Letter by Poullis Regarding Article, “Anatomic Properties of Myocardial Bridge Predisposing to Myocardial Infarction”
To the Editor:
Ishikawa et al1 provide important data on the correlation between myocardial bridges and the predisposition to myocardial infarction. They confirm the 2 everyday findings of coronary artery surgeons: First, that intramyocardial epicardial coronary artery segments, whether in the left anterior descending territory or the obtuse marginal territory, are rarely involved in the atherosclerotic process, and second, that atherosclerotic lesions always seem to be proximal to the muscle bridge. The findings by Ishikawa et al1 raise a number of interesting points that were not answered in their report, however.
Patients with a history of myocardial infarction were more likely than patients with no such history to have significantly increased intima-media ratios, regardless of the presence of muscle bridges, which implies that muscle bridges play a minor role in the cause of atherosclerosis, because there was no significant difference between intima-media ratios in those who had no history of myocardial infarction and no muscle bridges versus those with no history of myocardial infarction but who had muscle bridges. Retrograde flow secondary to muscle bridge spasm is not atherogenic; however, the reflected wave due to impedance mismatching of an epicardial artery meeting an intramyocardial artery, an analogous situation to prosthetic replacement of the aorta,2 results in localized arterial hypertension and, by increasing endothelial stress and strain, is atherogenic.
Systolic compression of epicardial arteries does not reduce myocardial blood supply to the left ventricle, because this is predominately diastolic. However, failure of relaxation in diastole may reduce coronary perfusion and subsequently affect myocardial blood supply. Interestingly, patients with infarcts in the study by Ishikawa et al1 had heavier hearts and a significantly higher incidence of hypertension, which implies that muscle bridges and the myocardial bridge muscle index were not the cause of myocardial infarction, but rather hypertension and diastolic dysfunction, as occurs with hypertrophic obstructive cardiomyopathy, were the cause.3 Analysis of the data in the report by Ishikawa et al1 according to the presence or absence of hypertension may negate the effect of their findings with regard to muscle bridges.
Table 2 in the article by Ishikawa et al1 demonstrates that patients with a history of myocardial infarction and revascularization, whether surgical or medical, had a 33% chance of having a muscle bridge, which is less than the 50% in the general population,4 which implies that muscle bridges are in fact not relevant in the generation of atherosclerotic lesions. Because 50% of autopsied hearts have muscle bridges4 and <5% of angiography cases do,5 this implies that muscle bridges are in fact protective and not a risk factor as concluded by Ishikawa et al.1
In summary, we agree that Ishikawa et al1 have elegantly confirmed that atherosclerosis occurs proximal to intramyocardial segments, but we would disagree that their data confirm that muscle bridges are the causative factor for an increased intima-media ratio and myocardial infarction, as they have concluded.
Ishikawa Y, Akasaka Y, Suzuki K, Fujiwara M, Ogawa T, Yamazaki K, Niino H, Tanaka M, Ogata K, Morinaga S, Ebihara Y, Kawahara Y, Sugiura H, Takimoto T, Komatsu A, Shinagawa T, Taki K, Satoh H, Yamada K, Yanagida-Iida M, Shimokawa R, Shimada K, Nishimura C, Ito K, Ishii T. Anatomic properties of myocardial bridge predisposing to myocardial infarction. Circulation. 2009; 120: 376–383.
Basso C, Thiene G, Mackey-Bojack S, Frigo AC, Corrado D, Maron BJ. Myocardial bridging, a frequent component of the hypertrophic cardiomyopathy phenotype, lacks systematic association with sudden cardiac death. Eur Heart J. 2009; 30: 1627–1634.
Möhlenkamp S, Hort W, Ge J, Erbel R. Update on myocardial bridging. Circulation. 2002; 106: 2616–2622.