Author + information
- Received May 22, 1989
- Revision received December 27, 1989
- Accepted March 14, 1990
- Published online August 1, 1990.
- Michael B. Honan, MD∗,
- Frank E. Harrell Jr., PhD,
- Keith A. Reimer, MD, PhD,
- Robert M. Califf, MD, FACC,
- Daniel B. Mark, MD, MPH, FACC,
- David B. Pryor, MD, FACC and
- Mark A. Hlatky, MD, FACC
- ↵∗Address for reprints: Michael B. Honan, MD. 880 Montclair Road, 1st Floor, Birmingham, Alabama 35213.
This study examined the relation between the risk of cardiac rupture and the timing of thrombolyiic therapy for acute myocardial infarction. To test the hypothesis that cardiac rapture is prevented by early thrombolytic therapy but is promoted by late treatment, randomized controlled trials or thrombolytk agents for myocardial infarction were pooled. A logistic regression model including 58 cases of cardiac rupture among 1,638 patients from four trials showed that the odds ratio (treated/control) of cardiac rapture was directly correlated with time to treatment (p = 0.01); at 7 h, the odds ratio was 0.4 (95% confidence limits 0.17 to 0.93); at 11 h, it was 0.93 (0.53 to 1.60) and at 17 h, it was 3.21 (1.10 to 10.1).
Analysis of data from the Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) trial independently confirmed the relation between time to thrombolytic therapy and risk of cardiac rapture (p = 0.03). Analysis of 4,692 deaths in 44346 patients demonstrated that the odds ratio of death was also directly correlated with time to treatment (p = 0.006); at 3 h, the odds ratio for death was 0.72 (0.67 to 0.77); at 14 h, it was 0.88 (0.77 to 1.06) and at 21 h, it was 1 (0.82 to 1.37). Thrombolytic therapy early after acute myocardial infarction improves survival and decreases the risk of cardiac rupture. Late administration of thrombolytic therapy also appears to improve survival but may increase the risk of cardiac rupture.
☆ This work was supported in part by Research Grants HS-05635 and HS-04873 from the National Center for Health Services Research, Hyattsville, Maryland, Research Grant HL-17670 and HL-36587 from the National Heart, Lung, and Blood Institute, Bethesda, Maryland and grants from the Andrew W. Mellon Foundation, New York, New York and the Robert Wood Johnson Foundation, Princeton, New Jersey. It was presented in part at the 61st Annual Scientific Session of the American Heart Association, Washington. D.C., November 1988.
- Received May 22, 1989.
- Revision received December 27, 1989.
- Accepted March 14, 1990.