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Myocardial bridging of the coronary arteries

Myocardial bridging of the coronary arteries
Literature review current through: Jan 2024.
This topic last updated: Jul 31, 2023.

INTRODUCTION — The major coronary arteries, which are distributed over the epicardial surface of the heart, occasionally have a segment that is intramyocardial. The muscle overlying the intramyocardial segment of an epicardial coronary artery (most often the left anterior descending artery) is referred to as a "myocardial bridge."

This topic will review the epidemiology, anatomy, physiology, diagnosis, and clinical management of myocardial bridging. Other relevant topics include:

(See "Myocardial infarction or ischemia with no obstructive coronary atherosclerosis", section on 'Coronary artery spasm'.)

(See "Approach to the patient with suspected angina pectoris", section on 'Conditions causing or worsening angina'.)

(See "Congenital and pediatric coronary artery abnormalities", section on 'Causes'.)

(See "Hypertrophic cardiomyopathy: Clinical manifestations, diagnosis, and evaluation", section on 'Clinical manifestations'.)

PREVALENCE — The prevalence of bridging varies according to the population studied and the method used to assess the coronary anatomy. Pathologic studies have found a mean frequency of myocardial bridging of 25 percent (range 5 to 86 percent), similar to that observed in noninvasive imaging studies using coronary computed tomography [1-7]. In one autopsy study, the prevalence was 50 percent [3]

Angiographic studies have noted somewhat different findings. Among patients undergoing coronary angiography, the reported prevalence of myocardial bridging is 1.7 percent (range 0.5 to 16 percent), which is almost always confined to the left anterior descending coronary artery (image 1) [1,2,8-13]. A higher prevalence has been observed in patients with hypertrophic cardiomyopathy and in recipients of cardiac transplants [1,13-15]. (See 'Patients with hypertrophic cardiomyopathy' below.)

Among patients with myocardial infarction with nonobstructive coronary arteries (MINOCA), the prevalence of bridging is higher (2.9 percent) than observed in patients with coronary artery disease [16].

The difference in prevalence when estimated by these modalities reflects the fact that angiographic evidence of myocardial bridging depends upon a variety of factors, including the thickness of the myocardium, the length of the bridged segment, the orientation of the coronary artery to the myocardial fibers, the nature of the tissue interposed between the coronary artery and the myocardium, the observer's experience, and the intensity with which bridging is sought. We believe bridging often goes unrecognized on angiography.

In one study of 100 patients using computed tomography angiography (CTA), myocardial bridging of coronary arteries was found in 34 percent, but only approximately one-third of these showed systolic compression [17]. In another study using CTA, myocardial bridging was found to be a common anatomic variant [18]. (See 'Diagnosis' below.)

ANATOMY — The site, length, and severity of bridging vary from patient to patient and may vary in the same patient from one examination to another. Although all major epicardial coronary arteries can be affected, involvement of the left anterior descending coronary artery (LAD) is the most common.

The degree of bridging is usually neither extensive nor severe. However, there is a large degree of variability among patients:

Bridging may vary in terms of depth (superficial [>1 to 2 mm] versus deep [>2 mm]) and length of the tunneled artery encasement. When a large segment of the vessel is involved, extending from the origin to more than two-thirds of the vessel length, bridging may jeopardize the flow to secondary branches [19].

In some cases, bridging is so severe that there is almost complete obliteration of the vessel lumen during systole (image 1) [5].

Bridging can involve the secondary branches, especially the septal perforators (picture 1). Systolic compression of septal perforators appears to be more common in patients with hypertrophic cardiomyopathy, in whom it has been postulated to be one of several mechanisms responsible for myocardial ischemia. (See 'Patients with hypertrophic cardiomyopathy' below.)

PATHOPHYSIOLOGY — Most instances of bridging are of little clinical significance. However, severe bridging of the major coronary arteries can produce myocardial ischemia, coronary thrombosis, myocardial infarction, and stress cardiomyopathy (see "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy"), and can predispose the patient to sudden death [3,8,20-26].

Effects on coronary blood flow — The effects of myocardial bridging on myocardial blood flow vary from patient to patient and within the same patient.

This variability arises from variation in the extent of myocardial bridging, the fact that myocardial blood flow occurs predominantly during diastole, when bridging is not usually present, and challenges in methods of detection of ischemia due to myocardial bridging.

Frame-by-frame analysis of cine coronary angiograms has shown a "spill-over" phenomenon that is characterized by persistence of narrowing of the bridged segment in early diastole. In general, the more severe the systolic narrowing is, the more likely that the phasic coronary spasm will prolong into diastole.

With tachycardia, there is more systolic compression of the bridged segment, and systole occupies a greater percentage of the cardiac cycle because of shortening of diastolic filling period.

During left ventricular systole, the intramuscular segment of the vessel is compressed, a condition referred to as "milking" [1,2]. Myocardial bridge "milking" might also cause ischemia by "intramural steal" or "branch steal" mechanism, which are linked to decreased perfusion pressure of septal branches and blood suction [25].

In vitro models show that regardless of the degree of stenosis, myocardial bridges have a higher maximum and lower mean pressure drop than typical atherosclerotic lesions [27].

Myocardial bridging may cause myocardial ischemia by impairing coronary vasomotility. To this regard, it has been associated with a higher incidence of endothelial dysfunction and coronary artery spasm. Provocation test using incremental acetylcholine dose infusion may reveal coronary vasospasm in patients with bridging [28,29].

Quantitative coronary angiography has been combined with intravascular ultrasound (IVUS) and Doppler flow measurements in patients with isolated bridging of the proximal left anterior descending coronary artery [1,9-13,30-32]. (See "Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation" and "Clinical use of coronary artery pressure flow measurements".)

The following observations have been made [9,10]:

A specific, echolucent half-moon phenomenon over the bridge segment, which exists throughout the cardiac cycle and whose etiology is not completely understood.

A characteristic systolic compression (either concentric or eccentric) with delayed relaxation in diastole of the myocardial bridging segment.

Accelerated flow at early diastole (finger-tip phenomenon) with either no or reduced systolic antegrade flow (figure 1).

Decreased diastolic/systolic velocity ratio.

Retrograde flow in the proximal segment, which is provoked and enhanced by nitroglycerin injection.

The cross-sectional lumen area variation in one report was 40±25 percent in the bridging segments versus 9±7 percent in the normal segments. Atherosclerotic lesions occurred proximal to, but not within or distal to, the bridging segments [9].

A highly characteristic pattern showing a prominent peak in coronary velocity in early diastole was seen in 86 percent of patients (figure 1).

The coronary flow velocity reserve ratio (peak/resting ratio) was 2.2, which is below normal, possibly due to delayed release of bridging and/or proximal atherosclerosis; this finding may explain signs of ischemia in some of these patients.

Fractional flow reserve (FFR) was measured at baseline and during dobutamine infusion in a study of 12 patients with myocardial bridging [32]. The mean and diastolic FFR decreased from baseline with dobutamine, with the diastolic change being more prominent. The authors postulated that overshooting of systolic pressure interferes with and is a cause of error in FFR measurement based upon mean pressures, while the diastolic FFR appears to be the method of choice. Other reports have emphasized the use of dobutamine rather than adenosine when assessing myocardial bridging with FFR [33].

Another study found that in the presence of a myocardial bridge, instantaneous wave free-ratio (iFR), a lesion-specific, diastole-only index, has a greater correlation to anginal symptoms or presence of myocardial ischemia as compared with FFR [34]. Out of 20 patients with angina, no significant coronary artery disease, and angiographic evidence of a myocardial bridge, 65 percent had positive iFR at rest (with a clear step-up across the myocardial bridge, as shown during pressure wire pullback), while FFR was negative in all patients. Moreover, after dobutamine infusion, when vessel compression was maximal and patients developed symptoms, FFR did not significantly change while iFR (better defined as "hyperemic wave-free period pressure ratio") dropped in all cases.

Even if the diagnostic and prognostic values of the latter index remain to be established, these findings show that iFR seems more reliable than FFR to detect myocardial bridge-related ischemia, being that iFR is a diastolic-specific parameter and therefore not hampered by systolic-pressure overshooting.

Bridging and atherosclerosis — It has been postulated that the intramyocardial course of the coronary artery has a "protective" effect on the development of atherosclerosis at the site of the myocardial bridge [35]. However, some studies have reported concentric intimal thickening of the artery underneath the bridges, and increased atherosclerotic plaques proximal to the bridging [3,12]. This has been seen both pathologically and with the use of IVUS [10]. Increased wall shear stress proximal to bridging segment is thought to predispose to the development of atherosclerosis [36].

Myocardial bridging can occur in patients with and without coronary artery disease, including disease in the same vessel. In addition, we have seen patients in whom bridging became apparent only after percutaneous coronary intervention of a more proximal segment with fixed stenosis.

CLINICAL RELEVANCE — In the majority of patients, myocardial bridging is not associated with adverse clinical sequelae.

However, patients may present with silent ischemia, stable angina, acute coronary syndromes, stress cardiomyopathy, or malignant arrhythmias possibly leading to sudden cardiac death [1,37-39]. The following are representative findings from small series:

In clinical studies using stress myocardial perfusion imaging, the rate of myocardial ischemia has varied widely (21 to 88 percent) [40]. This variation is likely due to differences in the populations studied and the type of stress and imaging performed.

In a study of 11 patients with bridging who were evaluated with both pacing and exercise, five patients had more than 75 percent systolic narrowing [8]. Of these, four had ST-segment depression and increased coronary sinus lactate production with pacing at 150 beats per minute (bpm). Of the four patients with 50 to 75 percent systolic narrowing, two had angina and electrocardiogram (ECG) changes with pacing at 150 bpm. In the two patients with less than 50 percent bridging, neither had ECG changes, lactate production, or symptoms with either pacing or exercise.

In a report of 39 patients with myocardial bridging who underwent stress myocardial perfusion imaging, eight (20.5 percent) were found to have perfusion defects in the distribution of the bridge [40]. The myocardial ischemia was associated more closely with the degree of systolic narrowing than with the length of the tunneled artery or the location of the bridge.

There are few reports of survival rates but, when studied, five-year survival ranges between 85 and 98 percent [12,13,41].

Bridging may affect survival of pediatric patients with hypertrophic cardiomyopathy (HCM) but has not been found to influence prognosis of adult patients. (See 'Patients with hypertrophic cardiomyopathy' below.)

Myocardial bridging has been linked in selected cases to acute myocardial infarction [21,42,43], paroxysmal supraventricular tachycardia [21], ventricular tachycardia [2,37,43], exercise-induced atrioventricular conduction block [44], and sudden death [2,45].

One study showed that myocardial bridging with systolic-dynamic compression of a left anterior descending coronary artery (LAD) segment is a frequent finding in patients with stress cardiomyopathy, suggesting a role of myocardial bridging as a potential substrate in the pathogenesis of this condition [46]. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

Some previously asymptomatic individuals may become symptomatic. Pathophysiologic factors that may unmask or exacerbate myocardial bridges are a patient's age, heart rate, left ventricular hypertrophy, and the presence of coronary atherosclerosis, since all of these may worsen the supply-demand mismatch imposed by the bridge, reducing coronary reserve [41].

Patients with hypertrophic cardiomyopathy — HCM in children is associated with a 2 to 6 percent annual mortality, primarily due to sudden cardiac death, which may result from arrhythmias or myocardial ischemia. One possible cause for myocardial ischemia and a poorer outcome in these children is myocardial bridging, which appears to be especially common in this population. (See "Hypertrophic cardiomyopathy in children: Clinical manifestations and diagnosis", section on 'Signs and symptoms'.)

Reports have suggested that bridging in children with HCM is an important risk factor for cardiac complications [47,48]. The potential risk was illustrated in an angiographic study of 36 children with HCM, 10 of whom (28 percent) had myocardial bridging of the LAD persisting for 50 percent of diastole [47]. The following findings were noted:

Compared with patients without bridging, those with bridging had a significantly greater incidence of chest pain (60 versus 19 percent), history of resuscitated cardiac arrest (50 versus 4 percent), and ventricular tachycardia on ambulatory monitoring (80 versus 8 percent).

With exercise testing, the patients with myocardial bridging had a reduction in blood pressure (rather than the increase seen in those without bridging), a greater degree of ST-segment depression, and more QT dispersion.

The estimated proportion of patients free from death or resuscitated cardiac arrest at five years was significantly lower among those with bridging (67 versus 94 percent).

A later report evaluated 57 children with HCM, 23 of whom (40 percent) had myocardial bridging [48]. Bridging was associated with more severe left ventricular hypertrophy but not ischemia or sudden death [48].

In adults with HCM, a high prevalence of myocardial bridging also has been observed, with bridging observed in 15 percent of patients undergoing coronary angiography and in 41 percent in a necropsy study [30,49]. The link between the presence of bridging and impairment of survival, including risk of sudden death, has not been demonstrated in some studies [13,50], though there is controversy, as other studies have described such association with adverse events [51,52].

CLINICAL MANIFESTATIONS — In the majority of patients, myocardial bridging is asymptomatic. Symptomatic patients may present with clinical manifestations of myocardial ischemia that are similar to those in patients with fixed obstructive coronary artery disease such as an acute coronary syndrome, coronary spasm, exercise-induced dysrhythmias, atrioventricular conduction block, myocardial stunning, transient ventricular dysfunction, syncope, or sudden death [41]. (See "Approach to the patient with suspected angina pectoris", section on 'History' and 'Clinical relevance' above.)

DIAGNOSIS — The diagnosis of myocardial bridging is made when a section of an epicardial coronary artery (usually the left anterior descending coronary artery [LAD]) is found to be entirely or substantially within the myocardium (intramyocardial). This may be documented at the time of diagnostic coronary angiography, computed tomographic angiography, intraoperatively, or at postmortem examination.

With diagnostic coronary angiography, bridging is recognized as compression of a segment of a coronary artery during systole, resulting in narrowing that reverses during diastole (image 1). The dynamic and phasic nature of the obstruction serves to differentiate bridging from fixed coronary stenosis. Bridging is easier to recognize in the left anterior oblique than right anterior oblique projection.

Provocation with nitroglycerin may be useful during coronary angiography, with careful attention to coronary filling during systole. Nitroglycerin augments the severity of compression, probably by reflex sympathetic stimulation of contractility and/or a lower intraluminal pressure in the coronary artery [4].

The diagnosis of myocardial bridging of the LAD should be considered in patients at low risk for atherosclerotic coronary artery disease, such as younger individuals or those with no atherosclerotic risk factors, who have exertional angina and an anteroseptal perfusion defect.

Additional testing — For some patients in whom the diagnosis of myocardial bridging has been secured, additional testing may be considered.

Intravascular ultrasound is useful to better characterize the length, thickness, and location of the myocardial bridge, as well as the presence, severity, and distribution of sub-angiographic atherosclerosis. Cardiac computed tomography is able to easily detect and characterize myocardial bridging, given its three-dimensional capability and high spatial and contrast resolution. It can visualize the coronary lumen, the vessel wall, and the myocardial wall, hence allowing accurate definition of the myocardial bridge's morphologic features and precise definition of the myocardial bridge's length and depth.

Diagnostic workup of a myocardial bridge should not be limited to its anatomic definition, but rather include physiologic evaluation of its hemodynamic significance. To this regard, Doppler-flow catheters or intracoronary pressure-wire evaluation with instantaneous wave-free ratio rather than fractional flow reserve seem to be informative, and should be performed at rest and after inotropic stimulus. (See "Intravascular ultrasound, optical coherence tomography, and angioscopy of coronary circulation" and "Clinical use of coronary artery pressure flow measurements".)

TREATMENT — Only symptomatic patients or those with objective signs of ischemia require treatment. Such individuals respond well to pharmacologic therapy, which appears to be the treatment of choice for the vast majority of subjects [53,54]. Only patients with symptoms refractory to medical therapy should be considered for percutaneous or surgical treatment.

Medical therapy — Pharmacologic treatment includes beta blockers, ivabradine, and possibly nondihydropyridine calcium channel blockers. These agents reduce heart rate and myocardial contractility. In particular, beta blockers are able to revert intracoronary-pressure changes and angina symptoms induced by inotropic infusion, and should therefore be considered as first-line therapy [34].

Nitrates, by reducing the intrinsic coronary wall tension and increasing reflex sympathetic stimulation of contractility, may worsen symptoms, and their use is contraindicated [2].

In the absence of evidence for atherosclerosis, we do not treat with aspirin or a statin.

Revascularization — Preliminary studies suggest that intracoronary stent placement may normalize disturbed intracoronary hemodynamics and improve clinical symptoms in patients with symptomatic bridging [55,56]. However, relatively higher rates of target lesion revascularization (sometimes secondary to stent fracture [57]) may occur with stenting segments containing myocardial bridging [49,58]. In one study of 70 patients with myocardial bridging who had percutaneous coronary intervention predominantly with drug-eluting stents, target-lesion revascularization at mean follow-up of 358 days was 24 percent among patients who had stenting that extended into the segment containing myocardial bridging, in comparison to 3 percent among patients whose stent was implanted only in the epicardial obstructive lesion [49]. Of note, coronary artery perforation during stenting for myocardial bridging has been reported in several instances [59,60]. (See "Intracoronary stent restenosis".)

Surgical therapy should be reserved for patients with persistent symptoms, in whom ischemic changes are proven, and for those with a high-risk marker (such as life-threatening ventricular arrhythmias, aborted sudden death, or nonfatal myocardial infarction), in whom a trial of medical therapy has failed. In patients with severe bridging and concomitant coronary artery disease who are undergoing coronary artery bypass surgery, an attempt should be made to relieve the bridge, which may compromise flow to proximal branches despite a patent graft to the distal vessel.

The operative procedure of choice is resection of the muscle bridge using cardiopulmonary bypass [61-63]. Dissection of the overlying myocardial fibers with complete exposure of the coronary artery is essential if recurrence is to be avoided. Some have combined this procedure with bypass grafting. Perforation of the right ventricle is a recognized complication; epicardial echocardiography with a high-frequency probe may help to identify the course of the vessel and thereby help reduce the risk of this complication [64].

SUMMARY AND RECOMMENDATIONS

Introduction – The major coronary arteries may have a segmental intramyocardial course. During systole, this segment of the vessel is compressed, a condition referred to as "myocardial bridging." (See 'Introduction' above.)

Pathophysiology and clinical relevance – Most instances of bridging have no clinical significance. However, severe bridging of the major coronary arteries can produce myocardial ischemia, coronary thrombosis, myocardial infarction, and stress cardiomyopathy. (See 'Pathophysiology' above and 'Clinical manifestations' above and 'Clinical relevance' above.)

Diagnosis – The diagnosis of myocardial bridging is made when a section of an epicardial coronary artery (usually the left anterior descending coronary artery) is found to be entirely or substantially within the myocardium (intramyocardial). This may be documented at the time of diagnostic coronary angiography, computed tomographic angiography, intraoperatively, or at postmortem examination. (See 'Diagnosis' above.)

Treatment – Medical therapy with beta blockers, ivabradine, and calcium channel blockers is effective in reducing symptoms in the vast majority of patients. However, nitroglycerin or other nitrate drugs may exacerbate bridging and are contraindicated. Coronary artery stent implantation and coronary artery surgery may be used to improve symptoms in patients who are refractory to medical therapy. (See 'Treatment' above.)

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