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Guidelines on the Diagnosis and Management of Pericardial
European Heart Journal (2004) Ã, 1–28 ESC Guidelines Guidelines on the Diagnosis and Management of Pericardial Diseases Full Text The Task Force on the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology Task Force members, Bernhard Maisch, Chairperson* (Germany), Petar M. Seferovic (Serbia and Montenegro), Arsen D. Ristic (Serbia and Montenegro), Raimund Erbel (Germany), Reiner Rienmuller€ (Austria), Yehuda Adler (Israel), Witold Z. Tomkowski (Poland), Gaetano Thiene (Italy), Magdi H. Yacoub (UK) ESC Committee for Practice Guidelines (CPG), Silvia G. Priori (Chairperson) (Italy), Maria Angeles Alonso Garcia (Spain), Jean-Jacques Blanc (France), Andrzej Budaj (Poland), Martin Cowie (UK), Veronica Dean (France), Jaap Deckers (The Netherlands), Enrique Fernandez Burgos (Spain), John Lekakis (Greece), Bertil Lindahl (Sweden), Gianfranco Mazzotta (Italy), Joa~o Morais (Portugal), Ali Oto (Turkey), Otto A. Smiseth (Norway) Document Reviewers, Gianfranco Mazzotta, CPG Review Coordinator (Italy), Jean Acar (France), Eloisa Arbustini (Italy), Anton E. Becker (The Netherlands), Giacomo Chiaranda (Italy), Yonathan Hasin (Israel), Rolf Jenni (Switzerland), Werner Klein (Austria), Irene Lang (Austria), Thomas F. Luscher€ (Switzerland), Fausto J. Pinto (Portugal), Ralph Shabetai (USA), Maarten L. Simoons (The Netherlands), Jordi Soler Soler (Spain), David H. Spodick (USA) Table of contents Constrictive pericarditis . 9 Pericardial cysts . 13 Preamble . 2 Specific forms of pericarditis . 13 Introduction. 2 Viral pericarditis . 13 Aetiology and classification of pericardial disease. 2 Bacterial pericarditis . 14 Pericardial syndromes . ..................... 2 Tuberculous pericarditis . 14 Congenital defects of the pericardium . 2 Pericarditis in renal failure . 16 Acute pericarditis . 2 Autoreactive pericarditis and pericardial Chronic pericarditis . 6 involvement in systemic autoimmune Recurrent pericarditis . 6 diseases . 16 Pericardial effusion and cardiac tamponade . -
Myocarditis, Pericarditis and Other Pericardial Diseases
Heart 2000;84:449–454 Diagnosis is easiest during epidemics of cox- GENERAL CARDIOLOGY sackie infections but diYcult in isolated cases. Heart: first published as 10.1136/heart.84.4.449 on 1 October 2000. Downloaded from These are not seen by cardiologists unless they develop arrhythmia, collapse or suVer chest Myocarditis, pericarditis and other pain, the majority being dealt with in the primary care system. pericardial diseases Acute onset of chest pain is usual and may mimic myocardial infarction or be associated 449 Celia M Oakley with pericarditis. Arrhythmias or conduction Imperial College School of Medicine, Hammersmith Hospital, disturbances may be life threatening despite London, UK only mild focal injury, whereas more wide- spread inflammation is necessary before car- diac dysfunction is suYcient to cause symp- his article discusses the diagnosis and toms. management of myocarditis and peri- Tcarditis (both acute and recurrent), as Investigations well as other pericardial diseases. The ECG may show sinus tachycardia, focal or generalised abnormality, ST segment eleva- tion, fascicular blocks or atrioventricular con- Myocarditis duction disturbances. Although the ECG abnormalities are non-specific, the ECG has Myocarditis is the term used to indicate acute the virtue of drawing attention to the heart and infective, toxic or autoimmune inflammation of leading to echocardiographic and other investi- the heart. Reversible toxic myocarditis occurs gations. Echocardiography may reveal segmen- in diphtheria and sometimes in infective endo- -
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. -
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. -
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. -
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. -
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. -
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. -
Pericardial Disease and Other Acquired Heart Diseases
Royal Brompton & Harefield NHS Foundation Trust Pericardial disease and other acquired heart diseases Sylvia Krupickova Exam oriented Echocardiography course, 4th November 2016 Normal Pericardium: 2 layers – fibrous - serous – visceral and parietal layer 2 pericardial sinuses – (not continuous with one another): • Transverse sinus – between in front aorta and pulmonary artery and posterior vena cava superior • Oblique sinus - posterior to the heart, with the vena cava inferior on the right side and left pulmonary veins on the left side Normal pericardium is not seen usually on normal echocardiogram, neither the pericardial fluid Acute Pericarditis: • How big is the effusion? (always measure in diastole) • Where is it? (appears first behind the LV) • Is it causing haemodynamic compromise? Small effusion – <10mm, black space posterior to the heart in parasternal short and long axis views, seen only in systole Moderate – 10-20 mm, more than 25 ml in adult, echo free space is all around the heart throughout the cardiac cycle Large – >20 mm, swinging motion of the heart in the pericardial cavity Pericardiocentesis Constrictive pericarditis Constriction of LV filling by pericardium Restriction versus Constriction: Restrictive cardiomyopathy Impaired relaxation of LV Constriction versus Restriction Both have affected left ventricular filling Constriction E´ velocity is normal as there is no impediment to relaxation of the left ventricle. Restriction E´ velocity is low (less than 5 cm/s) due to impaired filling of the ventricle (impaired relaxation) -
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.