of heart. The next in the Order techniques have been applied to model order is the fractional order technique that addresses phenomenon like charging and discharge of the cardiac dynamics. The latest in the que is capacitors7 as well as the visco-elasticity Magnetocardiography using SQID (Semiconductor phenomenon and this approach has been extended quantum interface device) to the modeling of human heart as a natural 6,8 Key words : Electrical modeling, heart, fractional corollary . order technique In the recent past, some studies have revealed a Introduction : Electrical modeling of the human magnetic eld generated by the heart. Interaction of heart as a dynamic system has been attempted since this magnetic eld with electromagnetic probe long by contemporary researchers and these models beams have also been a focus of research and some researchers have been able to extract footprints of fall under two major genre viz. electrical models to 9 generate ECG likes signals which serve as heart malfunctioning. from Magnetocardiography indicators to different malfunctions associated with using a Semiconductor Quantum Interface Device the heart's rhythm and mathematical models to (SQID) has been used to map the magnetic eld represent the physiological phenomena associated produced by the heart to locate sources of arythmia. with the heart and the cardio-vascular system. This paper reviews some of these recent trends in The models belonging to the rst genre can be used the following sections. to actually simulate ECG like response in different Modeling human heart using circuit conditions of heart malfunction with varying components degree of accuracy.These methods range from Van- Modeling a human heart has been attempted by der-Pol oscillator based circuits in various 1,2 contemporary researchers to produce analog combinations to combined hydro- models of the following genre: Physical Models of electromechanical system modeling which uses the Total Arti cial Heart(TAH) for example10 capable concept of ow resistance due to the cardio- 3 of simulating physiological phenomenain the heart, vascular system . The focus of these methods is baro-receptor models, electro-mechanical model mainly simulation of the P-wave and the QRS and models using circuit components for generating complex. The analysis of the heart as an oscillator ECG signals. A combination of different concepts has received considerable merit in contemporary 4 yields a hybrid modeling methodology termed as literature. For example, Babloyantzet al in have the Hydro-electromechanical system modeling3 . attempted to analyze the heart as a perfect oscillator Physical models normally use the electrical circuit by proposing circuits to simulate the P-wave and the analogy where charge is analogous to rate of ow of QRS complex and their study establishes the blood, current is analogous to rate of change of ow bandwidth of the signals. Frequency domain and its second derivative represents the rate of treatment of signals using micro-waves have also change of current. A valve is usually represented by been proposed to detect congestive heart failures at 5 a diode –which is a unidirectional circuit early stages. component allowing current to ow in a particular
30 BENGAL HEART JOURNAL direction only- and a resistance. A typical example switching sequence of the diodes in Fig. 1 can be is the work by Shi et. al in [10] as shown in Fig. 1 used to model the ow of arterial and venous blood which is derived from the gure presented in [10] through the heart. Simulation of physiological The basis of this model is the seminal work by phenomena can be achieved by altering the circuit Reulet. al. which uses the analogy between Pressure parameters. A baro-receptor model can be used to ()PVand Voltage () and that between Flow rate () f of sequence the switching of the diodes and hence blood and current()i in an electric circuit to model pressure build up, thus simulating the nervous the ow of blood in a part human cardio-vascular system component in the control of the heart rate. system as aRLC-- circuit described electrically as Combined Electro-Hydro-Mechanical Models shown in Fig. 1. The circuit shown depicts the part The fact that the TAH approach can be used to corresponding to the ow from the Right Atrium, simulate physiological phenomena in the heart, for Right Ventricle, the Pulmonary Artery, through the example, by varying the various circuit parameters, lungs and then through the Pulmonary Vein and it is worthwhile to explore the possibility of then to the Left Atrium. The symmetrical circuit synchronizing these parameter variations with the representing the ow from the Left Atrium, the variation of pressure gradients rhythmically. One circulatory network and then to the Right Atrium is way of doing this is the combined Hydro- not shown. The R-L-C networks serve either as ow Electromechanical System Modelling10 . The element simulators or as phase shifters which add principle behind this modeling approach is to link delays so that the diodes representing the valves the compliance, Inertance and laminar resistance to turn on is a pre-determined sequence. Thus, a model the wall motion of the heart and hence the represented by Fig. 1 can be used different corresponding capacitance, inductance and conditions associated with the vascular as well as resistance. Clearly, this would involve modeling the rhythmic attributes of the human heart, though capacitors with time-varying characteristics to choice of parametric values are extremely subject simulate polarization and de-polarization of heart speci c. muscles, usually represented by complex non- The inductance acts as an inertial element for the linear functions. In the recent past, charging and applied voltage and initially acts as an open circuit discharge phenomena of such capacitors have been which causes a delay in the voltage build up at the very effectively modeled using Fractional Order anode (positive terminal ) of a diode which systems [references] and this has opened a new conducts only when there is a positive potential domain of research in the modeling of the human difference across its terminals exactly like a heart. The other simpler approach is to use mechanical valve which opens only when there oscillators which generate the pacemaker signals exists a positive pressure gradient in the direction of and the corresponding models for the heart, the ow across it. Once the valve conducts, the cardio-vascular system and the appropriate capacitor charges and this neutralizes the gradient simulated sensor generating thesynthetic ECG across the diode which then stops conduction (the signals as shown in Fig.2.which is a computer valve closes) and remains in this state till the generated replica. capacitor discharges by some means and a fresh It is a well-known fact that a heartbeat is initiated cycle starts. Once the diode conducts, the following by a series of electrical events in the heart tissues. equation holds for the circuit shown in Fig. 2 Each event isinitiated by changes in electric potential between the exterior and interior cells of the heart tissue producing the cardiac action potential in the form of spikes8 . Such spikes are generated due to the movement of ions across the and its ow analog transmembrane ion channels present in the cardiac cells. Acardiac myocyte model has been proposed in [8] to model the ionic phenomenon at the cellular level and the generation and propagation of the cardiac action potential. Cardiac cell modeling is where the resistanceR is analogous to the laminar inspired by the Hodgkin-Huxley (HH) model which resistance to owR , the inductanceL is analogous utilizes the similarity between the neurons and the to the inertanceL and the capacitanceC is cardiac cells since they have similar ion exchange analogous to the complianceC . mechanisms. From (2) it is clear that controlling the pressure gradient actually alters the ow rate and the
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FO models of the heart origin of this magnetic eld could be traced to It is clear that the simple models of the human heart bioelctromagnetism a phenomenon where electric often has many inadequacies – as the models and magnetic elds are produced by periodic translate to a set of Linear Differential Equations change in charge conduction in a biological tissue which entail higher order dynamics to model a –such as the heart. This has given rise to a whole heart. The solution to such a modeling problem is new technology where the heart's magnetic eld is the Fractional Order (FO) system modeling – an mapped and used for detection of heart approach which uses a set FO differential equations malfunctioning and even for ow visualization. The to model cardiac dynamics which can be used either extremely low magnetic eld which is of the order to model transmembrane ionic conduction6,8 . For of a few pico-Tesla is picked up using a SQID – a example,FO modeling has been used very technology already in use in a few German effectively in modeling the electrical impedance of hospitals. the electrode–tissue interface in the heart and for Conclusion modeling the stress–strain behavior of arterial The emergence of enabling tools and techniques for viscoelasticity and hysteresis. Some authors have 8 understanding biological phenomena together with also used FO models to model heart myocytes .FO advanced methodologies for modeling of order viscoelasticity based modeling of heart valves dynamical systems has produced a platform for has been attempted by some contemporary development of models that can simulate different researchers as well. These modern models can very aspects of a human heart. While studies on heart effectively simulate heart dynamics and can rhythms require electrical models, combined hydo- generate almost accurate ECG signals2. electromechanical models can be used to combine The magnetic eld of the heart and the the electrical and vascular aspects of the human magnetocardiography heart which could lend a much larger dimension to a Recent research has shown that the heart like the simple ECG. human brain produces its own magnetic eld9 . The
Fig. 1. 1TAH representation of the human heart with circuit elements
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Fig. 2.Asample computer generated ECG signal using simulated model of a human heart
References : 1. Gois, S.R. and Savi, M.A., An analysis of heart rhythm dynamics using a three coupled oscillator model, Chaos, Solitons& Fractals, vol. 41, no. 5, pp. 2553–2565,2009 2. Das, S. and Maharatha, K., Fractional Dynamical Model for the Generation of ECG like Signals from Filtered Coupled Van-derPol Oscillators, Computer Methods and Programs in Biomedicine 112 (3), 490–507,2013 3. YALCINKAYA,F., KIZILKAPLAN,E. and ERBAS, A., Mathematical Modelling of Human Heart as a Hydro- electromechanical System, 8th International Conference on Electrical and Electronics Engineering (ELECO), 2013 4. Babloyantz,A. and Destexhe, Is the normal heart a periodic oscillator?,Biological Cybernetics, Volume58, Issue3, pp 203–211, 1988. 5. Zamani, A.,Rezaeieh,S.A. and Abbosh, A. M., Frequency domain method for early stage detection of congestive heart failure, Proceedings of the 2014 IEEE MTT-S International Microwave Workshop Series onRF and Wireless Technologies for Biomedical and HealthcareApplications (IMWS-Bio), 2014 6. Carew, E. O., Doehring, T. C., Barber, E. J., Freed, A.D. and Vesely, I., FRACTIONAL-ORDER VISCOELASTICITYAPPLIED TO HEARTVALVETISSUES 7. Calik, A.E.,Sirin, H.,Ertik,H. and Sen,M, Analysis of charge variation in fractional order LC electrical circuit, Revista Mexicana de F´ısica 62 (2016) 437–441,2016 8. Wardhan, H. and Singh, S., Modeling of generation and propagation of cardiac action potential using fractional capacitance, IOSR Journal of Biotechnology and Biochemistry,Vol.1,Issue(2),pp 1-11,2015 9. MAGNETOCARDIOGRAPHY(MCG) EXPLAINED, http://www.w2agz.com/Library/Electronic%20Applications/SQUIDS/CardioMag%20Imaging%20Product%20I nformation/MCG%20Introduction/MCG%20Explained.pdf 10. Shi, W. and Chew, M. , Mathematical and Physical Models of a Total Arti cial Heart, 2009 IEEE International Conference on Control andAutomationChristchurch, New Zealand, December 9-11, 2009
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Image corner Many a Times ECG Holds the Clue Dr. Soumitra Kumar Professor & HOD, Dept. of Cardiology, Vivekananda Institute of Medical Sciences, Kolkata
56 years old diabetic male presented with acute l ST elevation in aVR onset severe central chest pain for previous four l ST elevation I V1 > 2.5 mm hours. On interrogation, he mentioned that he has been experiencing similar but milder chest pain on l Complete RBBB exertion for past one year. His vitals were stable on l ST depression in V5 examination : Heart rate 90/min; BP 130/80mmHg; plus : ST-elevation in aVL and > 1 mm ST - SaO2 99% on room air. His ECG however was quite alarming.(Fig.1) Ten hours later ECG was depression in inferior leads. indicative of ostial LAD occlusion (septal STEMI) A multivariate analysis from the GUSTO-1 (Fig.2). database of 41,021 patients found that the following ECG variables were predictive of 30 days mortality. l Sum of the absolute ST-segment deviation, both elevation and depression, ≥ 19mm (odds ratio 1.53) l Evidence of prior infarction for new inferior infarction (odds ratio 2.47) l Heart rate >84 beats per min (odds ratio 1.49) l QRS duration ≥ 100 msec for anterior infarction Fig. 1. ECG on admission (odds ratio 1.55) However this patient's ECG differed in the following aspects: l Lesser magnitude of ST elevation in aVR and V1 l Lesser magnitude of ST-depression in inferior leads l Alternate incomplete and complete RBBB and lesser average QRS width overall However, still on suspicion of a proximal LAD Fig. 2. ECG ten hours later indicative of ostial LAD occlusion occlusion the patient was immediately take up for (septal STEMI) primary PCI, which revealed the following (Fig.4 and 5).
Fig. 3. Typical features of an osteoproximal LAD occlusion presenting as STEMI. Usual Signs of basal septal involvement are as follows(Fig.3) : Fig. 4. Coronary angiogram of LMCA-LAD
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develop cardiogenic shock. However, this patient during his hospital stay continued to maintain stable vital signs with usual medical management and was eventually discharged after a week. The Cardiac Surgeon opined not to operate on the subject before three weeks. The patient reported at OPD after two weeks post-discharge in a stable condition and has been referred for consideration of CABG. Reasons for the stable clinical course of the patient can only be explained by “acute on chronic” nature Fig. 4. Coronary angiogram of RCA of the lesion in question which allowed for signi cant collateral support and ischaemic LMCA showed 50% mid to distal lesion with preconditioning. These explain the less severe ECG heavily calci ed LAD showing total occlusion manifestations in this patient compared to usual before S1 origin without hint of a nipple. As ECG ndings of LAD occlusion proximal to S1. anticipated the lesion could not be crossed despite Collateral ow and ischemic pre-conditioning were use of intermediate stiffness Guidewires. PPCI was shown to reduce the degree of ST elevation and QT abandoned. There is always an apprehension (in this prolongation in such cases.1 type of a lesion) of the patient progressing to
References : 1. Floyd JS, Maynard C, Johanson P, Jennings RB, Wanger GS; effects of ischemic preconditioning and arterial collateral ow on ST-segment elevation and QRS complex prolongation in a canine model of acute coronary occlusion: J Electrocardiol 2009 Jan-Feb;42(1): 19-26.
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