Detection of myocardial damage in patients with sarcoidosis.
Detection of myocardial damage in patients with sarcoidosis.
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DOI：
10.1161/circulationaha.109.851352
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发表时间：
2009-11-17
期刊：
影响因子：
37.8
通讯作者：
Kim RJ
中科院分区：
文献类型：
--
作者：
Patel MR;Cawley PJ;Heitner JF;Klem I;Parker MA;Jaroudi WA;Meine TJ;White JB;Elliott MD;Kim HW;Judd RM;Kim RJ
在结节病患者中，猝死是死亡的主要原因，这可能代表未被识别的心脏受累。延迟增强心血管磁共振（DE-CMR）可以检测到微量的心肌损伤。我们试图将DE-CMR与标准临床评价进行比较，以确定心脏受累。前瞻性招募了81例经活检证实的心外结节病患者，对（1）DE-CMR和（2）使用共识标准（修订的日本卫生部[JMH]指南）进行标准临床评价之间的心脏受累进行平行和盲法比较。标准评估包括12导联心电图和至少一项专门的非CMR心脏研究（超声心动图、放射性核素闪烁扫描或心导管插入术）。对患者进行了21±8个月的主要不良事件（死亡、除颤器电击或起搏器要求）随访。患者主要为中年（46±11岁）、女性（62%）、非洲裔美国人（73%），患有慢性结节病（中位数，7年），LVEF保留（中位数，56%）。DE-CMR确定了21例患者（26%）的心脏受累，JMH标准确定了10例患者（12%，8例重叠），DE-CMR的发生率高出两倍以上（p=0.005）。所有在DE-CMR上出现心肌损伤的患者均经X线血管造影排除了冠状动脉疾病。15例患者（19%）的病理学评估确定了4例心脏结节病;所有4例均为DE-CMR阳性，而2例为JMH阳性。随访时，8例发生不良事件，包括5例心源性死亡。DE-CMR组中有心肌损伤的患者的不良事件发生率是无损伤患者的9倍，心源性死亡率是无损伤患者的11.5倍。在结节病患者中，DE-CMR对心脏受累的敏感性是目前共识标准的两倍多。DE-CMR检测到的心肌损伤似乎与未来的不良事件（包括心源性死亡）相关，但事件很少，这需要在更大的队列中确认。
In patients with sarcoidosis, sudden death is a leading cause of mortality, which may represent unrecognized cardiac involvement. Delayed-enhancement cardiovascular magnetic resonance (DE-CMR) can detect minute amounts of myocardial damage. We sought to compare DE-CMR with standard clinical evaluation for the identification of cardiac involvement. Eighty-one consecutive patients with biopsy proven extra-cardiac sarcoidosis were prospectively recruited for a parallel and masked comparison of cardiac involvement between: (1) DE-CMR, and (2) standard clinical evaluation using consensus criteria (modified Japanese Ministry of Health [JMH] guidelines). Standard evaluation included 12-lead electrocardiography and at least one dedicated non-CMR cardiac study (echocardiography, radionuclide scintigraphy, or cardiac catheterization). Patients were followed 21±8 months for major adverse events (death, defibrillator shock, or pacemaker requirement). Patients were predominantly middle-aged (46±11 years), female (62%), African-American (73%), had chronic sarcoidosis (median, 7 years), and preserved LVEF (median, 56%). DE-CMR identified cardiac involvement in 21 patients (26%) and JMH criteria in 10 (12%, 8 overlapping), a more than two-fold higher rate for DE-CMR (p=0.005). All patients with myocardial damage on DE-CMR had coronary disease excluded by x-ray angiography. Pathology evaluation in 15 patients (19%) identified 4 with cardiac sarcoidosis; all 4 were positive by DE-CMR whereas 2 were JMH positive. On follow-up, 8 had adverse events including 5 cardiac deaths. Patients with myocardial damage on DE-CMR had a 9-fold higher rate of adverse events and a 11.5-fold higher rate of cardiac death than patients without damage. In patients with sarcoidosis, DE-CMR is more than twice as sensitive for cardiac involvement than current consensus criteria. Myocardial damage detected by DE-CMR appears to be associated with future adverse events including cardiac death, but events were few and this needs confirmation in a larger cohort.