INDEPENDENT IMPACT OF THROMBOLYTIC THERAPY AND VESSEL PATENCY ON LEFT-VENTRICULAR DILATION AFTER MYOCARDIAL-INFARCTION - SERIAL ECHOCARDIOGRAPHIC FOLLOW-UP

Citation
Ad. Popovic et al., INDEPENDENT IMPACT OF THROMBOLYTIC THERAPY AND VESSEL PATENCY ON LEFT-VENTRICULAR DILATION AFTER MYOCARDIAL-INFARCTION - SERIAL ECHOCARDIOGRAPHIC FOLLOW-UP, Circulation, 90(2), 1994, pp. 800-807
Citations number
22
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
90
Issue
2
Year of publication
1994
Pages
800 - 807
Database
ISI
SICI code
0009-7322(1994)90:2<800:IIOTTA>2.0.ZU;2-B
Abstract
Background It has been shown that successful reperfusion of the infarc t-related artery by thrombolysis can prevent left ventricular dilation after acute myocardial infarction; these beneficial effects were dete cted from several days to several months after infarction. To date, ho wever, no study has shown that these effects can be demonstrated withi n hours after the onset of infarction. Furthermore, data are scarce on the independent impact of thrombolytic therapy and late vessel patenc y on ventricular volume and function. The aim of this study was to ass ess separate effects of thrombolysis and patency of the infarct-reiate d artery on left ventricular size and function by serial two-dimension al echocardiographic examinations. Methods and Results We evaluated 13 1 consecutive patients with first acute myocardial infarction by two-d imensional 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. Lef t 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. Coro nary 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 (T IMI 3) and 53 with TIMI grade <3. On day 1, end-systolic volume was si gnificantly higher in patients not receiving thrombolysis (37.7+/-15.3 versus 33.0+/-10.6 mL/m(2), P=.045). End-systolic volume (ESVi) was s ignificantly higher in patients treated without thrombolysis throughou t the study, whereas significant differences in end-diastolic volume ( EDVi) were detected from day 3 (P=.041) onward and in ejection fractio n (EF) from day 2 (P=.025) onward, all differences becoming progressiv ely more significant with time (6-week values: EDVi, 78.8+/-4 versus 6 5.9+/-7 mL/m(2), P=.001; ESWi, 45.4+/-22.6 versus 33.9+/-15.1 mL/m(2), 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 signi ficant differences at 6 weeks compared with patients with patent vesse ls (EDWi, 76.81+/-24.7 versus 65.2+/-15.6 mL/m(2), P=.006; ESVi, 44.6/-23.3 versus 31.9+/-12.2 mL/m(2), P=.001; EF, 45.0+/-11.6% versus 52. 1+/-9.0%, P<.001), but these differences developed more slowly than th at seen among the thrombolytic subgroups. Indeed, multivariate analysi s demonstrated that thrombolysis was the major determinant of initial volumes (P=.08, .02, and .08 for EDVi, ESVi, and EF, respectively), wh ile vessel patency was the overwhelming determinant of subsequent chan ges (P=.0033, .0002, and .0024 for EDVi, ESVi, and EF, respectively). Additionally, ventricular volumes were significantly higher and ejecti on fractions lower in patients with anterior versus inferior infarctio n, but even adjusting for these differences as well as those associate d with age, sex, and initial ventricular volume, the additive and inde pendent impact of thrombolysis and infarct vessel patency persisted. C onclusions These data indicate that the beneficial effect of thromboly sis on left ventricular size and function can be demonstrated in the e arliest phases of acute myocardial infarction and that subsequent chan ges are mediated primarily through patency of the infarct-related arte ry. Thrombolytic therapy and late vessel patency thus have an additive and complementary impact in reducing ventricular dilation after myoca rdial infarction.