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Journal of Renin-Angiotensin-Aldosterone System
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Cardiac aldosterone in subjects with hypertrophic cardiomyopathy

Wenxia Chai

Department of Clinical Genetics, Erasmus MC

Yvonne M Hoedemaekers

Department of Clinical Genetics, Erasmus MC

Ron HN van Schaik

Department of Clinical Chemistry, Erasmus MC

Marianne van Fessem

Department of Clinical Chemistry, Erasmus MC

Ingrid M Garrelds

Department of Clinical Genetics, Erasmus MC

Jasper J Saris

Department of Clinical Genetics, Erasmus MC

Dennis Dooijes

Department of Clinical Genetics, Erasmus MC

Folkert J ten Cate

Department of Cardiology, Erasmus MC, Rotterdam, The Netherlands

Marcel MJ Kofflard

Department of Cardiology, Erasmus MC, Rotterdam, The Netherlands

AH Jan Danser

Department of Pharmacology, Erasmus MC, a.danser{at}erasmusmc.nl

Left ventricular (LV) hypertrophy in subjects with hypertrophic cardiomyopathy (HCM) is variable, suggesting a role for modifying factors. Here, we determined whether aldosterone modulates hypertrophy in HCM. Cardiac and/or plasma aldosterone were measured in organ donors and HCM patients.The effect of the aldosterone synthase (CYP11B2 ) C-344T polymorphism on LV mass index (LVMI) and interventricular septum thickness (IVS) was determined in 79 genetically independent subjects with HCM. Aldosterone in HCM hearts and plasma was similar to that in normal hearts and plasma. In HCM women, no associations between CYP11B2 genotype and any of the measured parameters were observed, whereas in HCM men, LVMI increased with the presence of the T allele. Similar T allele-related increases were observed for IVS. Multiple regression analysis revealed that the T allele-related effect on IVS occurred independently of renin, the ACE I/D polymorphism, the AT1-receptor A/C 1166 polymorphism and the AT -receptor A/C 3123 polymorphism. In conclusion, circulating and cardiac aldosterone are normal in HCM, thereby arguing against selectively increased cardiac aldosterone production in HCM.Thus, the association between the CYP11B2 C-344T polymorphism and hypertrophy in HCM most likely relates to the T allele-related increases in circulating aldosterone.This finding raises the need for studies determining the benefit of aldosterone blockade in HCM.

Key Words: aldosterone • hypertrophy • polymorphism • angiotensin • gender

Journal of Renin-Angiotensin-Aldosterone System, Vol. 7, No. 4, 225-230 (2006)
DOI: 10.3317/jraas.2006.042


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