The direct manipulation of coronary blood flow to induce regional myocardial ischemia has been almost entirely limited to experimental animal models. Thus, the detection of ischemia-induced left ventricular dysfunction in human subjects has been generally limited to observations made under conditions of diagnostic loading or during spontaneous clinical events. Percutaneous coronary angioplasty requires repeated interruptions of coronary blood flow for periods as long as 1 minute. The resulting appearance of or increase in ischemia-produced changes in myocardial function were detected by two-dimensional echocardiography in 18 patients undergoing angioplasty of 22 coronary stenoses. Accordingly, left ventricular contraction was studied during 52 episodes of regional coronary blood flow interruption and reperfusion in the process of inflating and deflating the angioplasty balloon. Before angioplasty, left ventricular wall motion was normal in 14 patients. There was mild anteroapical hypokinesia in two patients, anteroapical akinesia in one and mild inferior hypokinesia in one. Balloon inflations repeatedly produced new or increased wall motion abnormalities in the distribution of the instrumented coronary artery in 19 (86.4%) of the 22 procedures, but did not alter wall motion during angioplasty of one left circumflex artery lesion, one highly collateralized left anterior descending artery stenosis and one left anterior descending stenosis that had already caused severe anteroapical dyssynergy. Hypokinesia, usually rapidly progressing to dyskinesia, began 19 +/- 8 seconds (mean +/- SD) after coronary occlusion. Wall motion began to normalize 17 +/- 8 seconds after reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
These findings demonstrate that in patients with unstable ischemic syndromes undergoing coronary angioplasty, the use of ionic low osmolar contrast media reduces the risk of ischemic complications acutely and at 1 month after the procedure. Therefore, low osmolar ionic contrast media should be strongly considered when performing interventions in patients with unstable angina or myocardial infarction.
Adjunctive intravenous streptokinase therapy does not enhance early preservation of ventricular function, improve arterial patency rates, or lower restenosis rates after PTCA therapy of acute MI. Hospital course is longer, more expensive, and more complicated. For these reasons, PTCA therapy of acute MI should not be routinely performed with adjunctive intravenous streptokinase therapy.
Omission of routine heparin therapy after successful coronary angioplasty reduces bleeding complications without increasing patient risk. Earlier discharge and significant cost savings are possible under proper conditions.
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