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Detection of Myocardial Bridging with ECG-Gated MDCT and Multiplanar Reconstruction

¹ Department of Radiology, Medical Faculty, Atatürk University, 200 Evler Mah. 14. Sok No: 5, Dadaskent, Erzurum 25090, Turkey.
² Department of Radiology, Florence Nightingale Hospital, Istanbul, Turkey.
³ Department of Cardiology, Florence Nightingale Hospital, Istanbul, Turkey.

Received February 23, 2005; accepted after revision May 6, 2005.

 
Address correspondence to M. Kantarci (akkanrad{at}hotmail.com).

Abstract

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OBJECTIVE. The aim of this study was to evaluate the incidence of myocardial bridging in 626 patients examined with MDCT angiography of the coronary arteries.

MATERIALS AND METHODS. Six hundred twenty-six patients who were referred to Florence Nightingale and Atatürk University Hospitals were involved in this study. These patients had atypical chest pain, symptoms suggestive of coronary artery disease, or no significant cardiac complaint. Patients were in sinus rhythm and were premedicated with metoprolol tartrate (5 mg/mL IV bolus) to decrease the heart rate and nitroglycerin (5 mg sublingual 1 min before the examination) to dilate the coronary arteries. MDCT was performed on two different 16-MDCT scanners.

RESULTS. Among the 626 patients, 22 cases (3.5%) of myocardial bridging were detected. Fifteen cases of myocardial bridging (2.4%) were located at the middle third of the left anterior descending coronary artery (LAD), five (0.8%) were at the distal third of the LAD, and two (0.3%) were at the proximal third of the LAD. In these patients, the length of tunneled artery was between 6 and 22 mm, with a mean of 17 mm, and the depth of tunneled artery was between 1.2 and 3.3 mm, with a mean of 2.5 mm.

CONCLUSION. We found the incidence of myocardial bridging in this patient group to be 3.5%. This result is in agreement with some of the angiographic studies in the literature. Our study showed that MDCT is a reliable and noninvasive tool for diagnosing coronary myocardial bridging. After evaluating resource axial images, it is necessary to also evaluate the sagittal multiplanar reconstruction images for myocardial bridging.

Keywords: cardiac imaging • coronary arteries • CT angiography • MDCT • myocardial bridging

Introduction

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Myocardial bridging is one of the nonatherosclerotic anatomic abnormalities of the coronary arteries [1]. Muscle overlying a segment of a coronary artery causes myocardial bridging. Myocardial bridging of coronary arteries in systole was long considered an incidental finding; however, now there is ample evidence in the literature to document its association with compromised coronary flow causing clinical symptoms including angina, myocardial infarction, life-threatening arrhythmias, and sudden death [2-6]. Because of the complications associated with myocardial bridging, diagnosis and treatment are important.

Although conventional angiography is the gold standard, some other imaging techniques have been used, such as intravascular sonography and MDCT [7]. Recent advances in CT techniques, such as MDCT scanners, make it possible to visualize the coronary arteries. MDCT is a reliable and noninvasive tool for diagnosing coronary stenoses and abnormalities [8-12]. For this reason, it can also be used to evaluate the real incidence of myocardial bridging in vivo. We evaluated the incidence of myocardial bridging in 626 patients who were examined with MDCT coronary angiography. In the English-language literature, this study is the first, to our knowledge, in which such a large group of patients was evaluated.

Materials and Methods

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Six hundred twenty-six patients with atypical chest pain, symptoms suggestive of coronary artery disease, or no significant cardiac complaint were referred to Florence Nightingale Hospital or Atatürk University Hospital. Each patient had one or more risk factors of coronary artery disease such as family history, smoking, hypertension, diabetes mellitus, hyperlipidemia, and so on. Echocardiograms were normal. The patients were between the ages of 35 and 75 years (mean ± SD, 58 ± 12.28 years). Four hundred thirty-eight patients were male (70%), and 188 (30%) were female. The procedures used were in accordance with the recommendations found in the Helsinki Declaration.

Premedication
Patients were in sinus rhythm and were always premedicated with nitroglycerin (5 mg sublingual 1 min before the examination) to dilate the coronary arteries and, if necessary, with metoprolol tartrate (5 mg/mL IV bolus; Beloc ampule, AstraZeneca) to decrease the heart rate; patients with arrhythmia were excluded from the study. The heart rate of all the patients ranged between 55 and 75 beats per minute (bpm) with or without premedication.

MDCT Scan Protocol
MDCT was performed on two different 16-MDCT scanners (Sensation 16, Siemens Medical Solutions; or Aquilon, Toshiba Medical Systems) during one breath-hold (16-24 sec). With the first scanner, the following parameters were applied: 12 x 0.75 mm collimation, 1-mm slice thickness, and 0.6-mm reconstruction interval. On the second scanner, images were obtained with 16 x 0.5 mm collimation, 1.0-mm slice thickness, and 1.0-mm reconstruction interval. Eighty-five milliliters of iodinated contrast medium (iohexol [Omnipaque, Amersham Health]) was injected IV at 4.5 mL/sec followed by 40 mL of saline at 2.5 mL/sec. Retrospective ECG-gated reconstructions were generated at 50%, 60%, and 70% of the R-R interval.

Among these different data sets, the best ones for evaluation of the right coronary artery (RCA), left anterior descending coronary artery (LAD), and left circumflex coronary artery (LCX) were chosen by a radiologist and a cardiologist. First, axial resource images and then multiplanar reconstructions were evaluated for all patients. If findings suggestive of myocardial bridging, such as the vessel coursing in the muscle or getting closer to the septum, were detected, then the images were reevaluated in the sagittal plane. However, we evaluated images from all planes for each patient whether we suspected myocardial bridging or not. The depth of the myocardial bridging was evaluated in the sagittal plane. Also, the length was measured in the same plane (Figs. 1A and 1B). For evaluation of myocardial bridging, 3D volume rendering was also used (Fig. 1C). By means of changing the window width and level, the muscle fibers overlying the vessel and the narrowing of the vessel at this area could be detected. This last technique (3D images) is not diagnostic, but it may be useful when explaining the problem to the clinician and the patient.

View larger version (123K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1A —16-MDCT contrast-enhanced coronary angiography images of 37-year-old man with myocardial bridging. Axial image shows suspicious intramyocardial course of middle left anterior descending coronary artery (LAD) (white arrows). Locations of aorta (A) and right coronary artery (RCA) are indicated.

View larger version (122K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1B —16-MDCT contrast-enhanced coronary angiography images of 37-year-old man with myocardial bridging. Sagittal multiplanar reconstruction image shows intramyocardial course and shifting into myocardium of middle LAD (arrows). Length and depth of tunneled segment can be clearly measured using this image. Location of left ventricle (LV) is indicated.

View larger version (96K): [in this window] [in a new window] [as a PowerPoint slide]   Fig. 1C —16-MDCT contrast-enhanced coronary angiography images of 37-year-old man with myocardial bridging. Volume-rendering 3D image shows myocardial bridging at middle third of LAD (arrowheads). At this tunneled segment, caliber of LAD appears thinner. Locations of aorta (A), left main coronary artery (LMCA), circumflex artery (Cx), LAD, and diagonal branch of LAD (D) are indicated.

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Discussion

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Muscle overlying a segment of a coronary artery causes myocardial bridging, and the artery coursing within the myocardium is called a "tunneled artery." Myocardial bridging is characterized by systolic compression of the tunneled segment, which remains clinically silent in most cases. Although it is silent in most cases, sometimes it causes severe ischemia. Several mechanisms have been postulated to explain ischemia resulting from myocardial bridging, including vasospasm and systolic kinking of the artery, resulting in direct physical damage to the underlying endothelial cells. Exercise-induced high heart rate, shortened diastolic perfusion time, increased contractility, compression of an artery, and increased flow velocity may cause ischemia [7, 14, 15]. The likelihood of ischemia also increases with the intramyocardial depth of the tunneled segment [16]. Suspected sequelae of myocardial bridging are angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, myocardial stunning, paroxysmal arteriovenous blockade, exercise-induced ventricular tachycardia, and sudden cardiac death [17-20]. Myocardial bridging is also an intraoperative problem during bypass surgery.

In a previous study, researchers reported that myocardial bridging must be considered in patients at low risk for coronary atherosclerosis and with anginalike chest pain or established myocardial ischemia [21]. Despite those features associated with myocardial bridging, our patients with myocardial bridging were young (mean ± SD, 41.9 ± 5.87 years); therefore, we concluded that myocardial bridging must also be considered in symptomatic young patients at low risk for coronary atherosclerosis.

Because of the complications associated with myocardial bridging, diagnosis and treatment are important. The current gold standard for diagnosing myocardial bridges is coronary angiography with the typical "milking effect" and a "step down-step up" phenomenon induced by systolic compression of the tunneled segment [21]. Although angiography is the gold standard, it is an invasive procedure. On angiography, myocardial bridging can occur in different forms during the systolic and diastolic phases. In addition, interpretation of angiography findings requires an experienced eye and only the deep type of bridges may be apparent on angiography [22].

With the use of MDCT, intravascular sonography, intracoronary Doppler sonography, and intracoronary pressure devices, morphologic and functional features of myocardial bridging can be visualized and quantified [7, 23, 24]. Standard MDCT protocols for coronary evaluation are focused on obtaining images at the time of maximal vasodilatation and minimal motion. Development of the multidetector scanner made it possible to visualize the coronary arteries by means of CT. This approach allows unveiling, if present, of the intramyocardial course of a coronary artery. MDCT is a reliable and noninvasive tool for diagnosing coronary stenoses and abnormalities [8-12]. Coronary arteries normally are superficial to myocardium. In our study, we could recognize the length and depth of myocardial bridging on sagittal multiplanar reconstruction images easily. Even when a few muscle fibers cause myocardial bridging, MDCT can also reveal the vessel shifting into the myocardium and 3D volume-rendering images make it possible for the clinician and patient to see the problem. In addition, MDCT provides the evaluation of the real incidence of myocardial bridging in vivo.

Myocardial bridging is confined mostly to the LAD, and muscle bridges occur between the proximal third and middle third portions of the vessel. In our study, we assessed 15 cases of myocardial bridging (2.4%) at the middle third of the LAD, five (0.8%) at the distal third of the LAD, and two (0.3%) at the proximal third of the LAD. The incidence of myocardial bridging on angiography has been reported to be less than 5% [17, 21]. We found the rate of myocardial bridging in our patient group to be 3.5% by evaluating not only the axial resource images but also the sagittal reformatted images. Our results are in agreement with some angiography studies in the literature. The length of tunneled artery was between 6 and 22 mm (mean, 17 mm). The depth of tunneled artery was between 1.2 and 3.3 mm (mean, 2.5 mm).

No myocardial bridging was detected in other arteries in our study. Although myocardial bridging of the other coronary arteries is rare, it must also be kept in mind [4, 5, 22, 25, 26]. Each of our patients had one or more risk factors, but most had no significant symptoms suggestive of coronary artery disease. They were scanned just for screening; however, two patients had angina pectoris and five patients had atypical chest pain.

In symptomatic patients, treatment is usually medical and rarely surgical. In the past few years, angioplasty and stenting have been used more frequently in cases resistant to medical therapy and this appears to be an effective alternative to surgery [27]. All of our patients were treated medically, and they all responded to medical treatment.

This study is the first to investigate such a large patient group (n = 626 patients). However, a limitation of our technique is that it does not work for patients with arrhythmia or patients who cannot hold their breath. Multicenter clinical studies of larger groups are required to determine whether myocardial bridging is responsible for symptoms such as angina, myocardial infarction, life-threatening arrhythmias, and so on.

In conclusion, because of advances in CT technology, radiologists have begun diagnosing diseases of the coronary arteries. Patients should be evaluated with great attention to the possibility of myocardial bridging because it is a variation that is not rare and can cause important complications. The results of our study showed that MDCT is a reliable and noninvasive tool for diagnosing coronary myocardial bridging. To diagnose myocardial bridging in patients, sagittal multiplanar reconstruction images, in addition to axial images, should be evaluated.

References

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