The Canadian journal of cardiology
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Oxidant injury contributes to myocardial stunning, and cardiac ischemic and reperfusion injury. Vitamin E is the major--and perhaps the only--lipid soluble, chain-breaking antioxidant in the heart. Vitamin E and its analogues potentially offer significant advantages for the prevention of ischemic and reperfusion injury. Recent investigations have suggested that modified vitamin E analogues may be more efficacious than vitamin E and may permit myocardial salvage from acute myocardial ischemic injury.
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To determine whether myocardial infarct size in rabbits could be reduced by pretreatment with vitamin E, either as a dietary supplement over 10 days or as a single oral dose either 24 or 72 h before coronary artery occlusion and reperfusion. ⋯ Myocardial infarct size in rabbits can be reduced by 10 days of supplemental dietary vitamin E or a single oral dose of vitamin E 72 h before ischemia. The current results suggest possible clinical potential for oral vitamin E to be used as prophylaxis against myocardial ischemia and reperfusion injury.
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Two patients with the acquired immune deficiency syndrome developed acute pulmonary edema following intravenous fluid administration. Both recovered with diuretic therapy. In neither case was there evidence of persistent severe left ventricular dysfunction, nor was there evidence (either clinically or by thallium study) of flow limiting coronary lesions or of cardiac uptake of iodine-123 meta-iodobenzylguanidine, pointing to ventricular sympathetic neuropathy. It is hypothesized that destruction of the cardiac sympathetics contributed importantly to the development of pulmonary edema following the intravenous fluid load.