Author + information
- Received October 29, 1992
- Revision received March 8, 1993
- Accepted March 10, 1993
- Published online September 1, 1993.
- Kenneth G Lehmann, MD, FACC∗∗,
- Charles K Francis, MD, FACC∗,
- Florence H Sheehan, MD∗∗,
- Harold T Dodge, MD, FACC∗∗,
- The TIMI study Group†
- ↵∗Address for correspondence: Kenneth G. Lehmann, MD, Section of Cardiology (111C), Seattle Veterans Affairs Medical Center, 1660 South Columbian Way, Seattle, Washington 98108.
Objective. This study was undertaken to determine whether early successful thrombolysis can reverse infarct-associated mitral valve dysfunction.
Background. Mitral regurgitation is a common complication of acute myocardial infarction and has been shown to adversely affect both short and long-term prognosis. Although anecdotal reports have suggested that reperfusion of the infarct-related artery may restore normal function to the mitral valve, this theory has not been subjected to formal investigation.
Method. Patients with total or partial obstruction of the infarct-related artery received intravenous thrombolytic therapy with either streptokinase or recombinant tissue-type plasminogen activator within 7 h of symptom onset (mean 4.8 h) as part of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial. Repeat coronary angiography assessed arterial patency at 90 min and 10 days after attempted reperfusion. The presence and severity of mitral regurgitation were determined by contrast ventriculography both before thrombolysis and before hospital discharge.
Result. Overall, 21 (16%) of the 132 study ptients 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). Although coronary artery perfusion increased overall during sequential measurement (mean TIMI grade was 0.4 ± 0.6 initially, 1.5 ± 1.3 at 90 min and 2.2 ± 1.0 at 10 days), the pattern of reperfusion observed could 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 regurgitation during the recovery period (6%) was also unrelated to improved perfusion (7% vs. 4%).
Conclusions. Acute mitral regurgitation developing during myocardial infarction shows frequent changes in its presence or severity during the 1st 10 days, appears independent of coronary artery patency both early and late after thrombolysis and cannot be reliably treated by improving arterial perfusion with thrombolytic agents.
↵† A complete list of the TIMI Study Group appears in Reference 3.
☆ This study was presented in part at the 62nd Scientific Sessions of the American Heart Association, New Orleans, Louisiana, November 1989. It was supported by research contracts and grants from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland.
- Received October 29, 1992.
- Revision received March 8, 1993.
- Accepted March 10, 1993.