Theerasuwipakorn Nonthikorn, Montrivade Sakolwat, Kosum Paisit, Chattranukulchai Pairoj
Division of Cardiovascular Medicine, Department of Medicine, Faculty of Medicine, Chulalongkorn University, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
Cardiac Center, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
Radiol Case Rep. 2025 Jan 15;20(4):1854-1857. doi: 10.1016/j.radcr.2024.12.048. eCollection 2025 Apr.
Hypertrophic cardiomyopathy (HCM) is characterized by myocardial hypertrophy and can lead to significant complications including left ventricular outflow tract obstruction (LVOTO) and myocardial ischemia. Microvascular dysfunction (MVD) is a less recognized but crucial cause of myocardial ischemia in HCM, contributing to myocardial injury in the absence of obstructive coronary artery disease. We presented a case of a 48-year-old male with retrosternal chest tightness radiating to the left arm for 3 h. Electrocardiography revealed left ventricular (LV) hypertrophy with ST-segment depression and T wave inversion. High-sensitivity troponin T levels were elevated. Echocardiography showed marked LV wall thickness, predominantly at the basal septum, with systolic anterior motion of anterior mitral valve leaflet causing LVOTO. Adenosine stress cardiac magnetic resonance imaging demonstrated faint patchy scars in the hypertrophied ventricular septum and significant stress-induced perfusion defects beyond the area of myocardial scarring. Coronary angiography showed normal epicardial arteries, suggesting MVD as the underlying cause of ischemia. The patient was treated with nebivolol and verapamil, leading to symptom relief and a reduction in the pressure gradient of LVOTO at follow-up. This case highlights the role of MVD in causing myocardial ischemia in patients with HCM. Effective management of HCM with MVD includes pharmacological therapy to alleviate outflow obstruction and improve myocardial perfusion. Comprehensive diagnostic and treatment approaches are essential for optimizing outcomes in patients with this complex condition.
肥厚型心肌病(HCM)的特征是心肌肥厚,并可导致包括左心室流出道梗阻(LVOTO)和心肌缺血在内的严重并发症。微血管功能障碍(MVD)是HCM中一种较少被认识但至关重要的心肌缺血原因,在无阻塞性冠状动脉疾病的情况下导致心肌损伤。我们报告了一例48岁男性患者,其胸骨后胸闷向左臂放射3小时。心电图显示左心室(LV)肥厚伴ST段压低和T波倒置。高敏肌钙蛋白T水平升高。超声心动图显示左心室壁明显增厚,主要位于基底间隔,二尖瓣前叶收缩期前向运动导致LVOTO。腺苷负荷心脏磁共振成像显示肥厚的室间隔有模糊的片状瘢痕,心肌瘢痕区域以外有明显的负荷诱导灌注缺损。冠状动脉造影显示心外膜动脉正常,提示MVD是缺血的潜在原因。患者接受奈必洛尔和维拉帕米治疗,随访时症状缓解,LVOTO压力梯度降低。该病例突出了MVD在HCM患者心肌缺血中的作用。对伴有MVD的HCM进行有效管理包括药物治疗以减轻流出道梗阻并改善心肌灌注。综合的诊断和治疗方法对于优化这种复杂疾病患者的治疗效果至关重要。