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Pathophysiology of stunned or hibernating myocardium

INTRODUCTION

Left ventricular (LV) dysfunction, an important consequence of coronary artery disease, can result from myocardial ischemia or myocardial infarction [1,2]. In some patients, transient ischemia can lead to a period of persistent dysfunction after the restoration of flow while in others persistent, asymptomatic ischemia produces LV dysfunction that can mimic nonischemic causes of heart failure. The former phenomenon is referred to as myocardial stunning and the latter as hibernating myocardium.

The definitions and pathophysiology of myocardial stunning and hibernation will be reviewed here. The approach to diagnosis and therapy of hibernation, the clinical syndromes associated with stunned or hibernating myocardium, and the role of nuclear imaging and dobutamine echocardiography to assess myocardial viability are discussed elsewhere. (See "Evaluation of hibernating myocardium" and "Clinical syndromes of stunned or hibernating myocardium" and "Assessment of myocardial viability by nuclear imaging in coronary heart disease" and "Dobutamine stress echocardiography in the evaluation of hibernating myocardium".)

DEFINITIONS

Hibernating myocardium must be distinguished from the stunned myocardium and from transient LV dysfunction that is a result of ischemia induced by stress (eg, exercise, dobutamine). However, hibernating myocardium can coexist with both conditions.

Stunned myocardium — Stunned myocardium was the term initially used to describe a condition demonstrated in the laboratory in which total coronary artery occlusion lasting only 5 to 15 minutes (a period not associated with cell death) produced an abnormality in regional LV wall motion that persisted for hours or days following reperfusion [3-7]. Thus, the key elements of the stunned myocardium are:

  • Short-term, total or near total reduction of coronary blood flow
  • Reestablishment of coronary blood flow
  • Subsequent LV dysfunction of limited duration
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