Abstract and Introduction
Sudden cardiac death is an important cause of cardiovascular mortality with the majority of cases occurring in low-risk groups. HMG-CoA reductase inhibitors (statins) have recently been shown to reduce the incidence of ventricular tachycardia (VT)/fibrillation (VF) and sudden cardiac death, and this has been attributed to their pleiotropic effects. However, it is unclear whether this occurs through an 'indirect' anti-ischemic or 'direct' antiarrhythmic effect. We systematically reviewed articles published on MEDLINE between January 1996 and December 2009 focusing on the reduction of VT/VF and sudden cardiac death by statins and the potential mechanisms. Studies reporting sudden cardiac death or VT/VF outcomes with statin use (n = 23) or the pathophysiology of sudden cardiac death reduction by statins (n = 19) were included. We found that statins have been shown to reduce VT/VF and sudden cardiac death only in subjects with underlying coronary artery disease or ischemic cardiomyopathy. No definite benefits were seen with statins in sudden cardiac death and VT/VF in patients with non-ischemic cardiomyopathy. There is insufficient evidence to point toward a benefit in populations at low risk for VT/VF. In conclusion, an anti-ischemic rather than a primary antiarrhythmic effect emerges as the likely mechanism of sudden cardiac death reduction with statins.
Sudden cardiac death is defined as unexpected death from a cardiac etiology after cardiac arrest within 1 hour of the onset of acute symptoms. Though significant developments have occurred in the management of cardiovascular disease, sudden cardiac death remains an important global health concern with more than 3 million worldwide deaths annually. The estimated incidence in the US is about 1 per 1000 person-years in the general population, with similar numbers reported from other parts of the world.[4–7]
Arrhythmias are the most common cause of sudden cardiac death, with ventricular tachycardia (VT)/fibrillation (VF) being responsible for the vast majority (83.4%) of cases. Coronary artery disease is the underlying etiology for approximately 80% of these fatal ventricular arrhythmias, the remainder being accounted for by hypertrophic or dilated cardiomyopathy, congenital heart disease, primary electrophysiological abnormalities, valvular heart disease, and infiltrative myocardial disorders. A smaller fraction (16%) of sudden cardiac death is attributed to bradyarrhythmias and electromechanical dissociation.
Certain groups have been identified as being at high risk for sudden cardiac death, but the majority of the sudden death burden exists in the larger, lower risk population.[10,11] Given the low incidence in this low-risk population, any attempt at reducing sudden cardiac death would require specific screening and risk-stratifying strategies as well as safe, effective yet economical interventions.
A protective effect of HMG-CoA reductase inhibitors (statins) in sudden cardiac death has been demonstrated in recent studies. This has been partly attributed to their 'pleiotropic' (i.e. beyond lipid-lowering) effects, such as atherosclerotic plaque stabilization, reduction in systemic inflammation and thrombogenicity, as well as changes in membrane ion channel conduction. We conducted a systematic review of published literature on the efficacy of statins in lowering the incidence of sudden cardiac death and explored the underlying mechanisms.
Am J Cardiovasc Drugs. 2010;10(3):155-164. © 2010 Adis Data Information BV
Cite this: Statins and the Reduction of Sudden Cardiac Death: Antiarrhythmic or Anti-Ischemic Effect? - Medscape - Jun 01, 2010.