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GENETIC VARIANTS OF PROTEINS FROM THE RENIN ANGIOTENSIN SYSTEM ARE ASSOCIATED WITH PRESSURE LOAD CARDIAC HYPERTROPHY
Author(s) -
Wong KK,
Summers KM,
Burstow DJ,
West MJ
Publication year - 1996
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1996.tb02788.x
Subject(s) - renin–angiotensin system , cardiac hypertrophy , muscle hypertrophy , medicine , blood pressure , genetic variants , angiotensin ii , peptidyl dipeptidase a , endocrinology , cardiology , biology , genotype , genetics , gene
SUMMARY 1. The relationship between the angiotensinogen (AGT) T 174 M, angiotensin converting enzyme (ACE) insertion/deletion (I/D) and the angiotensin II type 1 receptor (AT 1 ) genetic markers and left ventricular hypertrophy was examined in normal subjects and those with aortic stenosis. 2. Subjects with aortic stenosis had higher left ventricular systolic pressure and relative wall thickness (RWT) compared with normal. However, within aortic stenosis subjects, left ventricular RWT did not correlate with left ventricular systolic pressure or with aortic valve area. 3. In subjects with aortic stenosis, left ventricular RWT was higher in those with ACE DD ( P <0.05) or AGT T 174 M ( P <0.06) compared with those with the ACE II or ID genotype or AGT TT 174 genotype. No relationship was observed with any of the AT 1 alleles. The ACE and AGT genetic markers independently predicted left ventricular RWT in aortic stenosis. No association was observed between these genotypes and left ventricular RWT in normal subjects. 4. The data suggest that the AGT T 174 M and ACE I/D genotypes may act together to influence the degree of hypertrophy in subjects with aortic stenosis. 5. In patients with aortic stenosis, genetic variants of proteins from the renin angiotensin system may be at least as important as left ventricular systolic pressure in determining the degree of left ventricular hypertrophy and could therefore explain the clinical variation observed in the progression to cardiac dysfunction.