Independent impact of thrombolytic therapy and vessel patency on left ventricular dilation after myocardial infarction. Serial echocardiographic follow-up.

BACKGROUND: It has been shown that successful reperfusion of the infarct-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were detected from several days to several months after infarction. To date, however, no study has shown that these effects can be demonstrated within hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patency on ventricular volume and function. The aim of this study was to assess separate effects of thrombolysis and patency of the infarct-related artery on left ventricular size and function by serial two-dimensional echocardiographic examinations. METHODS AND RESULTS: We evaluated 131 consecutive patients with first acute myocardial infarction by two-dimensional echocardiography in the following sequence: days 1, 2, 3, 7, and after 3 and 6 weeks. Intravenous streptokinase was administered in 81 patients, and 50 patients were treated without thrombolysis. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were determined from apical two- and four-chamber views using the Simpson biplane formula and normalized to body surface area. Coronary angiography was performed in 107 patients after a mean of 26.0 +/- 20.2 (mean +/- SD) days after infarction. Patency of the infarct-related artery was assessed using TIMI criteria, with 54 considered patent (TIMI 3) and 53 with TIMI grade < 3. On day 1, end-systolic volume was significantly higher in patients not receiving thrombolysis (37.7 +/- 15.3 versus 33.0 +/- 10.6 mL/m2, P = .045). End-systolic volume (ESVi) was significantly higher in patients treated without thrombolysis throughout the study, whereas significant differences in end-diastolic volume (EDVi) were detected from day 3 (P = .041) onward and in ejection fraction (EF) from day 2 (P = .025) onward, all differences becoming progressively more significant with time (6-week values: EDVi, 78.8 +/- 25.4 versus 65.9 +/- 15.7 mL/m2, P = .001; ESVi, 45.4 +/- 22.6 versus 33.9 +/- 15.1 mL/m2, P = .002; EF, 45.1 +/- 11.6% versus 50.2 +/- 10.1%, P = .018). Patients with an occluded infarct-related artery (TIMI < 3) demonstrated highly significant differences at 6 weeks compared with patients with patent vessels (EDVi, 76.8 +/- 24.7 versus 65.2 +/- 15.6 mL/m2, P = .006; ESVi, 44.6 +/- 23.3 versus 31.9 +/- 12.2 mL/m2, P = .001; EF, 45.0 +/- 11.6% versus 52.1 +/- 9.0%, P < .001), but these differences developed more slowly than that seen among the thrombolytic subgroups. Indeed, multivariate analysis demonstrated that thrombolysis was the major determinant of initial volumes (P = .08, .02, and .08 for EDVi, ESVi, and EF, respectively), while vessel patency was the overwhelming determinant of subsequent changes (P = .0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejection fractions lower in patients with anterior versus inferior infarction, but even adjusting for these differences as well as those associated with age, sex, and initial ventricular volume, the additive and independent impact of thrombolysis and infarct vessel patency persisted. CONCLUSIONS: These data indicate that the beneficial effect of thrombolysis on left ventricular size and function can be demonstrated in the earliest phases of acute myocardial infarction and that subsequent changes are mediated primarily through patency of the infarct-related artery. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myocardial infarction.