A changing heart in tako-tsubo syndrome.
A changing heart in tako-tsubo syndrome.
复制标题
tako-tsubo 综合征中心脏的变化。
DOI：
10.1093/ehjci/jead112
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发表时间：
2023
期刊：
影响因子：
--
通讯作者：
Sen G
中科院分区：
文献类型：
--
作者：
Sen G
一位63岁女性，因急性胸痛及心电图显示前下导联T波倒置而就诊。肌钙蛋白T（TnT）显著升高（峰值1378 ng/L;正常< 14 ng/L），NT-proBNP也是如此（3091 ng/L;正常< 400 ng/L）。有创血管造影显示冠状动脉通畅，心室造影（见在线补充数据，视频S1）和超声心动图（见在线补充数据，视频S2）显示心室中段球囊扩张和运动功能减退，提示心室中段tako-tsubo综合征（TTS）。预约了心脏磁共振（CMR），但患者无法参加。使用InterTAK诊断评分评估的重点病史显示无情绪或身体触发因素。患者6个月后再次出现类似症状和TnT升高。住院患者超声心动图显示反向TTS模式（参见在线补充数据，视频S3），1.5 T时的CMR显示基础运动功能减退，伴有匹配的自然T1（1220 ms;正常950-1100 ms）和T2（69 ms;正常< 48 ms）升高（图A-B）。研究微血管疾病的腺苷负荷灌注后定量灌注图显示基底至中周灌注不足，心尖心肌血流正常，未提示特定冠状动脉区域缺血（图D），无晚期钆增强（LGE）（图C），证实了反向TTS。两个月后，患者进一步出现胸痛和TnT升高。在这种情况下，重复住院患者CMR显示典型TTS模式，心尖运动功能减退，中间至心尖段T1和T2升高（分别为1261 ms和81 ms），无LGE（图E-G）。该病例被进一步探讨，但没有发现触发因素，包括神经或精神异常。具有不同表型的复发性TTS先前已被描述，但很罕见，特别是没有触发因素。我们的病例说明了多模态成像在TTS调查中的实用性，特别是CMR的多参数组织映射。此外，新的定量灌注图表征心肌血流增加了诊断效用。图A-B：四腔心切面显示在1.5 T下使用MOLLI时T1升高1220 ms（A，正常950-1100 ms），基底至中间隔下壁和基底前侧壁T2升高69 ms（B，正常< 48 ms）。图C：4腔造影后图像显示无LGE。图D：腺苷负荷后的定量灌注图显示基底至中周灌注不足，心尖心肌血流正常。
A 63-year-old female presented with acute chest pain and ECG showing T wave inversion in the anterior and inferior leads. Troponin T (TnT) was significantly elevated (peak 1378 ng/L; normal< 14 ng/L), as was NT-proBNP (3091 ng/L; normal< 400 ng/L). Invasive angiography showed unobstructed coronary arteries with mid-ventricular ballooning and hypokinesia on ventriculography (see Supplementary data online, Video S1) and echocardiography (see Supplementary data online, Video S2), suggesting a mid-ventricular tako-tsubo syndrome (TTS). Cardiac magnetic resonance (CMR) was booked but the patient was unable to attend. Focussed history using the InterTAK diagnostic score assessment revealed no emotional or physical triggers. The patient re-presented six months later with similar symptoms and elevated TnT. Inpatient echocardiography showed a reverse TTS pattern (see Supplementary data online, Video S3) and CMR at 1.5 T showed basal hypokinesia with matching elevated native T1 (1220 ms; normal 950–1100 ms) and T2 (69 ms; normal< 48 ms)(Panels A–B). Quantitative perfusion maps following adenosine stress perfusion to investigate microvascular disease showed basal to mid circumferential hypoperfusion with normal apical myocardial blood flow, not suggestive of specific coronary artery territory ischaemia (Panel D) and no late gadolinium enhancement (LGE)(Panel C), confirming a reverse TTS. The patient further presented two months later with chest pain and TnT elevation. Repeat inpatient CMR on this occasion showed a classic TTS pattern with apical hypokinesia and elevated T1 and T2 (1261 ms and 81 ms, respectively) at the mid to apical segments with no LGE (Panels E–G). The case was further explored but no triggers, including neurological or psychiatric abnormalities were found. Recurrent TTS with different phenotypes has previously been described but is rare, especially without a trigger. Our case illustrates the utility of multimodality imaging in the investigation of TTS; in particular, multiparametric tissue mapping by CMR. Furthermore, the novel quantitative perfusion maps characterising myocardial blood flow added diagnostic utility. Panel A–B: 4-chamber views showing elevated T1 of 1220 ms (A, normal 950–1100 ms) using MOLLI at 1.5 T and elevated T2 of 69 ms (B, normal< 48 ms) at basal to mid infero-septum and basal antero-lateral walls. Panel C: 4-chamber post-contrast images showing no LGE. Panel D: Quantitative perfusion maps following adenosine stress showed basal to mid circumferential hypoperfusion with normal apical myocardial blood flow.