Association polymorphism of guanine nucleotide-binding protein β3 subunit ( GNB3 ) C825T and insertion/deletion of the angiotensin-converting enzyme ( ACE ) gene with peripartum cardiomyopathy

• Published in: Frontiers in cardiovascular medicine Vol. 10; p. 1096514
• Main Authors: Dewi, Ivana Purnama, Wardhani, Louisa Fadjri Kusuma, Maghfirah, Irma, Dewi, Kristin Purnama, Subagjo, Agus, Alsagaff, Mochamad Yusuf, Nugroho, Johanes
• Format: Journal Article
• Language: English
• Published: Switzerland Frontiers Media S.A 2023
• Subjects: angiotensin-converting enzyme; Cardiovascular Medicine; guanine nucleotide–binding protein subunit β3; peripartum cardiomyopathy; PPCM; single nucleotide polymorphism; guanine nucleotide–binding protein subunit β3; single nucleotide polymorphism; peripartum cardiomyopathy; PPCM; angiotensin-converting enzyme
• ISSN: 2297-055X; 2297-055X
• DOI: 10.3389/fcvm.2023.1096514

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related heart disease. Genetic roles such as gene polymorphisms may relate to the etiology of PPCM. This study analyzes the association between single nucleotide gene polymorphism (SNP) guanine nucleotide-binding protein beta-3 subunit ( ) C825T and insertion/deletion (I/D) of the angiotensin-converting enzyme ( ) gene with the incidence of PPCM. An analytic observational study with a case-control design was conducted at the Integrated Cardiac Service Center of Dr. Soetomo General Hospital, Surabaya, Indonesia. PPCM patients of the case and control groups were enrolled. Baseline characteristic data were collected and blood samples were analyzed for SNP in the C825T gene and for I/D in the gene by using the polymerase chain reaction, restriction fragment length polymorphism, and Sanger sequencing. We also assessed levels among different genotypes using a sandwich-ELISA test. A total of 100 patients were included in this study, with 34 PPCM cases and 66 controls. There were significant differences in TT and TC genotypes in the case group compared with that in the control group (TT: 35.3% vs. 10.6%,  = 0.003; TC: 41.2% vs. 62.5%,  = 0.022). The TT genotype increased the risk of PPCM by 4.6-fold. There was also a significant difference in the DD genotype in the case group compared with that in the control group (26.5% vs. 9.1%,  = 0.021). DD genotypes increased the risk of PPCM by 3.6-fold. levels were significantly higher in the DD genotype group than in the ID and II genotype groups (4,356.88 ± 232.44 pg/mL vs. 3,980.91 ± 77.79 pg/mL vs. 3,679.94 ± 325.77 pg/mL,  < 0.001). The TT genotype of and the DD genotype of the are likely to increase the risk of PPCM. Therefore, these polymorphisms may be predisposing risk factors for PPCM incidence. levels were significantly higher in the DD genotype group, which certainly had clinical implications for the management of PPCM patients in the administration of inhibitors as one of the therapy options.