A myocardial bridge (MB) is an anatomical abnormality of the coronary artery and is characterized by the systolic narrowing of the epicardial coronary artery caused by myocardial compression during systole. An MB is frequently observed on cardiac computed tomography or coronary angiography and generally appears to be harmless in the majority of patients. However, the presence of MB is reportedly associated with abnormalities of the cardiovascular system, including coronary artery diseases, arrhythmia, certain types of cardiomyopathy, and cardiac death, indicating that MB serves a pivotal role in the occurrence and/or development of such cardiovascular events. Recently, there has been an increasing interest in the coexistence of MB and coronary spasm in research due to opposing aspects regarding their treatments. For example, monotherapy using β-blockers, which are effective in patients with MB, may worsen symptoms in patients with coronary spasm. By contrast, nitroglycerin, which is an effective treatment option for coronary spasm, may worsen symptoms in patients with MB. This review focuses on the pathophysiology and diagnosis of MB and MB-related cardiovascular diseases, including coronary spasm, and on the treatment strategies for MB.

Coronary spasm is caused by a transient coronary narrowing due to the constriction of epicardial coronary artery, which leads to myocardial ischemia. More than 50 years have passed since the first recognition of coronary spasm, and many findings on coronary spasm have been reported. Coronary spasm has been considered as having pivotal roles in the cause of not only rest angina but also exertional angina, acute coronary syndrome, and heart failure. In addition, several new findings of the mechanism of coronary spasm have emerged recently. The diagnosis based mainly on coronary angiography and spasm provocation test and the mainstream treatment with a focus on a calcium-channel blocker have been established. At a glance, coronary spasm or vasospastic angina (VSA) has become a common disease. On the contrary, there are several uncertain or unsolved problems regarding coronary spasm, including the presence of medically refractory coronary spasm (intractable VSA), or an appropriate use of implantable cardioverter defibrillator in patients with cardiac arrest who have been confirmed as having coronary spasm. This editorial focused on coronary spasm, including recent topics and unsolved problems.

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BACKGROUND Patients with vasospastic angina (VSA) sometimes experience prolonged chest symptoms. The clinical characteristics of these patients have not been clarified. AIM To investigate the clinical characteristics of prolonged VSA patients. METHODS This study included 167 patients with VSA diagnosed by spasm provocation tests (SPTs) using acetylcholine, which recorded the frequencies of positive reactions to a low dose of acetylcholine (L-ACh), total occlusion due to spasm (TOC), focal spasm, and the unavoidable use of nitroglycerin (unavoidable-NTG) during SPTs. The patients underwent a medical interview that investigated the maximum duration and frequency of chest symptoms as well as the frequencies of variant angina and other serious symptoms. The patients were divided into two groups based on the maximal duration: The short-duration group (< 15 min; n = 114) and the long-duration group (≥ 15 min; n = 53). They were also divided into two groups based on the frequency of chest symptoms: The low-frequency group (< 4/mo; n = 88) and the high-frequency group (≥ 4/mo; n = 79). RESULTS The long-duration group showed higher frequencies of other serious symptoms ( P < 0.001) and variant angina ( P < 0.05) as well as higher frequencies of spasm induction by L-ACh ( P < 0.05), TOC ( P < 0.05), focal spasm ( P < 0.01), and unavoidable-NTG ( P < 0.01) than the short-duration group. These parameters did not differ significantly between the low-frequency and high-frequency groups. CONCLUSION These findings suggest that patients with VSA who experience prolonged chest symptoms may have more severe characteristics of VSA.

(1) Background: We have sometimes experienced patients with vasospastic angina (VSA) who presented multi-vessel spasm (MVS) on coronary angiography and spasm provocation test (SPT). However, the clinical characteristics of VSA patients with MVS and the prognosis of such patients in the clinical setting have not been clarified. Therefore, we compared the clinical characteristics and prognosis in VSA patients with MVS with those in VSA patients with single-vessel spasm (SVS). (2) Methods: A total of 152 patients (mean age, 67 years, 74 men and 78 women) with VSA, in which the presence of coronary spasm was assessed in both left coronary artery (LCA) and right coronary artery (RCA) on SPT, were enrolled. We defined VSA as the presence of >90% narrowing of the epicardial coronary artery on angiograms, accompanied by usual chest symptoms and/or ischaemic ST-T changes on the electrocardiogram. On SPT, MVS was defined as the presence of spasms on ≥2 major coronary arteries. Based on the presence of MVS, patients were divided into the MVS group and the SVS group. The frequencies of conventional coronary risk factors, blood chemical parameters, average times of anginal attack, SPT findings such as spasm provocation induced by a low dose of acetylcholine (L-ACh) and total occlusion due to coronary spasm (TOC), number of coronary vasodilators at discharge and major cardiovascular events (MACE, including cardiac death and readmission due to any cause of cardiovascular diseases) were compared between the two groups. (3) Results: The MVS and SVS groups were comprised of 98 (64%) and 54 (36%) patients, respectively. The level of fasting blood glucose (FBS) was lower (p < 0.01), and the level of cystatin-C (n = 89) tended to be higher (p = 0.07) in the MVS group than in the SVS group. The frequencies of L-ACh-induced coronary spasm (33% in MVS and 17% in SVS, p = 0.04) and TOC (12% in MVS, 0% in SVS, p < 0.01) were higher in the MVS group than in the SVS group. The average number of coronary vasodilators at discharge was higher in the MVS group (1.2 ± 0.4) than in the SVS group (0.9 ± 0.5, p < 0.01). The frequency of MACE was not different between the two groups. (4) Conclusions: Patients with MVS may have higher VSA activity on SPT and have more aggressive medications, leading to a comparable prognosis in VSA patients with SVS. MVS is an important indicator of at least VSA activity, and cardiologists should confirm this in SPT whenever possible. Further studies should confirm whether lower FBS levels and higher cystatin-C levels are any markers of MVS.