Myocardial bridging does not predict sudden death in children with hypertrophic cardiomyopathy but is associated with more severe cardiac disease

OBJECTIVES We sought to examine the association between systolic compressio n of sections of epicardial coronary vessels (myocardial bridging) with myo cardial perfusion abnormalities and clinical outcome in children with hyper trophic cardiomyopathy (HCM). BACKGROUND It has recently been suggested that myocardial bridging is an im portant cause of myocardial ischemia and sudden death in children with HCM. METHODS Angiograms from 57 children with HCM were reviewed for the presence of bridging (50% or more maximum systolic arterial compression). QT interv al indices, echocardiographic and cardiac catheterization findings, treadmi ll exercise tests, exercise thallium scintigraphy, Holter monitoring and el ectrophysiologic study findings were compared in children with and without bridging. The findings were also related to the presence or absence of comp ression of septal branches of the left anterior descending artery (LAD). RESULTS Bridging was present in 23 (40%) of the children. Multiple coronary arteries were involved in four children. Bridging involved the LAD in 16 o f 28 (57%) affected vessels. Myocardial perfusion abnormalities were presen t in 14 of 30 (47%) children without bridging and in 17 of 22 (94%) childre n with bridging, p = 0.002. However, bridging was associated with more seve re septal hypertrophy (19 +/- 8 mm vs. 28 +/- 8 mm, p < 0.001), a higher se ptum:posterior wall thickness ratio (2.7 +/- 1.2 vs. 1.8 +/- 0.9, p < 0.001 ), and higher left ventricle (LV) outflow gradient (45 +/- 37 mm Hg vs. 16 +/- 28 mm Mg, p = 0.002). Compression of septal LAD branches was present in 37 (65%) of the children and was significantly associated with bridging, s everity of LV hypertrophy and outflow obstruction. Multivariate analysis de monstrated that LV septal thickness and septal branch compression, and not bridging, were independent predictors of thallium perfusion abnormalities. There was a 90% power at 5% significance to detect an effect of bridging on thallium abnormalities at an odds ratio of 3. CONCLUSIONS Bridging was also not associated with significantly greater sym ptoms, increased QT and QTc intervals and QTc dispersion, ventricular tachy cardia on Holter or induced at EP study, or a worse prognosis. Bridging and compression of septal branches of the LAD are common in HCM children and a re related to magnitude of LV hypertrophy. Left ventricular hypertrophy and compression of intramyocardial branches of the epicardial coronary arterie s may contribute to myocardial perfusion abnormalities. Our findings sugges t that bridging does not result in myocardial ischemia and may not cause ar rhythmias or sudden death in HCM children. (C) 2000 by the American College of Cardiology.