Reperfusion of the infarct-related coronary artery limits left ventricular expansion beyond myocardial salvage

Previous echocardiographic data from the Gruppo Italiano per lo Studio della Streptochinasi nell' Infarto Miocardico (GISSI 1) trial suggest that the relation between left ventricular end-systolic volume and infarct size could be altered by thrombolysis, which would exert a restraining effect on end-systolic volume beyond its reducing effect on infarct size. Thus in 63 patients with one-vessel disease and a recent anterior myocardial infarction, we tested at angiography (1) if perfusion of the anterior descending coronary artery exerts any restraining effect on end-systolic volume above and beyond infarct size reduction and (2) if ejection fraction reflects such an additional, beneficial difference in the ventricular remodeling process. End-systolic volume was calculated using the Dodge method and the right anterior oblique projection, while infarct size was quantified according to the number of ventricular radii whose percent shortening fell below the mean -2 SD of a group of normal individuals. Patients were then divided into two groups according to the perfusion status of the vessel using Thrombolysis In Myocardial Infarction (TIMI) criteria (TIMI grade 0 to 1: nonperfused vessel, 27 patients; TIMI grade 2 to 3: perfused vessel, 36 patients). For both groups there was a significant linear relation (p < 0.001) between end-systolic volume and infarct size; as in our echocardiographic data, the regression lines relating volume to infarct size showed a different slope in the two populations so that, for large and matched infarcts, end-systolic volume was smaller in patients with a perfused vessel (p < 0.05). This difference in ventricular topography was not reflected in any difference in the slopes of the regression lines relating ejection fraction to infarct size (p = NS) in the two groups. In conclusion, our data show that end-systolic volume is smaller in patients with a perfused infarct-related vessel and a large anterior infarction compared with patients with a nonperfused infarction of similar size. This suggests that reperfusion exerts a restraining effect on the process of infarct expansion that goes beyond its primary effect of infarct size reduction. Ejection fraction may not reflect any such additional beneficial contribution exerted by vessel patency on left ventricular remodeling, which calls into question its pivotal role in assessing the full benefit of reperfusion on ventricular function in trials devoted to thrombolysis.