Common Types of Supraventricular Tachycardia: Diagnosis and Management RANDALL A
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Cardiogenetics 2017; volume 7:6304 Sudden death in a young patient with atrial fibrillation Case Report Correspondence: María Angeles Espinosa Castro, Inherited Cardiovascular Disease A 22-year-old man suffered a sudden Program, Cardiology Department, Gregorio María Tamargo, cardiac arrest without previous symptoms Marañón Hospital, Dr. Esquerdo, 46, 28007, María Ángeles Espinosa, while he was at rest, waiting for a subway Madrid, Spain. Víctor Gómez-Carrillo, Miriam Juárez, train. Cardiopulmonary resuscitation was Tel.: +34.91.586.82.90. immediately started using an Automated E-mail: [email protected] Francisco Fernández-Avilés, External Defibrillation that identified the Raquel Yotti Key words: KCNQ1; mutation; channelopa- presence of ventricular fibrillation and thy; sudden cardiac death; atrial fibrillation. Inherited Cardiovascular Disease delivered a shock. Return of spontaneous Program, Cardiology Department, circulation was achieved after three Contributions: MT, acquisition and interpreta- Gregorio Marañón Hospital, Madrid, attempts, being atrial fibrillation (AF) the tion of data for the work, ensuring that ques- Spain patient’s rhythm at this point (Figure 1). tions related to the accuracy or integrity of any He was admitted to our Cardiovascular part of the work is appropriately investigated Intensive Care Unit and therapeutic and resolved; MAE, conception of the work, hypothermia was performed over a period critical revision of the intellectual content, final approval of the version to be published, Abstract of 24 h. After completing hypothermia, ensuring that questions related to the accuracy rewarming, and another 24 h of controlled of any part of the work is appropriately inves- Sudden cardiac death (SCD) in young normothermia the patient awakened with no tigated and resolved; VG-C, acquisition and patients without structural heart disease is residual neurologic damage. -
Antithrombotic Therapy in Atrial Fibrillation Associated with Valvular Heart Disease
Europace (2017) 0, 1–21 EHRA CONSENSUS DOCUMENT doi:10.1093/europace/eux240 Antithrombotic therapy in atrial fibrillation associated with valvular heart disease: a joint consensus document from the European Heart Rhythm Association (EHRA) and European Society of Cardiology Working Group on Thrombosis, endorsed by the ESC Working Group on Valvular Heart Disease, Cardiac Arrhythmia Society of Southern Africa (CASSA), Heart Rhythm Society (HRS), Asia Pacific Heart Rhythm Society (APHRS), South African Heart (SA Heart) Association and Sociedad Latinoamericana de Estimulacion Cardıaca y Electrofisiologıa (SOLEACE) Gregory Y. H. Lip1*, Jean Philippe Collet2, Raffaele de Caterina3, Laurent Fauchier4, Deirdre A. Lane5, Torben B. Larsen6, Francisco Marin7, Joao Morais8, Calambur Narasimhan9, Brian Olshansky10, Luc Pierard11, Tatjana Potpara12, Nizal Sarrafzadegan13, Karen Sliwa14, Gonzalo Varela15, Gemma Vilahur16, Thomas Weiss17, Giuseppe Boriani18 and Bianca Rocca19 Document Reviewers: Bulent Gorenek20 (Reviewer Coordinator), Irina Savelieva21, Christian Sticherling22, Gulmira Kudaiberdieva23, Tze-Fan Chao24, Francesco Violi25, Mohan Nair26, Leandro Zimerman27, Jonathan Piccini28, Robert Storey29, Sigrun Halvorsen30, Diana Gorog31, Andrea Rubboli32, Ashley Chin33 and Robert Scott-Millar34 * Corresponding author. Tel/fax: þ44 121 5075503. E-mail address: [email protected] Published on behalf of the European Society of Cardiology. All rights reserved. VC The Author 2017. For permissions, please email: [email protected]. 2 G.Y.H. Lip 1Institute of Cardiovascular Sciences, University of Birmingham and Aalborg Thrombosis Research Unit, Department of Clinical Medicine, Aalborg University, Denmark (Chair, representing EHRA); 2Sorbonne Universite´ Paris 6, ACTION Study Group, Institut De Cardiologie, Groupe Hoˆpital Pitie´-Salpetrie`re (APHP), INSERM UMRS 1166, Paris, France; 3Institute of Cardiology, ‘G. -
Constrictive Pericarditis Causing Ventricular Tachycardia.Pdf
EP CASE REPORT ....................................................................................................................................................... A visually striking calcific band causing monomorphic ventricular tachycardia as a first presentation of constrictive pericarditis Kian Sabzevari 1*, Eva Sammut2, and Palash Barman1 1Bristol Heart Institute, UH Bristol NHS Trust UK, UK; and 2Bristol Heart Institute, UH Bristol NHS Trust UK & University of Bristol, UK * Corresponding author. Tel: 447794900287; fax: 441173425926. E-mail address: [email protected] Introduction Constrictive pericarditis (CP) is a rare condition caused by thickening and stiffening of the pericar- dium manifesting in dia- stolic dysfunction and enhanced interventricu- lar dependence. In the developed world, most cases are idiopathic or are associated with pre- vious cardiac surgery or irradiation. Tuberculosis remains a leading cause in developing areas.1 Most commonly, CP presents with symptoms of heart failure and chest discomfort. Atrial arrhythmias have been described as a rare pre- sentation, but arrhyth- mias of ventricular origin have not been reported. Figure 1 (A) The 12 lead electrocardiogram during sustained ventricular tachycardia is shown; (B and C) Case report Different projections of three-dimensional reconstructions of cardiac computed tomography demonstrating a A 49-year-old man with a striking band of calcification around the annulus; (D) Carto 3DVR mapping—the left hand panel (i) demonstrates a background of diabetes, sinus beat with late potentials at the point of ablation in the coronary sinus, the right hand panel (iii) shows the hypertension, and hyper- pacemap with a 89% match to the clinical tachycardia [matching the morphology seen on 12 lead ECG (A)], and cholesterolaemia and a the middle panel (ii) displays the three-dimensional voltage map. -
J Wave Syndromes
Review Article http://dx.doi.org/10.4070/kcj.2016.46.5.601 Print ISSN 1738-5520 • On-line ISSN 1738-5555 Korean Circulation Journal J Wave Syndromes: History and Current Controversies Tong Liu, MD1, Jifeng Zheng, MD2, and Gan-Xin Yan, MD3,4 1Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, 2Department of cardiology, The Second Hospital of Jiaxing, Jiaxing, China, 3Lankenau Institute for Medical Research and Lankenau Medical Center, Wynnewood, Pennsylvania, USA, 4The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China The concept of J wave syndromes was first proposed in 2004 by Yan et al for a spectrum of electrocardiographic (ECG) manifestations of prominent J waves that are associated with a potential to predispose affected individuals to ventricular fibrillation (VF). Although the concept of J wave syndromes is widely used and accepted, there has been tremendous debate over the definition of J wave, its ionic and cellular basis and arrhythmogenic mechanism. In this review article, we attempted to discuss the history from which the concept of J wave syndromes (JWS) is evolved and current controversies in JWS. (Korean Circ J 2016;46(5):601-609) KEY WORDS: Brugada syndrome; Sudden cardiac death; Ventricular fibrillation. Introduction History of J wave and J wave syndromes The concept of J wave syndromes was first proposed in 2004 The J wave is a positive deflection seen at the end of the QRS by Yan et al.1) for a spectrum of electrocardiographic (ECG) complex; it may stand as a distinct “delta” wave following the QRS, manifestations of prominent J waves that are associated with a or be partially buried inside the QRS as QRS notching or slurring. -
The Syndrome of Alternating Bradycardia and Tachycardia by D
Br Heart J: first published as 10.1136/hrt.16.2.208 on 1 April 1954. Downloaded from THE SYNDROME OF ALTERNATING BRADYCARDIA AND TACHYCARDIA BY D. S. SHORT From the National Heart Hospita. Received September 15, 1953 Among the large number of patients suffering from syncopal attacks who attended the National Heart Hospital during a four-year period, there were four in whom examination revealed sinus bradycardia alternating with prolonged phases of auricular tachycardia. These patients presented a difficult problem in treatment. Each required at least one admission to hospital and in one case the symptoms were so intractable as to necessitate six admissions in five years. Two patients had mitral valve disease, one of them with left bundle branch block. One had aortic valve sclerosis while the fourth had no evidence of heart disease. THE HEART RATE The sinus rate usually lay between 30 and 50 a minute, a rate as slow as 22 a minute being observed in one patient (Table I). Sinus arrhythmia was noted in all four patients, wandering of TABLE I http://heart.bmj.com/ RATE IN SINus RHYTHM AND IN AURICULAR TACHYCARDIA Rate in Case Age Sex Associated Rate in auricular tachycardia heart disease sinus rhythm Auricular Venliicular 1 65 M Aortic valve sclerosis 28-48 220-250 60-120 2 47 F Mitral valve disease 35-75 180-130 90-180 on September 26, 2021 by guest. Protected copyright. 3 38 F Mitral valve disease 22-43 260 50-65 4 41 F None 35-45 270 110 the pacemaker in three, and periods of sinus standstill in two (Fig. -
Unstable Angina with Tachycardia: Clinical and Therapeutic Implications
Unstable angina with tachycardia: Clinical and therapeutic implications We prospectively evaluated 19 patients with prolonged chest pain not evolving to myocardiai infarction and accompanied with reversible ST-T changes and tachycardia (heart rate >lOO beats/min) in order to correlate heart rate reduction with ischemic electrocardiographic (ECG) changes. Fourteen patients (74%) received previous long-term combined treatment with nifedipine and nitrates. Continuous ECG monitoring was carried out until heart rate reduction and at least one of the following occurred: (1) relief of pain or (2) resolution of ischemic ECG changes. The study protocol consisted of carotid massage in three patients (IS%), intravenous propranolol in seven patients (37%), slow intravenous amiodarone infusion in two patients (lo%), and intravenous verapamil in four patients (21%) with atrial fibrillation. In three patients (16%) we observed a spontaneous heart rate reduction on admission. Patients responded with heart rate reduction from a mean of 126 + 10.4 beats/min to 64 k 7.5 beats/min (p < 0.005) and an ST segment shift of 4.3 k 2.13 mm to 0.89 k 0.74 mm (p < 0.005) within a mean interval of 13.2 + 12.7 minutes. Fifteen (79%) had complete response and the other four (21%) had partial relief of pain. A significant direct correlation was observed for heart rate reduction and ST segment deviation (depression or elevation) (f = 0.7527 and 0.8739, respectively). These patients represent a unique subgroup of unstable angina, in which the mechanism responsible for ischemia is excessive increase in heart rate. Conventional vasodilator therapy may be deleterious, and heart rate reduction Is mandatory. -
Tachycardia (Fast Heart Rate)
Tachycardia (fast heart rate) Working together to improve the diagnosis, treatment and quality of life for all those aff ected by arrhythmias www.heartrhythmalliance.org Registered Charity No. 1107496 Glossary Atrium Top chambers of the heart that receive Contents blood from the body and from the lungs. The right atrium is where the heart’s natural pacemaker (sino The normal electrical atrial node) can be found system of the heart Arrhythmia An abnormal heart rhythm What are arrhythmias? Bradycardia A slow heart rate, normally less than 60 beats per minute How do I know what arrhythmia I have? Cardiac Arrest the abrupt loss of heart function, breathing and consciousness Types of arrhythmia Cardioversion a procedure used to return an abnormal What treatments are heartbeat to a normal rhythm available to me? Defi brillation a treatment for life-threatening cardiac arrhythmias. A defibrillator delivers a dose of electric current to the heart Important information This booklet is intended for use by people who wish to understand more about Tachycardia. The information within this booklet comes from research and previous patients’ experiences. The booklet off ers an explanation of Tachycardia and how it is treated. This booklet should be used in addition to the information given to you by doctors, nurses and physiologists. If you have any questions about any of the information given in this booklet, please ask your nurse, doctor or cardiac physiologist. 2 Heart attack A medical emergency in which the blood supply to the heart is blocked, causing serious damage or even death of heart muscle Tachycardia Fast heart rate, more than 100 beats per minute Ventricles The two lower chambers of the heart. -
Original Article Reversibility of Both Sinus Node Dysfunction and Reduced HCN4 Mrna Expression Level in an Atrial Tachycardia
Int J Clin Exp Pathol 2016;9(8):8526-8531 www.ijcep.com /ISSN:1936-2625/IJCEP0023042 Original Article Reversibility of both sinus node dysfunction and reduced HCN4 mRNA expression level in an atrial tachycardia pacing model of tachycardia-bradycardia syndrome in rabbit hearts Zhisong Chen1*, Bing Sun1*, Gary Tse2, Jinfa Jiang1, Wenjun Xu1 1Department of Cardiovascular Diseases, Tongji Hospital of Tongji University, Shanghai, P. R. China; 2School of Biomedical Sciences, Li Ka Shing Faculty of Medicine, University of Hong Kong, Hong Kong, P. R. China. *Equal contributors. Received December 31, 2015; Accepted March 17, 2016; Epub August 1, 2016; Published August 15, 2016 Abstract: Objective: The aim of this study was to investigate potential reversible changes in sinus node function and mRNA expression levels of hyperpolarization-activated, cyclic nucleotide-gated ion channel subunit 4 (HCN4) in a tachycardia pacing model in rabbits. Methods: A total of 45 adult New Zealand white rabbits were randomized into the following three groups (n=15): pacing only, pacing-recovery and control. Following open thoracotomy, temporary pacing leads were attached to the right atrium. In the pacing only group, rapid atrial pacing was initiated at a rate of 350 stimuli per minute for 8 hours a day, continuing for 7 days. In the pacing-recovery group, the same pacing protocol was delivered, but pacing was then stopped for 7 days. In the control group, no tachycardia pacing was de- livered. The following parameters were measured before and after intervention, and compared between the groups: resting heart rate, intrinsic heart rate (measured after metoprolol and atropine administration) and corrected sinus node recovery time (CSNRT). -
Aberrated Supraventricular Tachycardia Associated with Neonatal Fever and COVID-19 Infection Kali a Hopkins ,1 Gregory Webster2
Case report BMJ Case Rep: first published as 10.1136/bcr-2021-241846 on 30 April 2021. Downloaded from Aberrated supraventricular tachycardia associated with neonatal fever and COVID-19 infection Kali A Hopkins ,1 Gregory Webster2 1Department of Paediatrics, SUMMARY Her blood pressure was 87/63 mm Hg and her Northwestern University A 9-day- old girl presented during the 2020 SARS- peripheral oxygen saturation was 97%. Her lungs Feinberg School of Medicine, CoV-2 pandemic in wide-complex tachycardia with were clear to auscultation. She had no murmur or Chicago, Illinois, USA acute, symptomatic COVID-19 infection. Because the hepatosplenomegaly, and her capillary refill was 2 s. 2Division of Cardiology, Ann potential cardiac complications of COVID-19 were Three- lead telemetry revealed a regular, WCT. Her and Robert H Lurie Children’s mother, the primary caregiver, was acutely symp- Hospital of Chicago, Chicago, unknown at the time of her presentation, we chose Illinois, USA to avoid the potential risks of haemodynamic collapse tomatic with suspected COVID-19 illness (later associated with afterload reduction from adenosine. verified by PCR) and other household contacts Correspondence to Instead, a transoesophageal pacing catheter was placed. were COVID-19 positive. The infant had no family Dr Kali A Hopkins; Supraventricular tachycardia (SVT) with an aberrated history of sudden death or rhythm disorders. kahopkins@ luriechildrens. org QRS morphology was diagnosed and the catheter was used to pace-terminate tachycardia. This presentation INVESTIGATIONS Accepted 18 April 2021 illustrates that the haemodynamic consequences of a The initial 12- lead ECG recorded regular tachy- concurrent infection with largely unknown neonatal cardia at 215 beats per minute (figure 1). -
Acute Non-Specific Pericarditis R
Postgrad Med J: first published as 10.1136/pgmj.43.502.534 on 1 August 1967. Downloaded from Postgrad. med. J. (August 1967) 43, 534-538. CURRENT SURVEY Acute non-specific pericarditis R. G. GOLD * M.B., B.S., M.RA.C.P., M.R.C.P. Senior Registrar, Cardiac Department, Brompton Hospital, London, S.W.3 Incidence neck, to either flank and frequently through to the Acute non-specific pericarditis (acute benign back. Occasionally pain is experienced on swallow- pericarditis; acute idiopathic pericarditis) has been ing (McGuire et al., 1954) and this was the pre- recognized for over 100 years (Christian, 1951). In senting symptom in one of our own patients. Mild 1942 Barnes & Burchell described fourteen cases attacks of premonitory chest pain may occur up to of the condition and since then several series of 4 weeks before the main onset of symptoms cases have been published (Krook, 1954; Scherl, (Martin, 1966). Malaise is very common, and is 1956; Swan, 1960; Martin, 1966; Logue & often severe and accompanied by listlessness and Wendkos, 1948). depression. The latter symptom is especially com- Until recently Swan's (1960) series of fourteen mon in patients suffering multiple relapses or patients was the largest collection of cases in this prolonged attacks, but is only partly related to the country. In 1966 Martin was able to collect most length of the illness and fluctuates markedly from of his nineteen cases within 1 year in a 550-bed day to day with the patient's general condition. hospital. The disease is thus by no means rare and Tachycardia occurs in almost every patient at warrants greater attention than has previously some stage of the illness. -
What Is Atrial Fibrillation?
ANSWERS Cardiovascular Conditions by heart What Is Atrial Fibrillation? Normally, your heart contracts and relaxes to a regular beat. Certain cells in your heart, called the sinus node, make electrical The illustrations above show normal conduction and contraction. signals that cause the heart to contract and pump blood. These electrical signals can be recorded using an electrocardiogram, or Sinus node ECG. Your doctor can read your ECG to find out if the electrical signals are normal. Left atrium In atrial fibrillation, or AFib, the heart’s Right atrium two small upper chambers (atria) beat irregularly and too fast, quivering instead of contracting properly. With atrial fibrillation, random electrical activity During AFib, some blood may not be interrupts the normal pumped efficiently from the atria into the conduction rhythm. ventricles. Blood that’s left behind can pool This prevents the atria from in the atria and form blood clots. properly contracting. How do I know I have atrial fibrillation? The risk of stroke is about five times higher in people with AFib. This is because blood can pool in the atria and blood Some people with AFib don’t have symptoms. Some of the clots can form. symptoms are: • Fast, irregular heartbeat What can be done to correct AFib? • Heart palpitations (rapid “flopping” or “fluttering” feeling in the chest) Treatment options may include one or more of the following: • Feeling lightheaded or faint • Medication to help slow your heart rate, such as beta • Chest pain or pressure blockers, certain calcium channel blockers or digoxin • Shortness of breath, especially when lying down • Medication to restore normal heart rhythm, such as • Tiring more easily (fatigue) beta blockers or antiarrhythmics • Procedures to stop or control the electrical impulses Can AFib lead to other problems? causing the AFib, such as electrical cardioversion or catheter ablation You can live with and manage AFib. -
Accuracy of the Single Cycle Length Method for Calculation of Aortic Effective Orifice Area in Irregular Heart Rhythms
AORTIC STENOSIS Accuracy of the Single Cycle Length Method for Calculation of Aortic Effective Orifice Area in Irregular Heart Rhythms Kerry A. Esquitin, MD, Omar K. Khalique, MD, Qi Liu, MD, Susheel K. Kodali, MD, Leo Marcoff, MD, Tamim M. Nazif, MD, Isaac George, MD, Torsten P. Vahl, MD, Martin B. Leon, MD, and Rebecca T. Hahn, MD, New York, New York; and Morristown, New Jersey Introduction: In irregular heart rhythms, echocardiographic calculation of aortic effective orifice area (EOA) re- quires averaging measurements from multiple cardiac cycles. Whether a single cycle length method can be used to calculate aortic EOA in aortic stenosis with nonsinus rhythms is not known. Methods: Transthoracic echocardiograms of 100 patients with aortic stenosis and either atrial fibrillation (AF) or frequent ectopy (FE) were retrospectively reviewed. The aortic valve velocity time integral (VTIAV) and the left ven- tricular outflow tract VTI (VTILVOT) were measured by two methods: the standard method (averaging multiple beats) and the single cycle length method. The latter matches the R-R intervals for VTIAV and VTILVOT.Stroke volume, EOA, and Doppler velocity index were calculated by both methods in all patients. The single cycle length method was used for short and long R-R cycles in AF and for postectopic beats (long R-R cycles) in FE. Results: In AF, long R-R cycles resulted in larger stroke volumes (73 6 21 vs 63 6 18 mL; P # .0001) but no difference in EOA (0.84 6 0.27 vs 0.82 6 0.27 cm2; P = .11), whereas short R-R cycles resulted in smaller stroke volumes (55 6 18 vs 63 6 18 mL, P # .0001) but a larger EOA (0.86 6 0.28 vs 0.82 6 0.27 cm2; P = .01).