Influence of angiotensin-I-converting-enzyme insertion/deletion gene polymorphism on perioperative hemodynamics after coronary bypass graft surgery.

The angiotensin I-converting enzyme insertion/ deletion polymorphism (ACE-I/D), including three genotypes (II, ID, DD), with a known impact on midterm mortality and morbidity in patients after coronary artery bypass graft surgery (CABG), was studied. Since this polymorphism has been linked with increased vascular response to phenylephrine during cardiopulmonary bypass (CPB), we investigated its possible effect on perioperative hemodynamics in patients undergoing CABG. Genotyping for the ACE-I/D was performed by polymerase chain reaction (PRC) amplification in 110 patients who underwent elective CABG with CPB. Patients were assigned to two groups according to their genotype (group II [II genotype] and group ID/DD [ID and DD genotypes]). Systemic hemodynamics were measured directly before and at 4 h, 9 h, and 19 h after CPB. Genotype distribution of ACE-I/D was 18%, 57%, and 25% in genotypes II, ID, and DD, respectively. The two groups were similar in age (group II: 66+/-6 years, group ID/DD: 66+/-8 years), body-mass-index (BMI) (group II: 28+/-2, group ID/DD: 29+/-5 kg/m2), male: female ratio (group II: 16: 4, group ID/DD: 63: 27) and Euroscore (group II: 3.1+/-1.9, group ID/DD: 3.5+/-2.1). There were no differences in mortality rate or perioperative systemic hemodynamics. The pulmonary vascular resistance before cardiopulmonary bypass was higher in the ID/DD genotypes than in the II genotypes (227+/-121 vs 297+/-169 dyn.s(-1).m2.cm(-5)). Four hours after CPB no difference remained; at 9 h after cardiopulmonary bypass there was a slight difference in pulmonary vascular resistance between the two groups (247+/-134 vs 290+/-117 dyn.s(-1).m2.cm(-5)) and a significant difference in pulmonary arterial pressure (19+/-6 vs 23+/-8); at 19 h after CPB the differences were no longer detectable. ACE-I/D had no influence on perioperative systemic hemodynamics. However, transitory differences in pulmonary hemodynamic were observed after CPB. These differences may have been due to changes in serum ACE activity during CPB.