Although the death rate from coronary artery disease has decreased over the past 20 years, the incidence of congestive heart failure (CHF) has increased. The most common cause of CHF is coronary artery disease. In addition to the implications from increased morbidity in an aging population, CHF has tremendous economic impact because it has become the highest cost Medicare diagnosis.<sup>16 Braunwald E., Grossman W. Clinical aspects of heart failure Heart Disease Philadelphia: WB Saunders (1992).  444

Haga clic aquí para ir a la sección de Referencias</sup> In spite of improvements in medical therapy, reversing the myocardial dysfunction cause of CHF provides the best treatment option. This is accomplished by revascularization of the dysfunctional myocardium usually by coronary artery bypass grafts or percutaneous angioplasty. New revascularization methods, such as transmyocardial laser therapy<sup>96 Scheinowitz M., Abramov D., Eldar M. The role of insulin-like and basic fibroblast growth factors on ischemic and infarcted myocardium: A mini review Int J Cardiol 1997 ;  59 : 1

Haga clic aquí para ir a la sección de Referencias</sup> and gene therapy,<sup>31 Frazier O.H., Kadipasaoglu K. Transmyocardial laser revascularization Curr Opin Cardiol 1996 ;  11 : 564

Haga clic aquí para ir a la sección de Referencias</sup> are currently under investigation. The planning and success of these procedures depend on the presence and amount of dysfunctional but viable myocardium present.

Viable myocardium may be normal, hibernating, or stunned, whereas nonviable myocardium represents scar. Stunned myocardium is found in the acute setting of myocardial ischemia.<sup>17 Braunwald E., Kloner R.A. The stunned myocardium: Prolonged, postischemic ventricular dysfunction Circulation 1982 ;  66 : 1146  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup> It represents dysfunctional myocardium, which persists following restoration of myocardial blood flow (e.g., following lytic therapy). Hibernating myocardium also is dysfunctional and represents a downregulation of contractile function secondary to persistent diminished myocardial blood flow or perfusion reserve.<sup>110 Vanoverschelde J.L., Wijns W., Borgers M. , y al. Chronic myocardial hibernation in humans: From bedside to bench Circulation 1997 ;  95 : 1961  [cross-ref]

Haga clic aquí para ir a la sección de Referencias</sup> Whereas the function of stunned myocardium spontaneously recovers over a period of weeks, hibernating myocardium remains dysfunctional until normal blood flow is restored. Hibernating myocardium represents myocardium that is at risk for infarction and contributes to CHF. There is no anticipated benefit from revascularizing either infarcted or stunned myocardium. Moreover, these procedures are expensive and carry undo risk for patients who likely do not benefit. Thus, it is the identification of hibernating myocardium that is paramount for the success and appropriate utilization of revascularization procedures.

Appropriate utilization of revascularization procedures should depend not only on the presence, but also the amount of hibernating myocardium relative to the dysfunctional area. Patients who have left ventricular ejection fractions less than 30% are known to have a poor prognosis. Thus, a patient with an ejection fraction of 10% to 20% should have more viable myocardium than a patient with an ejection fraction of 20% to 30% to warrant revascularization.

The gold standard for hibernating myocardium is recovery of function following revascularization. This is an imperfect reference because of difficulty in determining the completeness of the revascularization and the possibility of perioperative myocardial infarction. Moreover, the rate of recovery of function varies with the degree of adaptive structural changes within the myocardium. Complete recovery of function is usually achieved within the first 2 months following revascularization. If sufficiently long times for assessment are used to ensure recovery of function, there may be a confounding factor due to restenosis of vessels after angioplasty because of the high restenosis rate during the first 8 to 12 weeks.