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Association between a Deletion Polymorphism of the Angiotensin-Converting-Enzyme Gene and Left Ventricular Hypertrophy
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Association between a Deletion Polymorphism of the Angiotensin-Converting-Enzyme Gene and Left Ventricular Hypertrophy
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Journal Article
Association between a Deletion Polymorphism of the Angiotensin-Converting-Enzyme Gene and Left Ventricular Hypertrophy
1994
Overview
Left ventricular hypertrophy, a major independent risk factor for morbidity and mortality from cardiovascular disease,
1
–
4
is widely thought to be a consequence of left ventricular pressure overload
5
,
6
. However, the degree of such hypertrophy in patients with mildly elevated arterial pressure is not uniform and may range from normal ventricular mass to severe hypertrophy
6
,
7
. Furthermore, recent epidemiologic studies have shown that many subjects with left ventricular hypertrophy have normal blood pressure, suggesting that factors other than hemodynamic overload may contribute to the hypertrophy
4
.
Neuroendocrine factors such as angiotensin II and bradykinin have been implicated in . . .
Publisher
Massachusetts Medical Society
Subject
/ Aged
/ Alleles
/ Biological and medical sciences
/ Enzymes
/ Female
/ Genetics
/ Heart
/ Heart failure, cardiogenic pulmonary edema, cardiac enlargement
/ Humans
/ Hypertrophy, Left Ventricular - diagnosis
/ Hypertrophy, Left Ventricular - genetics
/ Male
/ Peptidyl-Dipeptidase A - genetics
/ Rodents
/ Women
