Cardiovascular Research

Morphologic and functional effects of piroxicam on myocardial scar formation after coronary occlusion in dogs.

Authors: H Hammerman|||K J Alker|||F J Schoen|||R A Kloner

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Abstract

To determine whether piroxicam, a widely used, long-acting anti-inflammatory agent, causes scar thinning after acute myocardial infarction (MI), MI was produced in 16 anesthetized, open-chest dogs by ligation of the proximal left anterior descending coronary artery. The dogs were randomized into 2 groups and treated in a blinded fashion, 8 with piroxicam, 1 mg/kg i.v. at 15 minutes and at 3 hours after ligation (Group 1) and 8 with saline solution (Group 2). Two-dimensional echocardiograms were performed 7 days and 6 weeks after ligation. At 6 weeks, the dogs were killed and the hearts examined. Scar thickness was 7.1 +/- 0.3 mm in control dogs and 5.2 +/- 0.4 mm in piroxicam-treated dogs (p less than 0.01). The ratio of scar thickness to noninfarcted wall thickness was 0.87 +/- 0.03 (mean +/- standard error of the mean) in the control group, and was significantly lower (0.62 +/- 0.04) in the piroxicam-treated group (p less than 0.001). Regional function, expressed as the percent change in the area of the left ventricular cavity (% delta A) from short-axis 2-dimensional echocardiograms, was 42 +/- 3% 7 days after occlusion in the control group and was not significantly different in the treated group (34 +/- 5%). At the end of 6 weeks % delta A had improved in the piroxicam-treated group to 44 +/- 3% (p less than 0.05 compared with the value after 7 days), and was similar to % delta A of the control group at 6 weeks (43 +/- 3%). Thus, clinical doses of piroxicam administered early after MI caused moderate scar thinning, which was not associated with impairment of regional left ventricular function 6 weeks later.

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Chemical List

Anti-Inflammatory Agents|||Thiazines|||Piroxicam