Does reperfusion injury exist in humans?
Timely coronary reperfusion as treatment for acute myocardial infarction reduces myocardial infarct size, improves left ventricular function and survival. There is still concern that at the time of reperfusion, a further injury occurs to the myocardium. Theoretically, if this "reperfusion injury" could be treated and eliminated, the outcome for patients with myocardial infarction might further improve. The concept of reperfusion injury is closely tied to the concept that oxygen radicals generated at the time of reperfusion cause tissue damage. There are four basic forms of reperfusion injury. Lethal reperfusion injury is described as myocyte cell death due to reperfusion itself rather than to the preceding ischemia. This concept continues to be controversial in both experimental animal and clinical studies. Vascular reperfusion injury refers to progressive damage to the vasculature over time during the phase of reperfusion. Manifestations of vascular reperfusion injury include an expanding zone of no reflow and a deterioration of coronary flow reserve. This form of reperfusion injury has been documented in animal models and probably occurs in humans. Stunned myocardium refers to postischemic ventricular dysfunction of viable myocytes and probably represents a form of "functional reperfusion injury." This phenomenon is well documented in both animal models and humans. Reperfusion arrhythmias represent the fourth form of reperfusion injury. They include ventricular tachycardia and fibrillation that occur within seconds to minutes of restoration of coronary flow after brief (5 to 15 min) episodes of myocardial ischemia. True reperfusion arrhythmias occur in only a small percentage of patients receiving thrombolytic therapy for acute myocardial infarction and are not a sensitive indicator for successful reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
Kloner
R A
RA
Heart Institute, Hospital of the Good Samaritan, Los Angeles, California 90017-2395.
D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D002470:Cell Survival; D005609:Free Radicals; D006801:Humans; D009203:Myocardial Infarction / Q000628:therapy; D015425:Myocardial Reperfusion / Q000379:methods; D015428:Myocardial Reperfusion Injury / Q000145:classification / Q000209:etiology / Q000503:physiopathology; D009206:Myocardium / Q000473:pathology; D010100:Oxygen / Q000009:adverse effects; D015912:Thrombolytic Therapy; D016276:Ventricular Function / Q000502:physiology
D005609:Free Radicals; D010100:Oxygen