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DOI:10.2214/AJR.06.0714
AJR 2007; 188:1069-1073
© American Roentgen Ray Society

Original Research

Myocardial Bridge: Evaluation on MDCT

Abdel-Rauf Zeina1,2, Majed Odeh2,3, Jorge Blinder4, Uri Rosenschein2,5 and Elisha Barmeir1,2

1 Department of Radiology and MAR Imaging Institute, Bnai Zion Medical Center, 47, Golomb St., P.O.B. 4940, Haifa, Israel.
2 Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
3 Department of Internal Medicine, Bnai Zion Medical Center, Haifa, Israel.
4 MAR Imaging Institute, Bikur Holim Hospital, Jerusalem, Israel.
5 Department of Cardiology, Bnai Zion Medical Center, Haifa, Israel.

Received May 27, 2006; accepted after revision September 12, 2006.

 
Address correspondence to A.-R. Zeina (raufzeina3{at}hotmail.com).


Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
OBJECTIVE. The correlation between myocardial bridge and atherosclerotic changes has been controversial. The aim of this study was to evaluate the relation between myocardial bridge and atheromatous coronary artery disease (CAD).

MATERIALS AND METHODS. Three hundred consecutive subjects who underwent coronary CT angiography (CTA) were included in this study. The prevalence, length, depth, precise location, and concomitant atheromatous changes were evaluated. The group of subjects with myocardial bridge was compared with another subgroup, the control group, which included subjects without myocardial bridge.

RESULTS. From a total of 300 subjects, 78 subjects (26%) were found to have one myocardial bridge each. The mid left anterior descending artery (LAD) was the most common coronary artery involved (48/78). A significant difference was found between the LAD myocardial bridge group and the control group regarding presence of atheromatous changes in a similar LAD segment proximal to the myocardial bridge (p < 0.0001) and in the severity of atheromatous changes in these segments (mild, p < 0.0001; moderate, p < 0.02; and severe, p < 0.0001). The presence of stenosis in the LAD proximal to the myocardial bridge correlated with the thickness and length of the bridge.

CONCLUSION. Myocardial bridge predisposes to the development of atherosclerosis in the coronary artery segment proximal to the bridge. This may indicate that myocardial bridge should be considered an anatomic risk factor in the evaluation of CAD.

Keywords: coronary anomalies • coronary CT angiography • intramyocardial coronary arterial segment • myocardial bridge • tunneled segment


Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Myocardial bridge is defined as an intramural segment of a coronary artery that normally courses epicardially. It is considered a benign congenital anomaly that most commonly affects the midportion of the left anterior descending artery (LAD) [1-4]. Myocardial bridge is usually asymptomatic and has a favorable long-term outcome [5]. However, this anomaly has been associated with various clinical manifestations such as unstable angina, myocardial infarction, arrhythmia, and sudden death [6-10]. The incidence of myocardial bridge varies considerably between angiographic (0.5-2.5%) and pathologic (15-85%) series [11].

The intramyocardial coronary arterial segment is termed a tunneled segment. Atherosclerotic changes have been shown to affect the segment immediately proximal to the myocardial bridge, whereas the occurrence of atheromatous changes in the tunneled coronary segment is still controversial. Some investigators think that the tunneled segment is spared [1-2, 12-17], but others believe that this segment is not protected [18].

Coronary CT angiography (CTA) is a noninvasive 3D technique with the advantages of vessel wall and plaque depiction in addition to its ability to assess the luminal diameter, course, and anatomic relationship of the coronary arteries [19-24]. Therefore, it offers a unique opportunity to evaluate the real incidence, location, and morphology of myocardial bridge in an in vivo setting. Previous studies have described the prevalence, location, and morphology of myocardial bridge on the basis of postmortem specimens and invasive studies such as conventional coronary angiography and intravascular sonography.

The goal of our study was to evaluate noninvasively the presence and distribution of atherosclerotic plaques in relation to evolved myocardial bridge coronary segments and to determine the prevalence of myocardial bridges and their location and morphology (length, thickness, and diameter) by using MDCT.


Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Population
Between October 2004 and September 2005, 307 consecutive subjects with atypical chest pain, inconclusive stress test results, and high risk for catheterization complications who had failed or on whom it was not possible to perform conventional coronary angiography and follow-up after coronary bypass surgery were referred to our department for coronary CTA. Coronary CTA was not performed in seven subjects because of the following exclusion criteria: presence of multiple ectopic beats, atrial fibrillation, heart rate greater than 75 beats per minute (bpm) despite therapy, renal failure, severe lung disease, and a history of allergic reaction to iodine-containing contrast material. Mean age of the 300 subjects (239 men and 61 women) included in the study was 56.2 ± 9.5 years (age range, 43-77 years). Subjects with myocardial bridge were compared with another subgroup of 78 subjects who did not have myocardial bridge (control group). The control group was also chosen from the total population of the study (300 subjects). This control group included the first 78 consecutive subjects who did not have myocardial bridge. The two groups matched in terms of age, sex, and risk factors for CAD (Table 1). Written informed consent was obtained from all subjects included in the study.


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  		TABLE 1: Baseline Characteristics of Subjects With and Without Myocardial Bridge

 

MDCT Scanning Protocol
Subjects received a ß-blocker 2 hours before the examination (atenolol 50-100 mg orally based on body mass) if the resting heart rate exceeded 70 bpm. All subjects were in sinus rhythm. The heart rate of all subjects ranged between 48 and 70 bpm (average, 58 ± 7 bpm) with or without premedication. Coronary CTA was performed using two different MDCT scanners: LightSpeed 16 Pro (226 subjects) and LightSpeed VCT (74 subjects) (GE Healthcare). With the first scanner, the following scanning parameters were applied: detector collimation, 16 x 0.625 mm; 120 kVp; 400-500 mAs; pitch range, 0.2-0.29; gantry rotation time, 0.42 second; slice thickness, 0.6 mm. On the second scanner, images were obtained with detector collimation, 64 x 0.625 mm; 120 kVp; 400-500 mAs; pitch range, 0.2-0.29; gantry rotation time, 0.35 second; slice thickness, 0.6 mm. ECG modulation was used in all coronary CTA examinations (ECG pulsing). The subjects were imaged in the supine position. The distance from the carina to 1 cm below the diaphragmatic face of the heart was covered. A bolus of 70-90 mL of Iomeron 400 (iomeprol 400 mgI/mL, Bracco) was IV injected (4 mL/s) via an 18-gauge catheter placed in the antecubital vein followed by a bolus of 40 mL of saline. Scanning delay was determined according to the Smart Prepare Protocol (GE Healthcare)—an automatic bolus test; the region of interest was placed on the ascending aorta. The subjects were instructed to maintain an inspiratory breath-hold during which the CT data and ECG trace were acquired.

Image Reconstruction
Image reconstruction was done using the retrospective ECG-gating method. Data sets were acquired at phases of 45%, 75%, and 85% of the R-R cycle. Other window positions within the cardiac cycle were reconstructed when unsatisfactory results were achieved. The image data sets were processed on a separate workstation (ADW 4.6, GE Healthcare) and analyzed using curved multiplanar reconstruction (MPR) in various planes and thin-slab maximum-intensity-projection (MIP) reconstructions in addition to the axial source images. Coronary artery findings were reviewed in consensus by two experienced radiologists and a cardiologist.

Data Analysis
In all cases, the diagnosis of myocardial bridge was established on the basis of the cross-sectional, thin-slab MIP and MPR images and the axial source images. Myocardial bridge was defined as an epicardial segment of a coronary artery that courses through the myocardium (Fig. 1A, 1B). Coronary artery disease (CAD) was defined as coronary wall atheromatous change (calcified and noncalcified plaque) with or without luminal reduction. Hemodynamically significant stenosis was defined as greater than 50% reduction of the lumen diameter. Each segment was assessed for the presence of atherosclerotic changes and the location of those changes in relation to the coronary segment under the bridge.


Figure 1
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  		Fig. 1A —58-year-old man with atypical chest pain. ECG-gated coronary CT angiography performed with 16-MDCT. Curved multiplanar reformat image shows band of myocardial muscle overlying mid left anterior descending artery (LAD) segment corresponding to myocardial bridge (arrows). No wall abnormality of coronary artery segment proximal to and under bridge is noted. LMCA = left main coronary artery, LCX = left circumflex artery, LV = left ventricle.

 

Figure 2
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  		Fig. 1B —58-year-old man with atypical chest pain. ECG-gated coronary CT angiography performed with 16-MDCT. Cross-section image shows tunneled segment completely surrounded by muscle fibers (arrow).

 
The length and maximum myocardial thickness overlying the coronary artery at the site of the bridge were measured using the same workstation. The relation between length, thickness of the bridge, and severity of the disease in the coronary artery proximal to the bridge was studied. The diameter of each tunneled segment was obtained in both end-diastolic and end-systolic phases. The coronary CTA findings were classified as the following: normal, no atheromatous changes or luminal narrowing; mild disease, atheromatous changes without luminal narrowing; moderate disease, atheromatous changes with insignificant stenosis; and severe disease, atheromatous changes with significant stenosis. The number and severity of lesions in segments other than the LAD—right coronary artery (RCA), posterior descending artery (PDA), left circumflex artery (LCX), and obtuse marginal artery (OM)—were compared between the two groups (subjects with myocardial bridge and subjects without). Because the LAD is the most common artery involved with myocardial bridge, we decided to compare coronary CTA findings in subjects with LAD myocardial bridge with those of the control group in the corresponding vessel.

Statistical Analysis
Statistical analysis was performed using version 12.0 (SPSS). Continuous variables are expressed as mean ± SD. Mean values were compared between groups by Student's t test. Two-tailed p < 0.05 was considered statistically significant.


Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
All coronary CTA examinations were performed without complications. Image quality was good, and all involved segments were considered to be assessable. Myocardial bridges were detected in 78 (26%) of the 300 subjects. The coronary arteries involved are presented in Table 2. No myocardial bridge was observed over the proximal segment of the LAD. About one quarter of the women (16/61) and men (62/239) examined had a myocardial bridge. Of those with LAD myocardial bridge (71/78), atherosclerotic changes were found in 52 subjects (73%) and were consistently localized in the coronary segment proximal to the bridge.


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  		TABLE 2: Location and Incidence of Myocardial Bridge in the Coronary Arteries

 

In addition, only three subjects had small atherosclerotic plaques in the distal coronary artery segment; whereas 12 subjects of the control group had such atherosclerotic changes in the distal LAD. A significant difference was found between these two groups in this regard (p = 0.02). The tunneled segment was intact in all subjects. The coronary CTA findings showed a significant difference between the LAD myocardial bridge group and the control group regarding the presence of atheromatous changes in a similar LAD segment proximal to the myocardial bridge (p < 0.0001) and in severity of atheromatous changes in these segments (mild, p < 0.0001; moderate, p <0.02; and severe, p < 0.0001) (Table 3).


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  		TABLE 3: Cardiac CT Angiography Findings in 71 Subjects With and 78 Subjects Without Left Anterior Descending Artery (LAD) Myocardial Bridge

 

A total of 41 coronary lesions in segments other than the LAD in the group with myocardial bridge were detected: RCA, 16 (6 significant); PDA, 3 (none significant); LCX, 12 (2 significant); and OM, 10 (4 significant). Thirty-four coronary lesions were detected in the control group: RCA, 11 (6 significant); PDA, 4 (1 significant); LCX, 16 (4 significant); and OM, 3 (none significant). No significant differences were found between these two groups regarding the number of lesions (p = 0.26) and the severity of lesions (p = 0.77). Clinical examples are shown in Figures 2 and 3.


Figure 3
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  		Fig. 2 —53-year-old man with typical chest pain but inconclusive stress tests. Coronary CT angiography was performed with 64-MDCT. Curved multiplanar reformat image shows atheromatous changes (calcified and soft plaques) only in left anterior descending artery (LAD) segment proximal to bridge (solid arrows), causing significant stenosis (open arrows). Note that tunneled segment and distal LAD segment are spared. LV = left ventricle.

 

Figure 4
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  		Fig. 3 —61-year-old man after percutaneous coronary intervention. Coronary CT angiography was performed with 64-MDCT. Curved multiplanar reformat image shows stent in mid left anterior descending artery (LAD), immediately before bridge (arrows). Arrowhead indicates mixed plaque. LV = left ventricle.

 
The overall mean length and maximum myocardial thickness overlying the bridge (depth) were 19.5 ± 5.7 mm (range, 8-30 mm) and 2 ± 0.6 mm (range, 1-3.1 mm), respectively. The mean length and mean thickness of the bridge in subjects with LAD myocardial bridge categorized as normal and mild on coronary CTA (46/71, Table 3) were 18 ± 5.6 mm and 1.8 ± 0.7 mm, respectively. The mean length and mean thickness of the bridge in subjects categorized as moderate and severe (25/71) were 22.9 ± 4.5 mm and 2.3 ± 0.37 mm, respectively. A significant difference was found between these two groups regarding the length (p < 0.0002) and thickness (p < 0.0014) of the bridge.

Of the 78 tunneled segments, 55 (70.5%) had insignificant segmental narrowing, and four (5.1%) had a significant segmental narrowing episode during the systolic phase. In the diastolic phase, these segments did not achieve normal diameter but still showed a mild segmental narrowing (about 30% of the normal adjacent coronary artery). The narrowing of the tunneled segment was due to compression of this segment by the myocardium but not due to atherosclerotic changes. The remaining 19 tunneled segments (24.4%) had a normal diameter.


Discussion
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 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The most common coronary artery involved by myocardial bridge is the LAD at the midportion, as indicated by our study and other studies [1-4]. The involvement of other coronary arteries, such as RCA, first diagonal, second diagonal, ramus, and the marginal branch, is far less common. The incidence of this anomaly, as has been previously reported, is higher in women than in men [24]. Our study, however, shows a similar incidence in both men and women. The incidence of myocardial bridge varies consistently between angiographic (0.5-2.5%) and pathologic (15-85%) series [11]. Recently Kantarci et al. [25] revealed an LAD myocardial bridge incidence of 3.5% among 626 patients who underwent coronary CTA, similar to that observed angiographically. Our results revealed an overall myocardial bridge incidence of 26% and an LAD myocardial bridge incidence of 24%. Our results are closer to those reported in autopsy studies, the ultimate gold standard for detecting this anomaly. Because even in autopsy studies a big variation of the myocardial bridge incidence has been reported, the difference between our results and those of Kantarci et al. could be related to ethnicity.

Regarding the occurrence of atherosclerotic plaques in the tunneled coronary segment, Geiringer [1] and other investigators [2, 12-16] reported that the tunneled segment is rarely affected by atherosclerosis, unlike the epicardial segments, in which atherosclerotic plaques are commonly found. The study by Ishikawa et al. [17] found the segments proximal to the bridge significantly narrowed, whereas the tunneled segment itself was free of atherosclerotic lesions. This phenomenon has been confirmed by our study, in which atherosclerotic lesions were found mainly in the coronary arteries proximal to the bridge, whereas the tunneled segment was always spared. In addition, significant cross-sectional stenosis was more frequently observed in subjects with LAD myocardial bridge compared with control subjects (18 [25%] vs 3 [4%], p < 0.0001).

Some authors [18, 26] claim that the atherosclerotic process occurs in the coronary segment under the bridge with the same severity and frequency as it does in the epicardial coronary segments. Our findings, however, indicate that the tunneled segment is consistently spared. Three hypotheses suggested for this phenomenon are as follows: First, the presence of myocardial bridge greatly alters the distribution of the physical forces against the arterial wall and influences the extent of atherosclerosis [15]. Second, the intima beneath the myocardial bridge is stressed by high shear force and the intima proximal to the myocardial bridge is stressed by low shear force. Thus, alteration of hemodynamic factors may contribute to atheromatous plaque formation proximal to the bridge and may have a protective role within the tunneled segment [27, 28]. Third, an increase in local wall tension and stretch may induce endothelial injury and plaque fissuring, with subsequent thrombus formation in the proximal segment [11, 28].

Despite the reported association of deep-tunneled segments with ischemia and sudden death [29], there is still no clear indication of what actually defines a deep-tunneled segment. As previously mentioned, those cases with LAD myocardial bridge without any diameter reduction proximal to the bridge (46/71) had a maximum myocardial thickness (at the site of the bridge) of 1.8 ± 0.7 mm, whereas those associated with a stenosis proximal to the bridge had a thickness of 2.3 ± 0.37 mm. We concluded, therefore, that a tunneled segment covered by a section of myocardium of 2.3 mm or more should be considered a deep segment.

The relationship between myocardial bridge and symptoms is still unclear; we believe that the clinical significance of myocardial bridge is most likely determined by the presence of concomitant atherosclerosis and stenosis in the coronary artery segment proximal to the bridge, rather than anatomic narrowing of the tunneled segment caused by the overlying myocardium. Ongoing investigations will probably clarify this issue.

So far, only symptomatic subjects with myocardial bridge have been treated. Management options can be either pharmacologic or interventional. Available medications include nitrates, ß-blockers, and calcium channel blockers [10, 30, 31]. Considering the consistent association of atherosclerotic changes with myocardial bridge as shown in our study, we think that pharmacologic therapy with antiaggregant agents and lipid-lowering drugs should be considered as an intervention to prevent further progression of the disease. Further systematic experimentation is required to validate this proposal.

Our study has some limitations. In the diagnosis of myocardial bridge, the ultimate gold standard is pathology. This, of course, was not attainable in our study. Thus, a consensus of the evaluation of myocardial bridge and the associated atherosclerotic changes with MDCT was considered to be the standard in this study. The relationship between myocardial bridge and symptoms is still unclear, particularly in those subjects with no stenosis in the coronary artery proximal the bridge or those with appreciable systolic narrowing in the tunneled segment. This issue was not evaluated in our study. In addition, asymptomatic patients who might have myocardial bridges but who might not have proximal atherosclerosis have not been studied.

The ability of coronary CTA to delineate calcified and noncalcified lesions that may or may not cause luminal stenosis within the coronary artery wall has been shown [32, 33]; however, lipid-rich soft plaque cannot be differentiated from fibrous plaque using this diagnostic technique. In addition, the accuracy of CT to detect intramyocardial vessel wall abnormality has never been determined. This would be a limitation of our study.

The applicability of this technique is dependent on a stable heart rate and is adversely affected by arrhythmia such as multiple ectopic beats and atrial fibrillation because data for each 3D volume set is acquired over multiple heart beats. The use of arrhythmia adjustment software in addition to ß-blockers can potentially solve this problem. Patient exposure to ionizing radiation represents, in fact, a major and still debated issue in coronary CTA. Overall, the effective dose can be substantially reduced by means of technical innovations, among which is ECG tube current modulation, consisting of a progressive online reduction of tube output during the systolic phases of each cardiac cycle [34, 35].

In conclusion, MDCT is a noninvasive 3D imaging technique possessing a unique diagnostic capability. It shows not only the coronary artery lumen and wall but also the surrounding myocardium. In addition, it accurately determines the location, depth, and length of myocardial bridge and any concomitant atherosclerotic changes.

The findings of our study show that myocardial bridge predisposes to development of atherosclerosis in the segment of the coronary artery proximal to the bridge and may protect against atheromatosis of both the tunneled segment and the coronary segment distal to the myocardial bridge. Thus, in view of its consistent association with atherosclerotic changes in the coronary artery proximal to the bridge, myocardial bridge should be considered an anatomic risk factor in evaluating CAD.


References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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