Parnham Susie, Gleadle Jonathan M, Bangalore Sripal, Grover Suchi, Perry Rebecca, Woodman Richard J, De Pasquale Carmine G, Selvanayagam Joseph B
Department of Cardiovascular Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (S.P., S.G., R.P., C.G.D.P., J.B.S.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.) South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia (S.P., S.G., J.B.S.).
Department of Renal Medicine, Flinders Medical Centre, Bedford Park, South Australia, Australia (J.M.G.) School of Medicine, Flinders University, Bedford Park, South Australia, Australia (S.P., J.M.G., R.P., C.G.D.P., J.B.S.).
J Am Heart Assoc. 2015 Aug 10;4(8):e002249. doi: 10.1161/JAHA.115.002249.
Coronary artery disease and left ventricular hypertrophy are prevalent in the chronic kidney disease (CKD) and renal transplant (RT) population. Advances in cardiovascular magnetic resonance (CMR) with blood oxygen level-dependent (BOLD) technique provides capability to assess myocardial oxygenation as a measure of ischemia. We hypothesized that the myocardial oxygenation response to stress would be impaired in CKD and RT patients.
Fifty-three subjects (23 subjects with CKD, 10 RT recipients, 10 hypertensive (HT) controls, and 10 normal controls without known coronary artery disease) underwent CMR scanning. All groups had cine and BOLD CMR at 3 T. The RT and HT groups also had late gadolinium CMR to assess infarction/replacement fibrosis. The CKD group underwent 2-dimensional echocardiography strain to assess fibrosis. Myocardial oxygenation was measured at rest and under stress with adenosine (140 μg/kg per minute) using BOLD signal intensity. A total of 2898 myocardial segments (1200 segments in CKD patients, 552 segments in RT, 480 segments in HT, and 666 segments in normal controls) were compared using linear mixed modeling. Diabetes mellitus (P=0.47) and hypertension (P=0.57) were similar between CKD, RT, and HT groups. The mean BOLD signal intensity change was significantly lower in the CKD and RT groups compared to HT controls and normal controls (-0.89±10.63% in CKD versus 5.66±7.87% in RT versus 15.54±9.58% in HT controls versus 16.19±11.11% in normal controls, P<0.0001). BOLD signal intensity change was associated with estimated glomerular filtration rate (β=0.16, 95% CI=0.10 to 0.22, P<0.0001). Left ventricular mass index and left ventricular septal wall diameter were similar between the CKD predialysis, RT, and HT groups. None of the CKD patients had impaired global longitudinal strain and none of the RT group had late gadolinium hyperenhancement.
Myocardial oxygenation response to stress is impaired in CKD patients and RT recipients without known coronary artery disease, and unlikely to be solely accounted for by the presence of diabetes mellitus, left ventricular hypertrophy, or myocardial scarring. The impaired myocardial oxygenation in CKD patients may be associated with declining renal function. Noncontrast BOLD CMR is a promising tool for detecting myocardial ischemia in the CKD population.
冠状动脉疾病和左心室肥厚在慢性肾脏病（CKD）和肾移植（RT）人群中很常见。心血管磁共振（CMR）结合血氧水平依赖（BOLD）技术的进展使得评估心肌氧合作为缺血的一种测量方法成为可能。我们假设CKD和RT患者对压力的心肌氧合反应会受损。
53名受试者（23名CKD患者、10名RT受者、10名高血压（HT）对照者和10名无已知冠状动脉疾病的正常对照者）接受了CMR扫描。所有组均在3T下进行电影CMR和BOLD CMR检查。RT组和HT组还进行了延迟钆增强CMR以评估梗死/替代纤维化。CKD组进行二维超声心动图应变检查以评估纤维化。使用BOLD信号强度在静息和使用腺苷（每分钟140μg/kg）激发状态下测量心肌氧合。使用线性混合模型比较了总共2898个心肌节段（CKD患者1200个节段、RT组552个节段、HT组480个节段和正常对照者666个节段）。CKD组、RT组和HT组之间的糖尿病（P=0.47）和高血压（P=0.57）情况相似。与HT对照者和正常对照者相比，CKD组和RT组的平均BOLD信号强度变化显著更低（CKD组为-0.89±10.63%，RT组为5.66±7.87%，HT对照者为15.54±9.58%，正常对照者为16.19±11.11%，P<0.0001）。BOLD信号强度变化与估计肾小球滤过率相关（β=0.16, 95%CI=0.10至0.22, P<0.0001）。CKD透析前组患者、RT组和HT组之间的左心室质量指数和左心室间隔壁直径相似。没有CKD患者出现整体纵向应变受损，也没有RT组患者出现延迟钆增强。
在无已知冠状动脉疾病的CKD患者和RT受者中，对压力的心肌氧合反应受损，不太可能仅由糖尿病、左心室肥厚或心肌瘢痕的存在来解释。CKD患者心肌氧合受损可能与肾功能下降有关。非对比BOLD CMR是检测CKD人群心肌缺血的一种有前景的工具。
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