Fujiwara Momo, Yamashita Soichiro, Takemoto Makoto, Hayashi Takatoshi
Hyogo Prefectural Awaji Medical Center, Hyogo Kenritsu Awaji Iryo Center, Shioya 1-1-137, Sumoto, Hyogo 6560021, Japan.
Eur Heart J Case Rep. 2022 Aug 16;6(8):ytac346. doi: 10.1093/ehjcr/ytac346. eCollection 2022 Aug.
Atrial infarction, usually concurrent with ventricular infarction, is under-recognized. Although most patients with atrial infarction have complicated supraventricular tachyarrhythmias, its mechanism is still unknown. We report a case of atrial tachycardia (AT) related to atrial infarction treated with catheter ablation.
A 51-year-old man was referred for acute chest pain. Electrocardiography showed a junctional rhythm with ST depression in the precordial leads. Emergency coronary angiography revealed an occluded dominant left circumflex coronary artery (LCX). A drug-eluting stent was deployed; however, the atrial branch from the distal side of the LCX was jailed by the stent and became occluded. On the 7th day, the premature atrial contractions (PACs) became frequent and changed to AT. Owing to its resistance to medication, we performed catheter ablation. The electro-anatomical map revealed counter-clockwise macro-reentrant tachycardia at the tricuspid valve annulus, with low-voltage and fragmented potential (FP) areas at the posterior wall of the right atrium (RA). After terminating the AT through linear ablation for the cavotricuspid isthmus, multiple-focus PACs originating from the FP area in the RA posterior wall were documented. Coronary angiography revealed that these damaged areas were perfused by the atrial branch of the LCX. Defragmentation in the FP area could eliminate PACs. The patient was discharged with sinus rhythm and without any complications.
We can perform electro-anatomical mapping to identify tachycardia circuit and PACs arising from the FP area in the posterior RA, where the atrial branch was perfusing. Multiple PACs from infarcted myocardium result in tachycardia.
心房梗死通常与心室梗死同时发生，目前尚未得到充分认识。尽管大多数心房梗死患者并发室上性快速心律失常，但其机制仍不清楚。我们报告一例与心房梗死相关的房性心动过速（AT）患者，经导管消融治疗。
一名51岁男性因急性胸痛就诊。心电图显示交界性心律，胸前导联ST段压低。急诊冠状动脉造影显示优势左旋支冠状动脉（LCX）闭塞。植入了药物洗脱支架；然而，LCX远端的心房分支被支架困住并闭塞。第7天，房性早搏（PACs）变得频繁并转变为AT。由于其对药物治疗有抵抗性，我们进行了导管消融。电解剖图显示三尖瓣环处逆时针方向的大折返性心动过速，右心房（RA）后壁存在低电压和碎裂电位（FP）区域。通过对三尖瓣峡部进行线性消融终止AT后，记录到起源于RA后壁FP区域的多灶性PACs。冠状动脉造影显示这些受损区域由LCX的心房分支供血。FP区域的碎裂电位消除可消除PACs。患者出院时为窦性心律，无任何并发症。
我们可以进行电解剖标测以识别心动过速环路以及起源于灌注心房分支的RA后壁FP区域的PACs。梗死心肌产生的多个PACs导致心动过速。
