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Original Research |
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
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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
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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.
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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.
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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.
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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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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.
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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.
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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.
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