In: Aortic Pressure5 Jan 2014
This study was designed to compare the effect of a mechanical vs a pharmacologic increase in BP on coronary artery blood flow and thrombolysis induced by IV administration of recombinant tissue plasminogen activator. We employed a canine model of coronary thrombosis induced by injection of radioactive blood clot in the left anterior descending coronary artery. Subsequently, all dogs underwent phlebotomy to decrease systolic BP to 75 mm Hg and this decreased coronary blood flow by 50%. BP was increased to 130 mm Hg by norepinephrine (NE) infusion or by inflation of a Fogarty catheter placed in the descending aorta. Interventions with NE or with a Fogarty balloon catheter increased coronary artery blood flow to similar values and rates of coronary thrombolysis were similar. However, cardiac output was significantly higher with NE. These results indicate coronary clot lysis is dependent on perfusion pressure and coronary blood flow, not cardiac output.
Several large clinical studies have demonstrated that thrombolytic therapy decreases mortality in patients with acute myocardial infarction. However, this therapeutic approach is not reported to affect mortality in the subset of patients with cardiogenic shock.x’ The failure for thrombolytic therapy to improve mortality in these patients may be due to the systemic hypotension impairing delivery of the thrombolytic agent, thus decreasing thrombolytic efficacy. Although previous studies have investigated the effect of different drugs, dosing regimens, and adjunctive therapy on thrombolytic efficacy, few studies have systematically investigated how changes in physiologic parameters, such as systolic BP, diastolic BP, and cardiac output, influence thrombolysis. A recent canine study demonstrated that a moderate increase in a low systolic pressure, attained by using a norepinephrine infusion, enhanced the rate of coronary thrombolysis induced by intracoronary administration of recombinant tissue plasminogen activator (rtPA). While we postulated that the increased thrombolysis was due to the increase in coronary perfusion pressure, it is conceivable that norepinephrine itself may have influenced thrombolysis. For example, in the presence of clot, norepinephrine may affect the regional coronary vascular resistance and thus, for a given coronary perfusion pressure, the delivery of the thrombolytic agent to the thrombus. That is, for the same increase in systolic pressure produced mechanically or by norepinephrine infusion, the delivery of the thrombolytic agent and thus the rates of thrombolysis could be different. Finally, we and others have speculated on the role of cardiac output itself in influencing coronary thrombolysis.
The current study compares the effect of a mechanical vs a pharmacologic increase in a low systolic BP on left anterior descending artery blood flow and coronary thrombolysis. Because cardiac output changes in different directions with these interventions, we also investigated the effect of cardiac output itself on coronaiy thrombolysis.
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