Left ventricular size, mass and function in relation to angiotensin-converting enzyme gene and angiotensin-II type 1 receptor gene polymorphisms in patients with coronary artery disease.
The objective of the present study was to analyse the potential synergistic influence of the insertion/deletion polymorphism of the angiotensin-converting enzyme gene (I/D ACE) and the A1166C polymorphism of the angiotensin-II type 1 receptor gene polymorphisms (A1166C AT1R) on the left ventricular size and performance. Three hundred sixty and one consecutive, Caucasian patients with angiographically confirmed coronary artery disease (CAD) were enrolled into the study. Left ventricular diameter, mass and function were evaluated by echocardiography. Screening for the I/D ACE and A1166C AT1R genotypes was performed by polymerase chain reaction of genomic DNA, followed by restriction enzyme digestion and agarose gel electrophoresis. The I/D ACE and A1166C AT1R genotypes separately were not significantly associated with the left ventricular size and function parameters in CAD patients. However, trends towards decreased left ventricular ejection fraction (LVEF) as well as increased left ventricular end-diastolic diameter (LVEDD) and left ventricular mass index (LVMI) were observed when patients with genotype DD+CC/AC and DD+CC were compared to patients homozygous only in one locus (DD or CC). Significant increase in LVEDD and LVMI was observed only in patients with a history of anterior myocardial infarction with combined genotype DD+CC/AC or DD+CC. This study does not support the role of the ACE I/D and AT1R A1166C polymorphisms in the determination of the left ventricular size and performance in patients with significant coronary atherosclerosis. However, it indicates that the influence of polymorphisms may be present in specific patient populations.
Gruchala
Marcin
M
First Department of Cardiology Medical University of Gdańsk, Gdańsk, Poland.
Ciećwierz
Dariusz
D
Ochman
Karolina
K
Wasag
Bartosz
B
Koprowski
Andrzej
A
Wojtowicz
Andrzej
A
Dubaniewicz
Witold
W
Targoński
Radosław
R
Sobiczewski
Wojciech
W
Grzybowski
Adam
A
Romanowski
Piotr
P
Limon
Janusz
J
Rynkiewicz
Andrzej
A
D000804:Angiotensin II; D003324:Coronary Artery Disease / Q000235:genetics*; D004247:DNA / Q000032:analysis; D017931:DNA Primers / Q000737:chemistry; D004452:Echocardiography; D005260:Female; D017353:Gene Deletion; D005838:Genotype; D006720:Homozygote; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000235:genetics; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic / Q000235:genetics*; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics*; D016277:Ventricular Function, Left / Q000235:genetics*; D044465:White People
D017931:DNA Primers; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D000804:Angiotensin II; D004247:DNA; D007703:Peptidyl-Dipeptidase A