Both environmental and genetic factors play an important role in the pathogenesis of coronary artery disease. In view of angiotensin-converting enzyme (ACE) role in physiology and pathology and benefits of ACE-inhibitors therapy, the gene coding this protein meets criteria for candidate gene for the susceptibility to cardiovascular disease including myocardial infarction. The goal of our research was to assess the association of ACE gene I/D polymorphism with myocardial infarction in Polish population regarding different variables related to the disease (smoking, concomitant hypertension, obesity, plasma cholesterol level and family history). To detect ACE I/D polymorphism method of Rigat with some modification was used. The study population consisted of 314 individuals of Polish origin. 178 of them suffered from acute myocardial infarction or have survived it. Another 136 people without apparent signs and symptoms of cardiovascular pathology or diabetes served as control subjects. No one from the control group reported positive family history. Both allele frequencies and genotype distribution did not differ substantially between study groups. They were similar to those reported in other Caucasian populations. Further analysis did not detect any important differences in allele and genotype frequencies between experimental and control subjects regarding body mass index, total plasma cholesterol level and concomitant arterial hypertension. Cigarette smoking status influenced allele frequencies and genotype distribution in the group of patients with premature myocardial infarction. DD genotype was observed more often among non-smoking patients who suffered from myocardial infarction before the age of 50. These differences had reached the level of statistical significance (p < 0.05).
Conclusions: 1. Insertion/deletion polymorphism in ACE gene does not seem to be associated with myocardial infarction in the studied Polish population. 2. The obtained results suggest that DD genotype may be associated with smoking-dependent risk of myocardial infarction. Further studies are needed to prove this hypothesis.