The Example of Short QT Syndrome Jules C
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WPW: WOLFF-PARKINSON-WHITE Syndrome
WPW: WOLFF-PARKINSON-WHITE Syndrome What is Wolff-Parkinson-White Syndrome? Wolff-Parkinson-White Syndrome, or WPW, is named for three physicians who described a syndrome in 1930 in young people with episodes of heart racing and an abnormal pattern on their electrocardiogram (ECG or EKG). Over the next few decades, it was discovered that this ECG pattern and the heart racing was due to an extra electrical pathway in the heart. Thus, WPW is a syndrome associated with an abnormal heart rhythm, or “arrhythmia”. Most people with WPW do not have any other problems with their heart. Normally, the electrical impulses in the heart originate in the atria or top chambers of the heart and spread across the atria. The electrical impulses are then conducted to the ventricles (the pumping/bottom chambers of the heart) through a group of specialized cells called the atrioventricular node or AV node. This is usually the only electrical pathway between the atria and ventricles. In WPW, there is an additional pathway made up of a few extra cells left over from when the heart formed. The conduction of electricity through the heart causes the contractions which are the “heartbeat”. What is WPW Syndrome as opposed to a WPW ECG? A person has WPW Syndrome if they experience symptoms from abnormal conduction through the heart by the WPW pathway. Most commonly, the symptom is heart racing, or “palpitations”. The particular type of arrhythmia in WPW is called “supraventricular tachycardia” or SVT. “Tachycardia” means fast heart rate; “supraventricular” means the arrhythmia requires the cells above the ventricles to be part of the abnormal circuit. -
Clinical Study of the Acute Effects of Intravenous Nifekalant on the Defibrillation Threshold in Patients with Persistent and Paroxysmal Atrial Fibrillation
Circ J 2008; 72: 76–80 Clinical Study of the Acute Effects of Intravenous Nifekalant on the Defibrillation Threshold in Patients With Persistent and Paroxysmal Atrial Fibrillation Kaoru Okishige, MD; Hiroki Uehara, MD; Naoto Miyagi, MD; Kentarou Nakamura, MD; Kouji Azegami, MD; Hirofumi Wakimoto, MD; Kageyuki Ohba, MD; Kenzo Hirao, MD*; Mitsuo Shimabukuro, MD**; Mistuaki Isobe, MD* Background Antiarrhythmic agents are considered to have significant effects on the defibrillation energy re- quirement, so this study investigated the effects of nifekalant on defibrillation. Methods and Results Forty-two patients with persistent atrial fibrillation (AF) underwent electrical cardiover- sion via intracardiac electrode catheters prior to and after the intravenous administration of nifekalant. The suc- cess rate of the defibrillation and change in the defibrillation threshold using sequential incremental defibrillation energy deliveries was investigated. In addition, the parameters that could predict the beneficial effects of nifekalant were also assessed. Nifekalant significantly decreased the defibrillation energy requirement in 13 of the 42 cases, and nifekalant also converted AF to sinus rhythm with an identical energy to that of the last unsuccessful defib- rillation in 21 of 42 cases. The success of defibrillation seemed to be dependent on significant prolongation of the intracardiac atrial electrogram intervals during AF by the nifekalant. Conclusions Intravenous nifekalant significantly improved the electrical defibrillation efficacy in patients with persistent -
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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. -
ILCOR Guidelines 2015 for Web.Pdf
Supplement to Circulation 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations Dallas, Texas February 1–3, 2015 Editors Mary Fran Hazinski (AHA) Jerry P. Nolan (ERC) International Liaison Committee on Resuscitation (ILCOR) Editorial Board Vinay M. Nadkarni (ILCOR Co-Chair, AHA) Eddy Lang (Grade Expert, HSFC) Gavin D. Perkins (ILCOR Co-Chair, ERC) Swee Han Lim (RCA) William H. Montgomery (C2015 Consensus Ian K. Maconochie (ERC) Conference Coordinator, AHA) Peter T. Morley (Evidence Monica E. Kleinman (Conference Evaluation Expert, ANZCOR) Co-Chair, AHA) Nikolaos I. Nikolaou (ERC) Maaret Castren (Conference Co-Chair, ERC) Robert W. Neumar (AHA) Richard Aickin (COI Co-Chair, ERC) Jeffrey M. Perlman (AHA) John E. Billi (COI Co-Chair, AHA) Eunice M. Singletary (AHA) Farhan Bhanji (HSFC) Jasmeet Soar (ERC) Clifton W. Callaway (AHA) Andrew H. Travers (HSFC) Allan R. de Caen (HSFC) Michelle Welsford (HSFC) Judith C. Finn (ANZCOR) Jonathan Wyllie (ERC) Lana M. Gent (AHA) David A. Zideman (ERC) Participating ILCOR Resuscitation Councils 2015 ILCOR Honorees Acknowledgments American Heart Association (AHA) Tom P. Aufderheide Alicia G. Pederson Australian and New Zealand Committee on Karl B. Kern Russell E. Griffin Resuscitation (ANZCOR) Vinay M. Nadkarni Jose Maria E. Ferrer European Resuscitation Council (ERC) Jerry P. Nolan Mandy L. Cootes Heart and Stroke Foundation of Canada (HSFC) Roger D. White Kara Robinson InterAmerican Heart Foundation (IAHF) Jody Hundley Resuscitation Council of Asia (RCA) Sandra Iverson Resuscitation Council of Southern Africa (RCSA) Joe Loftin We acknowledge the considerable contributions made by the late Professor Ian Jacobs, PhD, to this 2015 International Consensus on CPR Science. -
The In¯Uence of Medication on Erectile Function
International Journal of Impotence Research (1997) 9, 17±26 ß 1997 Stockton Press All rights reserved 0955-9930/97 $12.00 The in¯uence of medication on erectile function W Meinhardt1, RF Kropman2, P Vermeij3, AAB Lycklama aÁ Nijeholt4 and J Zwartendijk4 1Department of Urology, Netherlands Cancer Institute/Antoni van Leeuwenhoek Hospital, Plesmanlaan 121, 1066 CX Amsterdam, The Netherlands; 2Department of Urology, Leyenburg Hospital, Leyweg 275, 2545 CH The Hague, The Netherlands; 3Pharmacy; and 4Department of Urology, Leiden University Hospital, P.O. Box 9600, 2300 RC Leiden, The Netherlands Keywords: impotence; side-effect; antipsychotic; antihypertensive; physiology; erectile function Introduction stopped their antihypertensive treatment over a ®ve year period, because of side-effects on sexual function.5 In the drug registration procedures sexual Several physiological mechanisms are involved in function is not a major issue. This means that erectile function. A negative in¯uence of prescrip- knowledge of the problem is mainly dependent on tion-drugs on these mechanisms will not always case reports and the lists from side effect registries.6±8 come to the attention of the clinician, whereas a Another way of looking at the problem is drug causing priapism will rarely escape the atten- combining available data on mechanisms of action tion. of drugs with the knowledge of the physiological When erectile function is in¯uenced in a negative mechanisms involved in erectile function. The way compensation may occur. For example, age- advantage of this approach is that remedies may related penile sensory disorders may be compen- evolve from it. sated for by extra stimulation.1 Diminished in¯ux of In this paper we will discuss the subject in the blood will lead to a slower onset of the erection, but following order: may be accepted. -
Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: the Role of Multimodality Imaging to Detect High-Risk Features
diagnostics Review Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: The Role of Multimodality Imaging to Detect High-Risk Features Anna Giulia Pavon 1,2,*, Pierre Monney 1,2,3 and Juerg Schwitter 1,2,3 1 Cardiac MR Center (CRMC), Lausanne University Hospital (CHUV), 1100 Lausanne, Switzerland; [email protected] (P.M.); [email protected] (J.S.) 2 Cardiovascular Department, Division of Cardiology, Lausanne University Hospital (CHUV), 1100 Lausanne, Switzerland 3 Faculty of Biology and Medicine, University of Lausanne (UniL), 1100 Lausanne, Switzerland * Correspondence: [email protected]; Tel.: +41-775-566-983 Abstract: Mitral valve prolapse (MVP) was first described in the 1960s, and it is usually a benign condition. However, a subtype of patients are known to have a higher incidence of ventricular arrhythmias and sudden cardiac death, the so called “arrhythmic MVP.” In recent years, several studies have been published to identify the most important clinical features to distinguish the benign form from the potentially lethal one in order to personalize patient’s treatment and follow-up. In this review, we specifically focused on red flags for increased arrhythmic risk to whom the cardiologist must be aware of while performing a cardiovascular imaging evaluation in patients with MVP. Keywords: mitral valve prolapse; arrhythmias; cardiovascular magnetic resonance Citation: Pavon, A.G.; Monney, P.; Schwitter, J. Mitral Valve Prolapse, Arrhythmias, and Sudden Cardiac Death: The Role of Multimodality 1. Mitral Valve and Arrhythmias: A Long Story Short Imaging to Detect High-Risk Features. In the recent years, the scientific community has begun to pay increasing attention Diagnostics 2021, 11, 683. -
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. -
Modeling Atrial Fibrillation Using Human Embryonic Stem Cell
www.nature.com/scientificreports OPEN Modeling Atrial Fibrillation using Human Embryonic Stem Cell- Derived Atrial Tissue Received: 9 January 2017 Zachary Laksman1, Marianne Wauchop2, Eric Lin3, Stephanie Protze4, Jeehoon Lee5, Wallace Accepted: 1 June 2017 Yang6, Farzad Izaddoustdar7, Sanam Shafaattalab8, Lior Gepstein9, Glen F. Tibbits 10, Published: xx xx xxxx Gordon Keller11 & Peter H. Backx12 Since current experimental models of Atrial Fibrillation (AF) have significant limitations, we used human embryonic stem cells (hESCs) to generate an atrial-specific tissue model of AF for pharmacologic testing. We generated atrial-like cardiomyocytes (CMs) from hESCs which preferentially expressed atrial-specific genes, and had shorter action potential (AP) durations compared to ventricular-like CMs. We then generated confluent atrial-like CM sheets and interrogated them using optical mapping techniques. Atrial-like CM sheets (~1 cm in diameter) showed uniform AP propagation, and rapid re- entrant rotor patterns, as seen in AF could be induced. Anti-arrhythmic drugs were tested on single atrial-like CMs and cell sheets. Flecainide profoundly slowed upstroke velocity without affecting AP duration, leading to reduced conduction velocities (CVs), curvatures and cycle lengths of rotors, consistent with increased rotor organization and expansion. By contrast, consistent with block of rapid delayed rectifier +K currents (Ikr) and AP prolongation in isolated atrial-like CMs, dofetilide prolonged APs and reduced cycle lengths of rotors in cell sheets without affecting CV. In conclusion, using our hESC-derived atrial CM preparations, we demonstrate that flecainide and dofetilide modulate reentrant arrhythmogenic rotor activation patterns in a manner that helps explain their efficacy in treating and preventing AF. -
Effects of Nifekalant Injected Into the Pericardial Space on the Transmural Dispersion of Repolarization in Pig
Showa Univ J Med Sci 19(3), 123 135, September 2007 Original Effects of Nifekalant Injected into the Pericardial Space on the Transmural Dispersion of Repolarization in Pig Hiroyuki ITo, Taku ASANO, Youichi KOBAYASHI, Tatsuya ONUKI, Fumito MwosHI, Taka-aki MATSUYAMA, Yoshino MINOURA, Norikazu WATANABE, Mitsuharu KAWAMURA, Kaoru TANNO and Takashl KATAGIRI Abstract: Transmural dispersion of repolarization (TDR) has been implicated in the onset of ventricular arrhythmia. We investigated the effects of nifekalant (NIF) injected into the pericardial space on TDR and T wave in pig. We injected 50 or 100 mg of NIF into the pericardial space of 11 pigs, and measured the effective refractory period (ERP) between the endocardial and epicardial myocardial cells, as well as QT time and QT peak-end as an index of TDR and T waveforms, respectively. TDR decreased from 56•} 10 msec to 44•}8 msec (P < 0.01), 5.1 min after injection of 100 mg of NIF, although the QTc did not change. At a later time, QTc increased from 457 •} 44 msec before injection to 540•}49 msec (P < 0.01) and TDR recovered to the control level. When 50 mg of NIF was injected, the T wave amplitude decreased from 0.433 •}0.301 mV before injection to 0.107•}0.192 mV (P < 0.01) at 10 min after injection ; 100 mg of NIF caused the T wave amplitude to decrease more rapidly, reaching a negative value at 4.5 min after injection. Injecting NIF into the pericardial space altered ERP, QT, and T waveform, and also decreased TDR. -
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. -
Basic Arrhythmia Review Guide-Advanced
BASIC ARRHYTHMIA REVIEW GUIDE ADVANCED The following study guide provides a review of information covered in the basic arrhythmia competency. Preparation with this guide will help to achieve success on the exam. Sample questions and websites are provided at the end of this guide. DESCRIPTION OF THE HEART The adult heart is a muscular organ weighing less than a pound and about the size of a clenched fist. It lies between the right and Left left lung in an area called the mediastinal cavity behind the sternum of the breast bone. Approximately two-thirds of the heart Atrium lies to the left of the sternum and one-third to the right of the sternum. Right HEART MUSCLES Atrium The heart is composed of three layers each with its own special function. The outermost layer is called the pericardium, essentially a sac around the heart. The middle and thickest layer of the heart is called the Left myocardium. This layer contains all the atrial and ventricular Ventricle muscle fibers needed for contraction as well as the blood supply Right and electrical conduction system. Ventricle The innermost layer of the heart is the endocardium and is composed of endothelium and connective tissue. Any disruption or injury to this endothelium can lead to infection, which in turn can cause valve damage, sepsis, or death. CHAMBERS A normal human heart contains four separate chambers: right atrium, left atrium, right ventricle, and left ventricle. The right and left sides of the heart are divided by a septum. The right atrium (RA) receives oxygen-poor (venous) blood from the body’s organs via the superior and inferior vena cava (SVC and IVC). -
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.