Beta-blockers, ventricular arrhythmias, and sudden death in heart failure: not as simple as it seems

Patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) have arrhythmia-related symptoms or are identified during screening of an affected family. Heart failure symptoms occur late in the disease’s natural history. As strenuous exercise has been associated with disease acceleration and worsening of ventricular arrhythmias, lifestyle modification with restricted athletic activities is recommended upon disease diagnosis or even identification of mutation carrier status. An episode of an haemodynamically unstable, sustained ventricular tachycardia or ventricular fibrillation as well as severe systolic ventricular dysfunction constitute definitive indications for implantable cardioverter defibrillator (ICD) implantation, which should also be considered following tolerated sustained or non-sustained ventricular tachycardia episodes, syncope, or in the presence of moderate ventricular dysfunction. Antiarrhythmic medications are used as an adjunct to device therapy. Catheter ablation is recommended for incessant ventricular tachycardia or frequent appropriate ICD interventions despite maximal pharmacological therapy. Amiodarone alone or in combination with beta blockers is most effective for symptomatic ventricular arrhythmias. Beta blockers are considered for use in all patients with a definite diagnosis but evidence for their prognostic benefit is sparse. Heart failure symptoms are managed using standard protocols and heart transplantation is considered for severe ventricular dysfunction or much less commonly uncontrollable ventricular arrhythmias.

Download Full-text

Ambulatory Ventricular Arrhythmias in Patients With Heart Failure Do Not Specifically Predict an Increased Risk of Sudden Death

Circulation ◽

10.1161/01.cir.101.1.40 ◽

2000 ◽

Vol 101 (1) ◽

pp. 40-46 ◽

Cited By ~ 125

Author(s):

John R. Teerlink ◽

Muhammad Jalaluddin ◽

Susan Anderson ◽

Marrick L. Kukin ◽

Eric J. Eichhorn ◽

...

Keyword(s):

Heart Failure ◽

Sudden Death ◽

Ventricular Arrhythmias ◽

Increased Risk ◽

Patients With Heart Failure

Download Full-text

Inducible ventricular arrhythmias and sudden death during vasodilator therapy of severe heart failure

American Heart Journal ◽

10.1016/0002-8703(88)90727-2 ◽

1988 ◽

Vol 116 (6) ◽

pp. 1447-1454 ◽

Cited By ~ 74

Author(s):

William G Stevenson ◽

Lynne W Stevenson ◽

James Weiss ◽

Jan H Tillisch

Keyword(s):

Heart Failure ◽

Sudden Death ◽

Ventricular Arrhythmias ◽

Severe Heart Failure ◽

Vasodilator Therapy

Download Full-text

A Clinical Review of Ventricular Arrhythmias in Patients with Congestive Heart Failure

EMJ Cardiology ◽

10.33590/emjcardiol/18-00058r1 ◽

2019 ◽

Author(s):

Noel Boyle

Keyword(s):

Heart Failure ◽

Ejection Fraction ◽

Ventricular Arrhythmias ◽

Beta Blockers ◽

Management Strategies ◽

Significant Risk ◽

Holter Monitoring ◽

Current Evidence ◽

Compensatory Mechanisms ◽

Ventricular Ejection Fraction

Heart failure is an increasingly prevalent condition, which is associated with ventricular arrhythmias. The reduction in cardiac pumping efficiency leads to the activation of several compensatory mechanisms. These mechanisms eventually lead to cardiac remodelling and a decline in haemodynamic status, contributing to the formation of a substrate conducive to arrhythmias, including increased automaticity, triggered activity, and, most commonly, re-entry circuits. In turn, ventricular arrhythmias can lead to the worsening of heart failure. A diagnosis of heart failure and ventricular arrhythmias is obtained using the patient’s history, examination findings, and investigation results. A key tool in this is echocardiogram imaging, which visualises the cardiac chambers, determines ventricular ejection fraction, and identifies structural abnormalities. A reduction in ejection fraction is a significant risk factor for the development of ventricular arrhythmias. Arrhythmias are diagnosed by ECG, Holter monitoring, and telemetry or event monitoring, and should initially be treated by optimising the medical management of heart failure. Anti-arrhythmic drugs, including beta-blockers, are usually the first-line therapy. Sudden cardiac death is a significant cause of mortality in heart failure patients, and implantable cardioverter defibrillator devices are used in both primary and secondary prevention. Anti-arrhythmic drugs and catheter ablation are important adjunctives for minimising shock therapy. In addition, autonomic modulation may offer a novel method of controlling ventricular arrhythmias. The objective of this review is to provide a practical overview of this rapidly developing field in relation to current evidence regarding the underlying pathophysiology, burden of disease, and management strategies available.

Download Full-text

Primary prevention of sudden death in idiopathic dilated cardiomyopathy

ESC CardioMed ◽

10.1093/med/9780198784906.003.0554 ◽

2018 ◽

pp. 2341-2345

Author(s):

Riccardo Cappato

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Primary Prevention ◽

Sudden Death ◽

Dilated Cardiomyopathy ◽

Beta Blockers ◽

Idiopathic Dilated Cardiomyopathy ◽

Conduction Delay ◽

Converting Enzyme Inhibitors ◽

Icd Therapy

Idiopathic dilated cardiomyopathy is characterized by early ventricular enlargement and systolic contractile dysfunction with congestive heart failure not secondary to recognizable causes. Symptoms of congestive heart failure develop at a later stage, usually between 18 and 50 years of age, although they may occasionally occur earlier as a first manifestation of the underlying disease. Mechanisms of life-threatening arrhythmias are facilitated by subendocardial scarring, electrolyte unbalance, stretch-induced electrophysiological changes, autonomic impairment, conduction delay, or proarrhythmic effects of drug therapy. Sudden death may occur as a consequence of ventricular fibrillation, but electromechanical dissociation or bradycardia may also be a possible underlying cause. Most of the clinical characterization of idiopathic dilated cardiomyopathy is drawn from studies also enrolling patients with cardiomyopathies secondary to variable underlying conditions. Secular trends have improved the ability of early diagnosis, and the therapeutic strategies used to prevent sudden death. Among them are angiotensin-converting enzyme inhibitors, beta blockers, and mineralocorticoids/aldosterone receptor antagonists. The role of implantable cardioverter defibrillator (ICD) therapy for the primary prevention of all-cause mortality is controversial with some studies showing and others questioning the benefit of ICD in this population. Survivors of near-fatal arrhythmias have a high risk of recurrence, which may often be fatal. Idiopathic dilated cardiomyopathy contributes to less than 15% of all such patients. Previous randomized studies conducted in large heterogeneous populations showed that ICD therapy is beneficial and improves survival by about 30%. This therapy is currently recommended for all survivors of a near-fatal arrhythmia regardless of the underlying substrate.

Download Full-text

Arrhythmogenic right ventricular cardiomyopathy: management of symptoms and prevention of sudden cardiac death

ESC CardioMed ◽

10.1093/med/9780198784906.003.0361_update_001 ◽

2018 ◽

pp. 1502-1505

Author(s):

Alexandros Protonotarios ◽

Perry Elliott

Keyword(s):

Heart Failure ◽

Ventricular Tachycardia ◽

Right Ventricular ◽

Ventricular Arrhythmias ◽

Ventricular Dysfunction ◽

Beta Blockers ◽

Arrhythmogenic Right Ventricular Cardiomyopathy ◽

Pharmacological Therapy ◽

Sustained Ventricular Tachycardia ◽

Ventricular Cardiomyopathy

Patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) have arrhythmia-related symptoms or are identified during screening of an affected family. Heart failure symptoms occur late in the disease’s natural history. As strenuous exercise has been associated with disease acceleration and worsening of ventricular arrhythmias, lifestyle modification with restricted athletic activities is recommended upon disease diagnosis or even identification of mutation carrier status. An episode of an haemodynamically unstable, sustained ventricular tachycardia or ventricular fibrillation as well as severe systolic ventricular dysfunction constitute definitive indications for implantable cardioverter defibrillator (ICD) implantation, which should also be considered following tolerated sustained or non-sustained ventricular tachycardia episodes, syncope, or in the presence of moderate ventricular dysfunction. Antiarrhythmic medications are used as an adjunct to device therapy. Catheter ablation is recommended for incessant ventricular tachycardia or frequent appropriate ICD interventions despite maximal pharmacological therapy. Amiodarone alone or in combination with beta blockers is most effective for symptomatic ventricular arrhythmias. Beta blockers are considered for use in all patients with a definite diagnosis but evidence for their prognostic benefit is sparse. Heart failure symptoms are managed using standard protocols and heart transplantation is considered for severe ventricular dysfunction or much less commonly uncontrollable ventricular arrhythmias.

Download Full-text

Cellular basis of ventricular arrhythmias and abnormal automaticity in heart failure

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.277.1.h80 ◽

1999 ◽

Vol 277 (1) ◽

pp. H80-H91 ◽

Cited By ~ 50

Author(s):

H. Bradley Nuss ◽

Stefan Kääb ◽

David A. Kass ◽

Gordon F. Tomaselli ◽

Eduardo Marbán

Keyword(s):

Heart Failure ◽

Sudden Death ◽

Ventricular Arrhythmias ◽

Torsade De Pointes ◽

Resting Potential ◽

Unexpected Finding ◽

Early Afterdepolarizations ◽

Ventricular Cells ◽

High Incidence ◽

Delayed Afterdepolarizations

The high incidence of sudden death in heart failure may reflect an increased propensity to abnormal repolarization and long Q-T interval-related arrhythmias. If so, cells from failing hearts would logically be expected to exhibit a heightened susceptibility to early afterdepolarizations (EAD). We found that midmyocardial ventricular cells isolated from dogs with pacing-induced heart failure exhibited an increased action potential duration and many more EAD than cells from nonpaced controls; this was the case both under basal conditions ( P < 0.01) and after lowering external K+concentration ([K+]o) to 2 mM and exposing cells to cesium (3 mM; P < 0.05). An unexpected finding was the occurrence of spontaneous depolarizations (SD, >5 mV) from the resting potential that were not coupled to prior action potentials. These SD were observed in 20% of failing cells ( n = 5 of 25) under basal ionic conditions but in none of the normal cells ( n = 0 of 27, P < 0.05). The net inward current that underlies SD is not triggered by Ca2+ oscillations and thus differs fundamentally from the currents that underlie delayed afterdepolarizations. We conclude that cardiomyopathic canine ventricular cells are intrinsically predisposed to EAD and SD. Because EAD have been linked to the pathogenesis of torsade de pointes, our results support the hypothesis that sudden death in heart failure often arises from abnormalities of repolarization. The frequent occurrence of SD points to a novel cellular mechanism for abnormal automaticity in heart failure.

Download Full-text