scholarly journals Towards a better risk stratification for sudden cardiac death in patients with structural heart disease

2009 ◽  
Vol 17 (3) ◽  
pp. 101-106 ◽  
Author(s):  
K. Kraaier ◽  
P. M. J. Verhorst ◽  
P. F. H. M. van Dessel ◽  
A. A. M. Wilde ◽  
M. F. Scholten
ESC CardioMed ◽  
2018 ◽  
pp. 2363-2369
Author(s):  
Elena Arbelo ◽  
Josep Brugada

Cardiac channelopathies are genetically determined heart rhythm disorders affecting young individuals without structural heart disease, predisposing them to ventricular arrhythmias. Apart from avoiding triggers such as drugs, exercise, or fever, in most primary arrhythmia syndromes the only effective therapy for preventing sudden cardiac death is an implantable cardioverter defibrillator (ICD). However, in this group of a young, active population, ICD may cause a significant rate of device-related complications. Therefore, appropriate risk stratification and selective ICD indications are of utmost importance.


Heart Rhythm ◽  
2010 ◽  
Vol 7 (11) ◽  
pp. 1720-1721
Author(s):  
Peter Oosterhoff ◽  
Larisa G. Tereshchenko ◽  
Marcel A.G. van der Heyden ◽  
Raja N. Ghanem ◽  
Paul J. De Groot ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 2279-2288
Author(s):  
Tilman Maurer ◽  
William G. Stevenson ◽  
Karl-Heinz Kuck

Monomorphic ventricular tachycardia (VT) may occur in the presence or absence of structural heart disease. The standard therapy for patients with structural heart disease at high risk of sudden cardiac death due to VT is the implantable cardioverter defibrillator (ICD). While ICDs effectively terminate VT and prevent sudden cardiac death, they do not prevent recurrent episodes of VT, since the underlying arrhythmogenic substrate remains unchanged. However, shocks from an ICD increase mortality and impair quality of life. These limitations as well as continuous advancements in technology have made catheter ablation an important treatment strategy for patients with structural heart disease presenting with VT. Idiopathic ventricular arrhythmias include premature ventricular contractions and VT occurring in the absence of overt structural heart disease. In this setting, catheter ablation has evolved as the primary therapeutic option for symptomatic ventricular premature beats and sustained VTs and is curative in most cases. This chapter presents an overview of the principles of invasive diagnosis and treatment of monomorphic VTs in patients with and without structural heart disease and delineates the clinical outcome of catheter ablation. Finally, the chapter provides an outlook to the future, discussing potential directions and upcoming developments in the field of catheter ablation of monomorphic VT.


2020 ◽  
Vol 6 (5) ◽  
Author(s):  
Nabil El-Sherif ◽  
Mohamed Boutjdir ◽  
Gioia Turitto

Sudden cardiac death accounts for approximately 360,000 annually in the United States and is the cause of half of all cardiovascular deaths. Ischemic heart disease is the major cause of death in the general adult population. Sudden cardiac death can be due to arrhythmic or non-arrhythmic cardiac causes, for example, myocardial rupture. Arrhythmic sudden cardiac death may be caused by ventricular tachyarrhythmia (ventricular tachycardia/ventricular fibrillation) or pulseless electrical activity/asystole. The majority of research in risk stratification centers on ventricular tachyarrhythmias simply because of the availability of a successful management strategy, the implantable cardioverter/ defibrillator. Currently the main criterion of primary defibrillator prophylaxis is the presence of organic heart disease and depressed left ventricular systolic function assessed as left ventricular ejection fraction. However, only one third of eligible patients benefit from the implantable defibrillator, resulting in significant redundancy in the use of the device. The cost to the health care system of sustaining this approach is substantial. Further, the current low implantation rate among eligible population probably reflects a perceived low benefit-to-cost ratio of the device. Therefore, attempts to optimize the selection process for primary implantable defibrillator prophylaxis are paramount. The present report will review the most recent pathophysiology and risk stratification strategies for sudden cardiac death beyond the single criterion of depressed ejection fraction. Emphasis will be placed on electrophysiological surrogates of conduction disorder, dispersion of repolarization, and autonomic imbalance, which represent our current understanding of the electrophysiological mechanisms that underlie the initiation of ventricular tachyarrhythmias. Further, factors that modify arrhythmic death, including noninvasive risk variables, biomarkers, and genomics will be addressed. These factors may have great utility in predicting sudden cardiac arrhythmic death in the general public.


2016 ◽  
Vol 5 (1) ◽  
pp. 45 ◽  
Author(s):  
Krystien VV Lieve ◽  
◽  
Arthur A Wilde ◽  
Christian van der Werf ◽  
◽  
...  

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a rare but severe genetic cardiac arrhythmia disorder, with symptoms including syncope and sudden cardiac death due to polymorphic VT or ventricular fibrillation typically triggered by exercise or emotions in the absence of structural heart disease. The cornerstone of medical therapy for CPVT is β -blockers. However, recently flecainide has been added to the therapeutic arsenal for CPVT. In this review we summarise current data on the efficacy and role of flecainide in the treatment of CPVT.


2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Vago ◽  
L Szabo ◽  
C S Czimbalmos ◽  
Z S Dohy ◽  
I Csecs ◽  
...  

Abstract Introduction Sudden cardiac death (SCD) is the most common cause of death in athletes occurring usually during intensive training. Cardiac magnetic resonance (CMR) has a crucial role in the detection of structural myocardial abnormalities. Aims Our aim was to investigate the etiology of SCD and to estimate the prevalence of myocardial structural heart diseases among Hungarian athletes using CMR. Methods Between January 2011 and January 2019 we performed CMR scans on 228 athletes (199 males, age: 29.1±13.2) with suspected structural myocardial disease. Twelve athletes were investigated after aborted sudden cardiac death and normal coronary angiography. Results CMR confirmed the diagnosis of structural myocardial disease in 62 athletes (26.2%) (28.8±9.1 years, 59 male): hypertrophic cardiomyopathy (HCM) in 14 cases (22.6%), arrhythmogenic right ventricular cardiomyopathy (ARVC) in 9 cases (14.5%), noncompaction (NCCMP) in 6 cases (9.7%) and dilated cardiomyopathy (DCM) in 5 cases (8.1%). Subendocardial late gadolinium enhancement (LGE), reflecting myocardial scar, was typical of previous myocardial infarction (post MI) in 3 cases (5.5%). Acute myocarditis was found in 2 cases (3.6%). Nonischaemic LGE pattern was found in 20 cases (32.2%): patchy subepi-midmyocardial LGE suggesting previous myocarditis in 8 athletes, and with aspecific pattern in 12 athletes. Athletes with nonischaemic LGE had normal clinical and laboratory parameters without wall motion abnormalities, in their cases further investigations ruled out systemic disease. One athlete was diagnosed with Fabry-disease, one with coronary artery abnormality (anomalous origin of the left main coronary artery from the right sinus of Valsalva), one athlete showed pheochromocytoma-related Tako-Tsubo cardiomyopathy (each 1.6%). Five athletes with confirmed structural heart disease were investigated after sustained ventricular tachycardia, seven athletes after aborted SCD: ARVC (n=6), aspecific LGE pattern (n=4), HCM (n=1) and pheochromocytoma-related Tako-Tsubo cardiomyopathy (n=1) were diagnosed. RVOT movie of an ARVC pts Conclusion In our national CMR registry the most common structural alteration was nonischaemic fibrosis, the most common cardiomyopathy was HCM, and the leading cause of SCD in Hungarian competitive athletes was ARVC. The national registers are highly important for a better understanding the etiology and the geographical differences of SCD in athletes. Acknowledgement/Funding Project no. NVKP_16-1-2016-0017 has been implemented with the support provided from the National Research, Development and Innovation Fund of Hungary


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