Methods: A total of 48 patients (23 females, 25 males; mean age 60±13 years; range 42 to 78 years) were included in the study. Patients with PTE were classified according to carrying of ACE D allele. Group 1 consisted of patients with wild type, while group 2 consisted of patients with ACE D allele carrier.

Results: Tweny-eight patients (58%) had ACE ID (heterozygous) genotype, while six (13%) had ACE DD (homozygous) genotype. The remaining 14 (29%) had no deletion allele of ACE gene. The mean systolic pulmonary arterial pressure (sPAP) was 45.7±17 mmHg in patients with ID genotype, 70.1±20 mmHg in those with DD genotype, and 32.5±9 mmHg in those with II genotype. The comparison of the patients who carried ACE D allele with those who did not demonstrated that the former group had significantly higher levels of sPAP (32.5±8.8 versus 50.8±20 mmHg, p=0.017). It was found that carrying of ACE D allele (Exp(B): 7.331, p=0.032) was found to be independent predictor of pulmonary hypertension in patients with PTE.

Conclusion: In conclusion, we believe that the risk for the development of pulmonary hypertension is higher especially in PTE cases with deletion polymorphism of ACE gene. Therefore, evaluation of the ACE gene in these patients will contribute to shed light into the etiology and prognosis of the disease.