Effect of thrombolysis on acute mitral regurgitation during evolving myocardial infarction. Experience from the Thrombolysis in Myocardial Infarction (TIMI) Trial.
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.


METHODS
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.


RESULTS
Overall, 21 (16%) of the 132 study 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). 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.
Lehmann
K G
KG
Division of Cardiology, Yale University School of Medicine, New Haven, Connecticut.
Francis
C K
CK
Sheehan
F H
FH
Dodge
H T
HT
D000208:Acute Disease; D000328:Adult; D000368:Aged; D000704:Analysis of Variance; D006328:Cardiac Catheterization; D016009:Chi-Square Distribution; D017023:Coronary Angiography; D005260:Female; D006352:Heart Ventricles / Q000000981:diagnostic imaging; D006801:Humans; D008297:Male; D008875:Middle Aged; D008944:Mitral Valve Insufficiency / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000453:epidemiology / Q000209:etiology; D009203:Myocardial Infarction / Q000150:complications / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000453:epidemiology; D011994:Recombinant Proteins / Q000627:therapeutic use; D015912:Thrombolytic Therapy / Q000706:statistics & numerical data; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use
D011994:Recombinant Proteins; D010959:Tissue Plasminogen Activator