Statins and the Reduction of Sudden Cardiac Death: Antiarrhythmic or Anti-Ischemic Effect?

Abhimanyu Beri; Tahmeed Contractor; Atul Khasnis; Ranjan Thakur

Disclosures

Am J Cardiovasc Drugs. 2010;10(3):155-164. 

In This Article

2. Pathophysiology of Ventricular Tachycardia/Ventricular Fibrillation and Sudden Cardiac Death

Fatal ventricular arrhythmias can be initiated by underlying coronary artery disease through two mechanisms – acute myocardial ischemia or myocardial scarring. The relative incidence of these mechanisms is difficult to determine as acute ischemia frequently coexists at the scar border zone.[14] In acute ischemia, ventricular arrhythmias may be caused by abnormal impulse generation, abnormal automaticity, or triggered activity caused by early or delayed after depolarizations.[15] Reentrant arrhythmias can also occur, caused by an increased dispersion of refractoriness and conduction across the acute infarct zone[16,17] leading to polymorphic VT.[18,19]

Anisotropy is the conduction of impulses at different velocities across the normal myocardium depending on muscle fiber orientation. This is exacerbated in infarcted scar tissue as a result of islands of myocytes with altered orientations surviving among fibrotic tissue[20] predisposing to reentry.[21,22] With an underlying abnormal electrical substrate (scar), ventricular arrhythmias can also be triggered by neurohormonal mechanisms, electrolyte and acid-base disorders, hypoxemia, and proarrhythmic medications.[23] These often manifest with reentry monomorphic VT as the primary electrical event.[14,21]

Patients with genetic or acquired cardiac abnormalities, such as ion-channel abnormalities, acquired long-QT syndrome, or left ventricular hypertrophy may have polymorphic VT/torsades as the initial event.[24] The final cascade usually involves VT degenerating to VF and later into asystole.[9,10,14,25] Rarely, atrial fibrillation with high ventricular rates may also lead to VF by rapid antegrade conduction over an accessory pathway, for example in Wolff-Parkinson-White syndrome.[24]

Local and systemic autonomic influences may also play a role in sudden cardiac death. Decreased heart rate variability in post-myocardial infarction patients increases the risk of sudden cardiac death.[26–29] This may represent an increased sympathetic tone that lowers the threshold for VF.[30] Autonomic tone can also potentiate ischemia by influencing coronary circulation, free radical formation and platelet aggregation.[31]

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