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ACE I/D polymorphism in Indian patients with hypertrophic cardiomyopathy and dilated cardiomyopathy
Authors:Taranjit Singh Rai  Perundurai Subramaniam Dhandapany  Tarunveer Singh Ahluwalia  Monica Bhardwaj  Ajay Bahl  Kewal Krishan Talwar  Krishnakumar Nair  Andiappan Rathinavel  Madhu Khullar
Institution:(1) Department of Experimental Medicine and Biotechnology, Post Graduate Institute of Medical Education and Research, Chandigarh, 160012, India;(2) Department of Biochemisrty, Madurai Kamraj University, Madurai, India;(3) Department of Cardiology, Post Graduate of Institute of Medical Education and Research (PGIMER), Chandigarh, India;(4) Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences and Technology, Trivandrum, India;(5) Department of Cardiothoracic Surgery, Madurai Medical College and Rajaji Government Hosiptal, Madurai, India
Abstract:Aim The study was carried to determine the association of angiotensin converting enzyme (ACE) insertion/deletion (I/D) polymorphism with the risk of hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), and restrictive cardiomyopathy (RCM). Methods and results A total of 174 patients diagnosed with cardiomyopathy (118 with HCM, 51 with DCM, and 5 with RCM) and 164 ethnically, age- and gender-matched controls were included in the study. ACE I/D genotyping was performed by PCR. In total, 25.86% of the patients were in New York Heart Association (NYHA) class III and IV at presentation. A total of 67.24% patients had dyspnea, 56.89% had angina pectoris, and 25.28% of the patients had at least one event of syncope. Frequency of occurrence of the disease was more in male patients compared to female patients (P < 0.05). After adjustment for age, sex, body mass index (BMI), and smoking habit, the prevalence of ACE DD genotype, and ACE ‘D’ allele was significantly higher in patients as compared to controls and was associated with increased risk (DD: OR 2.11, 95% CI 1.27–3.52, P < 0.05; ‘D’: OR 1.91, 95% CI 1.08–3.35, P < 0.05). The mean septal thickness was higher for DD and ID genotypes (20.40 ± 3.73 mm and 21.82 ± 5.35 mm, respectively) when compared with II genotype (18.63 ± 6.69 mm) in HCM patients, however, the differences were not significant statistically (P > 0.05). The DCM patients with ID genotype showed significantly decreased left ventricular ejection fraction (LVEF) at enrolment (26.50 ± 8.04%) (P = 0.04). Conclusion Our results suggest that D allele of ACE I/D polymorphism significantly influences the HCM and DCM phenotypes.
Keywords:ACE I/D polymorphism  Hypertrophic cardiomyopathy  Dilated cardiomyopathy
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