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Myocardial bridging (MB) is a congenital variant in which a segment of a coronary artery follows an atypical intramural course under a “bridge” of myocardium and is notably common in hypertrophic cardiomyopathy (HCM). This systematic review and meta-analysis explored the clinical consequences of MB in patients with HCM. A total of 3 outcome domains were investigated: cardiovascular mortality, nonfatal adverse cardiac events, and investigative indicators of myocardial ischemia. A meta-analysis was performed on 10 observational studies comparing outcomes in patients with HCM with and without MB. Studies were identified through a systematic search of 4 databases (PubMed, Scopus, Medline Complete, and Web of Science). The quality of the studies was assessed using a modified version of the Downs and Black tool, from which studies could score a maximum of 23 points. The mean score was 17.5 ± 1.3 (good). The meta-analysis showed that MB was not associated with cardiovascular mortality (odds ratio [OR] 1.70, 95% confidence interval [CI] 0.56 to 5.15, p = 0.35) or nonfatal adverse cardiac events (OR 1.80, 95% CI 0.98 to 3.28, p = 0.06) but was associated with myocardial ischemia (OR 1.89, 95% CI 1.03 to 3.44, p = 0.04). In conclusion, the potential prognostic implications of MB in HCM, especially in those with hemodynamically significant bridges and/or severe underlying disease, should not be ignored. The focus of future studies should be to establish functional and morphologic thresholds, by which MB may adversely influence prognosis by corroborating imaging findings with clinical outcome data.

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 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.

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.

A 66-year-old man was transferred to a hospital after a cardiac arrest. Coronary angiography (shown in a video) revealed 50% stenosis in the middle LAD coronary artery during diastole with complete occlusion during systole.

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.

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. Summary 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.

To investigate the diagnostic performance of CT fractional flow reserve (CT-FFR) for myocardial bridging-related ischemia using dynamic CT myocardial perfusion imaging (CT-MPI) as a reference standard. Dynamic CT-MPI and coronary CT angiography (CCTA) data obtained from 498 symptomatic patients were retrospectively reviewed. Seventy-five patients (mean age ± standard deviation, 62.7 ± 13.2 years; 48 males) who showed myocardial bridging in the left anterior descending artery without concomitant obstructive stenosis on the imaging were included. The change in CT-FFR across myocardial bridging (ΔCT-FFR, defined as the difference in CT-FFR values between the proximal and distal ends of the myocardial bridging) in different cardiac phases, as well as other anatomical parameters, were measured to evaluate their performance for diagnosing myocardial bridging-related myocardial ischemia using dynamic CT-MPI as the reference standard (myocardial blood flow < 100 mL/100 mL/min or myocardial blood flow ratio ≤ 0.8). ΔCT-FFR (ΔCT-FFR calculated in the best systolic phase) was higher in patients with vs. without myocardial bridging-related myocardial ischemia (median [interquartile range], 0.12 [0.08-0.17] vs. 0.04 [0.01-0.07], < 0.001), while CT-FFR (CT-FFR distal to the myocardial bridging calculated in the best systolic phase) was lower (0.85 [0.81-0.89] vs. 0.91 [0.88-0.96], = 0.043). In contrast, ΔCT-FFR (ΔCT-FFR calculated in the best diastolic phase) and CT-FFR (CT-FFR distal to the myocardial bridging calculated in the best diastolic phase) did not differ significantly. Receiver operating characteristic curve analysis showed that ΔCT-FFR had largest area under the curve (0.822; 95% confidence interval, 0.717-0.901) for identifying myocardial bridging-related ischemia. ΔCT-FFR had the highest sensitivity (91.7%) and negative predictive value (NPV) (97.8%). ΔCT-FFR had the highest specificity (85.7%) for diagnosing myocardial bridging-related ischemia. The positive predictive values of all CT-related parameters were low. ΔCT-FFR reliably excluded myocardial bridging-related ischemia with high sensitivity and NPV. Myocardial bridging showing positive CT-FFR results requires further evaluation.

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.

Mounting evidence suggests an associated between myocardial bridging (MB) and coronary vasospasm (CVS); however, no consensus has been established on whether CVS worsens clinical outcomes in patients with MB. Therefore, this retrospective study aimed to compare the long-term clinical outcomes in patients with MB based on CVS presence. This retrospective study enrolled 254 consecutive patients with MB undergoing provocative testing for coronary reactivity between January 1, 2009 and December 30, 2015, and stratified them into 2 groups: (a) group A (with CVS, n = 168); and (b) group B (without CVS, n = 86). The primary endpoints were major adverse cardiovascular events (MACEs), a composite of cardiac death, cardiac arrest, non-fatal myocardial infarction, ischemia-driven revascularization, ischemia-driven coronary angiography, and ischemia-related hospitalization. Diverse Cox models were used to determine whether CVS independently influenced MACE. The mean age of study participants was 50.8 years, and 60.2% of them were male. The median follow-up period was 8.15 years. The rate of MACE was 35.1% and 26.7% in groups A and B, respectively. Group A had a significantly higher risk of MACE than group B (the reference group) in model 3 (hazard ratio [HR]:1.92; 95% confidence interval [CI]:1.12-3.29) and model 4 (adjusted HR: 1.94; 95% CI: 1.04-3.59). The presence of CVS adversely affects clinical outcomes in patients with MB. Further prospective clinical studies are required to confirm this association.