Evolution in the practice of primary angioplasty: effect of adjunctive coronary stenting and glycoprotein IIb/IIIa inhibitors on long-term outcomes.

Primary angioplasty strategies have evolved dramatically, including increasing adjunctive use of stents and glycoprotein (GP) IIb/IIIa inhibitors. The purpose of this study was to examine the specific effects of these adjunctive therapies on long-term outcomes after primary angioplasty. From 1996 to 1998, 257 unselected, consecutive patients underwent primary PTCI at our institution. In-hospital mortality was 5.4% (2.9% for patients without cardiogenic shock). The remaining 243 patients were followed for 2.0 +/- 0.7 years. Adjunctive stenting was associated with increased late mortality (8.7% vs. 2.3%, P = 0.02). GP IIb/IIIa inhibitors were associated with reduced late mortality among patients receiving stents (6.9% vs. 21.4%, P = 0.07), but not in those patients treated with balloon angioplasty alone (2.9% vs. 0%, P > 0.20). Coronary stenting remained a significant predictor of late mortality (hazard ratio 5.6, 95% CI 1.5-21.2) after adjustment for other established risk factors. In this unselected series, adjunctive coronary stenting was associated with higher late mortality among hospital discharge survivors. Concomitant GP IIb/IIIa inhibitors partially corrected for this increase. These results are limited by the small sample size and retrospective design of this study. Additional long-term studies are required to test these findings and evaluate for possible mechanisms.

Dobutamine effects on systole and diastole in rats with myocardial infarction.

In this article, the authors attempt to determine the effect of catecholamine stimulation on the systolic and diastolic properties of the left ventricle (LV) in rats with chronic infarction. Male Sprague-Dawley rats underwent coronary artery ligation at 8-10 weeks of age. Baseline hemodynamics were measured 1-2 months after infarction. Dobutamine was administered in bolus injections of increasing concentrations, and peak hemodynamic response after each dose was recorded. Rats were divided into three groups: controls (n = 14), rats with infarct size less than 30% of LV (n = 13), and rats with infarct size at least 30% of LV (n = 9). Baseline hemodynamics were similar among the three groups. There was no significant difference in the maximal response of LV systolic pressure and heart rate between the three groups. Left ventricle +dP/dt increased with dobutamine in all three groups, but rats with infarct size of at least 30% had a significantly smaller increase above baseline as compared with control rats. In contrast, LV -dP/dt increased to a similar degree in all three experimental groups with dobutamine. Although hemodynamics can be affected by loading conditions in the intact animal, the magnitude of the change in +dP/dt with unaltered -dP/dt suggests that there is an impaired inotropic but not lusitropic response to catecholamine stimulation in rats with large chronic myocardial infarcts. The findings imply a differential effect of beta-agonist stimulation on systolic and diastolic properties of the heart.

Mechanical abnormalities in the rat ischemic heart failure model which lie downstream to cAMP production.

OBJECTIVE: We previously showed diminished inotropic responses to isoproterenol in uninfarcted posterior papillary muscles of rats with anterior wall infarcts comprising > or = 30% of the left ventricle. We have also shown that this occurs in the absence of beta-receptor downregulation. Our objective was to show a mechanical defect in the rat infarct model which is secondary to cellular defects downstream to cAMP production. METHODS: Sprague-Dawley rats were infarcted via coronary ligation. After 3 weeks, the uninfarcted papillary muscle was placed in a muscle bath and exposed to increasing concentrations of dibutyryl cAMP while contracting isometrically at 28 degrees C. RESULTS: The large infarct group showed evidence of right ventricular hypertrophy which was manifested by an increased right ventricular mass. No differences were found in baseline measurements of developed tension (DT); rate of tension development (dT/dt); rate of relaxation (-dT/dt); time to peak tension (TPT); and relaxation time (t1/2R). When these muscles were stimulated with dibutyryl cAMP, the large infarct group had a reduced inotropic response as measured by +dT/dt and TPT. No consistent abnormalities were noted in relaxation. The findings are similar to those we noted previously with isoproterenol stimulation. CONCLUSION: The impaired response to beta stimulation in uninfarcted myocardium from rats with large myocardial infarctions is due to cellular defects which lie downstream to cAMP production.