Department of Cardiovascular Imaging Science, Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, United Kingdom (P.P.S., P.G., E.L., D.A.B., A.Z.-N., A.J.R.F., G.J.F., P.G.C., L.A.B., C.E.S., E.D., J.P.G., S.P.).
Medical Physics and Engineering, Leeds Teaching Hospitals NHS Trust, United Kingdom (D.A.B.).
Circ Cardiovasc Imaging. 2019 Sep;12(9):e009417. doi: 10.1161/CIRCIMAGING.119.009417. Epub 2019 Sep 11.
Athletic cardiac remodeling can occasionally be difficult to differentiate from pathological hypertrophy. Detraining is a commonly used diagnostic test to identify physiological hypertrophy, which can be diagnosed if hypertrophy regresses. We aimed to establish whether athletic cardiac remodeling assessed by cardiovascular magnetic resonance is mediated by changes in intracellular or extracellular compartments and whether this occurs by 1 or 3 months of detraining.
Twenty-eight athletes about to embark on a period of forced detraining due to incidental limb bone fracture underwent clinical assessment, ECG, and contrast-enhanced cardiovascular magnetic resonance within a week of their injury and then 1 month and 3 months later.
After 1 month of detraining, there was reduction in left ventricular (LV) mass (130±28 to 121±25 g; <0.0001), increase in native T1 (1225±30 to 1239±30 ms; =0.02), and extracellular volume fraction (24.5±2.3% to 26.0±2.6%; =0.0007) with no further changes by 3 months. The decrease in LV mass was mediated by a decrease in intracellular compartment volume (94±22 to 85±19 mL; <0.0001) with no significant change in the extracellular compartment volume. High LV mass index, low native T1, and low extracellular volume fraction at baseline were all predictive of regression in LV mass in the first month.
Regression of athletic LV hypertrophy can be detected after just 1 month of complete detraining and is mediated by a decrease in the intracellular myocardial compartment with no change in the extracellular compartment. Further studies are needed in athletes with overt and pathological hypertrophy to establish whether native T1 and extracellular volume fraction may complement electrocardiography, echocardiography, cardiopulmonary exercise testing, and genetic testing in predicting the outcome of detraining.
运动性心脏重构偶尔难以与病理性肥大区分。停训是一种常用于识别生理性肥大的诊断性试验，如果肥大消退即可诊断。我们旨在确定心血管磁共振评估的运动性心脏重构是否通过细胞内或细胞外间隙的变化来介导，以及这种变化是否在 1 或 3 个月的停训后发生。
28 名即将因意外肢体骨折而被迫停训的运动员在受伤后一周内接受了临床评估、心电图和对比增强心血管磁共振检查，然后在 1 个月和 3 个月后再次进行检查。
停训 1 个月后，左心室（LV）质量减少（130±28 至 121±25 g；<0.0001），本征 T1 增加（1225±30 至 1239±30 ms；=0.02），细胞外容积分数增加（24.5±2.3%至 26.0±2.6%；=0.0007），3 个月时无进一步变化。LV 质量的减少是由细胞内间隙体积减少（94±22 至 85±19 mL；<0.0001）介导的，而细胞外间隙体积无明显变化。基线时高 LV 质量指数、低本征 T1 和低细胞外容积分数均预测第一个月 LV 质量的回归。
在完全停训仅 1 个月后即可检测到运动性 LV 肥大的消退，并且是由细胞内心肌间隙减少介导的，而细胞外间隙无变化。需要对有明显和病理性肥大的运动员进行进一步研究，以确定本征 T1 和细胞外容积分数是否可以补充心电图、超声心动图、心肺运动试验和基因检测，预测停训的结果。
Zotero 插件
