Segment Of Epicardial Coronary Artery Research Articles

Cardiovascular disease among bariatric surgery candidates: coronary artery screening and the impact of metabolic syndrome

BackgroundObesity is known as a risk factor for cardiovascular disease (CVD). However, there is an absence of preoperative cardiac risk assessment in bariatric surgery candidates and the incidence of CVD among these high-risk patients is still unknown.MethodsA consecutive series of bariatric surgery candidates at two Chinese tertiary hospitals received coronary CT angiography or coronary angiography from 2017 to 2023. Patients were categorized as metabolically unhealthy obesity (MUO) and metabolically healthy obesity (MHO) based on the presence or absence of MetS. CVD was diagnosed based on the maximum intraluminal stenosis > 1% in any of the segments of the major epicardial coronary arteries. Obstructive CVD was defined as coronary stenosis ≥ 50%. Binary multivariable logistic regression was performed to analyze the association between CVD and metabolic status. The number of principal MetS components was categorized into zero (without glycemic, lipid, and BP components), one (with one of the components), two (with any two components), and three (with all components) to explore their association with CVD.ResultsA total of 1446 patients were included in the study. The incidence of CVD and obstructive CVD were 31.7% and 9.6%. Compared with MHO patients, MUO patients had a significantly higher incidence of mild (13.7% vs. 6.1%, P < 0.05), moderate (7.4% vs. 0.8%, P < 0.05), and severe CVD (3.1% vs. 0%, P < 0.05). Following complete adjustment, compared with zero or one component, two principal MetS components was found to be associated with a notable increase in the risk of CVD (OR 2.05, 95% CI 1.18–3.58, P < 0.05); three principal MetS components were observed to have a higher risk of CVD and obstructive CVD (OR 2.68, 95% CI 1.56–4.62, P < 0.001; OR 3.93, 95% CI 1.19–12.93, P < 0.05). Each increase in the number of principal MetS components correlated with a 1.47-fold (95% CI 1.20–1.81, P < 0.001) and 1.78-fold (95% CI 1.24–2.55, P < 0.05) higher risk of CVD and obstructive CVD, respectively.ConclusionThis study reported the incidence of CVD based on multicenter bariatric surgery cohorts. CVD is highly prevalent in patients with obesity, especially in MUO patients. Increased number of principal MetS components will significantly elevate the risk of CVD.

A 20-Year Autopsy Study of Myocardial Bridging Among Sudden Deaths

Myocardial bridging (MB) is a condition, where the cardiac muscle overlies the intramyocardial segment of the major epicardial coronary artery. This study aims to analyse the demographics and anatomical characteristics of MB within a pool of 2093 sudden cardiac-related death cases examined at the Forensic Unit of Universiti Kebangsaan Malaysia Medical Centre between 2000 and 2019. In this cross-sectional study, postmortem data collected were gender, racial affiliations, MB anatomical properties, and association with cardiac pathologies entered into the statistical software SPSS version 25 for analysis. The prevalence of MB was 12.9%. It was commoner in males (91.5%). MB was predominant between age 21-40 years old (50.2%). Chinese race showed the highest number of recorded MB cases (24.3%) among local races. MB was mostly found in left anterior descending (LAD) artery (98.2%), with the commonest length of 11-20mm (44.6%), depth of 1-5mm (49.8%), and distance from the ostium of 21-40mm (54.0%). The prevalence of isolated MB (43.2%) was nearly comparable to that of MB with cardiac pathologies (56.8%). MB was mostly associated with atherosclerosis (50.1%) and atheroma formation was mostly proximal to MB (78.3%). MB is a common occurrence and commonly found in the LAD as a single entity. It has a higher preponderance in the male gender among the adult population. In conclusion, the findings not only contribute to a deeper understanding of MB but also hold potential implications for identifying and managing risks related to sudden cardiac-related deaths. It is a pathological condition at a certain length and depth whether it exists as an isolated entity or associated with cardiac pathologies. Atherosclerosis tends to form proximal to MB and might pose a risk for myocardial infarction.

Prevalence of Myocardial Bridging in Angiography Study.

Myocardial bridging is a congenital anomaly in which a segment of epicardial coronary artery takes an intramyocardial course, the systolic compression of which could be asymptomatic or may lead to major hemodynamic changes such as myocardial ischemia, arrhythmias or sudden cardiac death. The prevalence is highly variable depending upon different investigational modalities to diagnose it. Here we have aimed to study the prevalence through invasive coronary angiography. This retrospective study was carried out at Manmohan Cardiothoracic Vascular and Transplant center, Kathmandu, Nepal. The invasive coronary angiography of 5096 patients were studied from March 2018 to April 2021 done for various indications. Among all the patients, the myocardial bridging was identified in 257 (5.04%) patients. About 177 (68.9%) were males and 80 (31.1%) were females. The mean age of the patients having myocardial bridging was 54.52 ± 10.31years. Diabetes mellitus was found in 33(12.8%) and hypertension was found in 77(29.9%) patients with myocardial bridging. Stable angina (29.2%) was the most common clinical presentation. Treadmill test was positive in about 70 (27.2%) patients. Majority of patients had myocardial bridge in left anterior descending artery alone (89.9%) and located mostly in mid-part (74.9%). The myocardial bridging is not an uncommon finding on invasive coronary angiography in middle aged people who present with typical angina.

Myocardial bridge analysis by multidetector computed tomography and its association with coronary atherosclerosis

Abstract Background Myocardial Bridging an inborn coronary abnormality, is defined as a segment of a major epicardial coronary artery, the tunneled artery, that goes intramurally through the myocardium beneath the muscle bridge. Objective To evaluate noninvasively the presence and distribution of atherosclerotic plaques in relation to myocardial bridge coronary segments and to determine the prevalence of myocardial bridges and their location and morphology by using MDCT. Patients and Methods The study population consisted of 55 patients presented with chest pain, referred for MDCT coronary angiography and found to have myocardial bridge at during the period from April 2018 and August 2019. 23 patients was found having Myocardial Bridge and coronary artery atherosclerotic plaques included in Group (A), 29 persons found having Myocardial Bridge without CAD included in Group (B). All patients were subjected to detailed history taking, clinical evaluation, ECG analysis and MSCT coronary angiography. Results In the present study, patients with atherosclerotic plaque (group A) (n = 29), mean age was 52.41 ± 10.55 years ranged from 35.0 to 73.0 years, 41.4% were males, while in Myocardial bridge without atherosclerotic lesion group (group B) (n = 26), mean age was 51.65 ± 7.58 ranged from 38.0 to 65.0 years., 30.8% were males. Conclusion Our study showed that diabetes mellitus and dyslipidemia are a significant risk factor for developing atherosclerotic plaque in the segment proximal to myocardial bridge. Myocardial bridge were usually located over the Mid segment of the left anterior descending coronary artery

Smooth Muscle Contraction Is Regulated by Chloride Channels: Functional Evidence for TMEM16A in Porcine Coronary Arteries

Contraction of coronary smooth muscle is influenced by ion channels that control membrane potential and, thus, Ca2+ influx. A great deal of attention has been focused on K+ channels, as their opening makes membrane potential more negative, reduces Ca2+ influx, and causes relaxation. Our objective was to investigate ion channels in coronary smooth muscle whose opening would depolarize membrane potential, increase Ca2+ influx, and promote contraction. One potential candidate for study is the Ca2+-activated Cl− channel TMEM16A, which is expressed in a variety of smooth muscle types. We tested the hypothesis that drugs which influence TMEM16A activity would alter contraction. Specifically, we tested the idea that coronary smooth muscle contraction would be enhanced by a TMEM16A activator (Eact), whereas coronary smooth muscle contraction would be attenuated by a TMEM16A inhibitor (T16Ainh-A01). We used isometric tension recording methods on epicardial coronary artery segments (3 mm length) from domestic swine to test the predictions. Contractions in response to elevated extracellular K+ (5-30 mM in 5 mM increments) were recorded before and after treatment with 5 μM Eact or 5 μM T16Ainh-01. Extracellular K+ was varied by adding potassium gluconate, rather than potassium chloride, in order to keep the Cl− concentration constant. Concentration-response curves were fit by nonlinear regression and compared with two-way repeated measures ANOVA. K+ contracted coronary artery rings with an EC50 of 19.1 ± 0.6 mM and a maximum of 11.8 ± 1.4 g. Drug vehicle (DMSO; 0.05%) had no effect on contraction (EC50 or maximum). EACT shifted K+-induced contraction to the left (17.8 ± 0.9 mM; P < 0.05), but did not affect the maximum (105 ± 3% of control). T16Ainh-A01 shifted K+-induced contraction to the right (20.4 ± 0.6 mM; P < 0.05), but did not affect the maximum (90 ± 1% of control). These data suggest that TMEM16A is expressed in the porcine coronary artery and can influence function through electromechanical coupling.

A case of myocardial infarction due to myocardial bridging alone

Myocardial bridging (MB) is characterised by a segment of a major epicardial coronary artery tunnelling through the myocardium, which is a frequent congenital anomaly, detected in 15–85% of autopsy series and in 0.5–33% of angiographic studies.[1,2][1] MB without critical stenosis is generally

Increased risk of coronary perforation during percutaneous intervention of myocardial bridge: What histopathology says.

Introduction: Myocardial bridge (MB) is a segment of a major epicardial coronary artery that goes intramurally under a bridge of overlying myocardium. Complications have been reported during or after stent implantation particularly coronary perforation. The aim of this study was to determine histological differences between proximal left anterior descending artery (LAD) and the tunneled segment that may have a possible role in increased risk of coronary artery perforation during percutaneous coronary intervention. Methods: Twenty specimens of MB were obtained from dissection of 45 cadavers. Sections were stained using hematoxylin and eosin (H&E), and trichrome methods. The proximal section and the tunneled artery were compared with a normal sample in terms of the characteristics of a muscle artery. Results: The findings of this study showed an MB prevalence of 51%, as 23 out of the 45 examined cadavers were discovered to be afflicted by the MB. The intima layer in the suffering artery had gone through significant hypertrophy, while it had remained thin in the tunneled artery section. The epithelial cells under the bridge were spindle-shaped, while they were polygonal in the proximal section. In the myocardium the nuclei of the muscle fibers in the MB section were smaller than the normal section. Adventitial layer was almost normal. Conclusion: The histopathological differences between MB and proximal part of vessel combined with small vessel diameter in the tunneled segment can explain the high incidence of the LAD rupture and perforation in the section under the bridge.

Aspirate from human stented saphenous vein grafts induces epicardial coronary vasoconstriction and impairs perfusion and left ventricular function in rat bioassay hearts with pharmacologically induced endothelial dysfunction.

Stent implantation into aortocoronary saphenous vein grafts (SVG) releases particulate debris and soluble vasoactive mediators, for example, serotonin. We now analyzed effects of the soluble mediators released into the coronary arterial blood during stent implantation on vasomotion of isolated rat epicardial coronary artery segments and on coronary flow and left ventricular developed pressure in isolated perfused rat hearts. Coronary blood was retrieved during percutaneous SVG intervention using a distal occlusion/aspiration protection device in nine symptomatic patients with stable angina pectoris and a flow‐limiting SVG stenosis. The blood was separated into particulate debris and plasma. Responses to coronary plasma were determined in isolated rat epicardial coronary arteries and in isolated, constant pressure‐perfused rat hearts (±nitric oxide synthase [NOS] inhibition and ±serotonin receptor blockade, respectively). Coronary aspirate plasma taken after stent implantation induced a stronger vasoconstriction of rat epicardial coronary arteries (52 ± 8% of maximal potassium chloride induced vasoconstriction [% KClmax = 100%]) than plasma taken before stent implantation (12 ± 8% of KClmax); NOS inhibition augmented this vasoconstrictor response (to 110 ± 15% and 24 ± 9% of KClmax). Coronary aspirate plasma taken after stent implantation reduced in isolated perfused rat hearts only under NOS inhibition coronary flow by 17 ± 3% and left ventricular developed pressure by 25 ± 4%. Blockade of serotonin receptors abrogated these effects. Coronary aspirate plasma taken after stent implantation induces vasoconstriction in isolated rat epicardial coronary arteries and reduces coronary flow and left ventricular developed pressure in isolated perfused rat hearts with pharmacologically induced endothelial dysfunction.

PERCENTAGE INCIDENCE, MORPHOLOGY AND MORPHOMETRY OF MYOCARDIAL BRIDGES: A CADAVERIC STUDY

Address for Correspondence: Ms. Sujatha Manupati, Ph.D. Scholar, Department of Anatomy, Sri Venkateswara Medical College, Tirupati, Andhra Pradesh. India. Mobile No.: +919246943011 E-Mail: manupatisujatha@gmail.com *1 Ph.D. Scholar, Department of Anatomy, S.V. Medical College, Tirupati, Andhra Pradesh, India. 2 Professor & Head, Department of Anatomy, S.V. Medical College,Tirupati, Andhra Pradesh, India. 3 Associate professor, Department of Forensic Medicine, RIMS Medical College, Kadapa, Andhra Pradesh, India. 4 Professor & Head, Dept of Anatomy, SVIMS, Sri Padmavathi Medical College for women, Tirupati, Andhra Pradesh India. Introduction: Myocardial bridging is the term used when a segment of major epicardial coronary artery runs intramuscularly under the tunnel formed by fibers of myocardium that bridges instead of it’s normal or routine epicardial path. In the literature there are varying reports on clinical implications of myocardial bridges from protection against atherosclerosis to myocardial ischemia, as well as leading to infarction and sudden cardiac death. Materials and Methods: 150 adult formalin fixed human hearts which were available in the department of Anatomy and Forensic Medicine, S.V.Medical College, Tirupati, Andhra Pradesh, India. These hearts were dissected and observed for the presence, location, type, number and direction of myocardial bridges and their association with coronary dominance. With the help of digital calipers morphometric parameters (length, width& thickness) of myocardial bridges and length of blood vessel underneath the myocardial bridge were measured, noted and photographs were taken. Results: The overall incidence of myocardial bridges was 20.6%( 31/150). Among these 18.6% (28/31) were on left anterior descending (LAD) artery and 2% (03/31) were on posterior interventricular (PIV) artery. The direction of muscle fibers in the bridges were oblique to the direction of the coronary vessels in majority of cases. Length, width and thickness of myocardial bridges were in the range of 12-69.7mm, 3.74-8.6mm and 1.3-3.87mm respectively. Conclusions: Myocardial bridges may be associated with wide range of clinical problems. Contraction of myocardial bridge may results in vascular compression and myocardial ischemia. Knowledge on morphology and morphometric details of myocardial bridges facilitates cardiologists in diagnosis, planning therapeutic strategies and prognostic predictions.

Intramyocardial bridges: anatomo-pathological characteristics, diagnosis, and therapeutic strategies

Intramyocardial bridge is defined as the segment of a major epicardial coronary artery that runs within the cardiac muscle wall (coronary tunneling). Usually, this kind of anatomic variant is asymptomatic but sometimes it may lead to acute coronary syndrome and/or arrhythmias, and more rarely to sudden cardiac death. Treatment for symptomatic patients is pharmacological, using beta-blockers.

Myocardial Ischemia by Aggravation of Myocardial Bridging

Myocardial bridging (MB) occurs when the myocardium covers a segment of a major epicardial coronary artery, resulting in a tunneled arterial segment. Although MB is generally considered benign, it has been associated with myocardial ischemia. A 70-year-old man with MB (50% luminal narrowing during systole) at the mid-left anterior descending artery (LAD) on previous coronary angiography (CAG) visited our hospital with worsening chest pain. His blood pressure (BP) was not well controlled because of poor compliance. Follow-up CAG showed that MB at the mid-LAD progressed to severe stenosis (>90% luminal narrowing during systole) and the total length of tunneled artery extended from 22.5 to 23.9 mm. His chest pain was relieved by BP control. This is the first report of myocardial ischemia secondary to progression of MB demonstrated by CAG in Korea.

Myocardial bridging and prognosis: more evidence but jury still out

Myocardial bridging (MB) is a congenital variant of coronary anatomy in which a segment of a major epicardial coronary artery that normally has an epicardial course runs intramurally through the myocardium beneath the muscle bridge. It occurs most frequently in the mid-portion of the left anterior descending ( Figure 1 ). It is also called ‘tunneled artery’. Geiringer1 first presented an in-depth analysis of autopsy samples in 1951, but clinical interest and systematic research were triggered by observed association of MB with myocardial ischaemia. In this regard, although traditionally considered a benign condition, MB may cause clinical symptoms including angina, myocardial infarction, life-threatening arrhythmias, and sudden death.2–4 It is widely accepted that MB might cause these ischaemic complications5,6 either from direct compression of the coronary artery during systolic contraction or by enhancement of the natural progression of atherosclerosis in the coronary segment. Both mechanisms are closely associated with changes in haemodynamic stress driven by the force of the MB compression through a combination of anatomical properties, such as the location, length, and thickness of the MB.7 Figure 1 Example of myocardial bridging (MB) of the middle tract of left anterior descending (LAD) coronary artery as displayed on Cardiac CT ( A –3D volume rendering—arrowhead). The longitudinal curved multiplanar views in orthogonal planes ( B and C ) show the location and length of the MB. Axial cross-section of the LAD performed proximal ( D ), distal ( F ) and within the MB ( E ) show the typical pattern of deep intra-myocardial course. The deep or complete intra-myocardial course consists of a 360° myocardium surrounded vessel ( E —arrowhead) as also displayed in pathology sample ( E ′—arrowhead). The true prevalence of MB is not fully known because it is largely underdiagnosed by conventional angiography. cardiac computed tomography (CCT) …

Miokardni mostovi - od slučajnog nalaza do miokardne ishemije

This article reviews current knowledge about morphology, pathophysiology, clinical relevance and treatment of myocardial bridges. Myocardial bridging (MB) is a congenital coronary abnormality defined as a segment of a major epicardial coronary artery running intramurally through the myocardium, usually affecting the left anterior descending artery (LAD). Because of incomplete understanding of the pathophysiology of MB, their clinical significance has been the subject of debate for the last 20 years. Although MB is generally considered as benign condition, there are many reports suggesting that this anomaly is associated with angina, acute coronary syndrome, myocardial infarction, arrhythmias and even sudden death. MB may cause ischemic heart disease by two distinct mechanisms. One is systolic compression of the intramural segment of LAD, resulting in delayed early diastolic artery relaxation, reduced blood flow reserve and decreased myocardial perfusion. The other is the development of atherosclerotic lesions of the LAD proximal to the MB, occurring because of hemodynamic disturbances influenced by retrograde blood flow up toward the LAD ostium at systole. New investigational tools in the cardiac catheterization laboratory (quantitative coronary angiography, intravascular ultrasound, intracoronary Doppler, fractional flow reserve) have revealed morphological and hemodynamical alterations during diastole. Medical therapy (beta-blockers, calcium channel-blockers) has a major role in the treatment of symptomatic patient with MB. Nitrates are contraindicated because they have been shown to increase the systolic compression of the affected portion of the vessel.

Does isolated myocardial bridge really interfere with coronary blood flow?

Myocardial bridge (MB) is defined as a segment of a major epicardial coronary artery the “tunneled artery” that goes intramurally through the myocardium beneath the muscle bridge. Multiple methods have been proposed to assess coronary flow rate among which thrombolysis in acute myocardial infarction frame count was a relatively new semiquantitative method. Our goal was to determine incidence of MB in the patients undergoing coronary angiography in Mansoura Specialized Hospital, Cardiac Catheterization Laboratory, also to investigate the hypothesis that slow coronary flow rate may be linked to angina or angina like symptoms in patients with MB without stenotic lesions in epicardial coronary arteries using TFC. Fifteen patients with MB (group I) were retrospectively collected from Mansoura Specialized Hospital, Cardiac Catheterization Laboratory, we review 3000 cases referred to diagnostic coronary angiography to exclude significant coronary artery disease. Fifteen patients with normal coronary angiography served as control (group II). We review the clinical presentations, risk factors, echocardiographic data for both test and control groups. TFC was calculated using a simple continuous index. The incidence of MB in our study was 0.5%. CTFC in LAD was significantly higher in the patients with MB compared with control. No significant correlation between TFC and echocardiographic parameters. Myocardial bridging must be considered especially in patients at low risk for coronary atherosclerosis but with angina like chest pain or established myocardial ischemia. We suggest that coronary blood flow is decreased in the patients with MB compared with the patients having normal coronary.

Myocardial bridging causing ischemia and recurrent chest pain: a case report

BackgroundMyocardial bridging is present when a segment of a major epicardial coronary artery runs intramurally through the myocardium. It usually has a benign prognosis, but in some cases myocardial ischemia, infarction and sudden cardiac death have been reported. We are here reporting a case of myocardial bridging which was complicated with recurrent chest pain and transient ST-segment elevation during exercise treadmill test.Case presentationA 40 year-old-man presented with recurrent retrosternal chest pain of 2 months duration. He had history of smoking and was obese, otherwise no physical abnormalities were detected by examination. Electrocardiogram and blood tests were normal apart from impaired glucose tolerance with elevated triglycerides and decreased level of high density lipoprotein cholesterol. While doing exercise treadmill test, the patient developed chest pain and significant ST-segment elevation in almost all precordial leads that persisted for about 15 minutes through recovery. We decided to admit the patient to the coronary care unit for further management and to perform coronary angiogram. Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery. Medical treatment was decided.At one year follow up, our patient was healthy and had no cardiac complaints. In conclusion, myocardial bridging may predispose to coronary vasospasm that may leads to ischemic complications.

Letter by Poullis Regarding Article, “Anatomic Properties of Myocardial Bridge Predisposing to Myocardial Infarction”

To the Editor: Ishikawa et al1 provide important data on the correlation between myocardial bridges and the predisposition to myocardial infarction. They confirm the 2 everyday findings of coronary artery surgeons: First, that intramyocardial epicardial coronary artery segments, whether in the left anterior descending territory or the obtuse marginal territory, are rarely involved in the atherosclerotic process, and second, that atherosclerotic lesions always seem to be proximal to the muscle bridge. The findings by Ishikawa et al1 raise a number of interesting points that were not answered in their report, however. Patients with a history of …

Myocardial Bridging in Taiwan: Depiction by Multidetector Computed Tomography Coronary Angiography

Myocardial bridging (MB) is a condition in which a segment of the major epicardial coronary artery is tunneled within and surrounded by the myocardium. This condition has been linked to severe complications. The aim of this study was to evaluate the incidence of MB in Taiwanese subjects examined with electrocardiogram-gated, 16-slice, multidetector computed tomography (MDCT) coronary angiography, as well as to determine the location, depth, and length of the bridged segments and the concomitant atherosclerosis of MB. From August 2004 to May 2005, 276 consecutive subjects referred to our department for MDCT coronary angiography were enrolled in the study after written informed consent was obtained from each participant. Twenty-four subjects (8.7%) had at least one coronary segment that was completely surrounded by myocardium. Patients ranged in age from 27 to 76 years, with an average of 54 +/- 12 years. Thirty coronary segments were found to have MB. The most common location of MB was in segment 7, which accounted for 14 coronary segments (46.7%) of the total number of bridged segments; left anterior descending artery (LAD) segments accounted for 23 (76.7%); and right coronary artery and left circumflex artery segments accounted for three (10%) and two (6.7%), respectively. The length of bridged segments ranged from 5.2 to 50.6 mm, with an average length of 24.6 +/- 11.8 mm, and the depth of the bridged segments ranged from 0.5 to 9.1 mm, with an average depth of 3.65 +/- 1.89 mm. Two bridged segments (6.7%) had concomitant atherosclerosis; these were located in segment 7 (24.0 mm long and 6.10 mm deep) and segment 8 (27.1 mm long and 7.0 mm deep). Bridged segments with concomitant atherosclerosis were deeper, but not longer, compared with bridged segments without concomitant atherosclerosis (p < 0.05). Electrocardiogram-gated MDCT is an effective noninvasive tool for evaluating MB in a clinical setting. The most common location of MB was in the LAD, especially in segment 7. Bridged segments with concomitant atherosclerosis were deeper, but not longer, compared with bridged segments without concomitant atherosclerosis.

The chance finding at multislice computed tomography coronary angiography of myocardial bridging

Myocardial bridging is present when a segment of a major epicardial coronary artery, the ‘tunnelled artery’, runs intramurally through the myocardium. With each systole, the coronary artery is compressed. The pathophysiology of myocardial bridging is incompletely understood. With each systole, the coronary artery is compressed. Moreover, intravascular ultrasound analysis revealed a delayed relaxation after systolic compression, which may extend significantly into diastole. This explains both the impaired coronary flow reserve and ischemia. Evidence indicates that the intima beneath the bridge is protected from atherosclerosis, and the proximal segment is more susceptible to the development of atherosclerotic lesions because of haemodynamic disturbances. Myocardial bridging is sometimes associated with overt pathology, as well as it can just be an incidental finding without any significance. Myocardial bridging may cause angina pectoris, myocardial infarction, life threatening arrhythmias and even sudden cardiac death but most of them are harmless. Furthermore depressed left ventricular function, myocardial stunning, early death after cardiac transplantation has been also reported. Although the exact management is not well known, beta blockers seem to be the first choice. Stenting is controversial and one must think “twice” before stenting the bridged coronary artery. We report a case of chance finding at multislice computed tomography coronary angiography of two myocardial bridging. Also this case focuses attention on myocardial bridging and it confirms that multislice computed tomography coronary angiography technology represents a useful, noninvasive imaging method of its assessment.

Prevalence of coronary artery intramyocardial course in a large population of clinical patients detected by multislice computed tomography coronary angiography

Intramyocardial course, an inborn coronary anomaly, is defined as a segment of a major epicardial coronary artery that runs intramurally through the myocardium; in particular, we distinguish myocardial bridging, in which the vessel returns to an epicardial position after the muscle bridge, and intramyocardial course, which is described as a vessel running and ending in the myocardium. To evaluate the prevalence of myocardial bridging and intramyocardial course of coronary arteries as defined by multidetector computed tomography (MDCT) angiography. The study population consisted of 242 consecutive patients (211 men, 31 women; mean age 59+/-6 years) with atypical chest pain admitted to our hospital between December 2004 and September 2006. All MDCT examinations were performed using a 16-detector-row scanner (Aquilion 16 CFX; Toshiba Medical System, Tokyo, Japan). Patients with heart rate above 65 bpm received 50 mg atenolol orally for 3 days prior to the MDCT scan, or they increased their usual therapy with beta-blockers, in order to obtain a prescan heart rate <60 bpm. Curved multiplanar and 3D volume reconstructions were performed to explore coronary anatomy. In 235 patients, the CT scan was successful and images were appropriate for evaluation. The prevalence of myocardial bridging and intramyocardial course of coronary arteries was 18.7% (47 cases) in our patient population. In 30 segments (63.8%), the vessels ran and ended in the myocardium. In the remaining 17 segments (36.2%), the vessels returned to an epicardial position after the muscle bridge. We found no difference in the prevalence of this inborn coronary anomaly when comparing different clinical characteristics of the study population (sex, age, body-mass index [BMI], etc.). The mean length of the subepicardial artery was 7 mm (range 5-12 mm), and the mean depth in the diastolic phase was 1.9 mm (range 1.2-2.3 mm). There was no significant difference of diameter in these segments between the different R-R phases examined. Our study is in agreement with major angiographic literature reporting a prevalence of myocardial bridging and intramyocardial course between 0.5% and 33%. MDCT technology represents a useful, noninvasive imaging method to assess and evaluate the location, depth, and length of this anatomical variation.

Influence of Ageing on Vasomotor Responses of Human Epicardial Coronary Arteries

Vasomotor responses to various agonists were studied on isolated circular segments of human epicardial coronary arteries from three different age groups; 23–38 years, 40–58 years and 63–86 years. Noradrenaline had no or only weak contractile effect on coronary arteries from younger patients but induced contraction of all artery segments from older patients. The Emax value was significantly (P<0.0001) higher in arteries from the oldest group compared to each of the two younger age groups, whereas the potency was similar in all three groups. Linear regression analysis of noradrenaline-induced contraction in individual patients revealed a significantly positive age-correlation (correlation coefficient 0.67, P<0.0001). Contraction induced by endothelin-1 and relaxation induced by substance P, calcitonin gene-related peptide and vasoactive intestinal peptide on arteries precontracted with U46619 showed no significant differences in maximum responses and potencies between the three age groups, and no significant linear age-correlation. These data demonstrate a large variability in contractile responses to noradrenaline with contractions seen mostly in coronary arteries from older patients. It thus seems that sympathetic activation could contribute to coronary ischaemia in some patients.