ADAPTATION TO CARDIAC DYSFUNCTION AFTER MYOCARDIAL-INFARCTION

Citation
P. Gaudron et al., ADAPTATION TO CARDIAC DYSFUNCTION AFTER MYOCARDIAL-INFARCTION, Circulation, 87(5), 1993, pp. 83-89
Citations number
28
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
87
Issue
5
Year of publication
1993
Supplement
4
Pages
83 - 89
Database
ISI
SICI code
0009-7322(1993)87:5<83:ATCDAM>2.0.ZU;2-Q
Abstract
Survival after myocardial infarction decreases with left ventricular d ilatation, although dilatation at 4 weeks was found to be compensatory . To study this apparent discrepancy, prospective simultaneous volume and hemodynamic measurements at rest were extended in 39 patients with small and 37 with large myocardial infarctions from 4 days (range, 2- 6 days) and 4 weeks (range, 3-5 weeks) to 6 months (range, 5-8 months) after infarction and were repeated during supine bicycle exercise at 50 W. In patients with small infarction, end-diastolic volume (mL/m2) decreased from 4 days to 6 months; ejection fraction (%), stroke volum e (mL/m2), and end-systolic volume (mL/m2) remained unchanged. Stroke index rose during exercise at 4 weeks and 6 months. In patients after large infarction (n=37), left ventricular end-systolic volume index (4 days, 38+/-3; 4 weeks, 47+/-3; 6 months, 52+/-3*; *p<0.05 versus 4 d ays) and end-diastolic volume indexes (4 days, 72+/-3; 4 weeks, 86+/-5 ; 6 months, 92+/-5*dagger; *p<0.05 versus 4 days, (dagger)p<0.05 vers us 4 weeks) increased at constant wedge pressure. Stroke index remaine d restored beyond 4 weeks after infarction (4 days, 35+/-2; 4 weeks, 4 2+/-2; 6 months, 42+/-2*; p<0.05 versus 4 days) and rose during exerc ise at 4 weeks (rest, 45+/-2; exercise, 55+/-3; p<0.05) but not at 6 m onths (rest, 42+/-3; exercise, 45+/-3; p=NS). These findings indicate that left ventricular dilatation and remodeling in its early phase (wi thin 4 weeks after myocardial infarction) are compensatory since hemod ynamics at rest are maintained and augmentation of stroke volume durin g exercise is possible. Progressive dilatation of the left ventricle b eyond 4 weeks after infarction, however, is noncompensatory since the capability to augment stroke volume during exercise was lost. Thus, pr ogressive left ventricular dilatation may cause an insidious transitio n to chronic cardiac dysfunction after myocardial infarction. This may explain the apparent discrepancy that left ventricular dilatation aft er infarction reduces survival late after infarction, although it may restore depressed stroke volume in its early phase.