Response to Letter Regarding Article, “Anatomic Properties of Myocardial Bridge Predisposing to Myocardial Infarction”
We appreciate Dr Poullis’ interest in our study on myocardial bridge (MB) predisposing to myocardial infarction.1 The MB-positive group without myocardial infarction in that study included case subjects who had short and thin MBs and atherosclerosis was more extensive in the left anterior descending coronary artery proximal to MBs that were long and thick.2 Hemodynamic change by retrograde blood flow at systole contributes to endothelial dysfunction, which leads to an atherogenic condition in the proximal left anterior descending coronary artery segments, and the endothelial morphology in the segment proximal to the MB clearly indicates the susceptibility to atherosclerosis in this segment, as noted in our previous study cited in the original article.
Dr Poullis suggests that a failure of arterial relaxation at diastole under MB may reduce coronary perfusion. We agree with this idea, which has been described previously. This MB effect has been reported in symptomatic patients who are young and lack significant coronary lesions other than tachycardia and/or arterial spasm, similar to the cases of hypertrophic cardiomyopathy described by Basso et al.3 However, we analyzed the MB effect on left anterior descending coronary artery atherosclerosis in patients who already had atherosclerosis and elucidated the importance of the MB muscle index for atherosclerosis distribution.
The lower frequency of MB by angiography is caused simply by underdiagnosis of thin or short MBs. By multidetector row computed tomography, the frequency of MBs with >1-mm thickness in ischemic hearts is similar to that of MBs of >1-mm thickness by autopsy.4 Our conclusion1 is that MBs are not always contributory to myocardial infarction, but MBs that exhibit a large muscle mass are associated with a shift of the coronary lesion more proximally and underlie the convergence of atherosclerosis evolution at 2.0 cm proximal to the MB entrance.
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.