Hermens Jeannine A J M, van Es Jan, von Birgelen Clemens, Op den Akker Jeroen W, Wagenaar Lodewijk J
Department of Cardiology, Thoraxcentrum Twente, Medisch Spectrum Twente, Haaksbergerstraat 55, 7513 ER, Enschede, The Netherlands,
Int J Cardiovasc Imaging. 2014 Aug;30(6):1097-103. doi: 10.1007/s10554-014-0435-7. Epub 2014 May 3.
Patients with acute chest pain, electrocardiographic ST-elevation and significant elevation of cardiac troponin but without obstructive coronary artery disease represent a diagnostic and therapeutic dilemma. Cardiac magnetic resonance imaging (CMR) can elucidate underlying alternative causes of troponin elevation including detection of (minor) myocardial infarction (MI) by identifying myocardial scarring as delayed enhancement. Of 77 patients, who were admitted between March 2009 and December 2012 with electrocardiographic (ECG) and biochemical evidence of acute MI without obstructive coronary artery disease, 45 patients underwent CMR that showed in 11/77 (14%) late gadolinium enhancement (LGE), compatible with myocardial scarring. We analyzed clinical, echocardiographic, and CMR data of these patients. Elevated troponin I levels were observed in all patients (median 1.3 ng/l, IQR 0.44-187) with median peak creatinine phosphokinase of 485 U/l (IQR 234-618). Echocardiographic wall motion abnormalities were detected in 8/11 (73%) patients; in 75% of these segments, ECG abnormalities were observed in corresponding leads. CMR detected LGE in the inferior (4/11), the inferolateral (5/11), the inferoseptal (2/11), the anterior (3/11), apical (3/11) and in the lateral segments (2/11). In addition, in all but two patients, these segments matched ECG abnormalities in corresponding leads. CMR identified microvascular obstruction in 4/11 (36%) patients. Patients with clinical, ECG, and biochemical signs of acute MI but unobstructed coronary arteries may have CMR-detectable myocardial scars. Information on myocardial scarring may help to make the diagnosis and draw therapeutic consequences. This case series underlines the value of contrast-enhanced CMR for myocardial tissue characterization.
患有急性胸痛、心电图ST段抬高且心肌肌钙蛋白显著升高但无阻塞性冠状动脉疾病的患者面临诊断和治疗困境。心脏磁共振成像(CMR)可阐明肌钙蛋白升高的潜在其他原因,包括通过将心肌瘢痕识别为延迟强化来检测(轻微)心肌梗死(MI)。在2009年3月至2012年12月期间入院的77例患者中,有心电图(ECG)和急性MI的生化证据但无阻塞性冠状动脉疾病,45例患者接受了CMR检查,其中11/77(14%)显示钆延迟强化(LGE),与心肌瘢痕相符。我们分析了这些患者的临床、超声心动图和CMR数据。所有患者均观察到肌钙蛋白I水平升高(中位数1.3 ng/l,四分位间距0.44 - 187),肌酐磷酸激酶峰值中位数为485 U/l(四分位间距234 - 618)。8/11(73%)患者检测到超声心动图壁运动异常;在这些节段的75%中,相应导联观察到心电图异常。CMR在下壁(4/11)、下侧壁(5/11)、下间隔(2/11)、前壁(3/11)、心尖(3/11)和侧壁节段(2/11)检测到LGE。此外,除两名患者外,所有这些节段均与相应导联的心电图异常相符。CMR在4/11(36%)患者中识别出微血管阻塞。有急性MI的临床、心电图和生化体征但冠状动脉未阻塞的患者可能有CMR可检测到的心肌瘢痕。关于心肌瘢痕的信息可能有助于做出诊断并得出治疗结论。该病例系列强调了对比增强CMR对心肌组织特征描述的价值。