Stunned and hibernating myocardium: Possibility of intervention

R. Ferrari, G. La Carina, R. Giubbini, O. Visioli

Research output: Contribution to journalArticlepeer-review

Abstract

There are several potential outcomes of myocardial ischemia. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When myocardial ischemia is less severe but still prolonged, myocytes may remain viable but exhibit depressed contractile function. Under these conditions, reperfusion restores complete contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed hibernating myocardium. The difference between this condition and that described before, i.e., prolonged ischemia, which results in further damage on reperfusion, is, most likely, related to residual coronary flow. In the hibernating myocardium, which is always supplied by a narrow coronary artery, blood flow is not low enough to cause progression toward tissue necrosis, but it is low enough to cause pH changes that, in turn, are responsible for the downregulation of myocardial contractility. The level of underperfusion is sufficient to maintain aerobic metabolism of the quiescient myocardium as demonstrated by the absence of lactate and creatine phosphokinase release. There are no doubts that revascularization is essential for hibernated myocardium, and the clinical goal to achieve is the possibility of accurately distinguishing viable from infarcted tissue. A third possible outcome of myocardial ischemia is a postischemic ventricular dysfunction or myocardial stunning. This term describes a transient mechanical dysfunction that persists on reperfusion after a short period of ischemia, despite the absence of irreversible damage. There are numerous clinical conditions in which stunning might manifest. These include spontaneous reperfusion after coronary artery spasm, unstable angina, exercise-induced ischemia, acute myocardial infarction with early reperfusion (either spontaneous or induced by thrombolytic therapy), angioplasty, open heart surgery, and transplantation. Calcium and oxygen might be involved in the pathophysiology of stunning as preventive pharmacological therapy with antioxidants and Ca2+antagonists improves this condition. The real need for stimulation of the stunned myocardium in the clinical setting, however, has been questioned, as by definition, such myocardium will eventually recover full contractile capacities. The clinical condition that requires specific treatment for stunning is the immediate postoperative period after cardiac surgery when the myocardium can undergo stunning as a result of the previous total and global period of ischemia. We report on our experience with nisoldipine in preventing stunning in either isolated and blood-perfused rabbit heart or patients with coronary artery disease subjected to coronary artery bypass.

Original languageEnglish
Pages (from-to)S5-S13
JournalJournal of Cardiovascular Pharmacology
Volume20
Issue number5
Publication statusPublished - 1992

Keywords

  • Calcium antagonist
  • Hibernating myocardium
  • Myocardial ischemia
  • Nisoldipine
  • Oxygen free radicals
  • Stunning

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Pharmacology

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