Frequency and Significance of Coronary Artery Disease and Myocardial Bridging in Patients With Hypertrophic Cardiomyopathy.

The etiology of chest pain in hypertrophic cardiomyopathy (HC) is diverse and includes coronary artery disease (CAD) as well as HC-specific causes. Myocardial bridging (MB) has been associated with HC, chest pain, and accelerated atherosclerosis. We compared HC patients with age-, gender- and CAD pre-test probability-matched outpatients presenting with chest pain to investigate differences in the presence of MB and CAD using coronary computed tomography angiography (CCTA). We studied 84 HC patients who underwent CCTA and compared these with 168 matched controls (age 54 ± 11 years, 70% men, pre-test probability 12% [5% to 32%]). MB, calcium score, plaque morphology and presence and extent of CAD were assessed for each patient. Linear mixed models were used to assess differences between cases and controls. MB was more often seen in HC patients (50% vs 25%, p <0.001). Calcium score and the presence of obstructive CAD were similar in both groups (9 [0 to 225] vs 4 [0 to 82] and 18% vs 19%; p = 0.22 and p = 0.82). In the HC group, MB was associated with pathogenic DNA variants (p = 0.04), but not with the presence of chest pain (74% vs 76%, p = 0.8), nor with worse outcome (log-rank p = 0.30). In conclusion, the prevalence and extent of CAD was equal among patients with and without HC, demonstrating that pre-test risk prediction using the CAD Consortium clinical risk score performs well in HC patients. MB was twice as prevalent in the HC group compared with matched controls, but was not associated with chest pain or decreased event-free survival in these patients.

Prevalence of myocardial bridging associated with coronary endothelial dysfunction in patients with chest pain and non-obstructive coronary artery disease.

AIMS: Myocardial bridging (MB), characterised by the epicardial coronary vessel diving into the myocardium, is present in up to one third of adults and is associated with angina and acute coronary syndromes. MB is accompanied by altered blood flow mechanics and regional changes in wall sheer stress. The purpose of this study was to determine the association between myocardial bridging and coronary endothelial dysfunction. METHODS AND RESULTS: Patients presenting with chest pain and found to have non-obstructive CAD (stenosis <40%) on angiography underwent an invasive assessment of epicardial and microvascular endothelial function. Epicardial endothelial function was assessed by measuring the percent change in coronary artery diameter in response to intracoronary infusions of acetylcholine (%ΔCADAch). Epicardial endothelial dysfunction was defined as a %ΔCADAch of <-20%. Microvascular endothelial function was assessed by the percent change in coronary blood flow in response to intracoronary infusions of acetylcholine (%ΔCBFAch), and microvascular endothelial dysfunction was defined as a %ΔCBFAch of <50%. MB was diagnosed angiographically by identifying the characteristic reduction in minimal luminal diameter during systole. Patients were divided into those with and those without MB, and the frequency of epicardial endothelial dysfunction and microvascular endothelial dysfunction was compared between patients with versus those without MB. Between 1993 and 2012, 1,469 patients (mean age 50.4 years, 35% male) underwent coronary angiography and invasive testing of endothelial function. Two hundred and eight (14.2%) patients were found to have MB in the LAD. Patients with any MB had a significantly higher frequency of endothelial dysfunction within the mid and/or distal vessel segment compared to patients without MB (60.1% vs 50.4%, p=0.012). In multivariate analyses, mid and/or distal vessel MB was a significant predictor of mid and/or distal vessel epicardial endothelial dysfunction (OR 1.44, 95% CI: 1.04-2.00, p=0.029) and of microvascular endothelial dysfunction (OR 1.34, 95% CI: 1.00-1.82, p=0.050). CONCLUSIONS: MB co-localises with epicardial endothelial dysfunction and is significantly associated with microvascular endothelial dysfunction in symptomatic patients with non-obstructive CAD, supporting its potential role as a mechanism for angina in symptomatic patients with MB.

Assessment of the Relationship between Monocyte to High-Density Lipoprotein Ratio and Myocardial Bridge.

BACKGROUND: Assessing the monocyte to high-density lipoprotein ratio (MHR) is a new tool for predicting inflamation, which plays a major role in atherosclerosis. Myocardial bridge (MB) is thought to be a benign condition with development of atherosclerosis, particularly at the proximal segment of the brigde. OBJECTIVE: To evaluate the relationhip between MHR and the presence of MB. METHODS: We consecutively scanned patients referred for coronary angiography between January 2013- December 2016, and a total of 160 patients who had a MB and normal coronary artery were enrolled in the study. The patients' angiographic, demographic and clinic characteristics of the patients were reviewed from medical records. Monocytes and HDL-cholesterols were measured via complete blood count. MHR was calculated as the ratio of the absolute monocyte count to the HDL-cholesterol value. MHR values were divided into three tertiles as follows: lower (8.25 ± 1.61), moderate (13.11 ± 1.46), and higher (21.21 ± 4.30) tertile. A p-value of < 0.05 was considered significant. RESULTS: MHR was significantly higher in the MB group compared to the control group with normal coronary arteries. We found the frequency of MB (p = 0.002) to increase as the MHR tertiles rose. The Monocyte-HDL ratio with a cut-point of 13.35 had 59% sensitivity and 65.0% specificity (ROC area under curve: 0.687, 95% CI: 0.606-0.769, p < 0.001) in accurately predicting a MB diagnosis. In the multivariate analysis, MHR (p = 0.013) was found to be a significant independent predictor of the presence of MB, after adjusting for other risk factors. CONCLUSION: The present study revealed a significant correlation between MHR and MB.

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.

Prediction of coronary plaque location on arteries having myocardial bridge, using finite element models.

This study was performed to evaluate the influences of the myocardial bridges on the plaque initializations and progression in the coronary arteries. The wall structure is changed due to the plaque presence, which could be the reason for multiple heart malfunctions. Using simplified parametric finite element model (FE model) of the coronary artery having myocardial bridge and analyzing different mechanical parameters from blood circulation through the artery (wall shear stress, oscillatory shear index, residence time), we investigated the prediction of "the best" position for plaque progression. We chose six patients from the angiography records and used data from DICOM images to generate FE models with our software tools for FE preprocessing, solving and post-processing. We found a good correlation between real positions of the plaque and the ones that we predicted to develop at the proximal part of the myocardial bridges with wall shear stress, oscillatory shear index and residence time. This computer model could be additional predictive tool for everyday clinical examination of the patient with myocardial bridge.

[Evaluation of association of myocardial bridge in the left anterior descending coronary with coronary atherosclerosis (stenosis > 50%) in the segment proximal to the site of bridge on coronary cta in hypertension subjects].

OBJECTIVE: To investigate whether myocardial bridging (MB) is an independent risk factor for coronary atherosclerosis (stenosis > 50%) proximal to MB in the left anterior descending coronary artery (LAD) in subjects with hypertension identified by coronary computed tomography angiography (CCTA). METHODS: From March 2011 to December 2012, Patients with suspected coronary disease underwent CCTA using dual-source CT scanner. The baseline clinical characteristics (age, gender, smoking history, presence of hypertension, dyslipidemia, diabetes mellitus, family history of heart attack and body mass index (BMI) ) and the results of CCTA were reviewed. Two radiologists evaluated the MB and more than 50% coronary atherosclerosis stenosis (CAS) in LAD and made a diagnosis by consensus. Significant independent risk factors for more than 50% CAS were investigated by Logistic regression analysis. All tests were two-tailed, the significance threshold was P value less than 0.05. RESULTS: The study included 9 862 patients, including 5 292 cases of patients with hypertension (MB in LAD 2 139 cases, more than 50% CAS proximal to MB 1 240 cases; no MB in 3 153 cases, more than 50% CAS in counterpart segment proximal to MB 898 cases); 4 570 cases of non-hypertensive patients (MB in LAD 1 043 cases, more than 50% CAS proximal to MB 418; no MB 3 527 cases, more than 50% CAS in counterpart segment proximal to MB 803 cases). After adjusted for clinical data, Logistic regression analysis showed that MB in LAD were significantly associated with CAS proximal to MB in LAD in hypertension and no hypertension subjects (OR, 3.17, 2.02, respectively, P < 0.05). CONCLUSION: MB in the LAD is an independent risk factor for more than 50% CAS in the proximal LAD in subjects with or without hypertension, and the OR of MB in subjects with hypertension is higher than that of MB in subjects without hypertension.

Increase in mean platelet volume in patients with myocardial bridge.

AIM: Myocardial bridge is associated with atherosclerosis altered in shear stress and endothelial dysfunction. Mean platelet volume (MPV), a determinant of platelet activation, is shown to be related with atherosclerosis and endothelial dysfunction. In this study, we aimed to evaluate platelet function assessed by MPV in patients with myocardial bridge. METHODS: Forty-two patients with myocardial bridge in the left anterior descending artery (LAD) and 43 age- and gender-matched healthy participants were included in the study. Myocardial bridging was defined as an intramyocardial systolic compression or milking of a segment of an epicardial coronary artery on angiography. For the entire study population, MPV was measured using an automatic blood counter. RESULTS: The study population consisted of 42 patients with myocardial bridge (52.7 ± 10.2, 76.2% male) and 43 age- and sex-matched healthy control participants (52.1 ± 10.4, 74.4% male). Compared to the control group, MPV value was significantly higher in patients with myocardial bridge (8.9 ± 1.24 vs 8.3 ± 0.78; P = .01). Further, there were no significant differences between groups regarding hemoglobin level, platelet count, fasting blood glucose, and creatinine levels. CONCLUSIONS: Our study findings indicated that myocardial bridge is associated with elevated MPV values. Our results might partly explain the increased cardiovascular events in patients with myocardial bridge.

Longitudinal rotating frame relaxation time measurements in infarcted mouse myocardium in vivo.

Longitudinal relaxation time in the rotating frame (T1ρ) was measured using continuous wave irradiation in normal and infarcted mouse myocardium in vivo. Significant increase in T1ρ was found after 7 days of infarction when compared with reference myocardium or in myocardium before infarction. Cine MRI and histology were performed to verify the severity of infarction. The time course of T1ρ in the infarct fits better with granulation and scar tissue formation than necrosis and edema. The results of the study show that T1ρ could potentially be a noninvasive quantitative marker for tissue remodeling after ischemic damage.

Myocardial bridging of the left anterior descending coronary artery and right coronary artery in a patient with mitral valve stenosis.

Myocardial bridging 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). Although it is considered to be a benign anomaly, it can lead to such complications as acute myocardial infarction, ventricular tachycardia, syncope, atrioventricular block and sudden cardiac death. Isolated myocardial bridging of the right coronary artery (RCA) and left circumflex artery have been reported in the literature In our case, myocardial bridging was observed in both the LAD and the RCA in a patient with mitral valve stenosis.

Transient myocardial bridging of the left anterior descending coronary artery in acute inferior myocardial infarction.

We observed transient myocardial bridging of left anterior descending coronary artery (LAD) in 18.75% (12 of the total 64) of the patients during acute inferior myocardial infarction (MI). Myocardial bridging occurred only in the acute phase of inferior MI and not in the chronic phase. In the acute phase of inferior MI, compensatory hypercontraction of the anterior wall is assumed to occur in response to the decrease in the movement of the infarct-related walls. In the chronic phase, disappearance of the myocardial bridging observed due to the resolution of compensatory anterior wall hypercontraction, as a result of the reperfusion of infarct-related coronary artery. Most of the myocardial bridges seen in autopsy series are not seen angiographically. Variation at angiography may in part be attributable to small and thin bridges causing little compression. Adrenergic stimulation or afterload reduction by nitroglycerin facilitates diagnosis of myocardial bridging by increasing coronary compression. Both of these conditions are almost always present in acute MI. We concluded that transient myocardial bridging of LAD can be observed in some patients with acute inferior MI during acute stage.

Myocardial Bridge in association with fixed atherosclerotic lesions treated with drug-eluting stents: a follow-up report with quantitative coronary analysis.

Stenting of muscle bridge is still a controversial issue with concerns regarding high restenosis rates, plaque prolapse and stent fracture. We report a case with significant atherosclerotic disease of right coronary artery and left anterior descending artery associated with a muscle bridge, proximal to the diseased segment which became more prominent after stenting the fixed lesion. This was managed by implanting another drug eluting stent, covering the bridge. Angiographic follow-up at 9 months revealed no difference in quantitative coronary angiography parameters in the stented segment of the bridge, as compared to other stented segments.