The possibility of regulating apoptosis in cardiac disease is such an exciting prospect that the reader might wonder why there has not been more public clamor for antiapoptosis therapies in cardiovascular disease. Because heart muscle is considered to be nonrenewable tissue, scenarios can be imagined in which health food stores promote specific antiapoptosis remedies. Although fads tend to focus on diseases of less obvious mechanical origin, part of the credit lies in the tendency of cardiologists to demand theoretic and experimental justification for adopting new procedures. Although research into apoptosis is likely to affect the management of cardiovascular disease, research ideas must first coalesce into a consensus, and, for that to occur, the ground rules must be defined clearly.

The term cardiovascular disease encompasses a wide range of problems, including acute emergencies, chronic stresses, infectious and inflammatory processes, and autoimmune disease. The role of apoptosis varies among these pathologies and frequently is simply one of the markers of an end-stage event: Apoptosis of a differentiated, adult cardiac myocyte may not be easily recognizable as apoptosis. To review the current state of affairs, several questions must be addressed: (1) the detection of apoptosis, (2) the evaluation of apoptosis and programmed cell death in culture and in developing embryos, (3) evidence for the induction of apoptosis in the mature heart, (4) the means by which apoptosis may be triggered (and by which it may be amenable to regulation), (5) and apoptosis in several pathologies threatening the heart. Each of these subjects is addressed in turn.