Myocardial Bridge: If You Wait Longer You Can Find It!

Dear Sir,

A case of myocardial bridge (MB) was reported in a previous issue of the Journal of Cardiovascular Echography.[1]

MB is a congenital coronary anomaly characterized by myocardial muscle overlying the intramyocardial segment of an epicardial coronary artery, usually the left descending artery (LDA).[2] As a consequence, it is responsible for a dynamic systolic compression of the entrapped coronary segment, which can persist into diastole, affecting coronary hemodynamics. A MB is usually an incident finding, not always responsible for symptoms. Even if it is generally considered a benign variant, it has been associated with acute myocardial infarction and also sudden cardiac death. It can be differentiated on the basis of depth and length of the encasement, with different potential factors favoring symptoms occurrence, such as heart rate, left ventricle (LV) hypertrophy, and coronary atherosclerosis.[34]

In a previous issue of the Journal of Cardiovascular Echography, Piccione et al. described a case of MB with positive dipyridamole stress test and mechanical cardiac alteration highlighted by speckle tracking echocardiography (STE).[1] Even if patient complained of mild chest discomfort at the end of dipyridamole infusion, neither electrocardiographic (ECG) changes nor wall motion abnormalities occurred. Subsequently, to the administration of atropine, it was possible to observe mild ECG changes and lower longitudinal strain of the anterior interventricular septum, with a more pronounced ST depression and T-wave inversion in V2–V4 only after aminophylline was administered. The interesting finding of this case was the possibility to use vasodilatory stress test also to unmask MB, while usually dobutamine and exercise test are employed in this subset and the peculiar response with only a late ECG changes’ appearance, after atropine and aminophylline administration. According to the authors, because of the dynamic nature of MB, a sustained elevated heart rate and a significant increase in LV contractility to provoke myocardial ischemia are necessary. This could explain the late occurrence of ECG alteration, only after the inotropic and chronotropic effects secondary to atropine and aminophylline administration. Another interesting finding of this case was the appearance, after dipyridamole infusion, of subtle myocardial mechanics alteration revealed by STE. The role of this technique to study myocardial deformation has been yet validated in different diseases, allowing to identify changes of myocardial mechanics also in early stage,[5] and interesting results were obtained also in the application to stress test.[6]

The mainstay of medical treatment of symptomatic MB relies on elimination of potential triggers such as hypertension/hypertrophy and increased heart rate, and use of beta-blocker or calcium-channel antagonists. As second option, in case of patients refractory to medical therapy, treatment can be percutaneous through stenting of coronary artery or, less frequently, surgical trough coronary artery bypass grafting or supra-arterial myotomy.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.