EFFECT OF THROMBOLYSIS ON ACUTE MITRAL REGURGITATION DURING EVOLVING MYOCARDIAL-INFARCTION - EXPERIENCE FROM THE THROMBOLYSIS IN MYOCARDIAL-INFARCTION (TIMI) TRIAL

Objectives. This study was undertaken to determine whether early succe ssful thrombolysis can reverse infarct-associated mitral valve dysfunc tion. Background. Mitral regurgitation is a common complication of acu te myocardial infarction and has been shown to adversely affect both s hort- and long-term prognosis. Although anecdotal reports have suggest ed that reperfusion of the infarct-related artery may restore normal f unction to the mitral valve, this theory has not been subjected to for mal investigation. Methods. Patients with total or partial obstruction of the infarct-related artery received intravenous thrombolytic thera py with either streptokinase or recombinant tissue-type plasminogen ac tivator within 7 h of symptom onset (mean 4.8 h) as part of the Thromb olysis in Myocardial Infarction (TIMI) Phase I trial. Repeat coronary angiography assessed arterial patency at 90 min and 10 days after atte mpted reperfusion. The presence and severity of mitral regurgitation w ere determined by contrast ventriculography both before thrombolysis a nd before hospital discharge. Results. Overall, 21 (16%) of the 132 st udy patients exhibited mitral regurgitation on either their initial or their predischarge ventriculogram. The proportion of infarct-related arteries found to be patent (TIMI flow grade 2 or 3) was statistically similar in patients with and without mitral regurgitation during each angiographic evaluation period (initial, 90 min and 10 days). Althoug h coronary artery perfusion increased overall during sequential measur ement (mean TIMI grade was 0.4 +/- 0.6 initially, 1.5 +/- 1.3 at 90 mi n and 2.2 +/- 1.0 at 10 days), the pattern of reperfusion observed cou ld not predict an increase or decrease in regurgitant severity (p = NS ). Early mitral regurgitation resolved in 57% of patients by 10 days, but this resolution appeared independent of the presence or absence of improved coronary perfusion (60% vs. 50%). The development of new reg urgitation during the recovery period (6%) was also unrelated to impro ved perfusion (7% vs. 4%). Conclusions. Acute mitral regurgitation dev eloping during myocardial infarction shows frequent changes in its pre sence or severity during the lst 10 days, appears independent of coron ary artery patency both early and late after thrombolysis and cannot b e reliably treated by improving arterial perfusion with thrombolytic a gents.