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.