Journal of Cardiovascular Computed Tomography
Volume 6, Issue 1 , Pages 3-13, January 2012

Myocardial bridging on coronary CTA: An innocent bystander or a culprit in myocardial infarction?

  • Rine Nakanishi, MD, PhD

      Affiliations

    • Department of Imaging and Medicine, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA
    • ,
  • Ronak Rajani, MD, MRCP

      Affiliations

    • Department of Imaging and Medicine, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA
    • ,
  • Yukio Ishikawa, MD, PhD

      Affiliations

    • Department of Pathology, Toho University School of Medicine, 5-21-16 Omori-nishi, Ota-ku, Tokyo 143-8540, Japan
    • ,
  • Toshiharu Ishii, MD, PhD

      Affiliations

    • Department of Pathology, Toho University School of Medicine, 5-21-16 Omori-nishi, Ota-ku, Tokyo 143-8540, Japan
    • ,
  • Daniel S. Berman, MD, FACC

      Affiliations

    • Department of Imaging and Medicine, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, 8700 Beverly Boulevard, Los Angeles, CA 90048, USA
    • Corresponding Author InformationCorresponding author.

Received 28 January 2011; accepted 20 October 2011. published online 21 November 2011.

Article Outline

Abstract 

Myocardial bridging describes the clinical entity whereby a segment of coronary artery is either partially or completely covered by surrounding myocardium. It represents the most frequent congenital coronary anomaly and has an estimated prevalence of ≤13% on angiographic series. With the emergence of cardiac computed tomography and its ability to simultaneously image the coronary arteries and also the myocardium, there has been an apparent increase in the detection rates of myocardial bridges (prevalence as high as 44%). It has now become important to evaluate their clinical significance. Myocardial bridging is generally considered a benign entity with survival rates of 97% at 5 years; however, there is now emerging evidence that certain myocardial bridge characteristics may be associated with cardiovascular morbidity. The length and depth of myocardial bridges have been associated with increased atherosclerosis, whereas the degree of systolic compression has been associated with ischemia on myocardial perfusion single-photon emission tomography. On the basis of current evidence, it appears that limiting further testing for ischemia to symptomatic patients with long and/or deep myocardial brides would be appropriate.

Keywords: Myocardial bridge, Coronary artery, Cardiac computed tomography, Myocardial infarction

 

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Introduction 

Myocardial bridging describes the anatomical entity whereby a segment of coronary artery is covered by a bridge of myocardium. It was first recognized on autopsy by Reyman in 17371 and first described angiographically by Portmann and Iwig in 1960.2 These investigators described a characteristic “milking effect” seen at the site of a myocardial bridge.2 This characteristic appearance of myocardial bridging represents systolic constriction of a coronary artery that is embedded in the myocardium for a variable distance. This segment is squeezed (milked) in systole by contraction of the surrounding muscle and disappears during diastole.3 The incidence of myocardial bridging in the population varies substantially between invasive coronary angiography (ICA; ≤13%) and on autopsy (15%–85%).4, 5 Given its frequency, myocardial bridging represents the most common congenital coronary abnormality. As such, it is by far the most common congenital abnormality encountered on coronary computed tomographic angiography (CTA). This review is intended cover multiple aspects of bridging, particularly its frequency, pathophysiology, clinical implications, and approaches to interpretation and determining the need for ischemia testing.

Frequency and distribution of myocardial bridges on coronary CTA 

Multiple studies have reported myocardial bridging by coronary CTA, showing a wide range of frequency (Table 1). With the use of 16-slice CT, Ko et al14 observed an occurrence of only 5.7%, whereas Lubarsky et al21 observed a rate of 44% in 245 patients undergoing 64-slice coronary CTA. In a consecutive group of 300 patients, Kim et al20 reported a 58% rate of bridging. Other studies have shown intermediate rates of myocardial bridging (20%–30%) on 64-slice coronary CTA.17, 19, 25 The variance in the frequency of reported myocardial bridging on CT most likely reflects the evolution in CT technology over the past decade. It is unknown whether environmental and geographical factors also play a contributory role.

Table 1. Autopsy, angiography, and coronary CTA studies that report the frequency and common sites of myocardial bridging
NumberCommon sites (%)Incidence of bridging, %
Autopsy studies
Geiringer5100LAD23
Risse and Weiler et al61056LAD (88)26
Polacek et al770LAD (60)86
Lee et al8108LAD58
Ishii et al9642LAD45
Angiographic studies
Noble et al105250LAD0.5
Ishimori et al11313LAD1.6
Greenspan et al121600LAD0.9
Angelini et al41100LAD5.5
Cay et al1325,982LAD11.8
Coronary CTA studies
16-slice
Ko et al14401p-LAD (4)
m-LAD (91)
d-LAD (4)		5.7
Kawawa et al15148p-LAD (4)
m-LAD (83)
d-LAD (4.3)
OM1 (4.3)
D2 (4.3)		15.8
40- and 64-slice
Koen et al16118m-LAD (75)
d-LAD (19)
Diagonal branches (17)
Intermediate (11)
OM (8)		30.5
64-slice
Leschke et al17150m-LAD (51)
d-LAD (47)
p-RCA (2)		28.7
Jodocy et al18221p-LAD (11)
m-LAD (77)
d-LAD (12)		23
La Grutta et al19277LAD (85)30
Kim et al20300 58 (partial, 33) (complete, 67)
Lubarsky et al21245p-LAD (8.5)
m-LAD (66)
d-LAD (25.5)		44
Cademartiri et al22543 10.9
Zeina et al23300p-LAD (0)
m-LAD (61.5)
d-LAD (29.5)
D1 (1.3)
D2 (1.3)
Ramus (2.6)
OM1 (2.6)
RCA (1.3)		26
Atar et al24169LAD (60)
D1 (8.5)
LCX (2.8)		7
128-slice
Lazoura et al25875p-LAD(3.2)
m-LAD (67.9)
d-LAD (28.8)		21

P, proximal; m, mid; d, distal; LAD, left anterior descending artery; LCX, left circumflex; RCA, right coronary artery; OM, obtuse marginal; D, diagonal.

The mid segment of the left anterior descending artery (LAD) is the most frequent site of bridging, followed by the distal LAD (Table 1). Muscle bridging can occur in almost any coronary segment, but the reported rates are exceptionally low for other segments and vessels. Although the precise mechanism for this anatomic variance is unknown, it has been shown that the location of myocardial bridges is associated with coronary dominance; that is, most commonly seen in the LAD in patients with left coronary dominance and in the right coronary artery in those with a dominant right coronary artery. This potentially suggests a common embryologic developmental pattern between coronary dominance and myocardial bridges.26, 27

Comparison with invasive coronary angiography 

Although ICA has been used extensively to evaluate the presence and functional significance of myocardial bridges, the prevalence of bridging on ICA has been lower than that reported with coronary CTA. In one study, Leshcka et al17 studied 100 patients who underwent both 64-slice CT and ICA and observed that myocardial bridges were detected in 26% of the patients by coronary CTA compared with only 12% by ICA. In the study of Kim et al,20 13.3% of patients showed myocardial bridges on ICA compared with 58% on coronary CTA. The lower frequency of finding bridging on ICA rather than on coronary CTA is probably explained by the differences in how myocardial bridges are detected by the 2 techniques. Whereas coronary CTA looks at the relation of the coronary to the surrounding myocardium, ICA predominantly looks at systolic changes in vessel caliber to suggest the presence of a bridge. ICA may therefore fail to detect superficial myocardial bridges that do not show systolic compression.

Approach to evaluation and classification of myocardial bridges by coronary CTA 

Curved multiplanar reformations are superior to axial imaging to assess for the presence of myocardial bridges, because of the improved ability to detect myocardium overlying the coronary artery, particularly in the LAD (Fig. 1). We suggest that when present, myocardial bridges should be described by the anatomic location, length, and depth of the tunneled segment (Fig. 2 and Fig. 3).

  • View full-size image.
  • Figure 2 

    Example of a deep myocardial bridge located within the mid segment of the LAD. Short-axis plane showing the locality and depth of the myocardial bridge (A), long-axis plane showing the length of the myocardial bridge (B), and long-axis plane showing an absence of proximal atherosclerotic disease (C).

  • View full-size image.
  • Figure 3 

    Example of a deep myocardial bridge located within the mid segment of the LAD. Short-axis plane showing the locality and depth of the myocardial bridge (A), long-axis plane showing the length of the myocardial bridge (B), and long-axis plane showing the presence of a proximal calcified plaque within the LAD (C).

Evaluation of systolic changes in bridged segments requires high-resolution imaging in both systole and diastole. Because myocardial bridges are common and usually not of clinical significance as noted below, the routine evaluation of systolic compression is not recommended, because of the increased radiation dose associated with multiphase imaging. In the case in which a myocardial bridge might be suspected, dose modulation should not be used, so that systolic and diastolic phases of the cardiac cycle can be observed with sufficient image quality.17

Myocardial bridges vary in size with a reported length ranging from 4 to 40 mm by autopsy,9, 28 8–50 mm by coronary CTA,15, 23 and a width and depth between 1 and 4 mm by autopsy9, 28 and 1–3mm by coronary CTA.15, 23 Longer and deeper bridges and those that exhibit greater degrees of systolic compression (>70%) are more common in symptomatic patients.29, 30, 31 Although attempts have been made to classify myocardial bridging, there is no consensus as to which has the most clinical utility. On coronary CTA, the length and the depth of myocardial bridging are most used to describe bridges. In general, a depth of bridging of ≥2 mm is considered deep.18 Another method is to describe muscle bridging as being partial or complete, depending on the extent to which the coronary artery segment with bridging is surrounded by myocardium. A partial myocardial bridge is one in which >75% but <100% of the coronary artery is encased by myocardium, and a complete bridge is one that is entirely encased by myocardium.20 With the use of this classification, Kim et al20 reported that 33% of myocardial bridges were partial and 67% were complete. Conventional angiography in the same group showed dynamic compression in 13.3% of patients. Of the 40 patients with myocardial bridging detected by systolic compression on ICA, only one patient (2.5%) had a partial bridge, and 39 patients (97.5%) had a complete bridge.

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Clinical significance 

In most patients, myocardial bridging is an incidental finding associated with an excellent survival rate of 97% at 5 years.32 However, it is not entirely a benign entity. There have been reported associations with myocardial ischemia,33 myocardial infarction,34, 35, 36, 37 arrhythmia,38 and sudden death.39, 40, 41 The clinical significance of a myocardial bridge appears to be related to (1) the anatomic properties of tunneled segment of coronary artery, (2) the presence of associated myocardial ischemia, and (3) the presence of proximal and distal atherosclerotic disease. With increasing systolic compression, to levels > 75%, the obstruction may persist into diastole (4%–50% of diastole).42, 43 This systolic milking effect3 along with associated altered coronary flow dynamics within the bridged segments (increased diastolic flow velocity and average flow velocity)30, 31, 44, 45 may result in impaired coronary flow reserve and ischemia.

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Pathophysiologic relation to myocardial ischemia and infarction 

Two mechanisms have been postulated to explain the relation of myocardial bridges to myocardial ischemia and infarction: direct compression of the coronary artery by the myocardial bridge and the development of atherosclerosis proximal and distal to the bridged segment.

Coronary flow and systolic compression in myocardial bridging 

In nonpathologic states, ∼80% of coronary flow occurs in diastole and 20% in systole. In myocardial bridging, this pattern is altered when systolic compression of the tunneled coronary artery may affect not only systolic coronary flow but also early and mid-diastolic flow. Klues et al46 performed intracoronary Doppler flow studies on 12 patients with myocardial bridges on ICA and demonstrated a characteristic “finger-tip” pattern of flow within the bridged segments. They observed an acceleration of flow in early diastole followed by an immediate deceleration and a mid-diastolic plateau. This phenomenon was observed within, as well as just proximal to, the myocardial bridge31, 46 and has been associated with an increased pressure gradient in early diastole as a result of reduced distal coronary resistance, delayed relaxation of the myocardial fibers, and the ensuing relative luminal dilatation.47 Concomitant changes have also been reported in systole with reduced, absent, or even retrograde systolic flow and secondary fluid waves and nonlaminar flow within the myocardial bridge,31, 48 caused by a persistent reduction in luminal diameter in systole.46, 49 These phasic compression patterns and associated alterations in coronary flow, along with the nonuniformity of tunneled segments, increase the propensity to myocardial ischemia.46, 50

In states of tachycardia, this phenomenon of reduced systolic and diastolic flow is further exacerbated by the shortened diastolic period associated with tachycardia, potentially resulting in ischemia. This may explain reported cases of sudden death in athletes with myocardial bridges in the absence of obstructive coronary disease, proven by autopsy.51, 52 In addition, it has been reported that endothelium-mediated vasodilators enhance vasoconstriction at the myocardial bridge, indicating endothelial dysfunction in the bridged coronary artery segment.53 This endothelial dysfunction may stimulate coronary vasospasm, platelet aggregation, and thrombus formation either within or proximal to the myocardial bridge.47

The degree of systolic compression appears to be of clinical importance. Angiographic studies have shown that myocardial ischemia is more likely when there is >75% systolic compression of the bridged coronary artery.10 This finding has been replicated in studies that evaluated the presence of ischemia by myocardial perfusion scintigraphy in which greater degrees of systolic compression were more often associated with perfusion defects.54, 55, 56 The magnitude of systolic compression is in turn related to the contractile force of the myocardial bridge which is governed by its length57 and thickness.58, 59 In angiographic studies with intravascular ultrasound scans, longer bridges have been associated with more severe systolic compression57 and on multidetector CT deeper bridges with more severe systolic compression.58, 59 These reports suggest that the anatomic properties of a myocardial bridge may influence the degree of systolic compression, the presence and magnitude of myocardial ischemia, and the subsequent occurrence of myocardial infarction.

Myocardial bridging and atherosclerosis 

Although bridged segments of coronary arteries are spared from atherosclerosis, it has been suggested that atherosclerosis may be more frequent in segments proximal to the bridging. These changes in atherosclerotic distribution have been recognized in autopsy5, 9 and in angiographic57 and coronary CTA15, 60 studies. Myocardial bridging has been reported to result in retrograde systolic blood flow in proximal segments from myocardial bridging squeezing.50, 61 This results in a lower mean shear wall stress and nonlaminar or oscillatory blood flow, which can increase endothelial dysfunction and atherosclerosis in proximal segments.62, 63, 64, 65 Conversely, within the bridged segments there is moderate-to-high shear wall stress that leads to atherosclerosis suppression by decreasing the bioavailability of nitric oxide and endothelin-1.66 This dissociation from classical endothelial dysfunction and its relation to atherosclerosis may be explained by systolic compression of the bridged segments causing changes to the endothelial cell structure from flat and polygonal to spindle-shaped, engorged, and aligned with the direction of blood flow.67 In addition, systolic compression of the bridged coronary artery potentially prevents the deposition of lipid molecules and the subsequent formation of atherosclerosis.68

Histopathological evidence: Myocardial bridge characteristics and atherosclerosis development 

Ishikawa et al69 performed a histomorphometric study to assess whether anatomic features of myocardial bridges were associated with myocardial infarction. The researchers compared 100 autopsied hearts with myocardial infarction (46 with and 54 without myocardial bridges) to 200 hearts without myocardial infarction (100 with and 100 without myocardial bridges). They reported that patients with myocardial infarction had an increased muscle thickness and muscle bridge index (length × depth of muscle bridge) compared than patients without myocardial infarction with myocardial bridges. They also observed increased intima/media ratios at distances ≤2 cm proximal to the myocardial bridge, thus indicating that alterations in flow dynamics in coronary segments proximal to bridging may predispose to advanced atherosclerotic change.

Evidence is also emerging that myocardial bridging may be associated with ultrastructural changes in the myocardium. Brodsky et al70 studied 6 autopsy hearts with an intramural course of the LAD (deep myocardial bridges) and compared the presence of myocardial fibrosis with 10 age-matched controls. They observed a significantly increased degree of myocardial fibrosis compared with the controls, suggesting that myocardial bridging may be associated with ischemia and interstitial fibrosis. Morales et al59 similarly demonstrated myocardial fibrosis and contraction band necrosis in myocardium distal to a myocardial bridge in 22 of 39 hearts. In the 13 subjects who died suddenly the tunneled segments were significantly deeper in the myocardium (intramural/deep myocardial bridges) than subjects who did not die suddenly.

Other factors predisposing to ischemia 

As well as flow alterations induced by systolic compression of a myocardial bridge, other factors may also modulate symptom occurrence. Tachycardia, hypertension, coronary vasospasm, the presence of proximal or distal atherosclerotic disease, and left ventricular hypertrophy may augment symptoms by directly reducing the coronary flow to already compromised myocardium or by accentuating the degree of systolic compression (hypertrophic cardiomyopathy and hypertensive cardiomyopathy). The influence of conventional cardiovascular risk factors on symptoms in patients with myocardial bridges is unknown.

Frequency of ischemia in myocardial bridges detected by ICA 

A number of studies have reported the frequency of ischemia in patients with myocardial bridging detected by ICA with the use of various modalities, including exercise stress testing, myocardial perfusion single-photon emission CT (SPECT), dobutamine stress echocardiography (DSE), and fractional flow reserve (FFR).

Exercise stress testing 

When bridges have been detected at ICA, the frequency of a positive exercise treadmill test (ETT) in patients with symptomatic myocardial bridges has been reported to be highly variable (28%–67%). Schwarz et al30 found positive ETT findings in 60% of 35 patients with a myocardial bridge, Klues et al46 found positive exercise tests in 67% of 12 patients, Ge et al31 found positive exercise tests in 28% of 64 patients, and Haager et al44 found positive findings in 36% of 11 symptomatic patients.

Myocardial perfusion scintigraphy 

Several studies have reported the frequency of ischemia on myocardial perfusion SPECT of myocardial bridging by ICA. The frequency of reported perfusion abnormalities in patients with myocardial bridges by ICA varies significantly from 21% to 88%.30, 44, 45, 54, 55, 56 Gawor et al71 studied 42 patients with isolated myocardial bridges, who had no prior history of myocardial infarction, with attenuation-corrected gated myocardial SPECT. The researchers observed significant perfusion defects in 29% of patients. Stress-induced perfusion defects were seen in 63% of patients with angiographic systolic compression > 50%, 35% of patients with 50% systolic compression, and in 0% of patients with <50% systolic compression. Tang et al54 studied 39 patients with myocardial bridging of the LAD and showed that 8 patients (21%) were found to have SPECT perfusion defects in the corresponding myocardial areas. The difference in the systolic compression of the coronary artery within the bridged segment was higher in patients with ischemia than without. Seven of 20 patients (35%) with severe systolic narrowing (>75%) and only 1 of 19 patients (5%) with mild narrowing (<50%) had significant perfusion defects. The researchers observed no difference in the length of the tunneled segment or the locality of the bridged segment.54 Vallejo et al56 performed both exercise and dipyridamole stress SPECT on 16 patients with angina and normal coronary arteries. They observed that 88% of patients who underwent exercise stress and 81% of patients who underwent dipyridamole had an abnormal scan and that there was no significant difference in the magnitude of perfusion defect between the 2 stress protocols. In the patients with abnormal scans, the mean angiographic systolic compression of the myocardial bridge was 73% ± 10%. In another small study, Lee et al55 performed dipyridamole SPECT in 12 patients with myocardial bridging all of whom had >50% of systolic compression. Similar to the work by Tang et al,54 Lee et al55 also found that the degree of systolic compression was related to the presence of reversible perfusion defects.

This high variability among these studies that evaluated the frequency of perfusion defects on myocardial SPECT in patients with myocardial bridges probably reflects the patient populations studied. Some studies investigated only symptomatic patients,56 whereas others investigated patients in whom a myocardial bridge was found incidentally.54 Furthermore, not all studies controlled for additional factors that may have contributed to the perfusion defects detected such as concomitant atherosclerotic disease, left ventricular hypertrophy, and myocardial disease.56

Dobutamine stress echocardiography 

A single small study has reported evaluation of ischemia with the use of DSE in patients with myocardial bridges. Duygu et al72 investigated the sensitivities of DSE and integrated backscatter in detecting myocardial ischemia in 14 patients with myocardial bridging of the LAD detected on coronary angiography. They observed that, although 57% of their patients developed angina during DSE, only 14% developed regional wall motion abnormalities. The researchers concluded that patients with myocardial bridging and angina rarely develop regional wall motion abnormalities on DSE and that DSE alone was accordingly not sufficiently sensitive to detect ischemia in patients with myocardial bridging.

Cardiac magnetic resonance imaging 

For stress cardiac magnetic resonance imaging and myocardial bridging, there have only been isolated case reports.73, 74

Fractional flow reserve 

FFR has been used to guide percutaneous coronary intervention strategies in patients with atherosclerotic lesions. FFR represents the ratio of the mean distal intracoronary pressure to the mean aortic pressure measured at maximum hyperemia, and an FFR < 0.75 has been shown to correlate well with ischemia on functional testing.75 FFR is generally considered to be highly specific and to have a high positive predictive value.75 It has been suggested that measurement of FFR might be useful to guide treatment strategies in patients with myocardial bridges.76, 77 In a small but interesting study by Escaned et al,76 12 symptomatic patients with myocardial bridging that caused >50% systolic narrowing in the mid LAD underwent FFR assessment at rest and during dobutamine infusion. The researchers found that abnormalities of FFR were more common when diastolic rather than mean FFR was measured. Although only 1 patient had abnormal diastolic FFR at rest, 5 of the 12 had abnormality at stress. These findings suggest that FFR may be useful to assess the functional severity of myocardial bridging and that, when used, it should be performed during inotropic stimulation.

Frequency of ischemia in myocardial bridges detected by coronary CTA 

One study reported the frequency of ischemia in myocardial bridging detected by coronary CTA. Jodocy et al18 studied 221 consecutive patients with 64-slice coronary CTA and myocardial bridging was detected in 51 patients (23%). In patients with LAD bridging, the rate of an abnormal ETT (≥1 mm ST depression in ≥1 anterior lead) was higher in patients with than in patients without bridging (68% vs 19.4%, respectively). The researchers did not describe whether the patients had rest electrocardiogram (ECG) abnormalities, left ventricular hypertrophy, or other causes of false-positive ETT studies. In that study, no relation was observed between an abnormal ETT and the length and depth of myocardial bridging.

The studies that identified the bridging at the time of ICA rely heavily on the presence of systolic narrowing of the coronary arteries which is considered to be a strong factor in producing inducible ischemia. Even when systole and diastole are both imaged during coronary CTA, it is difficult to detect systolic narrowing, because of the relatively lower spatial resolution of this method compared with ICA. On coronary CTA, the bridging is more directly observed than it is with ICA because of the improved myocardial definition on CT. It is likely that the frequency of ischemia in bridging detected on coronary CTA will prove to be much lower than that seen in patients with bridging detected by ICA.

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Treatment 

No clear guidelines are available as to the optimal treatment for patients with myocardial bridges. For asymptomatic patients, no treatment is necessary. In common clinical practice, the combination of the anatomic and functional findings helps guide treatment for symptomatic patients. Pharmacologic therapy with β-blockers or calcium channel blockers is useful for symptomatic patients.45, 47, 68, 78 β-Blockers theoretically reduce tachycardia and increase the diastolic coronary filling time with a decrease in myocardial contractility and compression of the coronary arteries, and they normalize coronary flow reserve within myocardial bridging. For patients with severe symptoms refractory to medical treatment and recurrent clinical events, percutaneous or surgical intervention may be considered. Coronary stenting of the tunneled coronary artery has been proposed as a treatment strategy for patients with marked systolic compression.79 A few studies have suggested the FFR may be useful in judging the need for and guiding percutaneous coronary intervention.80, 81, 82 The use of stenting, however, is controversial, because of reported peri-procedural complications, including coronary perforation,83 and high reported rates of in-stent restenosis that occur after bare metal stent deployment (45% within 7 weeks) by neointimal proliferation and increase of extrinsic stent compressive forces from the myocardial bridge.44 The mainstay of surgical therapy is coronary artery bypass grafting to segments distal to the myocardial bridging to improve the blood flow to compromised areas, or surgical unroofing of the intramyocardial coronary segment (myotomy) to relieve the systolic compression and to directly correct the congenital anatomical defect.84, 85

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Conclusions 

Myocardial bridging is a common anatomic variant on coronary CTA. The frequency of bridging on coronary CTA is higher than that reported for ICA, because of the strong reliance of the latter of the finding of systolic compression of the involved segment in establishing the diagnosis. Emerging data suggest that certain anatomic characteristics of myocardial bridges, such as length and depth, may contribute to the development of atherosclerosis and be related to subsequent cardiac events as well to the presence of ischemia. However, the frequency of inducible ischemia in symptomatic patients, or in patients in whom myocardial bridging is found incidentally, has not been well studied by coronary CTA. It thus still remains unclear as to which patients require further testing after the detection of a myocardial bridge. On the basis of current evidence, it appears as if most myocardial bridges are incidental findings, associated with a good prognosis, and that ischemia testing should be reserved for symptomatic patients with long or deep bridges.

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Acknowledgments 

Dr Rine Nakanishi is supported in part by research fellowship awards from the Society of Nuclear Medicine and Toho University School of Medicine, Tokyo, Japan. Dr Ronak Rajani is currently funded by the American College of Cardiology and the British Cardiovascular Society.

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 Conflict of interest: The authors report no conflicts of interest.

 Drs Nakanishi and Rajani contributed equally to this work.

PII: S1934-5925(11)00414-X

doi:10.1016/j.jcct.2011.10.015

Journal of Cardiovascular Computed Tomography
Volume 6, Issue 1 , Pages 3-13, January 2012

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