Abstract
Whether antecedent systemic hypertension influences the risk of subsequent left ventricular
(LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction
is unclear. We assessed echocardiographic evidence of ventricular remodeling from
baseline (mean ± SD 11 ± 3 days) to 2 years after an acute myocardial infarction in
122 hypertensive (defined as a history of treated hypertension, baseline systolic
blood pressure ≥140 or baseline diastolic blood pressure ≥90 mm Hg) and 334 nonhypertensive
patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared
with nonhypertensives, baseline heart size, defined as the sum of the average short-
and long-axis LV cavity areas, was similar (70.1 ± 11.9 vs 68.8 ± 11.2 cm2, p = 0.33 at end-diastole; 50.1 ± 11.3 vs 48.8 ± 10.8 cm2, p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 ± 4.3 vs 25.7
± 5.0 cm2, p = 0.043) and wall thickness (1.15 ± 0.16 vs 1.21 ± 0.17 cm, p = 0.004) at end-diastole
were greater among hypertensives. The myocardial infarct segment lengths were similar
in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the
2 groups from baseline to 2 years (p ≤0.001), the increase was significantly greater
in hypertensives than in nonhypertensives (+5.6 ± 11.5 vs +2.2 ± 10.7 cm2, p = 0.005 at end-diastole; +6.23 ± 12.75 vs +2.94 ± 11.4 cm2, p = 0.012 at end-systole). There was no concomitant difference in the change in
LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting
for known confounders, antecedent hypertension was associated with a doubling of the
risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27
to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial
infarct segment length, or captopril use (all p values for interaction >0.10). We
conclude that antecedent hypertension is associated with subsequent LV dilation in
patients after acute myocardial infarction with LV systolic dysfunction.
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Article info
Publication history
Accepted:
March 12,
2004
Received in revised form:
March 12,
2004
Received:
January 19,
2004
Footnotes
☆The Survival and Ventricular Enlargement Trial was originally supported by a grant from the Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, New Jersey. No additional funding was provided for this analysis.
Identification
Copyright
© 2004 Excerpta Medica Inc. Published by Elsevier Inc. All rights reserved.
