DOCSLIB.ORG

Cardiac Characteristics in the Premature Ventricular Contraction Patients with Or Without Ventricular Tachycardia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Cardiac Characteristics in the Premature Ventricular Contraction Patients with Or Without Ventricular Tachycardia Int J Clin Exp Med 2018;11(6):6106-6112 www.ijcem.com /ISSN:1940-5901/IJCEM0064109 Original Article Cardiac characteristics in the premature ventricular contraction patients with or without ventricular tachycardia Yafen Su1*, Meng Xia2,3*, Junxian Cao2, Qianping Gao2 1Ambulatory Electrocardiogram Room, The First Affiliated Hospital of Harbin Medical University, China; 2Unit of Cardiology, The First Affiliated Hospital of Harbin Medical University, China; 3Unit of Cardiology, Liaoyang Central Hospital, China. *Equal contributors. Received August 21, 2017; Accepted March 22, 2018; Epub June 15, 2018; Published June 30, 2018 Abstract: Background/Aims: Frequent (sustained) premature ventricular contractions (PVCs) lead to ventricu- lar tachycardia (VT), which triggers ventricular fibrillation and sudden cardiac death. The cardiac characteristics and risk prediction in frequent/sustained PVC patients with or without VT have been still in need of investigation. Methods: The data from patients with frequent PVCs via 24 h ambulatory electrocardiogram (ECG) monitor were collected at the Department of Cardiology in the First Affiliated Hospital of Harbin Medical University from January 1, 2012 to August 31, 2015. Total 342 patients were grouped into VT group (n=136) and Non-VT group (n=206) based on the presence or absence of VT. Cardiac functional examination and blood tests were carried out on the second day of admission. Independent risk factors related to the occurrence of VT were identified. The receiver operating characteristic (ROC) curves was established to evaluate the accuracy of the risk factors and VT. Results: The baseline characteristics were similar between the two groups. The blood potassium, extensive PVC burden, left ventricular ejection fraction (LVEF), PVC couplets, and alcohol consumption were associated with the occurrence of VT. Of them, the occurrence of PVC couplets was an independent high risk factor for the development of VT in the patients with frequent PVCs. Based on the weight of these risk factors for the occurrence of VT, a simple scoring method for VT prediction was set up in this study. The area under curve (AUC) for receiver operating characteristic (ROC) curves of the new scores resulted from the scoring method was 0.8874, indicating a valuable predictor for VT occurrence. Conclusion: The PVC couplets is an independent high risk factor for the development of VT in the patients with frequent PVCs. Keywords: Sudden cardiac death, ventricular tachycardia, premature ventricular contractions, left ventricular ejec- tion fraction, electrocardiogram Introduction structural cardiopathy such as coronary artery disease (CAD), aortic stenosis, cardiomyopathy The premature ventricular contractions (PVCs) and electrolyte problem. The electrical events are early depolarization of the myocardium of the heart detected with the ECG allow the caused by an electrical impulse or ectopic PVC to be easily distinguished from a normal rhythm from any part of the ventricles, includ- heart beat. PVCs can be observed in both ing the ventricular septum, before the sinoatrial healthy people and patients with or without impulse has reached the ventricles. According structural cardiopathy [2, 3]. Frequent PVCs, to the frequency of ventricular premature beats also called sustained PVCs, is a risk factor that (VPB), PVCs can be divided into sporadic and leads to ventricular tachycardia. frequent [1]. Sporadic PVCs are, also called functional premature beats, defined as less Ventricular tachycardia (VT) is the myocardial than 6 pules/min, which can occur in healthy arrhythmias under His bundle branch and myo- people; while frequent PVCs, defined as more cardial conduction fiber. Wellens [4] defined VT than 6 pules/min, can occur in patients with as more than 100 beats/min, and three or more Cardiac characteristics in the premature ventricular contractions patients Table 1. Basic characteristics and medical history of the two First Affiliated Hospital of Harbin groups (n (%)) Medical University from January 1, Parameter VT (n=136) Non-VT (n=206) P 2012 to August 31, 2015. Inclusion criteria for the study were: 1) with Ages (years), mean ± SD 58.10 ± 13.50 56.44 ± 15.17 0.300 a more than 30-beat of ventricular Male 70 (51.47) 83 (40.29) 0.042 premature per hour; 2) the frequ- Smoking 44 (32.35) 56 (27.18) 0.304 ency of PVCs ranged from 746 to Drinking alcohol 38 (27.94) 32 (15.53) 0.005 47083 per 24 h. Exclusion criteria CAD 54 (39.71) 94 (45.63) 0.279 were: 1) pulmonary heart disease, OMI 11 (8.09) 7 (3.40) 0.057 severe dysfunction of kidney and Hypertension 45 (33.09) 83 (40.29) 0.178 liver, rheumatic disease, and tu- Diabetes 20 (14.71) 24 (11.65) 0.409 mor: 2) receiving the treatment with digitalis, quinidine and tricyclic DCM 48 (35.29) 11 (5.34) < 0.001 antidepressant. The 342 patients Alcoholic myocardiopathy 5 (3.68) 0 (0.00) 0.021 were assigned into VT group (136) ICM 18 (13.24) 6 (2.91) < 0.001 and non-VT group (206) based on Valvular heart disease 4 (2.94) 4 (1.94) 0.816 the presence or absence of VT. The HCM 1 (0.74) 0 (0.00) 0.398 study was approved by the Ethical Tachycardiomyopathy 1 (0.74) 0 (0.00) 0.398 Committee of Institutional Review VT: ventricular tachycardia, CAD: coronary artery disease, OMI: old myocar- Board at the First Affiliated Hospital dial infarction, DCM: Dilated Cardiomyopathy, ICM: ischemic cardiomyopathy, of Harbin Medical University. HCM: hypertrophic cardiomyopathy. Information collection consecutive spontaneous PVCs. Six or more The baseline information was collected at ad- rapid ventricular beats (frequency > 100/min) mission, including gender, age, blood pressure, are considered as persistent VT (longer than and heart rate. Medical history included hyper- 30 seconds), while less than 6 beats as non- tension, coronary artery disease (CAD), dilated persistent VT (episodes less than 30 seconds). cardiomyopathy (DCM), ischemic cardiomyopa- Persistent VT is very dangerous, as it can trig- thy (ICM), smoking and drinking (alcohol). Heart ger ventricular fibrillation and sudden cardiac function examination and blood tests were car- death. ried out on the second day of hospitalization. Measurements of LVEF, left ventricular end-dia- Although clinical and electrophysiological stud- stolic diameter (LVEDD), inter-ventricular septal ies have featured the different initiation pat- thickness (IVST) and left ventricular posterior terns of VT [5, 6], studies on the cardiac char- wall thickness (LVPWT) were conducted by a acteristics in the PVC patients with or without cardiology specialist through Vivid Echocardio- VT have not been reported. Therefore, this stu- gram. The left ventricular muscle mass (LVM) dy was designed to explore the predictors for was calculated according to the Devereux for- the PVC patients who may develop into VT, and mula. Ambulatory monitoring was initiated in an evaluating method based on the weights the afternoon following the hospitalization. An of these predictors on VT. Due to a higher mor- electrocardiogram specialist was responsible bidity of cardiac diseases in the northeastern for recoding and analyzing the 24 h ambulatory part of China, where there have been a longer ECG monitoring results. The total heart beats, winter and the unhealthy diet, all patients in the frequency of PVCs, PVC burden, PVC couplets, current study were from one hospital in Harbin, polymorphic and multifocal PVCs, and VT were a representative city in the northeast of China. recorded. Patients and methods Statistical analysis Patients Normally distributed variables were compared with Student’s t-test, while non-normally distrib- This was a retrospective study. The medical uted variables were compared with Wilcoxon records were collected from 342 patients with two sample test. Qualitative data were com- frequent PVCs detected via 24 h ambulatory pared by X2 test. The receiver operating charac- ECG monitoring at Department of Cardiology in teristic (ROC) curves were drawn with the proc 6107 Int J Clin Exp Med 2018;11(6):6106-6112 Cardiac characteristics in the premature ventricular contractions patients Table 2. Comparison of laboratory blood examination in the two with SAS 9.3 software and the groups (mean ± SD) statistical significance was set at VT group Non-VT group P < 0.05 for two-tailed tests. Parameter P (n=136) (n=206) Results Glucose (mmol/L) 5.80 ± 2.28 5.30 ± 1.13 0.373 Cholesterol (mmol/L) 4.40 ± 1.13 4.69 ± 1.01 0.016 Comparisons of baseline charac- TG (mmol/L) 1.50 ± 1.02 1.58 ± 0.83 0.044 teristics and blood test results LDL (mmol/L) 3.01 ± 0.93 3.18 ± 0.89 0.065 K+ (mmol/L) 4.21 ± 0.44 4.05 ± 0.38 0.001 Of the 342 enrolled patients, 130 Mg2+ (mmol/L) 0.85 ± 0.08 0.87 ± 0.09 0.076 patients (38.0%) had no structural Ca2+ (mmol/L) 2.30 ± 0.14 2.31 ± 0.16 0.093 heart diseases, while 212 (62.0%) TNI (ng/mL) 0.10 ± 0.81 0.01 ± 0.08 < 0.001 did, including CAD, DCM, ICM, CKMB (u/L) 14.39 ± 13.25 11.71 ± 10.20 0.032 hypertension and valvular heart disease. The baseline characteris- Fibrinogen (g/L) 2.71 ± 0.76 2.68 ± 0.70 0.626 tics of the patients were shown in UA (umol/L) 361.8 ± 143.2 308.7 ± 87.94 0.003 Table 1. No significant differences VT: ventricular tachycardia, TG: triglyceride, LDL: low densitylipoproteins, TNI: in age, smoking history, systolic troponinI, CKMB: creatinekinase-MB, UA: uricacid. blood pressure (SBP), and diastol- ic blood pressure (DBP) were ob- Table 3. Cardiac parameters by Doppler echocardiography and served between the two groups. ambulatory electrocardiogram (mean ± SD) However, the ratios of patients with DCM (35.29% vs 5.34%), ICM Parameter VT (n=136) Non-VT (n=206) P (13.24% vs 2.91%), alcohol drink- VPCs (beats/24 h) 11628 ± 9227 8440 ± 8520 < 0.001 ing history (27.94% vs 15.53%), Heart rates (beats/24 h) 98662 ± 15947 104732 ± 64126 0.156 and gender (male/female ratio) LVPWT (mm) 9.13 ± 1.04 9.17 ± 1.05 0.797 (51.47% vs 40.29%) were signifi- IVST (mm) 9.35 ± 1.33 9.26 ± 1.23 0.714 cantly higher in VT group than that LVEDD (mm) 59.00 ± 12.07 49.16 ± 6.67 < 0.001 in non-VT group (P < 0.05).
Load more

Recommended publications
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • What Are Premature Ventricular Contractions?
    What Are Premature Ventricular Contractions? Premature ventricular contractions (VPCs or PVCs) are irregular beats that originate from the heart’s pumping chambers (ventricles). These beats interrupt the normal regular (sinus) rhythm, and result in irregularity to the heart rhythm. Although single PVCs are not life- threatening, they may indicate the presence of underlying heart disease, or when they become more severe can cause rapid and dangerous increases in heart rate (ventricular tachycardia). WHAT CAUSES PREMATURE VENTRICULAR CONTRACTIONS? PVCs can occur secondary to a variety of causes, most concerning being cardiac disease. PVCs are most commonly seen in dogs with Dilated Cardiomyopathy, but can also occur in the later stages of disease with Myxomatous Mitral Valve Degeneration. PVCs and other ventricular arrhythmias can also with no evidence of underlying structural heart disease. The workup for PVCs can be frustrating, because PVCs can also occur secondary to conditions unrelated to the heart. Most commonly they can occur secondary to gastrointestinal disease, systemic disease, and pain. HOW ARE PREMATURE VENTRICULAR CONTRACTIONS DIAGNOSED? Most commonly, your veterinarian will hear an irregular heart rhythm and recommend an electrocardiogram (ECG) to assess the heart rhythm. The ECG will enable your veterinarian to determine whether the irregular rhythm is due to PVCs. Following this diagnosis, there are several additional recommended tests. TESTING Following this diagnosis, there are several additional recommended tests. ECHOCARDIOGRAPHY Echocardiography (heart ultrasound) is recommended to make sure that there is no evidence of structural cardiac disease causing the abnormal heart rhythm. 24-HOUR HOLTER Single PVCs usually do not require treatment, however a Holter monitor will determine whether the frequency or severity of the MONITOR PVCs warrant anti-arrhythmic medication, and make sure that there is no evidence of ventricular tachycardia, which is a life threatening heart rhythm.
    [Show full text]
  • 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.
    [Show full text]
  • Basic Rhythm Recognition
    Electrocardiographic Interpretation Basic Rhythm Recognition William Brady, MD Department of Emergency Medicine Cardiac Rhythms Anatomy of a Rhythm Strip A Review of the Electrical System Intrinsic Pacemakers Cells These cells have property known as “Automaticity”— means they can spontaneously depolarize. Sinus Node Primary pacemaker Fires at a rate of 60-100 bpm AV Junction Fires at a rate of 40-60 bpm Ventricular (Purkinje Fibers) Less than 40 bpm What’s Normal P Wave Atrial Depolarization PR Interval (Normal 0.12-0.20) Beginning of the P to onset of QRS QRS Ventricular Depolarization QRS Interval (Normal <0.10) Period (or length of time) it takes for the ventricles to depolarize The Key to Success… …A systematic approach! Rate Rhythm P Waves PR Interval P and QRS Correlation QRS Rate Pacemaker A rather ill patient……… Very apparent inferolateral STEMI……with less apparent complete heart block RATE . Fast vs Slow . QRS Width Narrow QRS Wide QRS Narrow QRS Wide QRS Tachycardia Tachycardia Bradycardia Bradycardia Regular Irregular Regular Irregular Sinus Brady Idioventricular A-Fib / Flutter Bradycardia w/ BBB Sinus Tach A-Fib VT PVT Junctional 2 AVB / II PSVT A-Flutter SVT aberrant A-Fib 1 AVB 3 AVB A-Flutter MAT 2 AVB / I or II PAT PAT 3 AVB ST PAC / PVC Stability Hypotension / hypoperfusion Altered mental status Chest pain – Coronary ischemic Dyspnea – Pulmonary edema Sinus Rhythm Sinus Rhythm P Wave PR Interval QRS Rate Rhythm Pacemaker Comment . Before . Constant, . Rate 60-100 . Regular . SA Node Upright in each QRS regular . Interval =/< leads I, II, . Look . Interval .12- .10 & III alike .20 Conduction Image reference: Cardionetics/ http://www.cardionetics.com/docs/healthcr/ecg/arrhy/0100_bd.htm Sinus Pause A delay of activation within the atria for a period between 1.7 and 3 seconds A palpitation is likely to be felt by the patient as the sinus beat following the pause may be a heavy beat.
    [Show full text]
  • PAROXYSMAL VENTRICULAR TACHYCARDIA OCCURRING in a NORMAL HEART by DAVID ROMNEY, M.B., B.Ch.(Dub.) Ex-Senior House Officer in Medicine, St
    Postgrad Med J: first published as 10.1136/pgmj.31.354.191 on 1 April 1955. Downloaded from I9I -J PAROXYSMAL VENTRICULAR TACHYCARDIA OCCURRING IN A NORMAL HEART By DAVID ROMNEY, M.B., B.Ch.(Dub.) Ex-Senior House Officer in Medicine, St. James's Hospital, Balham It is widely taught-and rightly so-that by sinus pressure will, of course, not affect the paroxysmal ventricular tachycardia is one of the rate in ventricular tachycardia. rarer arrhythmias, and is associated with grave In I953 Froment, Gallavardin and Cahen myocardial damage, with special reference to myo- offered a classification of various forms of cardial infarction. It is the least common, and paroxysmal ventricular tachycardia, and included most serious of the paroxysmal tachycardias, some case report. They described the following which contain four varieties of arrhythmia: supra- groups:- ventricular (auricular and nodal) 60 per cent.; (i) Terminal prefibrillatory ventricular tachy- auricular fibrillation, 30 per cent.; auricular flutter, cardia. 6 per cent.; and ventricular tachycardia, 4 per (ii) Curable and mild monomorphic extra- cent. systoles, with paroxysms of tachycardia. Figures from various sources (Campbell, 1947) (iii) Paroxysmal ventricular tachycardia due toby copyright. would indicate that in the latter group, four-fifths a lesion of the ventricular septum. of the cases had seriously damaged hearts. In (iv) Persistent and prolonged ventricular tachy- the remaining fifth no cause was found for the cardia developing in sound hearts, usually paroxysms. Paroxysmal ventricular tachycardia is in young subjects. more common in men than in women in the proportion of about 3.2. This arrhythmia was Case Report first identified by Sir Thomas Lewis in I909 and A married woman, aged 48, first became aware Gallavardin (1920, I921, 1922) emphasized the in 1948 of a paroxysm which caused alarm, faint- seriousness of the 'terminal ven- ness and It lasted a short pre-fibrillatory collapse.
    [Show full text]
  • The Example of Short QT Syndrome Jules C
    Hancox et al. Journal of Congenital Cardiology (2019) 3:3 Journal of https://doi.org/10.1186/s40949-019-0024-7 Congenital Cardiology REVIEW Open Access Learning from studying very rare cardiac conditions: the example of short QT syndrome Jules C. Hancox1,4* , Dominic G. Whittaker2,3, Henggui Zhang4 and Alan G. Stuart5,6 Abstract Background: Some congenital heart conditions are very rare. In a climate of limited resources, a viewpoint could be advanced that identifying diagnostic criteria for such conditions and, through empiricism, effective treatments should suffice and that extensive mechanistic research is unnecessary. Taking the rare but dangerous short QT syndrome (SQTS) as an example, this article makes the case for the imperative to study such rare conditions, highlighting that this yields substantial and sometimes unanticipated benefits. Genetic forms of SQTS are rare, but the condition may be under-diagnosed and carries a risk of sudden death. Genotyping of SQTS patients has led to identification of clear ion channel/transporter culprits in < 30% of cases, highlighting a role for as yet unidentified modulators of repolarization. For example, recent exome sequencing in SQTS has identified SLC4A3 as a novel modifier of ventricular repolarization. The need to distinguish “healthy” from “unhealthy” short QT intervals has led to a search for additional markers of arrhythmia risk. Some overlap may exist between SQTS, Brugada Syndrome, early repolarization and sinus bradycardia. Genotype-phenotype studies have led to identification of arrhythmia substrates and both realistic and theoretical pharmacological approaches for particular forms of SQTS. In turn this has increased understanding of underlying cardiac ion channels.
    [Show full text]
  • Ventricular Tachycardia Drugs Versus Devices John Camm St
    Cardiology Update 2015 Davos, Switzerland: 8-12th February 2015 Ventricular Arrhythmias Ventricular Tachycardia Drugs versus Devices John Camm St. George’s University of London, UK Imperial College, London, UK Declaration of Interests Chairman: NICE Guidelines on AF, 2006; ESC Guidelines on Atrial Fibrillation, 2010 and Update, 2012; ACC/AHA/ESC Guidelines on VAs and SCD; 2006; NICE Guidelines on ACS and NSTEMI, 2012; NICE Guidelines on heart failure, 2008; NICE Guidelines on Atrial Fibrillation, 2006; ESC VA and SCD Guidelines, 2015 Steering Committees: multiple trials including novel anticoagulants DSMBs: multiple trials including BEAUTIFUL, SHIFT, SIGNIFY, AVERROES, CASTLE- AF, STAR-AF II, INOVATE, and others Events Committees: one trial of novel oral anticoagulants and multiple trials of miscellaneous agents with CV adverse effects Editorial Role: Editor-in-Chief, EP-Europace and Clinical Cardiology; Editor, European Textbook of Cardiology, European Heart Journal, Electrophysiology of the Heart, and Evidence Based Cardiology Consultant/Advisor/Speaker: Astellas, Astra Zeneca, ChanRX, Gilead, Merck, Menarini, Otsuka, Sanofi, Servier, Xention, Bayer, Boehringer Ingelheim, Bristol- Myers Squibb, Daiichi Sankyo, Pfizer, Boston Scientific, Biotronik, Medtronic, St. Jude Medical, Actelion, GlaxoSmithKline, InfoBionic, Incarda, Johnson and Johnson, Mitsubishi, Novartis, Takeda Therapy for Ventricular Tachycardia Medical therapy Antiarrhythmic drugs Autonomic management Ventricular tachycardia Monomorphic Polymorphic Ventricular fibrillation Ventricular storms Ablation therapy Device therapy Surgical Defibrillation Catheter Antitachycardia pacing History of Antiarrhythmic Drugs 1914 - Quinidine 1950 - Lidocaine 1951 - Procainamide 1946 – Digitalis 1956 – Ajmaline 1962 - Verapamil 1962 – Disopyramide 1964 - Propranolol 1967 – Amiodarone 1965 – Bretylium 1972 – Mexiletine 1973 – Aprindine, Tocainide 1969 - Diltiazem 1975- Flecainide 1976 – Propafenone Encainide Ethmozine 2000 - Sotalol D-sotalol 1995 - Ibutilide (US) Recainam 2000 – Dofetilide US) IndecainideX Etc.
    [Show full text]
  • Common Types of Supraventricular Tachycardia: Diagnosis and Management RANDALL A
    Common Types of Supraventricular Tachycardia: Diagnosis and Management RANDALL A. COLUCCI, DO, MPH, Ohio University College of Osteopathic Medicine, Athens, Ohio MITCHELL J. SILVER, DO, McConnell Heart Hospital, Columbus, Ohio JAY SHUBROOK, DO, Ohio University College of Osteopathic Medicine, Athens, Ohio The most common types of supraventricular tachycardia are caused by a reentry phenomenon producing acceler- ated heart rates. Symptoms may include palpitations (including possible pulsations in the neck), chest pain, fatigue, lightheadedness or dizziness, and dyspnea. It is unusual for supraventricular tachycardia to be caused by structurally abnormal hearts. Diagnosis is often delayed because of the misdiagnosis of anxiety or panic disorder. Patient history is important in uncovering the diagnosis, whereas the physical examination may or may not be helpful. A Holter moni- tor or an event recorder is usually needed to capture the arrhythmia and confirm a diagnosis. Treatment consists of short-term or as-needed pharmacotherapy using calcium channel or beta blockers when vagal maneuvers fail to halt or slow the rhythm. In those who require long-term pharmacotherapy, atrioventricular nodal blocking agents or class Ic or III antiarrhythmics can be used; however, these agents should generally be managed by a cardiologist. Catheter ablation is an option in patients with persistent or recurrent supraventricular tachycardia who are unable to tolerate long-term pharmacologic treatment. If Wolff-Parkinson-White syndrome is present, expedient referral
    [Show full text]
  • 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.
    [Show full text]