Key result
Treatment with a selective COX-2 inhibitor significantly improved left ventricular end-diastolic (P<0.05) and systolic pressures (P<0.01) and reduced infarct size (P<0.05) in rats with AMI.
Why the study?
Does a selective COX-2 inhibitor improve cardiac function and reduce infarct size in a rat model of acute myocardial infarction?
Does a selective COX-2 inhibitor improve cardiac function and reduce infarct size in a rat model of acute myocardial infarction?
p-value: p=<0.05
In a rat model of acute myocardial infarction, treatment with a selective COX-2 inhibitor improved hemodynamics and reduced infarct size, suggesting COX-2 contributes to myocardial injury.
COX-2 inhibition may improve LV function post-MI; extends preclinical RCT data but leaves clinical translation open.
Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery. Animals were either treated with a selective COX-2 inhibitor (5 mg x kg(-1) x day(-1)) or vehicle. Three days after ligation, cardiac function was assessed and infarct size was determined. Myocardial specimens were immunostained with antiserum to COX-2. Plasma concentration of prostanoids was measured by enzyme immunoassay. There was strong expression of COX-2 in the myocytes, endocardium, vascular endothelial cells, and macrophages in the infarcted zone of the myocardium. In contrast, little expression was seen in the myocardium of control rats. Animals treated with the COX-2 inhibitor showed a significant improvement in left ventricular (LV) end-diastolic pressure (P < 0.05) and LV systolic pressure (P < 0.01), and a reduction in infarct size (P < 0.05). Inhibition of COX-2 significantly decreased plasma concentration of thromboxane B2 (P < 0.05); however, it did not affect 6-keto-prostaglandin F1alpha. Induction of COX-2 during AMI appears to contribute to myocardial injury, and treatment with the specific inhibitor of the enzyme ameliorated the course of the disease.
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Saito et al. (2003) studied Acute myocardial infarction. Selective COX-2 inhibitor vs. Vehicle was evaluated on Left ventricular end-diastolic pressure, left ventricular systolic pressure, and infarct size (p=<0.05). Treatment with a selective COX-2 inhibitor significantly improved left ventricular end-diastolic (P<0.05) and systolic pressures (P<0.01) and reduced infarct size (P<0.05) in rats with AMI.
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