Myocardial Bridging: Diagnosis, Functional Assessment, and Management: JACC State-of-the-Art Review.

Myocardial bridging (MB) is a congenital coronary anomaly in which a segment of the epicardial coronary artery traverses through the myocardium for a portion of its length. The muscle overlying the artery is termed a myocardial bridge, and the intramyocardial segment is referred to as a tunneled artery. MB can occur in any coronary artery, although is most commonly seen in the left anterior descending artery. Although traditionally considered benign in nature, increasing attention is being given to specific subsets of MB associated with ischemic symptomatology. The advent of contemporary functional and anatomic imaging modalities, both invasive and noninvasive, have dramatically improved our understanding of dynamic pathophysiology associated with MBs. This review provides a contemporary overview of epidemiology, pathobiology, diagnosis, functional assessment, and management of MBs.

Functional Assessment of Myocardial Bridging With Conventional and Diastolic Fractional Flow Reserve: Vasodilator Versus Inotropic Provocation.

Background Functional assessment of myocardial bridging (MB) remains clinically challenging because of the dynamic nature of the extravascular coronary compression with a certain degree of intraluminal coronary reduction. The aim of our study was to assess performance and diagnostic value of diastolic-fractional flow reserve (d-FFR) during dobutamine provocation versus conventional-FFR during adenosine provocation with exercise-induced myocardial ischemia as reference. Methods and Results This prospective study includes 60 symptomatic patients (45 men, mean age 57±9 years) with MB on the left anterior descending artery and systolic compression ≥50% diameter stenosis. Patients were evaluated by exercise stress-echocardiography test, and both conventional-FFR and d-FFR in the distal segment of left anterior descending artery during intravenous infusion of adenosine (140 µg/kg per minute) and dobutamine (10-50 µg/kg per minute), separately. Exercise-stress-echocardiography test was positive for myocardial ischemia in 19/60 patients (32%). Conventional-FFR during adenosine and peak dobutamine had similar values (0.84±0.04 versus 0.84±0.06, P=0.852), but d-FFR during peak dobutamine was significantly lower than d-FFR during adenosine (0.76±0.08 versus 0.79±0.08, P=0.018). Diastolic-FFR during peak dobutamine was significantly lower in the exercise-stress-echocardiography test -positive group compared with the exercise- stress-echocardiography test -negative group (0.70±0.07 versus 0.79±0.06, P<0.001), but not during adenosine (0.79±0.07 versus 0.78±0.09, P=0.613). Among physiological indices, d-FFR during peak dobutamine was the only independent predictor of functionally significant MB (odds ratio, 0.870; 95% CI, 0.767-0.986, P=0.03). Receiver-operating characteristics curve analysis identifies the optimal d-FFR during peak dobutamine cut-off ≤0.76 (area under curve, 0.927; 95% CI, 0.833-1.000; P<0.001) with a sensitivity, specificity, and positive and negative predictive value of 95%, 95%, 90%, and 98%, respectively, for identifying MB associated with stress-induced ischemia. Conclusions Diastolic-FFR, but not conventional-FFR, during inotropic stimulation with high-dose dobutamine, in comparison to vasodilatation with adenosine, provides more reliable functional significance of MB in relation to stress-induced myocardial ischemia.

Impact of myocardial bridge on late lumen enlargement in distal reference segments after recanalization of coronary chronic total occlusion.

Successful recanalization of coronary chronic total occlusion (CTO) can induce subsequent positive vascular remodeling. Although myocardial bridge (MB) is known to alter endothelial function and wall shear stress, the impact of MB on late lumen enlargement in the distal segment is unclear. A total of 59 patients who underwent successful percutaneous coronary intervention (PCI) for CTO in the left anterior descending artery (LAD) under intravascular ultrasound (IVUS) guidance and follow-up angiography at 8-12 months were included. Gray-scale IVUS images were analyzed and MB was detected. Lumen diameter (LD) at distal reference at post-PCI was quantitatively compared with corresponding LD at follow-up coronary angiography to assess late lumen enlargement. MB on IVUS was detected in 17 patients (29%). The length from LAD ostium to the entry of CTO was shorter (11.7 ± 13.9 vs. 22.8 ± 13.4 mm, p = 0.006) and LD at distal reference at post-PCI was smaller (1.65 ± 0.54 vs. 1.97 ± 0.56 mm, p = 0.049) in patients with MB than those without. At the mean follow-up of 10.4 ± 2.4 months, LD at distal reference was significantly increased by 25% from baseline to follow-up in the overall population (1.88 ± 0.57 vs. 2.21 ± 0.41 mm, p < 0.001), with a greater increase in patients with MB compared to those without (46 ± 31% vs. 17 ± 29%, p < 0.001). Multivariable analysis indicated MB as an independent predictor of late lumen enlargement. In patients with MB on IVUS, CTO was located in more proximal segment of LAD than those without. Late lumen enlargement at follow-up was greater in patients with MB compared to the counterpart.

Myocardial bridging-an unusual cause of Wellens syndrome: A case report.

RATIONALE: Coronary chest pain is usually ischemic in etiology and has various electrocardiographic presentations. Lately, it has been recognized that myocardial bridging (MB) with severe externally mechanical compression of an epicardial coronary artery during systole may result in myocardial ischemia. Such a phenomenon can be associated with chronic angina pectoris, acute coronary syndromes (ACS), coronary spasm, ventricular septal rupture, arrhythmias, exercise-induced atrioventricular conduction blocks, transient ventricular dysfunction, and sudden death. PATIENT CONCERNS: We report the case of a 58-year-old woman presenting with recurrent episodes of constrictive chest pain during exercise within the last 2 weeks. Except for obesity, general and cardiovascular clinical examination on admission were normal. DIAGNOSES: The resting 12 lead electrocardiogram (ECG) revealed changes typically for Wellens syndrome. High-sensitive cardiac troponin I was normal. We established the diagnosis of low-risk non-ST-segment elevation acute coronary syndrome with a Global Registry of Acute Coronary Events risk score of 92 points. INTERVENTIONS: The patient underwent coronary angiography, who showed subocclusive dynamic obstruction of the left anterior descending artery due to MB. OUTCOMES: The patient was managed conservatively. Her hospital course was uneventful and she was discharged on pharmacological therapy (clopidogrel, bisoprolol, amlodipine, atorvastatin, and metformin) with well-controlled symptoms on followup. LESSONS: MB is an unusual cause of myocardial ischemia. Wellens syndrome is an unusual presentation of ACS. We present herein a rare case of Wellens syndrome caused by MB. This case highlights the importance of subtle and frequently overseen ECG findings when assessing patients with chest pain and second, the importance of considering nonatherosclerotic causes for ACS.

Recurrent attack of acute myocardial infarction complicated with ventricular fibrillation due to coronary vasospasm within a myocardial bridge: a case report.

BACKGROUND: Myocardial bridge (MB) often an inoffensive condition that goes in one or more of the coronary arteries through the heart muscle instead of lying on its surface. MBs sometimes leads to myocardial ischemic symptoms such as chest pain, even an occurrence of myocardial infarction. However, reports of severe and recurrent cardiac adverse events related to the MBs are rare. CASE PRESENTATION: A 44-year-old male patient who suffered from a four-hour crushing chest pain ten years ago, was diagnosed as acute anterior ST-elevation myocardial infarction (STEMI). The initial findings of coronary angiography (CAG) showed MB was located in the middle part of the left anterior descending coronary artery (LAD). The patient was managed medically. Another re-attack of similar previous chest pain characteristics occured just after 3 days of discharge. Supra-arterial myotomy and CABG were the next adopted management. Postoperative progression was uneventful. However, 32 months after surgical treatment, the patient experienced an abrupt onset of chest pain accompanied by loss of consciousness. The ECG showed ventricular fibrillation (VF). After electrical cardioversion, an immediate CAG followed by CTA was performed which excluded thrombus or acute occlusion in the native coronary artery and an occlusion was observed at the end of the left internal mammary artery. An implantable cardioverter-defibrillator (ICD) was successfully performed for prevention of malignant arrhythmia. During ten years of follow-up, no complications have been identified. CONCLUSIONS: Although MB is mostly benign, it may lead to significant cardiovascular consequences. Supra-arterial myotomy is an appropriate treatment option for this patient who failed to optimal medical therapy. Furthermore, ICD implantation must be considered in order to prevent malignant ventricular arrhythmia caused by continuous spasm resulting in ischemia. Further investigations are required to confirm the clinical effectiveness of these procedures.

Hemodynamic effects of myocardial bridging in patients with hypertrophic cardiomyopathy.

Myocardial bridging (MB) is linked to angina and myocardial ischemia and may lead to sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). However, it remains unclear how MB affect the coronary blood flow in HCM patients. The aim of this study was to assess the effects of MB on coronary hemodynamics in HCM patients. Fifteen patients with MB (7 HCM and 8 non-HCM controls) in their left anterior descending (LAD) coronary artery were chosen. Transient computational fluid dynamics (CFD) simulations were conducted in anatomically realistic models of diseased (with MB) and virtually healthy (without MB) LAD from these patients, reconstructed from biplane angiograms. Our CFD simulation results demonstrated that dynamic compression of MB led to diastolic flow disturbances and could significantly reduce the coronary flow in HCM patients as compared with non-HCM group (P < 0.01). The pressure drop coefficient was remarkably higher (P < 0.05) in HCM patients. The flow rate change is strongly correlated with both upstream Reynolds number and MB compression ratio, while the MB length has less impact on coronary flow. The hemodynamic results and clinical outcomes revealed that HCM patients with an MB compression ratio higher than 65% required a surgical intervention. In conclusion, the transient MB compression can significantly alter the diastolic flow pattern and wall shear stress distribution in HCM patients. HCM patients with severe MB may need a surgical intervention.NEW & NOTEWORTHY In this study, the hemodynamic significance of myocardial bridging (MB) in patients with hypertrophic cardiomyopathy (HCM) was investigated to provide valuable information for surgical decision-making. Our results illustrated that the transient MB compression led to complex flow patterns, which can significantly alter the diastolic flow and wall shear stress distribution. The hemodynamic results and clinical outcomes demonstrated that patients with HCM and an MB compression ratio higher than 65% required a surgical intervention.

Impact of heart rate on cross-bridge cycling kinetics in failing and nonfailing human myocardium.

The force-frequency relationship (FFR) is an important regulatory mechanism that increases the force-generating capacity as well as the contraction and relaxation kinetics in human cardiac muscle as the heart rate increases. In human heart failure, the normally positive FFR often becomes flat, or even negative. The rate of cross-bridge cycling, which has been reported to affect cardiac output, could be potentially dysregulated and contribute to blunted or negative FFR in heart failure. We recently developed and herein use a novel method for measuring the rate of tension redevelopment. This method allows us to obtain an index of the rate of cross-bridge cycling in intact contracting cardiac trabeculae at physiological temperature and assess physiological properties of cardiac muscles while preserving posttranslational modifications representative of those that occur in vivo. We observed that trabeculae from failing human hearts indeed exhibit an impaired FFR and a reduced speed of relaxation kinetics. However, stimulation frequencies in the lower spectrum did not majorly affect cross-bridge cycling kinetics in nonfailing and failing trabeculae when assessed at maximal activation. Trabeculae from failing human hearts had slightly slower cross-bridge kinetics at 3 Hz as well as reduced capacity to generate force upon K+ contracture at this frequency. We conclude that cross-bridge kinetics at maximal activation in the prevailing in vivo heart rates are not majorly impacted by frequency and are not majorly impacted by disease.NEW & NOTEWORTHY In this study, we confirm that cardiac relaxation kinetics are impaired in filing human myocardium and that cross-bridge cycling rate at resting heart rates does not contribute to this impaired relaxation. At high heart rates, failing myocardium cross-bridge rates are slower than in nonfailing myocardium.

Haemodynamic impacts of myocardial bridge length: A congenital heart disease.

OBJECTIVES: There is an association between long and thick myocardial bridging (MB), haemodynamic perturbations and increased risk of myocardial infarction. This study aims to investigate the alteration in coronary haemodynamics with increasing the length of MB. METHODS: Angiography and intravascular ultrasound were performed in 10 patients with varying length of MB in the left anterior descending (LAD) artery. In silico models of MB were developed based on the reconstructed three-dimensional model of the LAD. The entire LAD was divided into 3 segments, proximal (pre-bridge), bridge and distal (post-bridge). Transient computational fluid dynamics simulations were performed to derive distribution of blood residence time and wall shear stress (WSS) over entire vessel including proximal, bridge and distal segments. RESULTS: With increasing the length of MB, a decreasing trend was observed in the WSS over proximal segment whereas an increasing trend was found in the WSS over bridge segment. When patients were divided into 2 groups based on the average length of MB in the whole cohort (Lave = 23.92 mm), patients with bridges longer than Lave had smaller WSS and higher residence time in the proximal segment compared to those with bridges shorter than Lave (0.59 ± 0.31 vs 0.21 ± 0.14 Pa and 0.0021 ± 0.0015 vs 0.0045 ± 0.0021 s). In contrast, patients with bridges longer than Lave had greater WSS in the bridge segment compared to those with bridges shorter than Lave (1.37 ± 1.66 vs 2.53 ± 3.14 Pa). No significant difference was found in the distal WSS of patients with short and long bridges. CONCLUSION: Our findings revealed a direct relationship between the length of MB and haemodynamic perturbations in the proximal segment such that the increased length of MB is associated with decreased WSS and increased residence time.

Longitudinal strain measured by two-dimensional speckle tracking echocardiography to evaluate left ventricular function in patients with myocardial bridging of the left anterior descending coronary artery.

OBJECTIVES: Myocardial bridging (MB) can cause myocardial ischemia, myocardial infarction, or even sudden cardiac death. We aimed to evaluate the left ventricular function in patients with MB of the left anterior descending coronary artery (LAD) using longitudinal strain (LS) measured by two-dimensional speckle tracking echocardiography. METHODS: We enrolled 46 subjects with MB in the LAD diagnosed by coronary angiography. Patients were categorized into two groups according to the severity of tunneled artery stenosis: <50% as group I (23 patients) and ≥50% as group II (23 patients). Twenty-five gender- and age-matched subjects without MB confirmed by coronary angiography or with normal results on treadmill exercise test were included as controls. Two-dimensional strain software was applied to measure the territories systolic average peak LS of the LAD coronary artery (LAD-TPLS), right coronary artery (RCA-TPLS), and left circumflex coronary artery (LCX-TPLS) and to measure the global systolic peak LS of left ventricle (LV-GPLS). RESULTS: The ratio of mitral peak early (E) and late (A) filling velocity (E/A) and the average mitral annular velocity (e') were lower, and the mitral E/e' ratio was higher in group II than in group I and controls (P < 0.05). LV-GPLS and LAD-TPLS were significantly less negative in group II than in group I and controls (LV-GPLS: -19.77 ± 1.60% vs -21.10 ± 1.91% and -21.76 ± 1.23%; LAD-TPLS: -19.24 ± 2.22% vs -22.00 ± 2.22% and -22.74 ± 1.82%, P < 0.001). The systolic compression severity of the tunneled artery was significantly correlated with LAD-TPLS (r = -0.56, P < 0.001), but less strongly correlated with LV-GPLS (r = -0.40, P < 0.05). The area under the curves of LAD-TPLS was larger than that of LV-GPLS; a cutoff value for LAD-TPLS of -21.68% had 91.3% sensitivity and 73.9% specificity for detection of ≥50% of the tunneled artery stenosis. CONCLUSIONS: In patients with ≥50% systolic narrowing of the tunneled artery, left ventricular systolic function and diastolic function were impaired, and the LAD-TPLS is an excellent predictor of ≥50% systolic narrowing of the tunneled artery in patients with MB of the LAD.

Relationship between myocardial bridge compression severity and haemodynamic perturbations.

OBJECTIVES: This study aims to examine the alteration in coronary haemodynamics with increasing the severity of vessel compression caused by myocardial bridging (MB). METHODS: Angiography and intravascular ultrasound were performed in 10 patients with MB with varying severities of systolic compression in the left anterior descending (LAD) artery. Computer models of MB were developed and transient computational fluid dynamics simulations were performed to derive distribution of blood residence time and shear stress. RESULTS: With increasing the severity of bridge compression, a decreasing trend was observed in the shear stress over proximal segment whereas an increasing trend was found in the shear stress over bridge segment. When patients were divided into 2 groups based on the average systolic vessel compression in the whole cohort (%CRave = 27.38), patients with bridges with major systolic compression (>%CRave) had smaller shear stress and higher residence time in the proximal segment compared to those with bridges with minor systolic compression (<%CRave) (0.37 ± 0.23 vs 0.69 ± 0.29 Pa and 0.0037 ± 0.0069 vs 0.022 ± 0.0094 s). In contrast, patients with bridges with major systolic compression had greater shear stress in the bridge segment compared to those with bridges with minor systolic compression (2.49 ± 2.06 vs 1.13 ± 0.89 Pa). No significant difference was found in the distal shear stress of patients with bridges with major and minor systolic compression. CONCLUSION: Our findings revealed a direct relationship between the severity of systolic compression of MB and haemodynamic perturbations in the proximal segment such that the increased systolic vessel compression was associated with decreased shear stress and increased blood residence time.

Myocardial bridging and endothelial dysfunction - Computational fluid dynamics study.

Myocardial bridging (MB) is associated with endothelial dysfunction in patients with angina and non-obstructive coronary artery disease. This study aims to determine if there is a link between abnormal blood flow patterns and endothelial dysfunction in patients with MB. Ten patients with MB in their left anterior descending (LAD) artery were selected, 5 of whom had endothelial dysfunction and 5 had no endothelial dysfunction based on their response to acetylcholine. Similarly, 10 patients without MB in their LAD, 5 of whom had endothelial dysfunction and 5 of whom had no endothelial dysfunction, were studied as a control group. Transient computational fluid dynamics simulations were performed to derive wall shear stress (WSS) over the entire vessel including proximal, middle and distal segments. Patients with MB and endothelial dysfunction had lower WSS in the proximal LAD and greater WSS in the mid-LAD than patients with MB but without endothelial dysfunction. When comparing patients with endothelial dysfunction, those with MB had significantly lower shear stress in the proximal LAD (0.32 ±â€¯0.14 Pa (with MB) vs 0.71 ±â€¯0.38 Pa (without MB), p = 0.01) and greater shear stress in the mid-LAD (2.81 ±â€¯1.20 Pa (with MB) vs 1.66 ±â€¯0.31 Pa (without MB), p = 0.014) than patients without MB. Our findings demonstrated that the presence of MB significantly contributes to low WSS and endothelial dysfunction relationship.

Simulated coronary arterial hemodynamics of myocardial bridging.

The objective of this study was to explore the effects of myocardial bridge compression on blood flow, normal stress, circumferential stress and shear stress in mural coronary artery. An original mural coronary artery simulative device has been greatly improved and its measured hemodynamic parameters have been expanded from a single stress (normal stress) to multiple stresses to more fully and accurately simulate the true hemodynamic environment under normal stress, circumferential stress and shear stress. This device was used to more fully explore the relationship between hemodynamics and mural coronary atherosclerosis under the combined effects of multiple stresses. Results obtained from the mural coronary artery simulator showed stress abnormality to be mainly located in the proximal mural coronary artery where myocardial bridge compression was intensified and average and fluctuation values (maximum minus minimum) of proximal stress were significantly increased by 27.8% and 139%, respectively. It is concluded that myocardial bridge compression causes abnormalities in the proximal hemodynamics of the mural coronary artery. This is of great significance for understanding the hemodynamic mechanism of coronary atherosclerosis and has potential clinical value for the pathological effect and treatment of myocardial bridge.

Myocardial bridging of the left anterior descending coronary artery is associated with reduced myocardial perfusion reserve: a 13N-ammonia PET study.

Myocardial Bridging (MB) refers to the band of myocardium that abnormally overlies a segment of a coronary artery. This paper quantitatively evaluates the influence of MB of the left anterior descending artery (LAD) on myocardial perfusion of the entire left ventricle. We studied 131 consecutive patients who underwent hybrid rest/stress 13N-ammonia positron emission tomography (PET) and coronary computed tomography angiography (CCTA) due to suspected myocardial ischemia. Patients with previous myocardial infarction and/or significant coronary artery disease (≥ 50% stenosis) were excluded. Myocardial perfusion measurements were compared between patients with and without LAD-MB. Additionally, we evaluated the relationship between anatomical characteristics (length and depth) of LAD-MB and myocardial perfusion measurements. 17 (13%) patients presented a single LAD-MB. Global myocardial perfusion reserve (MPR) was lower in patients with LAD-MB than in patients without LAD-MB (1.9 ± 0.5 vs. 2.3 ± 0.6, p < 0.01). Global stress myocardial blood flow (MBF) was similar in patients with and without LAD-MB (2.2 ± 0.4 vs. 2.3 ± 0.7 ml/g/min, p = 0.40). Global rest MBF was higher in patients with LAD-MB than in patients without LAD-MB (1.2 ± 0.3 vs. 1.0 ± 0.2 ml/g/min, p < 0.01). Global rest MBF, stress MBF, and MPR quantifications were similar in patients with superficial and deep LAD-MB (all p = NS). We did not find any correlation between length and global rest MBF, stress MBF nor MPR (r = - 0.14, p = 0.59; r = 0.44, p = 0.07; and r = 0.45, p = 0.07 respectively). Quantitative myocardial perfusion suggests that LAD-MB may be related to impaired perfusion reserve, an indicator of microvascular dysfunction. Anatomical characteristics of LAD-MB were not related to changes in myocardial perfusion.

Fractional flow reserve derived from CCTA may have a prognostic role in myocardial bridging.

PURPOSE: To evaluate the feasibility of fractional flow reserve (cFFR) derivation from coronary CT angiography (CCTA) in patients with myocardial bridging (MB), its relationship with MB anatomical features, and clinical relevance. METHODS: This retrospective study included 120 patients with MB of the left anterior descending artery (LAD) and 41 controls. MB location, length, depth, muscle index, instance, and stenosis rate were measured. cFFR values were compared between superficial MB (≤ 2 mm), deep MB (> 2 mm), and control groups. Factors associated with abnormal cFFR values (≤ 0.80) were analyzed. RESULTS: MB patients demonstrated lower cFFR values in MB and distal segments than controls (all p < 0.05). A significant cFFR difference was only found in the MB segment during systole between superficial (0.94, 0.90-0.96) and deep MB (0.91, 0.83-0.95) (p = 0.018). Abnormal cFFR values were found in 69 (57.5%) MB patients (29 [49.2%] superficial vs. 40 [65.6%] deep; p = 0.069). MB length (OR = 1.06, 95% CI 1.03-1.10; p = 0.001) and systolic stenosis (OR = 1.04, 95% CI 1.01-1.07; p = 0.021) were the main predictors for abnormal cFFR, with an area under the curve of 0.774 (95% CI 0.689-0.858; p < 0.001). MB patients with abnormal cFFR reported more typical angina (18.8% vs 3.9%, p = 0.023) than patients with normal values. CONCLUSION: MB patients showed lower cFFR values than controls. Abnormal cFFR values have a positive association with symptoms of typical angina. MB length and systolic stenosis demonstrate moderate predictive value for an abnormal cFFR value. KEY POINTS: • MB patients showed lower cFFR values than controls. • Abnormal cFFR values have a positive association with typical angina symptoms. • MB length and systolic stenosis demonstrate moderate predictive value for an abnormal cFFR value .

Surgical unroofing of hemodynamically significant myocardial bridges in a pediatric population.

BACKGROUND: Although myocardial bridges (MBs) are traditionally regarded as incidental findings, it has been reported that adult patients with symptomatic MBs refractory to medical therapy benefit from unroofing. However, there is limited literature in the pediatric population. The aim of our study was to evaluate the indications and outcomes for unroofing in pediatric patients. METHODS: We retrospectively reviewed all pediatric patients with MB in our institution who underwent surgical relief. Clinical characteristics, relevant diagnostic data, intraoperative findings, and postoperative outcomes were evaluated. RESULTS: Between 2012 and 2016, 14 pediatric patients underwent surgical unroofing of left anterior descending artery MBs. Thirteen patients had anginal symptoms refractory to medical therapy, and 1 patient was asymptomatic until experiencing aborted sudden cardiac arrest during exercise. Thirteen patients underwent exercise stress echocardiography, all of which showed mid-septal dys-synergy. Coronary computed tomography imaging confirmed the presence of MBs in all patients. Intravascular ultrasound imaging confirmed the length of MBs: 28.2 ± 16.3 mm, halo thickness: 0.59 ± 0.24 mm, and compression of left anterior descending artery at resting heart rate: 33.0 ± 11.6%. Invasive hemodynamic assessment with dobutamine confirmed the physiologic significance of the MBs with diastolic fractional flow reserve: 0.59 ± 0.13. Unroofing was performed with the patient under cardiopulmonary bypass (CPB) in the initial 9 cases and without CPB in the subsequent 5 cases. All patients were discharged without complications. The 13 symptomatic patients reported resolution of symptoms on follow-up, and improvement in symptoms and quality of life was documented using the Seattle Angina Questionnaire version 7. CONCLUSIONS: Unroofing of MBs can be safely performed in pediatric patients, with or without use of CPB. In symptomatic patients, unroofing can provide relief of symptoms refractory to medical therapy.

Chest Pain During Chemotherapy: A Case of Severe Myocardial Bridging.

A cancer patient presented with acute chest pain at rest 40 hours after IV fluorouracil infusion. Angiography showed evidence of myocardial bridging.