Myocardial bridging and sudden cardiac death: Is the actual classification exhaustive?

Myocardial bridging (MB) is a congenital coronary anomaly charac-terizedbythepresenceofabandofcardiacmuscleoverlyingasegmentof a coronary artery along its normal course in the epicardial adiposetissue [1]. The tract of the coronary artery that penetrates within themyocardium and lies beneath the muscle is called “tunnelled artery”and the presence of the MB allows dividing the vessel in three sectors:proximal, underneath and distal to the bridge [2–4]. The incidenceranges from 1.5 to 16% when assessed by angiography [4] and up to80% in some autopsy series [3,5].(SeeFig. 1.)The left anterior descending coronary (LAD) is the most frequentlyaffected vessel (70% in an autopsy series) and in some cases heartscontain more than one bridge, affecting the same vessel or differentcoronaries [1,2,4,5]. Particularly, MBs are most commonly localized inthe middle segment of the LAD [3]. MBs were also detected above acoronary vein, albeit they appear to have no clinical relevance [3].The bridge of myocardial fibers passing over the tunneled segmentcan cause narrowing of the artery during each systolic contraction.However,coronaryflowismaximalduringdiastolicphaseofthecardiaccycle and not systole. Therefore, it appeared unlikely that this systolicphenomenon could by itself result in myocardial ischemia andmyocardial bridges have long been considered as a normal anatomicalvariant without any hemodynamic or physiological relevance [6].This hypothesis was disproved by ultrasound evaluations demon-strating that during early diastole, the period of highest coronaryblood flow,theMBisresponsibleforthedelayedrelaxation,thusreduc-ing the distal coronary pressure [2,4,6]. This mechanism represents themain functional consequence of this coronary anomaly.Recently,MBshave beenclassified inbenignorpathologicalaccord-ingto the intra-myocardiallength and depth.This anomaly is thereforeconsideredpathologicalwhenthetunneledsegmentis20–30 mmlongand 2–3 mm deep [5].Pathological myocardial bridges may, in some cases, lead to is-chemia, infarction, malignant ventricular arrhythmias, and suddencardiac deaths [1,5,7,8]. Ischemic damage has been reported inshorter bridges [5], demonstrating that benign bridges can be clini-cally significant.Themechanismforischemiaiscomplexandisrelatedtothedelayedrelaxationintheearly diastole. Infact, after releasingthesystolicocclu-sion due to MB, diastolic flow increased proportionally with the dura-tion of vessel occlusion, albeit the increase in diastolic flow is not fullycompensatory. As a result, the main diastolic flow and the coronaryflow reserve are both reduced [3,6]. The likelihood of ischemia alsoincreases if MBs are located more proximally in the vessel and thetunneled segment tends to be longer and/or deeper [3].Stresses or exercises produce a rise in sympathetic drive thus facili-tating ischemia through tachycardia and increased contractility. In fact,the positive chronotropic effect leads to an increase of the systolic–diastolictimeratioandtoadecreaseofdiastolicflow,whilethepositiveinotropic effect further aggravates systolic and diastolic compression[3]. Finally, during tachycardia diastole shortens more than systole.We hereby discuss four cases of MB with heterogeneous anatomiccharacteristics and clinical presentation, summarized in Table 1.According to the actual classification based on the intra-myocardiallength and depth, the first and the second case should be consideredbenign, while the third and the fourth a pathological variant.In particular, thefirst case presented a MB over the LAD at 3 cmfrom its origin which was 18 mm long and 3 mm deep. Nonethelessthe clinical and autopticalfinding respectively of fever and divertic-ulitis could be considered the stressors capable of producing anincrease in heart rhythm. In other meanings, they represented thetrigger of sudden death in presence of a benign MB. In fact, neither