Canadian Health&Care Mall: Discussion of Low-Dose Vasopressin Infusions
Defects on myocardial scans that improve on serial imaging are considered an expression of regional reductions in coronary blood flow. Resting 201Tl scans obtained in patients with known coronary heart disease at a time when they are angina-free can show reversible abnormalities of myocardial uptake, but only in the area of distribution of severely stenotic coronary arteries. Our findings indicate that similar abnormalities can frequently be identified in patients without known previous heart disease during the administration of vasopressin at low doses. Even individuals with insignificant or nonexistent coronary artery disease can show abnormal xaH scintigraphy in this setting. This phenomenon most likely reflects the capacity of vasopressin to increase coronary vascular resistance even at blood levels that are within the physiologic range.
The contribution of a simultaneous increase in myocardial oxygen demands must also be addressed since vasopressin has a powerful systemic vasoconstrictive action that can significantly augment cardiac afterload. This was investigated in the present series by resorting to the heart rate-blood pressure product, an accurate indirect measure of myocardial oxygen consumption. With the cessation of the vasopressin infusion, the average heart rate rose, and the blood pressure did not change. Thus, the heart rate-blood pressure product actually increased at the time when the 201Tl distribution became normal, suggesting that changes in myocardial oxygen consumption were not significantly involved in the abnormal scintigraphy. Vasopressin infusions that achieve plasma levels comparable to those observed during stress have been associated with hemostatic changes consistent with low-level activation of the coagulation mechanism. Although it is possible that intravascular thrombus formation contributed to the abnormalities in 201Tl distribution that were detected, the prompt reversibility of the scintigraphic defects strongly militates against this interpretation. The source: canadian health care mall can attract people by its interesting articles on the medical science.
The present series demonstrates that abnormalities in myocardial perfusion induced by vasopressin remain largely undetected by standard monitoring techniques. Under these circumstances, serious cardiovascular events can supervene without forewarning. An example of such is torsade des pointes, a life-threatening arrhythmia that has been documented during vasopressin therapy, with and without concomitant hypokalemia but invariably associated with prolongation of the QTc interval. Since QTc interval prolongation has been identified in the course of coronary artery spasm, it is tempting to speculate that torsade des pointes is yet another expression of vasopressin-induced alterations in coronary blood flow.
Two controlled studies, performed two decades apart, failed to demonstrate that vasopressin favorably alters the outcome of patients with active upper gastrointestinal bleeding. With this in mind, the wisdom of therapy with an agent that has such powerful yet subtle effect on the coronary circulation must be seriously challenged. Animal experimentation suggests that the concurrent administration of intravenous nitroglycerin is able to reverse the reduction in coronary blood flow induced by vasopressin without altering its beneficial effects on the portal circulation. Were this approach to be tested in humans, 201Tl scintigraphy would be a valuable tool to evaluate its impact on the coronary circulation.