Author + information
- Received August 5, 1991
- Revision received October 18, 1991
- Accepted November 15, 1991
- Published online May 1, 1992.
- Gary F. Mitchell, MD∗,1,
- Gervasio A. Lamas, MD, FACC,
- Douglas E. Vaughan, MD, FACC and
- Marc A. Pfeffer, MD, PhD, FACC2
- ↵∗Address for reprints: Gary F. Mitchell, MD, Cardiovascular Division, Brigham and Women's Hospital, 75 Francis Street, Boston, Massachusetts 02115.
Infarct expansion after myocardial infarction results in early ventricular enlargement and distortion of ventricular geometry. To characterize the components of late volume enlargement, biplane left ventriculography was performed in 52 patients 3 weeks and 1 year after a first anterior myocardial infarction. Biplane diastolic circumference and contractile and noncontractile segment lengths were measured. Global geometry was evaluated by using a sphericity index (angiographic volume of the ventricle divided by the volume of a sphere with the same circumference). Regional geometry was assessed by measurement of endocardial curvature, an important determinant of wall tension.
End-diastolic volume was enlarged at baseline and increased at 1 year (230 ± 42 to 244 ± 55 ml, p = 0.01) as a result of increases in contractile segment length (34 ± 5 to 37 ± 5 cm, p < 0.001) and sphericity index (0.74 ± 0.07 to 0.76 ± 0.08, p < 0.001), whereas the noncontractile segment length decreased (15 ± 6 to 12 ± 6 cm, p < 0.005). Curvature analysis revealed a flattening of presumably high tension concavity at the anterobasal (−6.0 ± 4.0 to −4.5 ± 3.7, p < 0.01) and inferior (−4.5 ± 2.0 to −3.6 ± 2.1, p < 0.005) margins of the infarct and less bulging of the anterior wall (9.4 ± 2.5 to 8.2 ± 2.3, p < 0.001). Patients selected for late enlargement (diastolic volume increase >20 ml, n = 19) had an increase in sphericity (0.75 ± 0.05 to 0.80 ± 0.08, p < 0.005) and in diastolic circumference (54 ± 3 to 56 ± 4 cm, p < 0.001) secondary to elongation of the contractile segment (32 ± 4 to 36 ±4 cm, p = 0.001) at 1 year.
Thus, late ventricular enlargement after anterior infarction results from an increase in contractile segment length and a change in ventricular geometry and is not a result of progressive infarct expansion. In the group of patients at high risk for late ventricular enlargement because of persistent occlusion of the infarct-related vessel, captopril therapy attenuated late volume enlargement by preventing these changes in contractile segment length and chamber geometry.
↵1 During this study, Dr. Mitchell was a recipient of training Grant T32-HL-07604 from the National Institutes of Health and of a Physician-Investigator Fellowship from the Massachusetts Affiliate of the American Heart Association. Needham, Massachusetts.
↵2 Dr. Pfeffer was a recipient of an Established Investigatorship of the American Heart Association, Dallas, Texas.
☆ This study was supported in part by a grant from E. R. Squibb and Sons, Princeton, New Jersey and by Clinical Research Center Grant RR-02635 from the National Institutes of Health, Bethesda, Maryland.
- Received August 5, 1991.
- Revision received October 18, 1991.
- Accepted November 15, 1991.