Myocardial Bridge and Atherosclerosis, an Intimal Relationship.

PURPOSE OF REVIEW: This review investigates the relationship between myocardial bridges (MBs), intimal thickening in coronary arteries, and Atherosclerotic cardiovascular disease. It focuses on the role of mechanical forces, such as circumferential strain, in arterial wall remodeling and aims to clarify how MBs affect coronary artery pathology. REVIEW FINDINGS: MBs have been identified as influential in modulating coronary artery intimal thickness, demonstrating a protective effect against thickening within the MB segment and an increase in thickness proximal to the MB. This is attributed to changes in mechanical stress and hemodynamics. Research involving arterial hypertension models and vein graft disease has underscored the importance of circumferential strain in vascular remodeling and intimal hyperplasia. Understanding the complex dynamics between MBs, mechanical strain, and vascular remodeling is crucial for advancing our knowledge of coronary artery disease mechanisms. This could lead to improved management strategies for cardiovascular diseases, highlighting the need for further research into MB-related vascular changes.

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.

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.

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.

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.

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 .

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.

Myocardial bridging is associated with exercise-induced ventricular arrhythmia and increases in QT dispersion.

BACKGROUND: A myocardial bridge (MB) has been associated with ventricular arrhythmia and sudden death during exercise. QT dispersion (QTd) is a measure of abnormal repolarization and may predict ventricular arrhythmia. We investigated the frequency of ventricular arrhythmias during exercise and the QTd at rest and after exercise, in patients with an MB compared to a normal cohort. METHODS: We studied the rest and stress ECG tracings of patients with an MB suspected by focal septal buckling on exercise echocardiography (EE) (Echo-MB group, N = 510), those with an MB confirmed by another examination (MB group, N = 110), and healthy controls (Control group, N = 198). RESULTS: The frequency of exercise-induced premature ventricular contractions (PVCs) was significantly higher in the Echo-MB and MB groups compared with the Control group (both p < .001). In all, 25 patients (4.9%) in the Echo-MB group, seven patients (6.4%) in the MB group and no patients in the Control group had exercise-induced non-sustained ventricular tachycardia (NSVT). There was no difference in the baseline QTd between the groups. In the Echo-MB and MB groups, QTd postexercise increased significantly when compared with baseline (both p < .001). Patients with NSVT had a higher frequency of male gender and an even greater increase in QTd with exercise compared with the non-NSVT group. DISCUSSION: There is an increased frequency of exercise-induced PVCs and NSVT in patients with MBs. Exercise significantly increases QTd in MB patients, with an even greater increase in QTd in MB patients with NSVT. Exercise in MB patients results in ventricular arrhythmias and abnormalities in repolarization.

Development of a Computational Fluid Dynamics Model for Myocardial Bridging.

Computational fluid dynamics (CFD) modeling of myocardial bridging (MB) remains challenging due to its dynamic and phasic nature. This study aims to develop a patient-specific CFD model of MB. There were two parts to this study. The first part consisted of developing an in silico model of the left anterior descending (LAD) coronary artery of a patient with MB. In this regard, a moving-boundary CFD algorithm was developed to simulate the patient-specific muscle compression caused by MB. A second simulation was also performed with the bridge artificially removed to determine the hemodynamics in the same vessel in the absence of MB. The second part of the study consisted of hemodynamic analysis of three patients with mild and moderate and severe MB in their LAD by means of the developed in silico model in the first part. The average shear stress in the proximal and bridge segments for model with MB were significantly different from those for model without MB (proximal segment: 0.32 ± 0.14 Pa (with MB) versus 0.97 ± 0.39 Pa (without MB), P < 0.0001 - bridge segment: 2.60 ± 0.94 Pa (with MB) versus 1.50 ± 0.64 Pa (without MB), P < 0.0001). When all three patients were evaluated, increasing the degree of vessel compression shear stress in the proximal segment decreased, whereas the shear stress in the bridge segment increased. The presence of MB resulted in hemodynamic abnormalities in the proximal segment, whereas segments within the bridge exhibited hemodynamic patterns which tend to discourage atheroma development.

Multimodality Imaging in the Assessment of the Physiological Significance of Myocardial Bridging.

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.

Impact of Myocardial Bridge-mural Coronary Artery on Myocardial Blood Supply.

Objective To explore the impact of myocardial bridge-mural coronary artery (MB-MCA) on myocardial blood supply. Methods The imaging data of 74 patients with the isolate MB in the left anterior descending artery undergoing 256-slice CT coronary angiography and myocardial perfusion imaging (MPI) were retrospectively analyzed. The subjects were divided into incomplete and complete MB types. The length of MB and the systolic stenosis degree of MCA were measured.The type and length of MB and the systolic stenosis degree of MCA (according to Noble grade) were compared between the normal and abnormal MPI groups. The clinical characteristics including age, gender, body mass index, hypertension, dyslipidemia, diabetes mellitus, and smoking history were also reviewed. Results There were 38 incomplete MB cases and 13 complete MB cases in the normal MPI group,and 5 and 18 in the abnormal MPI group (χ2=18.134,P=0.000). The MB length in the normal and abnormal MPI group were (14.7±3.7) mm and (15.5±4.5) mm (t=0.804,P=0.424). However, the systolic stenosis degree of MCA showed significant difference (χ2=17.839,P=0.000). The clinical characteristics were not significantly differentt between the normal and abnormal MPI groups (P>0.05). Conclusions The MB type and the systolic stenosis degree of MCA can affect myocardial perfusion.Patients with complete MB and the moderate-to-severe systolic stenosis degree of MCA are more susceptible to myocardial ischemia. However, the MB length is not correlated with myocardial ischemia.

A case of myocardial muscular bridging causing severe hypotension during exercise-electrocardiography test.

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.

Myocardia ischemia associated with a myocardial bridge with no significant atherosclerotic stenosis.

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.

Myocardial bridging: a review with emphasis on electrocardiographic findings.

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.

Exercise-Induced Repolarization Changes in Patients with Isolated Myocardial Bridging.

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.

The morphologic and functional features of LAD myocardial bridging at multi-detector computed tomography coronary angiography: correlation with coronary artery disease.

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.

Disappearance of myocardial bridging of the left anterior descending coronary artery after inferior myocardial infarction.

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.

Efficacy of calcium channel blockers in the treatment of the myocardial bridging: a pilot study.

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 bridge: an unusual cause of asymptomatic ST-elevation during treadmill stress test causing functional ischaemia.

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.