Deletion polymorphism of the angiotensin-converting enzyme gene is independently associated with left ventricular mass and geometric remodeling in systemic hypertension Academic Article Article uri icon


MeSH Major

  • Masked Hypertension


  • An insertion/deletion (I/D) polymorphism of the angiotensin-converting enzyme (ACE) gene is associated with myocardial infarction, cardiomyopathy, and left ventricular (LV) hypertrophy. LV mass and geometry are related to cardiovascular morbidity and mortality. Two-dimensional directed M-mode echocardiograms and 24-hour ambulatory blood pressure monitoring were performed in 67 hypertensive subjects. Echocardiographic measurements were assessed in blinded fashion. LV mass index and relative wall thickness were calculated. ACE genotypes were determined by polymerase chain reaction amplification of deoxyribonucleic acid prepared from leukocytes, using primers that encompass the polymorphic segment. Systolic ambulatory blood pressure was higher in subjects with the II genotype. All other patient characteristics were similar across genotype groups. After adjustment for other covariables, the DD and ID genotypes were associated with significantly higher LV mass index than was the II genotype. Adjusted relative wall thickness was also higher in subjects with the DD genotype than in subjects with the ID and II genotypes. On multiple regression analysis, systolic ambulatory blood pressure, gender, body mass index, and the ACE genotype were each independently related to LV mass index (R2 = 0.53). Systolic ambulatory blood pressure, race, and ACE genotype were each independently related to relative wall thickness (R2 = 0.34). The ACE genotype explained an additional 3% and 4% of the variations of LV mass index and relative wall thickness, respectively. In conclusion, ACE polymorphism accounted for a small but statistically significant proportion of the variation in LV mass and geometry in our hypertensive subjects.

publication date

  • June 15, 1996



  • Academic Article


Digital Object Identifier (DOI)

  • 10.1016/S0002-9149(96)00198-1

PubMed ID

  • 8677872

Additional Document Info

start page

  • 1315

end page

  • 9


  • 77


  • 15