Guevara-Bermudez Liliana P, Toleva Olga
Department of Hospital Medicine, Emory Saint Joseph's Hospital, Atlanta, USA.
Department of Medicine, Division of Hospital Medicine, Emory University School of Medicine, Atlanta, USA.
Cureus. 2023 Jun 7;15(6):e40091. doi: 10.7759/cureus.40091. eCollection 2023 Jun.
Myocardial bridge (MB) is a congenital abnormality where part of a coronary epicardial artery runs under the myocardium fibers and is compressed in systole; this becomes more pronounced when nitroglycerin (NTG) is administered. In this report, we describe the case of a 40-year-old African American man who presented with chest pain that did not respond to NTG or isosorbide mononitrate and was only partially relieved by narcotics. His past medical history was significant for coronary artery disease (CAD) with a stent into the left anterior descending artery (LAD) several months prior, hypertension, hyperlipidemia, paroxysmal atrial fibrillation, sick sinus syndrome, permanent pacemaker, pulmonary embolism, and cerebral vascular accident. No explanation for his angina was found either in the previous outpatient left heart catheterization (LHC) procedures demonstrating LAD stent patency or initial chest pain workup upon admission. Functional LHC procedure with adenosine infusion and acetylcholine provocation demonstrated endothelial dysfunction with notable epicardial spasm and MB of the LAD that worsened with NTG. Cardiology advised dual antiplatelet therapy and a statin as part of treatment for CAD and a calcium channel blocker with a bradycardic effect (e.g., diltiazem, verapamil) for the MB and coronary vasospasm, and avoidance of NTG and long-acting nitrates (e.g., isosorbide mononitrate), which can cause reflex tachycardia and worsen angina from MB. A selective serotonin reuptake inhibitor was added for increased cardiac nociception. The patient's pain resolved, and he was discharged. MB is an important alternate etiology to consider when chest pain does not respond to NTG administration for adjustment of treatment modalities. The initial treatment for this patient's pain with NTG likely exacerbated symptoms by reducing intrinsic coronary wall tension and subsequently increasing reflex sympathetic stimulation of contractility of the left ventricular myocardium, which can, in turn, increase anginal symptoms and ischemia.
心肌桥（MB）是一种先天性异常，即部分冠状动脉心外膜动脉走行于心肌纤维下方，并在收缩期受压；使用硝酸甘油（NTG）时这种情况会更加明显。在本报告中，我们描述了一名40岁非裔美国男性的病例，他出现胸痛，对NTG或单硝酸异山梨酯无反应，仅用麻醉剂部分缓解。他既往有冠状动脉疾病（CAD）病史，数月前左前降支（LAD）置入支架，还有高血压、高脂血症、阵发性心房颤动、病态窦房结综合征、永久性起搏器、肺栓塞和脑血管意外。在之前显示LAD支架通畅的门诊左心导管检查（LHC）过程中，或入院时最初的胸痛检查中，均未发现其心绞痛的原因。使用腺苷输注和乙酰胆碱激发的功能性LHC程序显示存在内皮功能障碍，伴有明显的心外膜痉挛和LAD的MB，NTG会使其加重。心脏病学建议双联抗血小板治疗和他汀类药物作为CAD治疗的一部分，以及使用具有减慢心率作用的钙通道阻滞剂（如地尔硫䓬、维拉帕米）治疗MB和冠状动脉痉挛，避免使用NTG和长效硝酸盐（如单硝酸异山梨酯），因为它们可引起反射性心动过速并加重MB所致的心绞痛。添加了一种选择性5-羟色胺再摄取抑制剂以增强心脏伤害感受。患者疼痛缓解并出院。当胸痛对NTG给药无反应时，MB是调整治疗方式时需要考虑的一个重要的替代病因。该患者最初使用NTG治疗疼痛可能通过降低冠状动脉固有壁张力，随后增加左心室心肌收缩力的反射性交感神经刺激而加重了症状，进而可增加心绞痛症状和缺血。
