DOCSLIB.ORG

Chronic Recurrent Ventricular Tachycardia

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Chronic Recurrent Ventricular Tachycardia LONDON, SATURDAY 8 SEPTEMBER 1979 BRITISH Br Med J: first published as 10.1136/bmj.2.6190.561 on 8 September 1979. Downloaded from MEDICAL JOURNAl ai Chronic recurrent ventricular tachycardia Chronic recurrent ventricular tachycardia is always a serious In other cases the initiating ventricular beat occurs after full arrhythmia since it may deteriorate into fatal ventricular inscription of the T wave of the preceding sinus beat, and the fibrillation. Chronic recurrent ventricular tachycardia at a complexes vary in form from beat to beat. One type is known rate of 250 beats/minute may cause syncope, but at a rate of as Torsades de Pointe because of progressive and cyclical 100-150 may not cause any symptoms. Often, but not always, twisting in the electrical axis of each complex. This form of a signal to serious underlying heart disease, the arrhythmia ventricular tachycardia is often self-terminating, but also may recur or may disappear as mysteriously as it came. particularly likely to deteriorate into ventricular fibrillation. Treatment usually demands long-term drugs, and control may It may occur as a complication of drugs that prolong re- prove difficult. polarisation, or may signify a metabolic abnormality, par- Chronic recurrent ventricular tachycardia may complicate ticularly potassium and magnesium deficiency.' A prolonged ischaemic heart disease and almost any heart-muscle disease. QT interval is familial in the cardioauditory syndrome of It is more likely when the QT interval is prolonged, when Jervell and Lange-Nielson in which ventricular tachycardia both recurrence and conversion to ventricular fibrillation may or ventricular fibrillation may occur.2 This condition may be be encouraged by quinidine-like antiarrhythmic drugs that perplexing because the QT prolongation is not always present http://www.bmj.com/ further prolong repolarisation. Chronic recurrent ventricular on the ECG, though it may often be recorded after exercise. tachycardia seems to have become more common-possibly as Emergency treatment of ventricular tachycardia is usually a result of increased survival of patients after myocardial by intravenous lignocaine, but DC counter shock is often infarction. required. Lignocaine should be avoided when the arrhythmia Chronic recurrent ventricular tachycardia may be the first complicates a prolonged QT interval. In such cases the heart sign ofheart disease. The symptoms depend on the ventricular rate should be accelerated by isoprenaline or temporary pacing. rate and the underlying cardiac disorder, patients complaining The aim, often impossible, is to identify and correct any of blackouts, angina, or palpitations, but they are often un- underlying cardiac fault. Serum potassium concentrations on 26 September 2021 by guest. Protected copyright. aware of any change in heart rate. Repeated Holter ECG tape should be measured and then kept as close as possible to recording may help to detect the arrhythmia in patients with 5 mmol(mEq)/l. Treatment must be continued with anti- fainting attacks or other poorly defined symptoms; monitoring arrhythmic drugs, whose initial selection is usually empirical. is also valuable in assessing the response to treatment. When These drugs are often only partially effective, and, reflecting chronic recurrent ventricular tachycardia is associated with this, the prognosis of chronic recurrent ventricular tachycardia ischaemia it tends to be provoked by tachycardia, so that is poor. Careful trials of antiarrhythmic drugs are time con- exercise or emotion may then precipitate both the arrhythmia suming, and the patient must be in hospital for his safety and and angina. In other cases the arrhythmia may occur at any to measure the response. Because of the deficiencies of drug time. Sudden, unexpected death is a feature of hypertrophic treatment, purpose-built implanted pacemakers,3 and surgical cardiomyopathy, but may be prevented if an occult ventricular excision or exclusion of arrhythmogenic foci have been tried.4 arrhythmia is detected and treated. Chronic recurrent ventri- Classically chronic recurrent ventricular tachycardia complicat- cular tachycardia is also common in dilated (congestive) ing a ventricular aneurysm has been an indication for excising cardiomyopathy, when it may bring on heart failure. If this, but any ventricular scar, either visible or theoretical, may tachycardia is prolonged cardiac failure may develop even in be equally culpable. These scars can be located by ECG map- subjects without organic heart disease. ping at operation. Whether excision, encirclement, or cryo- The appearance of ventricular tachycardia on the electro- therapy is used, however, a further scar results and so re- cardiogram varies. Typically the arrhythmia starts with a pre- currences of chronic recurrent ventricular tachycardia are mature ventricular beat occurring on, or close to, the T wave possible. of the preceding sinus beat. The premature beat initiates a These difficulties have led to an aggressive and invasive self-sustaining tachycardia with uniformly wide and bizarre approach, where ventricular tachycardia is induced by elec- QRS complexes, whose initial inscription is slow, with a mean trode stimulation of the heart during catheterisation and the axis different from that of the normal complexes. effect of drugs can then be studied.5 These studies may take C BRITISH MEDICAL JOURNAL 1979. All reproduction rights reserved. NO 6190 PAGE 561 562 BRITISH MEDICAL JOURNAL 8 SEPTEMBER 1979 several days.6-9 Induction of supraventricular arrhythmia has in which patients with soft-tissue sarcomas of the arms or legs Br Med J: first published as 10.1136/bmj.2.6190.561 on 8 September 1979. Downloaded from been employed for some years to assess drug effects, but were randomised to receive either amputation or a limb- electrophysiological studies of ventricular tachycardia have sparing operation and postoperative radiotherapy. All patients hitherto been less informative. Moreover, the deliberate in- received adjuvant chemotherapy (adriamycin, cyclophospha- duction ofa potentially fatal cardiac arrhythmia is a frightening mide, and methotrexate). So far local recurrence has been procedure. To induce these arrhythmias multiple multipolar reported in only one ofthe 16 patients treated by limb-sparing electrode catheters are positioned in the heart (usually through surgery and radiotherapy, and there have been no local the femoral veins) for the delivery, by programmed electrical recurrences in the group treated with amputation (10 patients). stimulation, ofsingle or multiple extra stimuli to chosen points Comparison of the results in all 49 patients in the study (with at predetermined phases of the cardiac cycle. It is usually limb, trunk, and head and neck lesions) with historical controls possible to induce ventricular tachycardia similar in morpho- treated with radical surgery alone shows improvements in both logy and rate to the spontaneously occurring arrhythmia, and disease-free survival and overall survival. So far too few patients then to terminate it by similar means. Techniques for inducing have relapsed to distinguish between the two randomised ventricular tachycardia include rapid atrial or ventricular pacing, subgroups. bursts ofextra stimuli, and combinations ofthese. The arrhyth- Morton et al5 used a regimen which included radiotherapy mia is usually terminated by a single or short burst of extra and intra-arterial adriamycin (without proximal vascular stimuli, or by ventricular or atrial overdrive at rapid rates. compression) with local resection. Postoperatively some Thus the mechanism and origin of ventricular tachycardia can patients also received chemotherapy, with or without immuno- be characterised, and serial electrophysiological studies per- therapy. Of the 17 patients treated with surgery alone, 11 formed after giving drugs. Patients selected for the prolonged have had local recurrence and required amputation. None of studies have usually been refractory to medical treatment. the five who had postoperative radiotherapy have had local Though induction of ventricular arrhythmias is still con- recurrences. Of the eight patients who received preoperative tentious, and possible only in specialist units, the speedier intra-arterial adriamycin, five had shrinkage of tumour, but formulation of an optimum drug regimen for the individual by the limb was salvaged in only one patient. Thirteen of 14 these means would represent an important advance. patients treated with intra-arterial adriamycin and radiotherapy had sufficient shrinkage of the tumour to allow local resection. IKrikler, D M, and Curry, P V L, British Heart Journal, 1976, 38, 117. this 2 Jervell, A, and Lange-Nielsen, F, American Heart Journal, 1957, 54, 59. All patients treated with combined approach have 3Moss, A J, and Rivers, R J, Circulation, 1974, 50, 942. remained free of local or distant recurrence for four to 34 4 Spurrell, R A J, et al, British Heart Journal, 1975, 37, 115. months. When these preliminary results are compared with 5 Wellens, H J J, Lie, K I, and Durrer, D, Circulation, 1974, 49, 647. 6 Mason, J W, and Winkle, R A, Circulation, 1978, 58, 971. those achieved in the unrandomised group of 17 patients 7Horowitz, L N, et al, Circulation, 1978, 58, 986. managed by surgery alone, the combined modality approach 8 Scheinman, M M, Circulation, 1978, 58, 998. seems superior. 9 Fisher, J D, Circulation, 1978, 58, 1000. Karakousis et a18 have recently reported the results of concomitant radiotherapy
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]