Hibernating, stunning and ischemic preconditioning of the myocardium: therapeutic implications.
Hibernating myocardium, as a compensatory mechanism to chronic ischemia caused by a tight coronary stenosis is best treated by restoration of blood flow. Hence in this condition the therapeutic implications are rather obvious and the problem is how to diagnose hibernating myocardium. Provocation tests and/or scintigraphic methods are usually used to show viability of an akinetic myocardial area. These tests, however, can be expected to be clearly positive only if hibernating myocardium is not mixed with patchy scar tissue. Physicians should be aware of myocardial stunning, when left ventricular function remains impaired immediately after revascularization, for example, after cardiac surgery of the totally ischemic organ or after thrombolytic therapy of acute myocardial infarction. Due to the self-recovery of this condition, therapeutic implications are given only when symptoms and signs of impaired ventricular function are present. Positive inotropic agents have been shown to be effective in experimental conditions and are widely accepted to be beneficial in clinical use. Based on experimental observations the term "ischemic preconditioning" has been introduced to describe a condition of increased ischemic tolerance after a short preceding period of ischemia and reperfusion. This condition, however, has never been proven to be of clinical significance in the treatment of patients with ischemic heart disease. According to some clinical observations, repeated episodes of ischemia are even associated with a worse prognosis. Therapeutic implications may arise from understanding the mechanisms involved in this cardioprotective process, for example, activation of adenosine A1 receptors.
Niroomand
F
F
Universität Heidelberg, Germany.
Kübler
W
W
D000818:Animals; D002921:Cicatrix / Q000473:pathology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000150:complications* / Q000601:surgery; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D009203:Myocardial Infarction / Q000628:therapy; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009204:Myocardial Revascularization; D017682:Myocardial Stunning / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D009336:Necrosis; D011942:Receptors, Adrenergic, alpha / Q000502:physiology; D011976:Receptors, Muscarinic / Q000502:physiology; D015398:Signal Transduction; D015912:Thrombolytic Therapy; D016277:Ventricular Function, Left
D011942:Receptors, Adrenergic, alpha; D011976:Receptors, Muscarinic