Normal and abnormal consequences of apoptosis in the human heart: from postnatal morphogenesis to paroxysmal arrhythmias.

Abstract

Apoptosis and necrosis are two distinctly different forms of cell death and both occur in the human heart. In contrast to necrosis, apoptosis is not associated with inflammation and there are two reasons for this. The apoptotic cell does not swell or rupture prior to its being engulfed by either a macrophage or even a neighboring like cell. And the phagocytosis occurs with unusual rapidity. Apoptosis, also thought of as cell suicide, is a tidy way of removing cells no longer useful, in essence a form of selective deletion. These features make apoptosis a valuable component of morphogenesis, mediation of hormonal and immunological responses, and the homeostatic balance between hypertrophy and atrophy or involution. In the human heart apoptosis has been found in the sinus node of patients with the long QT syndrome. It most likely participates in the important postnatal morphogenesis of the sinus node, AV (atrioventricular) node and His bundle. Apoptosis may also participate in the genesis and pathophysiology of cardiomyopathy, paroxysmal arrhythmias or conduction disturbances (some of which may be responsible for sudden death), focal fibromuscular dysplasia of small coronary arteries, hereditary medial degeneration of the tunica media of coronary arteries, and arrhythmogenic right ventricular dysplasia. The possible role of apoptosis in numerous other changes in the human heart merit future investigation, among them being the pathogenesis of atherosclerosis and mechanisms of ageing in the myocardium.

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