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CLINICAL STUDY: PEDIATRIC CARDIOLOGY

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

Saidi A. Mohiddin, MB, ChB, MRCP^*, David Begley, MB, ChB, MRCP^*, Joanna Shih, PhD and Lameh Fananapazir, MD, FRCP^*

^* Section of Electrophysiology and Inherited Heart Diseases, Cardiology Branch, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
Office of Biostatistics Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA

Manuscript received February 14, 2000; revised manuscript received June 1, 2000, accepted July 14, 2000.

Reprint requests and correspondence: Dr. Lameh Fananapazir, Electrophysiology and Inherited Heart Diseases Section, Cardiology Branch, Building 10, Room 7B-15, 10 Center Dr., MSC 1650, Bethesda, Maryland 20892-1650
fananapa{at}nih.gov

OBJECTIVES

We sought to examine the association between systolic compression of sections of epicardial coronary vessels (myocardial bridging) with myocardial perfusion abnormalities and clinical outcome in children with hypertrophic cardiomyopathy (HCM).

BACKGROUND

It has recently been suggested that myocardial bridging is an important 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 interval indices, echocardiographic and cardiac catheterization findings, treadmill exercise tests, exercise thallium scintigraphy, Holter monitoring and electrophysiologic study findings were compared in children with and without bridging. The findings were also related to the presence or absence of compression 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 of 28 (57%) affected vessels. Myocardial perfusion abnormalities were present in 14 of 30 (47%) children without bridging and in 17 of 22 (94%) children with bridging, p = 0.002. However, bridging was associated with more severe septal hypertrophy (19 ± 8 mm vs. 28 ± 8 mm, p < 0.001), a higher septum: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 Hg, p = 0.002). Compression of septal LAD branches was present in 37 (65%) of the children and was significantly associated with bridging, severity of LV hypertrophy and outflow obstruction. Multivariate analysis demonstrated 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. Bridging was also not associated with significantly greater symptoms, increased QT and QTc intervals and QTc dispersion, ventricular tachycardia on Holter or induced at EP study, or a worse prognosis.

CONCLUSIONS

Bridging and compression of septal branches of the LAD are common in HCM children and are related to magnitude of LV hypertrophy. Left ventricular hypertrophy and compression of intramyocardial branches of the epicardial coronary arteries may contribute to myocardial perfusion abnormalities. Our findings suggest that bridging does not result in myocardial ischemia and may not cause arrhythmias or sudden death in HCM children.

Abbreviations and Acronyms   ECG = electrocardiogram   EP = electrophysiologic study   HCM = hypertrophic cardiomyopathy   LAD = left anterior descending artery   LV = left ventricle   QT = QT interval   QTc = corrected QT interval   VT = ventricular tachycardia

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