Search

Myocardial bridging is rare. Myocardial bridges are most commonly localized in the middle segment of the left anterior descending coronary artery. The anatomic features of the bridges vary significantly. Alterations of the endothelial morphology and the vasoactive agents impact on the progression of atherosclerosis of myocardial bridging. Patients may present with chest pain, myocardial infarction, arrhythmia and even sudden death. Patients who respond poorly to the medical treatment with β-blockers warrant a surgical intervention. Myotomy is a preferred surgical procedure for the symptomatic patients. Coronary stent deployment has been in limited use due to the unsatisfactory long-term results.

In myocardial bridging (MB) a segment of the coronary artery is covered by the myocardium. MB can be seen as a systolic compression by invasive coronary angiography (ICA) or as an intramural course by computed tomography angiography (CTA). Intramural course is a common incidental finding in CTA studies. Only minority of the bridging segments are associated with systolic compression causing a possible impairment of myocardial perfusion. The relationship between myocardial blood flow and MB is complex and poorly evaluated by anatomic imaging. Furthermore, provocation tests are frequently needed to uncover systolic compression. Fractional flow reserve can be used to assess the hemodynamic significance of MB. Nuclear perfusion imaging can demonstrate flow abnormalities associated with MB. Stress echocardiography can demonstrate ischemic wall motion abnormalities. They can be complemented by hybrid imaging with CTA to distinguish epicardial coronary artery disease and MB. This article will review different imaging modalities for the evaluation of the physiologic significance of MB.

Outlining the severity of the myocardial bridge (MB) is a critical step for selecting the appropriate option among medical, surgical, or angioplasty-based treatments. Invasive treatments are usually preferred if treatment-resistant symptoms are observed or ischemia is proven by tests such as fractional flow reserve or myocardial perfusion scintigraphy (MPS). In this report, we present a patient who developed severe hypotension during treadmill exercise test, even though there were no perfusion defects during adenosine-induced MPS. This case suggests MPS with adenosine is not a good choice for evaluating ischemia in MB patients, as it may cause false negative results.

Background: Heart rate (HR) recovery (HRR) reflects autonomic activity and predicts cardiovascular events. The aim of this study was to assess HRR in patients with myocardial bridge (MB)., Methods: Medical recordings of 93 patients with MB and appropriate age, compared to 78 sex-matched healthy subjects were analyzed. MB was diagnosed via coronary computed tomography angiography after a positive exercise stress test (EST). HRR indices were calculated by subtracting 1st (HRR1), 2nd (HRR2) and 3rd (HRR3) minute HR from the maximal HR during EST., Results: HRR1 (30.2 ± 13.3 bpm vs. 35.8 ± 10.4 bpm, p = 0.001) and HRR2 (52.3 ± 13.3 bpm vs. 57.1 ± 11.6 bpm, p = 0.013) were lower in patients with MB. In addition, HRR1 was lower in patients with left anterior descending (LAD) MB than non-LAD MB (28.5 ± 13.2 vs. 37.1 ± 11.4, p = 0.013). Presence of MB, deep MB, LAD MB and multi-vessel MB were predictors of HRR1 (p < 0.01 for all). In a multivariate analysis, LAD MB was the only significant independent predictor of HRR1 (b = -8.524, p = 0.009)., Conclusions: Patients with MB have impairment in HRR indices which is more pronounced among patients with LAD MB. Cardiac autonomic dysfunction in MB might be due to recurrent myocardial ischemia.

Background: Myocardial bridge refers to the myocardial tissue with which the coronary artery is partly covered. Though it has long been regarded to be benign, patients with myocardial bridges may present with myocardial ischemia, acute coronary syndromes, coronary spasm, sudden cardiac arrest or even sudden death., Case Presentation: In present study, we reviewed four cases with myocardial bridge and no stenosis of coronary artery, which included acute coronary syndrome and sudden cardiac arrest., Conclusions: These cases indicated that cardiac events in patients with myocardial bridge may be associated with coronary spasm, myocardial supply/demand mismatch or cardiac arrest.

Background: Although a myocardial bridge (MB) is often regarded as a benign coronary variant, recent studies have associated MB with focal myocardial ischemia. The physiological consequences of MB on ventricular function during stress have not been well established., Methods and Results: We enrolled 58 patients with MB of the left anterior descending artery, diagnosed by intravascular ultrasound. Patients underwent invasive physiological evaluation of the MB by diastolic fractional flow reserve during dobutamine challenge and exercise echocardiography. Septal and lateral longitudinal strain (LS) were assessed at rest and immediately after exercise and compared with strain of matched controls. Absolute and relative changes in strain were also calculated. The mean age was 42.5±16.0 years. Fifty-five patients had a diastolic fractional flow reserve ≤0.76. At rest, there was no significant difference between the 2 groups in septal LS (19.0±1.8% for patients with MB versus 19.2±1.5% for control, P=0.53) and lateral LS (20.1±2.0% versus 20.0±1.6%, P=0.83). With stress, compared with controls, patients with MB had a lower peak septal LS (18.9±2.6% versus 21.7±1.6%, P<0.001) and lower absolute (-0.1±2.1% versus 2.5±1.3%, P<0.001) and relative change (-0.6±11.2% versus 13.1±7.8%, P<0.001) in septal LS, whereas there was no significant difference in lateral LS. In multivariate analysis, diastolic fractional flow reserve and length were independent determinants of lower changes in septal LS., Conclusions: Patients with a hemodynamically significant MB, determined by invasive diastolic fractional flow reserve, have significantly lower change in septal LS on exercise echocardiography, suggesting that septal LS may be useful for noninvasively assessing the hemodynamic significance of an MB., (© 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.)

Myocardial noncompaction, namly isolated noncompaction of the left ventricular myocardium (NVM), is a rare congenital disease. It can be either seen in the absence of other cardiac anomalies, or associated with other congenital cardiac defects, mostly stenotic lesions of the left ventricular outflow tract. A myocardial bridge (MB) is thought being associated with coronary heart disease, such as coronary spasm, arrhythmia, and so on. The significance of MB in association with other congenital cardiac conditions is unknown.We report a novel case who was presented NVM and MB. A 34-year-old man complained of chest prickling-like pain and dizzy for 1 year. His blood pressure was 110/70 mm Hg. Echocardiograph revealed increased trabeculations below the level of papillary muscle of left ventricle (LV); deep intertrabecular recesses in the endocardial wall of LV particularly in apex free wall; and LV ejection fraction of 57%. A coronary computerized tomography scan showed that part, 38.9 cm, of left descending artery tunnel was surrounding by cardiac muscles rather than resting on top of the myocardium.The therapeutics interventions included lifestyle cares, agents of anti-ischemia and improvement myocardial cell metabolism. The patient was followed up for 2.6 years, and his general condition was stable.This case indicates that NVM can be developed with MB, and the complete diagnosis of NVM and MB should be made by different image studies.

Background: Although myocardial bridging (MB) is defined as an angiographic phenomenon with a benign course, it has also been associated with adverse cardiovascular events. The effects of exercise on myocardial repolarization in patients with MB were tested in this study, with Tp-e and Tp-e/QT repolarization indexes., Material and Methods: A total of 50 patients in whom isolated MB was diagnosed at coronary angiography (CAG) (Group I) and 48 patients with normal CAG results (Group II) were included in this study. The participants underwent treadmill exercise stress testing according to the Bruce protocol. QT dispersion (QTd) was defined as the minimum QT interval subtracted from the maximum. The Tp-e interval was defined as the difference between the QT and the QT peak time period. QTd and Tp-e intervals were calculated for all patients before and after exercise testing and differences between groups were compared., Results: At peak exercise, QTd and cQTd showed a significant increase in comparison to baseline values in the group of patients with myocardial bridges. Significant increases were also found with exercise in the Tp-e, cTp-e durations and Tp-e/QT ratio of the MB patient group in comparison to the baseline values. On the other hand, significant differences in QTd, cQTd, Tp-e, cTp-e intervals, and Tp-e/QT ratio during peak exercise in comparison with baseline values were not detected in the control group (p>0.05)., Conclusions: Significant increases in QTd, cQTd, Tp-e and cTp-e intervals and Tp-e/QT ratio were detected in the MB patients during exercise testing.

Objectives: This study observed hemodynamic consequences of myocardial bridging and its relation to coronary atherosclerosis., Background: Myocardial bridging is seen as intramural course by computed tomography angiography (CTA) or systolic compression by invasive coronary angiography. Segments with myocardial bridging are in previous studies closely associated with proximal atherosclerotic plaques., Methods: We prospectively studied 100 patients 63 ± 7 years of age with intermediate likelihood of coronary artery disease. Segments with superficial (>1 mm) or deep (>2 mm) intramural course were identified using CTA. Myocardial perfusion was studied by 15-Oxygen water positron emission tomography and systolic compression by invasive coronary angiography., Results: Myocardial bridging was detected in 34 (34%) patients in 48 different vascular segments. Of these, 24 (50%) were deep and systolic compression was present in 14 (29%). In patients without obstructive coronary artery disease, myocardial stress perfusion distal to myocardial bridging was comparable with remote control regions (3.3 ± 0.9 ml/g/min vs. 3.3 ± 0.7 ml/g/min, n = 24, p = 0.88). Stress perfusion was comparable in segments with and without systolic compression (3.0 ± 0.9 vs. 2.7 ± 1.0 ml/g/min, p = 0.43). Atherosclerotic plaques were more frequent in proximal (71%) than myocardial bridging (7%) or distal (21%) segments. The presence of atherosclerosis and the average number of plaques were comparable in coronary arteries with and without myocardial bridging (73% vs. 60%, p = 0.14 and 2.0 ± 1.7 vs. 1.5 ± 1.6, p = 0.06). Median Agatston coronary calcium score was not elevated in vessels with myocardial bridge (15 [interquartile range: 0, 129] vs. 50 [interquartile range: 0, 241], p = 0.21)., Conclusions: Myocardial bridging of coronary arteries is common on CTA, but only approximately one-third of these show systolic compression. Myocardial bridging is not associated with reduced myocardial perfusion during vasodilator stress. Atherosclerosis is located predominantly proximal to myocardial bridging but atherosclerotic burden and presence of vulnerable plaques were comparable., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objective: To study the imaging features of coronary competitive reverse flow and incidence of a "reverse attenuation gradient" in coronary CT angiography (CTA) with correlation to invasive coronary angiography (ICA)., Methods: Patients who had undergone coronary CTA and ICA within 2 weeks were retrospectively identified in our database and reviewed. All cases with ICA-confirmed competitive reverse flow or chronic total occlusions (CTOs) were included for further analysis. The "reverse attenuation gradient sign" was defined as a reverse intraluminal opacification gradient of vessels which showed higher opacification in more distal compared with proximal segments. ICA findings were recorded and served as the reference to identify the clinical implications of this sign., Results: In total, 134 patients (mean age, 68.1 ± 11.3 years; range, 38-90 years; 104 men) were included in our study. ICA revealed 11 cases of coronary competitive reverse flow and 123 cases of CTO. A reverse attenuation gradient sign was present in 9 of 11 patients (82%) with coronary competitive reverse flow and 72 of 123 (59%) chronically occluded coronary arteries. Myocardial bridges, distal collateral filling, as well as direct visualization of collateral connection were all more frequent in cases with coronary competitive reverse flow group compared with cases with a CTO., Conclusions: The reverse attenuation gradient sign distal to an upstream coronary severe stenosis indicates the presence of competitive collateral flow. Coronary CTA is able to correctly detect coronary competitive collateral flow and differentiate it from CTOs., (Copyright © 2015 Society of Cardiovascular Computed Tomography. Published by Elsevier Inc. All rights reserved.)

Aims: The aim of this study is to investigate how the myocardial bridge oppression affects the hoop stress of mural coronary artery., Methods: The "myocardial bridge - coronary artery" simulative device records the hoop stress which is changed by adjusting the external pressure of the simulated coronary artery and the oppression degree of the respectively., Results: Simulation experiment in vitro indicates that the abnormal hoop stress mainly occurs in the proximal end of mural coronary artery. As the oppression degree of myocardial bridge increases, the mean and the oscillatory value (maximum-minimum) of hoop stress in the proximal end increase markedly., Conclusions: The "myocardial bridge - coronary artery" simulation device can provide an experiment method of studying the hoop stress influence on mural coronary artery in vitro.

Background: Myocardial bridging (MB) occurs when a segment of an epicardial coronary artery takes an intra- myocardial course, thus leading to systolic compression. Most myocardial bridges involve the left anterior descending artery and are observed in 14-35% of patients. Different pathophysiological mechanisms can induce symptoms secondary to myocardial ischemia: systolic coronary compression, diastolic dysfunction associated with aging and coronary atherosclerosis, LV hypertrophy, vasospasm, microvascular and endothelial dysfunction, plaque development proximal to the bridge., Methods: We performed a literature review of MB, with a particular emphasis on electrocardiographic manifestations., Results: Stable angina-like chest pain is the usual presentation and MB should be suspected in patients at low risk for coronary atherosclerosis which refer this symptom or which present myocardial ischemia at instrumental examinations. ECG changes are not specific for MB and resting ECG is often normal or presents ST segment anomalies. Exercise stress test often shows non specific signs of ischemia, conduction disturbances or arrhythmias which do not allow the distinction between myocardial bridging and other causes of myocardial ischemia; angina often appears during exercise, even in the absence of ECG changes. Myocardial perfusion deficits at scintigraphy are neither obligatory nor specific. Although the clinical significance of MB is still debated, MB has been associated with acute coronary syndrome, coronary vasospasm, and even sudden cardiac death., Conclusion: Although MB may lead to myocardial ischemia during stress, its clinical presentation and electrocardiographic findings are not specific., (© 2014 Wiley Periodicals, Inc.)

Objectives: The aim of this study was to retrospectively evaluate the morphologic and functional features of myocardial bridging (MB) and to investigate the impact of morphologic features on presence of atherosclerosis with multi-detector computed tomography (MDCT) coronary angiography., Study Design: The study population consisted of 191 consecutive patients. Besides coronary lesions, morphologic features of the MB (depth, length and the distance of the tunneled artery from the left coronary ostium) were analyzed., Results: MDCT detected MB on left anterior descending artery in 41 patients (21.5%). The prevalence of atherosclerotic plaques proximal to the MB of LAD was 49% (20/41). There was a statistically significant correlation between percentage of systolic compression and depth of the tunneled segment (r=0.538, p<0.01). There was no relation between distance of the tunneled segment from the ostium and degree of systolic compression. No significant correlation was found between percentage of systolic compression and length of the tunneled segment (r=0.058, p=0.721). Morphologic features of MB were not related to the presence of CAD in proximal segments., Conclusion: MDCT coronary angiography depicts the morphologic and functional features of the MB in detail. The depth of MB segment was correlated with systolic compression of MB. There was no relationship between distance of the tunneled segment from the ostium and systolic compression.

Patients with myocardial bridging are often asymptomatic, but this anomaly may be associated with exertional angina, acute coronary syndromes, cardiac arrhythmias, syncope, or even sudden cardiac death. This review presents our understanding of the pathophysiology of myocardial bridging and describes prevailing diagnostic modalities and therapeutic options for this challenging clinical entity., (Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Myocardial bridging (MB) is defined as the intramural course of a major epicardial coronary artery, and is mostly confined to the left ventricle and the left anterior descending coronary artery (LAD). MB is a common congenital abnormality of a coronary artery, and is usually thought to be a benign anatomical variant. Although rare, previous studies have reported that patients with MB may suffer from myocardial ischemia, myocardial infarction (MI), arrhythmias, and even sudden death. Therefore, the diagnosis and treatment of MB are both important. Since MB is congenital, its disappearance is unlikely. We here report a very rare case of disappearance of MB after inferior MI.

Although some myocardial bridges can be asymptomatic, their presence often causes coronary disease either through direct compression of the "tunnel" segment or through stimulation and accelerated development of atherosclerosis in the segment proximally to the myocardial bridge. The studied material contained 30 human hearts received from the Department of Anatomy. The hearts were preserved 3 to 5 days in 10% formalin solution. Thereafter, the fatty tissue was removed and arterial blood vessels prepared by careful dissection with special reference to the presence of the myocardial bridges. Length and thickness of the bridges were measured by the precise electronic caliper. The angle between the myocardial bridge fibre axis and other axis of the crossed blood vessel was measured by a goniometer. The presence of the bridges was confirmed in 53.33% of the researched material, most frequently (43.33%) above the anterior interventricular branch. The mean length of the bridges was 14.64 ± 9.03 mm and the mean thickness was 1.23 ± 1.32 mm. Myocardial bridge fibres pass over the descending blood vessel at the angle of 10-90 degrees. The results obtained on a limited sample suggest that the muscular index of myocardial bridge is the highest for bridges located on RIA, but that the difference is not significant in relation to bridges located on other branches. The results obtained suggest that bridges located on other branches, not only those on RIA, could have a great contractive power and, consequently, a great compressive force, which would be exerted on the wall of a crossed blood vessel.

Objectives: The objective of this study was to determine the long-term efficacy and dynamics of systolic and diastolic luminal changes within the bridged segments of coronary arteries after intracoronary stenting with drug-eluting stent (DES) in patients (pts) with symptomatic myocardial bridging (SMB) in the absence of coronary atherosclerosis., Background: Although myocardial bridging (MB) represents a benign disease in the majority of pts, in its severest forms it is clinically manifested as typical or atypical angina, myocardial ischemia, myocardial infarction, left ventricular dysfunction, atrioventricular conduction disturbance, exercise-induced ventricular tachycardia, or sudden death. The only existing prospective study of 11 pts with SMB treated with bare-metal stent (BMS) reported a 36% in-stent restenosis (ISR) rate at 7 weeks repeated quantitative coronary angiography (QCA)., Methods: The study consisted of 15 consecutive patients (13 men and 2 women) with SMB of the mid-portion of the left anterior descending (LAD) coronary artery (and in 1 patient, concomitant MB of the left circumflex [LCX] coronary artery) and luminal diameter systolic narrowing of the tunneled segment of ≥50%, underwent percutaneous coronary intervention with DES. Clinical and non-invasive assessments of myocardial ischemia were determined every 6 months over 5 years and QCA was performed 12 and 24 months post procedure if not urged differently by deterioration of clinical symptoms and/or presence of positive ischemia tests. The minimal systolic and diastolic luminal diameters of the bridged/stented segments were measured before, immediately after, and 12 and 24 months post procedure by two independent observers blinded to each other's readings, using QCA commercial software. The endpoints of the study were ISR, target lesion revascularization (TLR) rate, in-stent diameter late luminal loss (LLL), and permanent disappearance or significant improvement of clinical symptoms., Results: After 12 months, ISR and TLR in 16 treated vessels was 18.7%, LLL was 0.2 ± 0.6 mm and permanent disappearance or significant improvement of symptoms was achieved in all 15 pts. In 3 pts, clinically-driven repeat revascularization was necessary within the first 6 months. In 1 patient, coronary perforation complicated stent deployment and was immediately resolved by stent-graft implantation, followed by completely uneventful recovery., Conclusions: DES implantation in pts with SMB resistant to medical treatment results in prompt and long-term increase of systolic and diastolic luminal diameters, and long-lasting relief of clinical symptoms. Compared to BMS, stenting of SMB with DES resulted in significantly lower ISR and TLR rate.

Background: Small case series have associated coronary myocardial bridging (MB) with adverse cardiac events. However, the clinical significance of MB in unselected patients with chest pain remains unclear. The purpose of this study was to explore the relation between the presence of isolated MB and subsequent adverse cardiac events in symptomatic patients referred for coronary computed tomography angiography (CCTA)., Methods and Results: Three hundred and thirty-four consecutive patients (age 57 ± 13 years, 43% female) with chest pain and no prior history of coronary artery disease (CAD) who underwent 64-slice CCTA and had no obstructive CAD (≥ 50% coronary luminal obstruction) were included. Patients were followed for cardiac events [cardiovascular (CV) death or non-fatal myocardial infarction (MI)] over 6.1 ± 1 years. Outcomes were compared between patients with MB vs. those without MB using the Cox models. MB was present in 117 out of 334 (35%) patients on CCTA and 80% of MB involved the mid-distal left anterior descending coronary artery. During a mean follow-up duration of 6.1 ± 1 years, cardiac events occurred in 6 out of 117 (5.1%) patients with, and 7 out of 217 (3.2%) patients without MB (P = 0.40). Univariate predictors of cardiac events were hypertension [hazards ratio (HR) = 10.6, P = 0.002], diabetes mellitus (HR = 4.8, P = 0.01), and older age (HR = 1.1, P = 0.0004). The association of hypertension and age with adverse cardiac events remained statistically significant after adjusting for other variables. Neither the presence nor the extent of MB was associated with an increased risk of cardiac events., Conclusion: MB is a common finding on CCTA among patients presenting with chest pain but no obstructive CAD. No association was evident between MB and the risk of CV death or MI.

Background: Patients with a myocardial bridge (MB) and no significant obstructive coronary artery disease (CAD) may experience angina presumably from ischemia, but noninvasive assessment has been limited and the underlying mechanism poorly understood. This study seeks to correlate a novel exercise echocardiography (EE) finding for MBs with invasive structural and hemodynamic measurements., Methods and Results: Eighteen patients with angina and an EE pattern of focal end-systolic to early-diastolic buckling in the septum with apical sparing were prospectively enrolled for invasive assessment. This included coronary angiography, left anterior descending artery (LAD) intravascular ultrasound (IVUS), and intracoronary pressure and Doppler measurements at rest and during dobutamine stress. All patients were found to have an LAD MB on IVUS. The ratios of diastolic intracoronary pressure divided by aortic pressure at rest (Pd/Pa) and during dobutamine stress (diastolic fractional flow reserve [dFFR]) and peak Doppler flow velocity recordings at rest and with stress were successfully performed in 14 patients. All had abnormal dFFR (≤0.75) at stress within the bridge, distally or in both positions, and on average showed a more than doubling in peak Doppler flow velocity inside the MB at stress. Seventy-five percent of patients had normalization of dFFR distal to the MB, with partial pressure recovery and a decrease in peak Doppler flow velocity., Conclusions: A distinctive septal wall motion abnormality with apical sparing on EE is associated with a documented MB by IVUS and a decreased dFFR. We posit that the septal wall motion abnormality on EE is due to dynamic ischemia local to the compressed segment of the LAD from the increase in velocity and decrease in perfusion pressure, consistent with the Venturi effect.

Objectives: This study sought to evaluate the prevalence and potential role of myocardial bridging in the pathogenesis of apical ballooning syndrome (ABS)., Background: ABS is characterized by reversible left ventricular dysfunction, frequently precipitated by a stressful event, but the pathogenesis remains still unclear., Methods: Forty-two consecutive patients (40 female, mean age 66 ± 7 years) with ABS underwent echocardiography, cardiac magnetic resonance, coronary angiography (CA) with intravascular ultrasound, and computed tomography angiography (CTA). Myocardial bridging was diagnosed by CA when a dynamic compression phenomenon was observed in the coronary artery and by CTA when a segment of coronary artery was completely (full encasement) or incompletely (partial encasement) surrounded by the myocardium. The prevalence of myocardial bridging detected by CTA and CA in ABS patients was compared with 401 controls without ABS who underwent both CTA and CA., Results: Myocardial bridging by CTA was observed in 32 ABS patients (76%): 23 with partial encasement and 9 with full encasement. All myocardial bridging was located in the mid segment of the left anterior descending coronary artery (LAD) with a mean length of 17 ± 9 mm. CA revealed myocardial bridging in 17 subjects (40%) (9 with partial encasement and 8 with full encasement by CTA). All subjects in which dynamic compression was observed by CA showed myocardial bridging by CTA, while none of the subjects with negative findings for myocardial bridging by CTA revealed dynamic compression by CA. Compared with controls, ABS patients showed a significant higher prevalence of myocardial bridging in the LAD either by CA (40% vs. 8%; p < 0.001) or by CTA (76% vs. 31%; p < 0.001)., Conclusions: Our study showed that myocardial bridging of the LAD is a frequent finding in ABS patients as revealed both by CA and, mostly, by CTA, suggesting a role of myocardial bridging as potential substrate in the pathogenesis of ABS., (Copyright © 2012 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Myocardial bridge (MB) is defined as compression of coronary artery during systole while it is normal in diastole. In angiographic series, the prevalence of this anomaly was reported between 0.5% and 2.5%. It is occasionally seen in the middle segment of the left anterior descending coronary artery. Although MB is considered to be a benign anomaly, the association of MB with ischemia, systolic dysfunction, conduction abnormality, arrhythmias, and sudden cardiac death were reported. Herein, we report 3 cases of MB that were diagnosed with coronary angiography and were associated with arrhythmic complications. In 2 patients, complete atrioventricular block was present, and another patient was diagnosed with sick sinus syndrome with the help of an electrophysiological study. All patients underwent permanent cardiac pacemaker implantation.

Background: Myocardial Bridging (MB) is defined as a segment of a major epicardial coronary artery, the "tunnelled artery", that goes intramurally through the myocardium beneath the muscle bridge., Materials and Methods: A 69-year-old male patient with a story of arterial hypertension and dyslipidemia in treatment with converting enzyme inhibitors (ACE-I), antiplatelet therapy and HMG-CoA reductase inhibitors and calcium channel blockers, presented with anginal-like chest pain and dyspnea. The coronary angiography showed a myocardial bridging and no hemodynamically significant coronary artery disease., Results: On admission in our Department, the exercise cyclo ergometer test was significant for > 3 mm ST segment depression in the anterior and lateral leads (V3, V4, V5, V6) associated with chest pain. The coronary angiography revealed a 40% stenosis of the distal tract of the right coronary artery (RCA), a 30% stenosis of the proximal tract of the left anterior descending artery (LAD) and 40% of the proximal tract of the first diagonal branch. A 30% stenosis in the middle tract of the left circumflex coronary artery (LCX) was then detected. A marked systolic localized narrowing (90%) on the middle tract of the LAD, after the second diagonal branch (a myocardial bridge) was also detected. After eight months, the exercise cyclo ergometer test using a standard Bruce protocol was normal and, after sixteen months, no significant coronary artery disease (< 50%) and no myocardial bridging were detected by the coronary 64-multislice spiral computed tomography. Two years later, the patient was readmitted to our Department because of angina-like chest pain during light exertion in the last two months. The coronary angiography of the right system revealed a 30% stenosis of the proximal tract and a 50% stenosis of the distal tract of the RCA. The coronary angiography of the left system showed a 30% stenosis of the proximal tract of the LAD and 85% of the middle tract of the first diagonal branch. A 40% stenosis in the middle tract of the left circumflex coronary artery (LCX) was then detected. No MB of the middle tract of the LAD was detected, and a bare metal stent (Presillion 2.5 x 12 mm) was deployed in the middle tract of the first diagonal branch., Conclusions: After 2 years, the administration of the calcium channel blockers has been effective in the treatment of the MB but no effect on the atherosclerotic plaque growth has been demonstrated.

Myocardial bridges are congenital structural abnormalities with debated clinical relevance; they may be traditionally asymptomatic or associated with various clinical manifestations, some of which may be potentially fatal. We report on a 60 years old man, who underwent a follow-up stress/rest myocardial perfusion scintigraphy developing asymptomatic exercise-induced ST-elevation and demonstrating completely reversible ischaemia in the scintigraphic images. Subsequent coronary angiography showed no artery stenosis, but revealed an intramyocardial pathway of the left anterior descending artery throughout a myocardial bridge. In conclusion, to our knowledge, this is the first reported case of asymptomatic exercise-induced ST-elevation secondary to a myocardial bridge.

Myocardial bridging is a common congenital abnormality of a coronary artery, and is usually thought to be a benign anatomical variant. Although rare, previous studies have reported that patients with myocardial bridging may suffer from myocardial ischemia, myocardial infarction (MI), arrhythmias and even sudden death. Here we report the case of an 18-year-old adolescent athlete with myocardial bridging resulting in MI. Coronary angiography revealed 80% luminal narrowing by systolic compression in the proximal and mid segments of the left anterior descending coronary artery, which returned to normal during diastole. We considered that heavy sports might be a potential trigger for his MI attack. Therefore, special attention should be paid to this kind of athlete, especially if adolescent.

Elevated levels of cardiac troponins are an established method of diagnosis of heart muscle necrosis. A case of a long distance amateur-marathon runner, who showed significant elevation of plasma troponin I after extreme physical effort is reported. The diagnostic examinations did not reveal atherosclerosis burden, but myocardial bridging of coronary artery. The authors describe the significance of the pathology in the view of extreme sport effort performed by the described patient.

To illustrate the effect of myocardial bridges on coronary vascular tone, we describe the cases of 2 patients with different clinical presentations in the context of reproducible increased spasticity at the site of myocardial bridging. One had an episode of takotsubo cardiomyopathy, and one developed typical Prinzmetal angina while receiving desmopressin treatment for pituitary insufficiency. In both patients, acetylcholine challenge clearly revealed both the presence and the severity of myocardial bridging while producing several recognizable degrees of abnormal spastic tendency.Both baseline functional states and responses to different medications correlate with spastic tendency and enable the characterization of individual cases. Understanding the spectrum of spastic conditions might help to clarify the causes of atypical ischemic events, especially in patients with myocardial bridging.

Unlabelled: Although myocardial bridging (MB) is a common coronary anomaly, its cardiovascular consequences are still disputed. A positive link between sudden cardiac death (SCD) and myocardial bridging has not yet been definitively proved, even though many case reports and small scale studies support this association. For myocardial bridging to be associated with sudden cardiac death it must exhibit certain specific characteristics involving coronary or myocardial changes sufficient to explain a terminal cardiac event. In this study we aimed to analyze the morphological changes (both myocardial and coronary) associated with hemodynamically significant myocardial bridging and the morphological differences between hemodynamically significant MB and MB considered to be non-hemodynamically significant., Material and Method: We analyzed 53 cases of sudden cardiac death, of which 21 cases had hemodynamically significant myocardial bridging, 14 had non-hemodynamically significant myocardial bridging and 20 cases suffered sudden cardiac death without myocardial bridging, using a morphological score with seven histological parameters., Results: Myocardial fibrosis and interstitial edema were found to be highly correlated with hemodynamically significant myocardial bridging (HSMB), as were interstitial edema and interstitial fibrosis., Conclusions: Hemodynamically significant myocardial bridging can be discovered during heart dissection by analyzing a series of morphological markers (width, distribution of atherosclerosis, distal hypoplasia). Our study showed that MB was associated with increased myocardial fibrosis and edema, both of which have an increased risk of electrical instability. Compared to non-hemodynamically significant myocardial bridging, HSMB shows a distinct histological pattern, with increased myocardial fibrosis and edema. The main cause of SCD in association with HSMB seems to be electrical due to increased electrical myocardial heterogeneity, but large scale studies are needed to test this., (© Georg Thieme Verlag KG Stuttgart · New York.)

Background: Myocardial bridging (MB) is the most common congenital coronary anomaly. However, the functional relevance of MB is not well understood., Methods: Eighteen patients with lone MB were consecutively enrolled. Fractional flow reserve (FFR) was measured before and after dobutamine infusion. Diastolic FFR was calculated by offline analysis. Cutoff values for functional significance of FFR and diastolic FFR were 0.75 and 0.76, respectively., Results: Baseline systolic percent diameter stenosis and lesion length of MB were 70 ± 16% and 24 ± 7 mm. FFR and diastolic FFR were 0.92 ± 0.05 and 0.89 ± 0.07 at maximal hyperemia induced by adenosine, respectively (P = 0.006). Despite the angiographic stenosis, only 1 lesion was functionally significant. After dobutamine infusion, percent diameter stenosis (84 ± 11%, P = 0.002) and lesion length (26 ± 6 mm, P = 0.019) were aggravated and diastolic FFR was lowered (0.84 ± 0.10, P = 0.006). Two additional lesions became functionally significant after dobutamine infusion. Angiographic percent diameter stenosis at diastole was correlated with dobutamine diastolic FFR (R = -0.58, P = 0.04), but stenosis at systole was not. During median follow-up of 54 months, 2 patients underwent target-lesion revascularization., Conclusions: Dobutamine increased the morphologic and functional severity of MB. Dobutamine-FFR seems to be helpful in the functional assessment of MB., (Copyright © 2011 Canadian Cardiovascular Society. Published by Elsevier Inc. All rights reserved.)

The authors present a case demonstrating the unusual combination of myocardial bridging with a coronary artery aneurysm complicated by acute transient left ventricular dysfunction due to myocardial stunning. The pathophysiology and current insights into myocardial bridging, coronary aneurysms and myocardial stunning are briefly discussed. The literature reveals only one other reported case of coronary aneurysms associated with myocardial bridging. In addition, although there are several reports of angina and myocardial infarction complicating bridging, there is only 1 other report of myocardial stunning specifically.

The association of variant angina (VA) and myocardial bridges is a rare finding. We describe a case of VA with recurrent coronary spasm triggered by different stimuli at the site of a myocardial bridge. The interplay of endothelial dysfunction, coronary vasoconstriction and myocardial bridging was detected by intracoronary acetylcholine test and IVUS. We speculate that mechanical stimulation at the bridge site caused endothelial dysfunction and enhanced local susceptibility to vasoconstrictor stimuli. Variant angina should always be suspected in cases of ST-elevation acute coronary syndrome without any significant angiographic coronary stenosis.

A myocardial bridge (MB), partially covering the coronary artery, is a congenital anatomical variant usually present in the left anterior descending coronary artery (LAD). MB causes coronary heart disease (CHD) by 2 distinct mechanisms influenced by the anatomical properties of the MB, such as its length, thickness, and location. One is direct MB compression of the LAD at cardiac systole, resulting in delayed arterial relaxation at diastole, reduced blood flow reserve, and decreased blood perfusion. The other is enhancement of coronary atherosclerosis causing stenosis of the LAD proximal to the MB, occurring because of endothelial injury arising from the abnormal hemodynamics provoked by retrograde blood flow up toward the left coronary ostium at cardiac systole. The magnitude of the effect of the 2 distinct mechanisms of the MB on LAD blood flow is prescribed by a common root of the MB-muscle mass volume generated by those properties. Furthermore, the anatomical properties of the MB are closely associated with the choice of treatment and therapeutic outcome in CHD patients having an MB. Thus, the anatomical properties of an MB should be considered in the diagnosis and management of CHD patients with this anomaly.

Background: It has been suggested that multidetector computed tomographic coronary angiography (MDCT-CA) may be a reliable modality for the diagnosis and assessment of myocardial bridge (MB). However, the correlation between MB measurements of MDCT-CA and conventional coronary angiography (CCA) has not been determined., Methods: We assessed the correlation between MDCT-CA and CCA in MB measurements. One hundred twenty consecutive patients (77 men, 61±12 yrs) underwent MDCT-CA and CCA simultaneously from suspected coronary artery disease. MB measurements on MDCT-CA included location, length, depth, within-MB diameter, reference luminal diameters of segment proximal and distal MB, and luminal narrowing. MB measurements on CCA included length, within-MB diameter, reference lumen diameters of segment proximal and distal to MB, and luminal narrowing., Results: We observed 38 MB segments in 30 patients (25%), with 6 patients having ≥2 MB segments. The within-MB diameters on MDCT-CA and CCA showed a significant correlation during systolic (1.3±0.3 mm vs. 1.2±0.5 mm: r=0.394, P=0.028) and diastolic phases (1.4±0.4 mm vs. 1.6±0.6 mm: r=0.524, P=0.001). Systolic luminal narrowing (SLN) on CCA ranged from 8% to 75% (38±16%), and a definite milking effect (defined as SLN>50%) was observed in only 7 segments (18.4% of 38 MBs, or 5.8% of all cohorts). In case of MB segments with a definite milking effect, length of MBs on MDCT-CA and CCA correlated significantly (systolic phase: r=0.794, P=0.033 and diastolic phase: r=0.766, P=0.045). SLN on CCA was not related with any MB measurement on MDCT-CA., Conclusions: In case of MBs with sufficient systolic compression, diameter and length of MBs correlates significantly between MDCT-CA and CCA analysis. The detection rate of MB on CCA may be associated with the degree of systolic compression, and systolic compression on CCA cannot be predicted by any measurement on MDCT-CA., (Copyright © 2009 Elsevier Ireland Ltd. All rights reserved.)

Compared to coronary angiography, both intravascular ultrasound (IVUS) and CT-angiography provide important information with respect to the morphological aspects of myocardial bridging (MB). However, these modalities are limited in defining the hemodynamic and clinical significance of MB. Intracoronary Doppler studies demonstrate a peculiar abnormal Doppler flow profile associated with MB. Fractional flow reserve (FFR) after adenosine infusion has been used to assess the hemodynamic significance of MB, but FFR after adenosine induced hyperemia underestimates the significance of MB. On the other hand, high-dose dobutamine by increasing the contractility of the bridging segment unmasks ischemia induced by MB. This review outlines the role of flow velocity measurement by intracoronary Doppler, FFR, and IVUS for assessment of patients with MB. In addition, we compared FFR measurements after adenosine versus dobutamine infusions for the hemodynamic assessment of MB in two patients.

An experimental model for heart-mural coronary artery-myocardial bridge was established based on the theory of haemodynamics. The application of the model demonstrated that it can repeat to great extent the phenomenon of the myocardial bridge compressing the mural coronary artery, which results in abnormal haemodynamic characteristics. The results of simulation experiments are mostly consistent with clinical research.

Medical treatments of coronary myocardial bridging (CMB) generally include beta-blockers and calcium channel blockers. Nitrates are avoided because symptoms may worsen. Nicorandil is a hybrid of a nitrate and a potassium channel opener. However, the effect of nicorandil on CMB is unknown. We analyzed nicorandil reactivity at the site with CMB in 51 patients. Maximal and minimal diameters of CMB were measured by quantitative angiography at baseline and at 60 seconds after intracoronary administration of 200 mg nicorandil. The maximal diameter during diastole increased from 2.15 + 0.42 mm to 2.34 + 0.44 mm after administration of nicorandil (P < .001), and the minimal diameter during systole increased from 1.24 + 0.63 mm to 1.67 + 0.64 mm (P < .001). Thus, nicorandil reduced the percentage vessel narrowing from 44.0 + 26.1% to 30.3 + 21.2% (P < .001). In 22 patients, we also evaluated the effect of nitroglycerin. The maximal diameter during diastole increased from 2.25 + 0.47 mm to 2.51 + 0.44 mm after administration of nitroglycerin (P < .019), and the minimal diameter during systole decreased from 1.28 + 0.64 mm to 1.14 + 0.60 mm (P = .276). Thus, nitroglycerin augmented the percentage vessel narrowing from 44.9% + 25.0% to 56.0% + 23.5% (P = .023). These results indicate that intracoronary administration of nicorandil could dilate coronary arteries during diastole as well as systole in patients with CMB during coronary angiography.

The myocardial tissue covering the artery is termed a myocardial bridge. But so far many researches on the myocardial bridge have been involved with clinical patients or animals, which have some limitations (e.g. lack of systematicness, difficulties in measuring the flow in the mural coronary artery and so on). Designing a "Heart-Mural coronary artery-Myocardial Bridge" Simulative Device provides a good approach to solve above problems; however, documents on this subject have seldom been reported until now. The heart pump as the key part of the whole simulative device should be able to simulate the waveform of blood pressure, adjust blood flow and regulate heart rate. Our experimental results basically met above requirements. The heart pump proposed in the paper presented an alternative experimental method to go further into other issues about the cardiovascular circulation system.

Several previous studies suggest that myocardial bridging (MB) is associated with ischemia and rhythm disturbances. We sought to examine exercise-induced changes in P wave duration and dispersion (PWD), the markers of atrial conduction abnormalities in patients with isolated MB of left anterior descending artery (LAD) and control subjects. Eighteen patients with MB of LAD (group-I) and 22 subjects with angiographically demonstrated normal coronary arteries (group-II) underwent treadmill exercise testing. Before and after exercise ECG was recorded at a paper speed of 50 mm/s. The change in maximum and minimum P wave duration was measured manually and difference between two values was defined as PWD. There was no difference between two groups in terms of demographic properties. Baseline maximum and minimum P wave duration and PWD durations were similar in both groups and they did not change after exercise. (Group-I: before and after test; 114 +/- 10 vs. 114 +/- 9, 66 +/- 13 vs. 67 +/- 10, and 47 +/- 9 vs. 45 +/- 13 ms, P > 0.05, group-II; 113 +/- 9 vs. 115 +/- 8, 68 +/- 11 vs. 68 +/- 11, 45 +/- 11 vs. 48 +/- 15 ms for each, respectively). In addition there was no significant correlation between PWD and P wave duration and echocardiographic variables. In patients with MB of LAD, PWD and P wave duration were not different than healthy subjects and treadmill exercise testing did not induce atrial conduction abnormalities in both groups.