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Myocardial bridging (MB) is a common anatomical variation in which myocardial fibers traverse over an epicardial coronary artery, potentially leading to angina or angina- equivalent symptoms. Ranolazine, known for its efficacy in chronic stable angina, might offer benefits in symptomatic MB, where traditional treatments often fall short. This prospective, parallel-group, double-blind, randomized add-on clinical trial was conducted at Al-Zahra Cardiovascular Teaching Hospital, Shiraz, Iran, from 2023 to 2024. We included patients with MB and angina symptoms who had normal epicardial coronary arteries. Participants were randomized into two groups: one receiving standard therapy (β-blockers) and the other receiving standard therapy plus ranolazine (500 mg twice daily). Outcomes were assessed using the Canadian Cardiovascular Society (CCS) classification of angina, echocardiographic left ventricular ejection fraction (LVEF), and electrocardiogram (ECG) parameters. Trial registry number: IRCT20230801059005N2 (08/11/2023). Among 52 participants, ranolazine addition significantly improved angina severity, with more patients transitioning to CCS grade I ( p  = 0.001 after adjusting for confounders). While univariate analysis showed no differences in ECG parameters, multivariate analysis revealed a modest but statistically significant QTc prolongation in the ranolazine group (OR = 1.055, 95%CI:1.012–1.100, p  = 0.012). PR and QRS intervals remained unaffected. Post-treatment LVEF was comparable between the two groups. Ranolazine, as an adjunct to β-blockers, significantly improved angina symptoms in patients with myocardial bridging and was associated with a mild but significant QTc prolongation, without causing substantial changes in LVEF or other ECG parameters. These findings suggest that ranolazine could be a beneficial addition to the management of angina in MB patients.

We aim to investigate if myocardial bridging (MB) provides predictive value beyond its association with non-obstructive coronary artery disease (CAD) burden in a long-term follow-up and multicenter study. This study included 4176 consecutive patients with suspected CAD underwent coronary computed tomography angiography (CTA) at two hospitals in Wuhan, China, between September 2016 and December 2017 for finial analysis. Kaplan-Meier method was used to estimate the cumulative event-free survival of non-obstructive CAD burden and MB burden classifications, respectively. Further, cox regression models were applied to calculate hazard ratios (HR) for increasing non-obstructive CAD and MB burden classifications. In total, during the 6.04 years (interquartile range 5.73–6.32) follow-up, 276 (6.61%) patients occurred main adverse cardiovascular events (MACE). MB was found in 44% of patients without CAD and in 40.5% of those with non-obstructive CAD. The annualized MACE rate was 1.07 (95% confidence interval (CI): 0.92–1.24) for the no MB group and 1.13 (95% CI: 0.95–1.34) for the MB group. Univarite and Multivariate Cox regression showed that neither the depth nor the length of MB was associated with the risk of MACE. However, after adjusting with sex, age, smoke, drink, hypertension and diabetes, 2-vessel non-obstructive CAD and 3-vessel non-obstructive CAD showed significant association with the risk of MACE, with HR of 1.53 (95% CI: 1.06–2.21, P  = 0.023) and 1.93 (95% CI: 1.32–2.82, P  = 0.001), respectively, using no CAD as the reference group. Non-obstructive CAD, not presence of MB, is the main predictor of risk for future MACE in patients without obstructive CAD. Prospective registries in the future should include validated quality of life measures and CT-FFR with long-term outcomes to enhance the understanding of symptomatic burden and functional assessment in MB risk stratification.

Background Myocardial bridging (MB) is common in patients with hypertrophic cardiomyopathy (HCM). There are sparse data on the impact of MB on myocardial fibrosis in HCM. This study was designed to evaluate the relationship between MB and myocardial fibrosis in patients with obstructive HCM. Methods In this cohort study, retrospective data were collected from a high-volume HCM center. Patients with obstructive HCM who underwent septal myectomy and preoperative cardiac magnetic resonance (CMR) were screened from 2011 to 2018. Results Finally, 492 patients were included in this study, with an average age of 45.7 years. Of these patients, 76 patients had MB. MB occurred mostly in the left anterior descending artery (73/76). The global extent of late gadolinium enhancement (LGE) was correlated with the degree of systolic compression ( r  = 0.33, p  = 0.003). Multivariable linear regression analysis revealed that the degree of systolic compression was an independent risk factor for LGE ( β  = 0.292, p  = 0.007). The LGE fraction of basal and mid anteroseptal segments in patients with severe MB (compression ratio ≥ 80%) was significantly greater than that in patients with mild to moderate MB (compression ratio < 80%). During a median follow-up of 28 (IQR: 15–52) months, 15 patients died. Kaplan–Meier analysis did not identify differences in all-cause death (log-rank p  = 0.63) or cardiovascular death (log-rank p  = 0.72) between patients undergoing MB-related surgery and those without MB. Conclusions MB with severe systolic compression was significantly associated with a high extent of fibrosis in patients with obstructive HCM. Concomitant myotomy or coronary artery bypass grafting might provide excellent survival similar to that of patients without MB. Identification of patients with severe MB and providing comprehensive management might help improve the prognosis of patients with HCM.

Background Myocardial bridging is a cardiac anomaly where a segment of epicardial coronary arteries runs through the myocardium and can rarely cause MI. Takotsubo syndrome is a stress-induced cardiomyopathy that can mimic MI. Catecholamine surge during stress can contribute to Takotsubo syndrome, but whether this surge can trigger an inconspicuous myocardial bridging to manifest symptomatically remains unclear, and alternately, whether a myocardial bridge might cause worsening of Takotsubo syndrome is also a matter that needs further research. Case presentation We report the case of a patient who initially presented with features of acute exacerbation of bronchiectasis and subsequently developed symptoms and ECG features suggestive of acute myocardial infarction. Echocardiography revealed features of takotsubo syndrome, and complete myocardial bridging was revealed via coronary angiography. The patient was managed conservatively with pharmacological treatment, and after a few days, echocardiographic features were reversed. As such, the diagnosis shifted toward Takotsubo syndrome with myocardial stunning due to co-existent myocardial bridging. Conclusion We report a rare case of a patient with acute bronchiectasis exacerbation with features suggestive of acute myocardial infarction who had findings of Takotsubo syndrome and complete myocardial bridging. In the beginning, it was difficult to determine whether the symptoms arose due to acute MI resulting from myocardial bridging or were solely due to takotsubo syndrome because of stress from bronchiectasis. Although myocardial bridging is often overlooked as an etiology for acute MI, this case highlights the importance of expanding the differential diagnosis to myocardial bridging in the work-up for the cause of acute MI and how Takotsubo syndrome can mimic acute MI and pose a diagnostic challenge.

A myocardial bridge (MB) is a condition where a segment of an epicardial coronary artery passes through the myocardial muscle. While traditionally regarded as benign, MBs have been associated with various cardiovascular conditions. Therefore, assessing their hemodynamic impact is crucial for informed treatment decisions. Intracoronary functional assessments, such as fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR), have proven useful, especially under inotropic stimulation. However, their invasive nature limits their widespread clinical application. The Quantitative Flow Ratio (QFR) has emerged as a minimally invasive alternative for functional evaluation of MBs, though data on its use are still limited. This study aims to compare the diagnostic efficacy of FFR, iFR, and QFR for evaluating MBs both at rest and under stress conditions. Patients with confirmed MB on the LAD and typical angina (or abnormal noninvasive tests indicating myocardial ischemia) were included. According to a prespecified protocol, all patients underwent functional intracoronary evaluation with FFR and iFR at rest and after dobutamine and atropine intravenous infusion. QFR was also calculated for all cases both at rest and during dobutamine infusion. FFR values ≤0.80, iFR values ≤0.89 and QFR values ≤0.84 were considered indicative of significant myocardial ischemia. A total of 21 patients were included. Median FFR remained unchanged from rest (0.85) to stress (0.85), with only 1 patient showing a positive stress-FFR. In contrast, median iFR significantly decreased from 0.91 to 0.79 (p <0.001), with stress-iFR ≤0.89 in 18 patients. Resting QFR did not indicate significant hemodynamic impact of the MB (median 0.90), but under inotropic stimulation, ischemia was detected in 18 patients (median 0.79, p <0.001). QFR and iFR were concordant during stress in 19 patients, showing a significant positive correlation (Spearman’s ρ = 0.702, p = 0.037) and comparable sensitivity (0.86). QFR, computed during inotropic infusion, shows high sensitivity for detecting MB-related ischemia, comparable to stress-iFR and superior to stress-FFR. The correlation between stress-induced iFR and QFR suggests QFR as a reliable, minimally invasive alternative for functional lesion-specific evaluation in MB patients. Larger studies are necessary to confirm these preliminary findings and standardize QFR use in dynamic coronary stenosis assessments. Central Illustration. Diagnostic work-up example. [Display omitted]

Myocardial bridging (MB) is a kind of congenital coronary abnormality. The functional impact of MB on coronary artery remains a subject of debate. This study aimed to assess the hemodynamic effects of MB using coronary angiography-derived fractional flow reserve (caFFR) and elucidate the relationship between MB anatomical parameters and diastolic caFFR (dcaFFR) in patients with isolated MB (iMB) and MB combined with proximal coronary atherosclerosis (MB+AS). A total of 683 patients diagnosed with MB located on left anterior descending (LAD) via coronary angiography (CAG) were retrospectively enrolled and categorized into two groups: iMB (n = 377) and MB+AS (n = 306). The dcaFFR was calculated to evaluate the hemodynamic impact of MB. Multivariate linear regression and mediation analysis were performed to identify predictors of dcaFFR. In the iMB group, diastolic minimal lumen diameter (MLD) of MB segment was the sole independent predictor of dcaFFR (B = 0.036, β = 0.253, p <0.001). In the group of MB+AS, the severity of proximal stenosis emerged as the only independent predictor of dcaFFR (B = −0.004, β = −0.674, p <0.001), with the hemodynamic effects of MB fully mediated by proximal stenosis. In conclusion, the hemodynamic impact of MB depends on the presence of proximal coronary atherosclerosis. In iMB cases, the diastolic MLD of MB segment directly determines hemodynamic impairment. However, the hemodynamic impact of MB is nonsignificant in cases of MB+AS, as its effect is fully mediated through proximal stenosis severity.

Myocardial bridging (MB) is a phenomenon that occurs when coronary arteries course through myocardial tissue rather than, as is normal, on the surface of the myocardium. Although often asymptomatic, contraction of the myocardium in the presence of a myocardial bridge can sometimes occlude the lumen of coronary arteries that penetrate the myocardium, resulting in symptoms, signs, and electrocardiographic changes indistinguishable from those associated with acute coronary syndromes (ACS) caused by intraluminal narrowing of coronary arteries or coronary artery plaque rupture. In this monograph, we present the case of a 45-year-old man who presented to the emergency department with typical chest pain accompanied by electrocardiographic changes consistent with acute occlusion of the left anterior descending artery. During percutaneous coronary intervention, fluoroscopically–obtained cine image loops revealed evidence of dynamic coronary artery narrowing due to myocardial bridging. There was no evidence of static coronary artery occlusion. Myocardial bridging is typically managed medically when symptomatic, although refractory cases may ultimately require invasive or surgical intervention. Given that emergency physicians are frequently the first providers to evaluate patients with acute coronary syndromes, myocardial bridging as an etiology for ACS is a clinical entity of which emergency physicians should be aware.

Background Clinical events such as angina pectoris, acute coronary syndrome, and sudden death caused by myocardial bridge (MB) have attracted increasing attention. It is still a challenge to diagnose whether MB can cause the symptoms of patients with MB. For most MB patients, medication remains the primary treatment. Case presentation This article reports a case of chest pain in a patient with MB in the middle segment of the left anterior descending artery (LAD m ) with moderate stenosis in the proximal segment (LAD p ). Through functional assessment, we found that neither MB nor fixed stenosis had sufficient effect on coronary blood flow to cause myocardial ischemia, but their synergistic effect resulted in myocardial ischemia. Finally, a stent was implanted in LAD p and good clinical results were achieved. Conclusions For symptomatic patients with MB combined with fixed stenosis, functional evaluation may be necessary, which has significant guiding significance for treatment strategy selection. For asymptomatic patients, early detection of myocardial ischemia may also improve the prognosis of patients.

Myocardial bridging (MB) is a congenital coronary anomaly characterized by systolic compression of the intramyocardial arterial segment and delayed early diastolic artery relaxation, resulting in reduced vessel luminal diameter in diastole. Current evidence suggests that MB, particularly in the left anterior descending artery, may cause anginal symptoms and/or myocardial ischemia through several different pathophysiological and cellular mechanisms acting independently or synergistically: (1) delayed early diastolic relaxation of intramyocardial arterial segment; (2) impaired endothelial-dependent vasodilation with vessel smooth muscle cell hyperactivity in the coronary artery with MB, especially within the bridged segment; (3) focal (septal) ischemia due to “septal steal” phenomenon; and (4) development and progression of an atherosclerotic lesion in the coronary artery segment proximal to MB. Patients with isolated-MB may also experience anginal pain and/or myocardial ischemia due to concomitant structural and/or functional abnormalities of the coronary microcirculation. Both MB and coronary microvascular dysfunction refer to a subgroup of patients with angina and/or ischemia with non-obstructive coronary arteries (ANOCA/INOCA). Therefore, it may be challenging to determine whether MB is causing anginal pain and/or ischemia, particularly since both phenomena have also been reported without MB’s existence. Therefore, comprehensive coronary physiology testing should be encouraged in patients with this coronary anomaly to identify the underlying cause of anginal pain and/or myocardial ischemia, enabling optimal therapeutic strategies in these patients. This review is focused on different pathophysiological and cellular mechanisms of MB-related angina and/or ischemia and future perspectives in the functional assessment of MB severity, bearing in mind the complexity of coronary physiology in the presence of this anomaly.

PurposeTo 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.MethodsThis 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.ResultsMB 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.ConclusionMB 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.