Author + information
- Mustafa Aparci1,
- Murat Yalcin2,
- Zafer Isilak2,
- Zekeriya Arslan3,
- Cengiz Ozturk4,
- Ugur Bozlar5 and
- Ejder Kardesoglu2
Myocardial bridging is a congenital abnormality of coronary arteries which may cause anatomically constriction of coronary lumen. Thus it may hemodynamically disturb and restrict the coronary flow at diastole when the myocardial oxygen demand extremely increased. So it may underlie in the etiology of left ventricular (LV) dysfunction such as left ventricular dilatation or systolic dysfunction. In the previous, young subjects with left ventricular dilatation had been diagnosed and followed as non-ischemic dilated cardiomyopathy. However myocardial bridging on coronary artery may be one of the causative factors in the etiology of LV dysfunction in young subjects. We retrospectively evaluated the findings on echocardiography and multisliced computerized tomography (MSCT) coronary angiography and the lesion properties in young subjects who presented with LV dysfunction.
Medical recordings of young patients with the diagnosis of dilated cardiomyopathy were retrospectively evaluated.
Young subjects with LV dysfunction were grouped according to results of MSCT Angiography such as normal (n=10, age 22.1±0.73, ranging 20,3-23.6 years old) and myocardial bridging (n=12, age 26.3±1.01, CI 24,1-28,5 years old). Both group had similarly increased left ventricular dimensions and reduced ejection fractions (Table 1). Young ones with LV dysfunction and normal coronary arteries presented mainly with dyspnea whereas those with myocardial bridging presented with angina or dyspnea on effort. Presence of wall motion abnormality of echocardiography in both of the groups was similar. LAD artery (n=11) was the mostly coexisting artery with presence of Intermediate, Cx and right coronary arteries (3, 4, and 1, respectively). Myocardial bridging was mainly located in the middle segment of the coronary arteries. Mild and moderately compression on coronary arteries were similar in rates.
Myocardial bridging on coronary arteries was not uncommon in the etiology of LV dysfunction in young subjects. So LV dysfunction in young ones should not be attributed to an idiopathic origin and may be referred to further imaging tests such as MSCT Angiography but not interventional coronary imaging. Since myocardial bridging may be highly overlooked in classical coronary angiography. Additionally myocardial bridging on coronary arteries detected on MSCT Angiography should strictly be sought, reported and also identified with its length, compression and luminal narrowing. Those subjects should be followed with the restriction from extremely strenuous exercise rather than mildly regular exercise. Beta blocking drugs may be the best options of therapy in order to reduce the myocardial oxygen demand and work load. Myocardial bridging may not be innocent due to its potential to induce ischemia and LV dysfunction especially in young subjects.