Intracoronary diltiazem limits infarct size during prolonged angioplasty balloon inflation

An animal model of failed coronary angioplasty was used to evaluate the effect of intracoronary diltiazem on regional ischemia and the degree of myocardial necrosis. Ischemia was produced in closed‐chest, pentobarbital‐anesthetized male mongrel dogs by inflation of 2.5–3.0 mm diameter balloons introduced under fluoroscopy into the left anterior descending or left circumflex coronary arteries. Animals were randomly assigned to control or diltiazem administered at the time of balloon inflation. Diltiazem, 900 μg/kg, was administered in divided doses through the lumen of the angioplasty balloon catheter. Diltiazem reduced the mean arterial pressure by 27 ± 6 mm Hg and blunted tachycardia following occlusion, which was also seen in controls. After 50 min of ischemia, a left thoracotomy was performed, and the left atrium was cannulated for injection of radiolabeled microspheres at 70 min. The animal was then reperfused by deflating the balloon. Regional segment function showed similar dyskinesis in the ischemic area of both groups. At 4 h the animal was sacrificed and the heart was removed for measurement of the area at risk and infarct size using a dual staining technique. Infarct size, when determined as the percent of the area at risk, was significantly reduced in diltiazem treated animals, 9 ± 2%, as compared to control animals, 22 ± 5%. Regional myocardial blood flow did not differ between groups. Therefore, intracoronary diltiazem produced a significant reduction in myocardial injury. This intervention may be useful to delay cell death in the setting of failed coronary angioplasty. © Wiley‐Liss, Inc.

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