期刊
EUROPEAN HEART JOURNAL
卷 36, 期 24, 页码 1547-1554出版社
OXFORD UNIV PRESS
DOI: 10.1093/eurheartj/ehv120
关键词
Hypertrophic Cardiomyopathy; (PMRS)-P-31; Exercise
资金
- British Heart Foundation [FS/07/030]
- Oxford NIHR Biomedical Research Centre
- Oxford BHF Centre of Research Excellence
- British Heart Foundation Intermediate Fellowship
- British Heart Foundation [RG/12/16/29939, FS/10/002/28078, FS/14/17/30634] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0512-10005, NF-SI-0508-10235] Funding Source: researchfish
Aims Hypertrophic cardiomyopathy (HCM) is the commonest cause of sudden cardiac death in the young, with an excess of exercise-related deaths. The HCM sarcomere mutations increase the energy cost of contraction and impaired resting cardiac energetics has been documented by measurement of phosphocreatine/ATP (PCr/ATP) using (31)Phosphorus MR Spectroscopy (P-31 MRS). We hypothesized that cardiac energetics are further impaired acutely during exercise in HCM and that this would have important functional consequences. Methods and results P-31 MRS was performed in 35 HCM patients and 20 age- and gender-matched normal volunteers at rest and during leg exercise with 2.5 kg ankle weights. Peak left-ventricular filling rates (PFRs) and myocardial perfusion reserve (MPRI) were calculated during adenosine stress. Resting PCr/ATP was significantly reduced in HCM (HCM: 1.71 +/- 0.35, normal 2.14 +/- 0.35 P < 0.0001). During exercise, there was a further reduction in PCr/ATP in HCM (1.56 +/- 0.29, P = 0.02 compared with rest) but not in normals (2.16 +/- 0.26, P = 0.98 compared with rest). There was no correlation between PCr/ATP reduction and cardiac mass, wall thickness, MPRI, or late-gadolinium enhancement. PFR and PCr/ATP were significantly correlated at rest (r = 0.48, P = 0.02) and stress (r = 0.53, P = 0.01). Conclusion During exercise, the pre-existing energetic deficit in HCM is further exacerbated independent of hypertrophy, perfusion reserve, or degree of fibrosis. This is in keeping with the change at the myofilament level. We offer a potential explanation for exercise-related diastolic dysfunction in HCM.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据