• left anterior descending artery
• minimally invasive cardiac surgery
• myocardial bridge
• robotic cardiac surgery
• unroofing

• Humans
• Female
• Middle Aged
• Male
• Robotic Surgical Procedures/methods
• Endoscopy/methods
• Treatment Outcome
• Myocardial Bridging/surgery
• Adult
• Coronary Angiography/methods
• Coronary Artery Bypass, Off-Pump/methods
• Retrospective Studies

• Atherosclerosis
• Coronary spasm
• Hypertrophic cardiomyopathy
• MINOCA
• Myocardial bridging

• Humans
• Myocardial Bridging/diagnosis
• Myocardial Bridging/therapy
• Coronary Artery Disease
• Myocardial Ischemia
• Coronary Artery Bypass
• Myocardial Infarction
• Coronary Angiography

• Coronary computed tomography angiography
• Intravascular ultrasound
• Ischemia with no obstructive coronary arteries
• Myocardial bridge
• Surgical unroofing

• Coronary
• Coronary computed tomographic angiography
• Myocardial bridging
• Myotomy
• Unroofing

• coronary artery bypass grafting
• myocardial bridging
• myotomy

Functional assessment of myocardial bridging (MB) remains clinically challenging because of the dynamic nature of the extravascular coronary compression with a certain degree of intraluminal coronary reduction. The aim of our study was to assess performance and diagnostic value of diastolic‐fractional flow reserve (d‐FFR) during dobutamine provocation versus conventional‐FFR during adenosine provocation with exercise‐induced myocardial ischemia as reference.

This prospective study includes 60 symptomatic patients (45 men, mean age 57±9 years) with MB on the left anterior descending artery and systolic compression ≥50% diameter stenosis. Patients were evaluated by exercise stress‐echocardiography test, and both conventional‐FFR and d‐FFR in the distal segment of left anterior descending artery during intravenous infusion of adenosine (140 μg/kg per minute) and dobutamine (10–50 μg/kg per minute), separately. Exercise–stress‐echocardiography test was positive for myocardial ischemia in 19/60 patients (32%). Conventional‐FFR during adenosine and peak dobutamine had similar values (0.84±0.04 versus 0.84±0.06, P=0.852), but d‐FFR during peak dobutamine was significantly lower than d‐FFR during adenosine (0.76±0.08 versus 0.79±0.08, P=0.018). Diastolic‐FFR during peak dobutamine was significantly lower in the exercise‐stress‐echocardiography test –positive group compared with the exercise‐ stress‐echocardiography test –negative group (0.70±0.07 versus 0.79±0.06, P<0.001), but not during adenosine (0.79±0.07 versus 0.78±0.09, P=0.613). Among physiological indices, d‐FFR during peak dobutamine was the only independent predictor of functionally significant MB (odds ratio, 0.870; 95% CI, 0.767–0.986, P=0.03). Receiver‐operating characteristics curve analysis identifies the optimal d‐FFR during peak dobutamine cut‐off ≤0.76 (area under curve, 0.927; 95% CI, 0.833–1.000; P<0.001) with a sensitivity, specificity, and positive and negative predictive value of 95%, 95%, 90%, and 98%, respectively, for identifying MB associated with stress‐induced ischemia.

Diastolic‐FFR, but not conventional‐FFR, during inotropic stimulation with high‐dose dobutamine, in comparison to vasodilatation with adenosine, provides more reliable functional significance of MB in relation to stress‐induced myocardial ischemia.

• adenosine
• dobutamine
• fractional flow reserve
• myocardial bridging
• myocardial ischemia
• stress‐echocardiography

• Guidelines
• adult congenital heart disease
• aortopathies
• arrhythmias
• cancer
• cardiomyopathy
• cardiovascular risk factors
• chronic coronary syndromes
• exercise
• heart failure
• peripheral vascular disease
• pregnancy
• recommendations
• risk stratification
• sport – special environments
• valvular heart disease

• Cardiology
• Cardiovascular Diseases/prevention & control
• Exercise
• Humans
• Sports

• IK6 RX002477 RRD VA

• Implantable Cardioverter-defibrillator
• Myocardial bridge
• Myocardial infarction
• Vasospasm
• Ventricular fibrillation

• Artery
• Bridging
• Coronary
• Ischemia
• Myocardium

• Bypass surgery
• Graft patency
• Major adverse cardiac events
• Myocardial bridge
• Myotomy

• Coronary artery disease
• athletes
• recommendations
• sports participation

Myocardial bridge (MB) will compress the mural coronary artery (MCA) during the systole and cause myocardial ischemia. In the diagnosis of coronary heart disease (CHD), because the structure of MB is difficult to be observed by coronary angiography (CAG), the clinical study of the influence of MB on CHD is lacking. With the advancement of computed tomography coronary angiography technology, detailed observations of the MB anatomy have realized.

To explore the main influencing factors of MB-related CHD and to find potential indicators for predicting MB-related CHD.

A total of 1718 patients with suspected CHD due to the symptoms of myocardial ischemia were enrolled as subjects. Patients diagnosed with CHD were included in a CHD group, and patients with no significant abnormalities were included in a control group. In the CHD group, patients were divided into an MB-CHD subgroup if MB-related CHD was found. In the control group, patients were divided into a simple MB subgroup if MB was found. The patient's clinical data and MB-related indicators, including the branch of MB, MB type (superficial/deep type), MB length, MB thickness, systolic and diastolic compression of the MCA, and MCA systolic stenosis rate were recorded and compared. Logistic regression analysis was used to explore the independent influencing factors of MD-related CHD. ROC curve was used to analyze the diagnostic efficacy of potential indicators for MB-related CHD.

There were 1060 cases in the CHD group and 658 cases in the control group, and there were 236 cases in the MB-CHD subgroup and 52 cases in the simple MB subgroup. Multivariate logistic regression analysis showed that the combined MB had a significant effect on the occurrence of CHD (P < 0.05). MB thickness, systolic compression, diastolic compression, and MCA systolic stenosis rate had significant effects on the occurrence of MB-related CHD (P < 0.05). The area under the curve (AUC) of the combination of these influencing factors for the diagnosis of MB-related CHD was 0.959, which was significantly higher than the AUCs of the four indicators separately (P < 0.05). The sensitivity was 97.06% and the specificity was 87.63%.

MB thickness, systolic compression, diastolic compression, and MCA systolic stenosis are independent influencing factors for MB-related CHD. The combination of these factors has potential diagnostic value for MB-related CHD.

• Myocardial bridge
• Coronary heart disease
• Mural coronary artery
• Computed tomography coronary angiography
• Independent influencing factor

• Arrhythmia
• CT angiography
• Coronary atherosclerosis
• ECG
• Myocardial bridge

Homocysteine has been long considered a risk factor for atherosclerosis. However, cardiovascular events cannot be reduced through homocysteine lowering by B vitamin supplements. Although several association studies have reported an elevation of serum homocysteine levels in cardiovascular diseases, the relationship of homocysteine with ST-segment elevation myocardial infarction (STEMI) is not well established.

We prospectively enrolled STEMI patients who were consecutively admitted to an intensive care unit following coronary intervention in a single medical center in Taiwan. Control subjects were individuals who presented to the outpatient or emergency department with acute chest pain but subsequently revealed patent coronary arteries by coronary arteriography. The association between serum homocysteine levels and STEMI was investigated. A culture system using human coronary artery endothelial cells was also established to examine the toxic effects of homocysteine at the cellular level.

Patients with chest pain were divided into two groups. The STEMI group included 56 patients who underwent a primary percutaneous coronary intervention. The control group included 17 subjects with patent coronary arteries. There was no difference in serum homocysteine levels (8.4 ± 2.2 vs. 7.6 ± 1.9 μmol/L, p = 0.142). When stratifying STEMI patients by the Killip classification into higher (Killip III-IV) and lower (Killip I-II) grades, CRP (3.3 ± 4.1 vs. 1.4 ± 2.3 mg/L, p = 0.032), peak creatine kinase (3796 ± 2163 vs. 2305 ± 1822 IU/L, p = 0.023), and SYNTAX scores (20.4 ± 11.1 vs. 14.8 ± 7.6, p = 0.033) were significantly higher in the higher grades, while serum homocysteine levels were similar. Homocysteine was not correlated with WBCs, CRP, or the SYNTAX score in STEMI patients. In a culture system, homocysteine at even a supraphysiological level of 100 μmol/L did not reduce the cell viability of human coronary artery endothelial cells.

Homocysteine was not elevated in STEMI patients regardless of Killip severity, suggesting that homocysteine is a bystander instead of a causative factor of STEMI. Our study therefore supports the current notion that homocysteine-lowering strategies are not essential in preventing cardiovascular disease.

• C-reactive protein (CRP)
• Coronary artery disease
• Homocysteine
• ST-segment elevation myocardial infarction (STEMI)
• White blood cell (WBC)

• interventional cardiology
• ischaemic heart disease