BACKGROUND AND AIM OF THE STUDY: Factors responsible for cardiac hypertrophy in patients with aortic stenosis (AS) are not well defined. The study aim was to examine the relationship between angiotensin-converting enzyme (ACE) I/D polymorphism and the degree of cardiac hypertrophy in patients with AS. METHODS: A total of 392 white patients (159 women, 233 men; age range: 32-82 years) with AS was analyzed, with clinical data, echocardiographic parameters and ACE I/D polymorphism being assessed. RESULTS: Left ventricular mass index (LVMI) and wall thickness (LVWT) were greater in men than in women (226 +/- 66 versus 200 +/- 68 g/m2, p <0.0001; and 28.4 +/- 4.5 versus 27.3 +/- 4.1 mm, p = 0.02, respectively). In all patients, LVMI was significantly correlated with the maximal aortic gradient, ejection fraction and gender, whereas LVWT was dependent upon maximal aortic gradient, ejection fraction, gender and history of hypertension. In women, cardiac hypertrophy increased with age. Hypertrophy in women aged <66 years correlated with an absence of the DD genotype. In men, a reverse correlation of both LVMI and LVWT with age was observed (higher in younger patients). The presence of a DD genotype in men seemed to have a significant impact on the degree of cardiac hypertrophy. CONCLUSION: The degree of left ventricular hypertrophy in patients with AS was higher in men than in women. ACE I/D polymorphism appeared to have a modulating impact on cardiac hypertrophy in patients with AS, notably those aged <66 years. A higher degree of cardiac hypertrophy was seen in men with the DD genotype, and in women without the DD genotype.
BACKGROUND AND AIM OF THE STUDY: Factors responsible for cardiac hypertrophy in patients with aortic stenosis (AS) are not well defined. The study aim was to examine the relationship between angiotensin-converting enzyme (ACE) I/D polymorphism and the degree of cardiac hypertrophy in patients with AS. METHODS: A total of 392 white patients (159 women, 233 men; age range: 32-82 years) with AS was analyzed, with clinical data, echocardiographic parameters and ACE I/D polymorphism being assessed. RESULTS: Left ventricular mass index (LVMI) and wall thickness (LVWT) were greater in men than in women (226 +/- 66 versus 200 +/- 68 g/m2, p <0.0001; and 28.4 +/- 4.5 versus 27.3 +/- 4.1 mm, p = 0.02, respectively). In all patients, LVMI was significantly correlated with the maximal aortic gradient, ejection fraction and gender, whereas LVWT was dependent upon maximal aortic gradient, ejection fraction, gender and history of hypertension. In women, cardiac hypertrophy increased with age. Hypertrophy in women aged <66 years correlated with an absence of the DD genotype. In men, a reverse correlation of both LVMI and LVWT with age was observed (higher in younger patients). The presence of a DD genotype in men seemed to have a significant impact on the degree of cardiac hypertrophy. CONCLUSION: The degree of left ventricular hypertrophy in patients with AS was higher in men than in women. ACE I/D polymorphism appeared to have a modulating impact on cardiac hypertrophy in patients with AS, notably those aged <66 years. A higher degree of cardiac hypertrophy was seen in men with the DD genotype, and in women without the DD genotype.
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