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Gender‐specific differences in left ventricular remodelling and fibrosis in hypertrophic cardiomyopathy: Insights from cardiovascular magnetic resonance
Author(s) -
SchulzMenger Jeanette,
AbdelAty Hassan,
Rudolph Andre,
Elgeti Thomas,
Messroghli Daniel,
Utz Wolfgang,
Boyé Philipp,
Bohl Steffen,
Busjahn Andreas,
Hamm Bernd,
Dietz Rainer
Publication year - 2008
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2008.06.021
Subject(s) - medicine , cardiology , hypertrophic cardiomyopathy , myocardial fibrosis , fibrosis , magnetic resonance imaging , heart failure , cardiomyopathy , cardiac magnetic resonance , ventricular remodeling , radiology
Background: Gender is an independent risk factor for heart failure mortality in hypertrophic cardiomyopathy (HCM). Aims: To explore the interaction between gender, myocardial fibrosis and remodelling in HCM. Methods: We studied 64 HCM patients (28 females, aged 51 ± 16 years) categorized as non‐obstructive (HNCM, n =31) or obstructive (HOCM, n =33) and 60 healthy subjects (31 females, aged 43 ± 14 years). Cine imaging was performed to assess left ventricular volumes and mass. LV remodelling index (LVRI) was calculated. Extension of late gadolinium enhancement (LGE) was quantified. Results: Females in the control group and in the HNCM group had a lower LVRI than males (control: 0.7±0.1 vs. 0.9±0.2 g/ml, <0.002; HNCM: 1.1±0.2 vs. 1.5±0.5 g/ml, p <0.001). In contrast, HOCM females had a similar LVRI compared to males (1.8±0.5 vs. 1.7±0.4 g/ml, p =ns). Thus the increase in LVRI was more pronounced in females compared to males. LGE was noted in 70% of the patients. No relation was found between the presence or the quantity of myocardial fibrosis and gender in any of the patient subgroups. Conclusion: Our data suggest a disproportionate degree of remodelling in different forms of HCM depending on gender. Gender does not appear to influence the quantity of fibrosis as defined by LGE.