Myocardial bridging: what have we learned in the past and will new diagnostic modalities provide new insights?

Abstract

The clinical significance of myocardial bridging has been a subject of discussion and controversy since the introduction of coronary arteriography (CAG) in the early 1960s. More recently computed tomography coronary angiography (CTCA) has made it possible to visualise the overlying muscular bands and appears to have a higher sensitivity for detecting myocardial bridging than CAG. Combining CTCA with invasive techniques such as CAG should make it possible to improve our understanding of the pathophysiology of myocardial bridging and to provide answers to hitherto unresolved questions. This paper critically reviews the outcomes of previous studies and defines remaining questions that should be answered to optimise the management of the presumably fast growing number of patients in whom a diagnosis of myocardial bridging has been made. Keywords Myocardial bridging . Computed tomography angiography . Coronary arteriographyAccording to the original definitions the term 'myocardial bridging' is used for an anatomic variation in which a band of cardiac muscle overlies a segment of an epicardial coronary artery while the artery involved is referred to as being 'tunnelled'. Initially the diagnosis could only be made at autopsy but soon after coronary arteriography (CAG) had become an established clinical diagnostic tool systolic compression of a coronary artery, usually the left anterior descending artery (LAD), was occasionally observed and correctly interpreted as evidence of myocardial bridging [1,2]. Since then the clinical significance of myocardial bridging has been a subject of discussion and controversy. In the last decade it was shown that myocardial bridging can be very well depicted by computed tomography coronary angiography (CTCA) [3,4] which has rekindled the interest in this anomaly. We expect that in the near future increasing numbers of patients with myocardial bridging will be detected by CTCA which may significantly enhance our understanding of the pathology and clinical consequences. At the same time, to ensure that these patients receive optimal treatment it is imperative that we stay aware of what previous studies have taught us. It is the purpose of this paper to critically review the outcomes of previous studies and to define remaining questions of clinical relevance that hopefully can be resolved with newer diagnostic modalities. DiagnosisAlthough myocardial bridging has been held responsible for a variety of symptoms in individual cases, ranging from atypical chest pain to sudden death, thus far clinical studies have been unable to identify specific diagnostic features that allow a diagnosis of myocardial bridging without visualisation of the coronary arteries [5][6][7][8][9][10][11]. The diagnosis is usually established by chance in patients who are examined by CAG or CTCA for various reasons but not because they are suspected of having myocardial bridging. It should be noted that there are essential differences between the diagnostic information provided by each of the two visualisati...

The Functional Effects of Intramural Course of Coronary Arteries and its Relation to Coronary Atherosclerosis

“…Absolute MBF during vasodilator stress was not influenced by myocardial bridges. Coronary atherosclerosis was predominantly localized proximal to the coronary segment with MB, which is known from previous studies(1,2,5,18). However, the atherosclerotic burden in coronary arteries and patients was not increased.…”

Myocardial Bridging in a Child With Hypertrophic Obstructive Cardiomyopathy

“…Usually, the diagnosis is established by chance in patients who are examined by coronary angiography or computerized tomography angiography for various reasons but not because they are suspected of having MB. 8 Echocardiographic features are associated with the severity of the disease or with its complications but not with MB. 3 On the other hand, LV wall thickness at the proximal interventricular septum, and the degree of asymmetrical septal hypertrophy are significantly greater in children with bridging.…”

“…8 Hypertrophic obstructive cardiomyopathy is the leading cause of sudden cardiac death in young patients, and the association of myocardial ischemia with sudden death has been recognized in patients with HCM. 8 The cause of ischemia may be intramural abnormalities of the small vessels, abnormal myocellular architecture, or massive hypertrophy. The role of MB in ischemia is controversial.…”

“…This prolongation may have a greater effect in young children because the heart rate is faster and the diastolic filling time is shorter, especially during exercise. 8 There is an ongoing debate whether hypertrophic cardiomyopathy-associated MB is an independent risk factor for ischemia and sudden cardiac death in children or simply an indicator of the severity of left ventricular hypertrophy. 9 A study of 36 pediatric patients with HCM showed evidence that significant MB of the LAD is characterized by greater than 90% systolic compression of the middle third of the LAD with ongoing compression during a mean of 50% of diastole.…”

Myocardial bridges and obstructive coronary atherosclerosis

“…При коронарной компьютерной томографической ангиографии туннелированный сегмент артерии обнаруживается у 20-30 % обследованных пациентов, хотя частота встречаемости этой врожденной аномалии развития, по данным отдельных авторов, колеблется в диапазоне от 5,7 до 58 % [7]. Такой же широкий диапазон колебаний (4,7-86 %) имеет распространенность ММ по данным аутопсии [8,9].…”