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Left Main Coronary Artery (leave + main_coronary_artery)
Selected AbstractsCongenital Atresia of the Ostium of Left Main Coronary Artery: A Rare Coronary Anomaly, Diagnostic Difficulty and Successful Surgical RevascularizationCONGENITAL HEART DISEASE, Issue 5 2007Philip Varghese MRCS ABSTRACT We report the case of an 8-month-old infant who was referred for mechanical circulatory support (extracorporeal membrane oxygenation). Aortogram was compatible with the diagnosis of anomalous origin of left coronary artery to pulmonary trunk. A definitive diagnosis of atresia of the left coronary ostium was only established intraoperatively. Patient underwent successful surgical angioplasty with an autologous pericardial patch. [source] Coronary Artery Fistulas: A Review of the Literature and Presentation of Two Cases of Coronary Fistulas with Drainage into the Left AtriumCONGENITAL HEART DISEASE, Issue 3 2007Scott Ceresnak MD Abstract We report 2 cases of infants presenting with a murmur shortly after birth and diagnosed with coronary artery fistulas with drainage into the left atrium. The first infant had a fistulous communication between the left main coronary artery and the left atrial appendage and presented with signs and symptoms of heart failure. The infant was repaired surgically in the first week of life. The second infant was asymptomatic and had a fistulous communication between the right coronary artery and the left atrium. The infant will have the fistula closed in the cardiac catheterization laboratory when the child is older. The literature on coronary artery fistulas is reviewed, and the diagnosis and management of coronary artery fistulas is discussed. [source] Effects of melatonin and caffeic acid phenethyl ester on testicular injury induced by myocardial ischemia/reperfusion in ratsFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005Mukaddes E Abstract Experimental studies indicate that ischemia/reperfusion (I/R) causes remote organ injury although the molecular mechanism has not been clearly defined. In this report, the role of oxidative injury on testicular damage following myocardial I/R injury and the effects of antioxidant agents, melatonin and caffeic acid phenethyl ester (CAPE), on testicular injury were investigated. As far as we know, this is the first report demonstrating that myocardial I/R induces damage to the testes. Thirty-two male Wistar rats were randomly divided into four groups: sham operation (SO), I/R + vehicle, I/R + melatonin, and I/R + caffeic acid phenethyl ester. To produce cardiac damage, the left main coronary artery was occluded for 30 min, followed by 120 min reperfusion, in anesthetized rats. Serum nitric oxide (NO) and malondialdehyde (MDA) levels and morphological changes were examined. I/R was accompanied by a significant increase in serum MDA and NO levels, whereas, melatonin and CAPE administration significantly reduced these values. Melatonin was more efficient in reducing MDA levels than CAPE (P < 0.05). I/R induced myocardial damage, manifested as the histopathological evidence of intracellular vacuolization, interstitial edema, neutrophil infiltration and coagulative necrosis. I/R + vehicle group showed many histological alterations such as focal tubular atrophy, and degeneration and disorganization of the seminiferous epithelium in testes. The number of atrophic tubules and degenerating cells was significantly higher in I/R + vehicle group than that of SO group. Melatonin and CAPE significantly reduced the number of degenerating cells; additionally, melatonin reduced the number of atrophic tubules (P < 0.05). Our results indicate that myocardial I/R induces severe testicular damage and antioxidant agents, especially melatonin, have protective effects on testicular injury after myocardial I/R. Our data emphasize that oxygen-based reactants may play a central role in remote organ injury. [source] Exercise-Attenuation of Q-Waves in II, III, and aVF, and R-Waves in V1 and V2 in a Patient with an Inferior Infarction and Anterior Wall IschemiaPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2008JOHN E. MADIAS M.D. A 63-year-old male patient with inferior infarction revealed transient attenuation of the Q-waves in II, III, and aVF, and R-waves in V1,V3 during an exercise stress test. Myocardial scintigraphy disclosed ischemia of the anterior wall and coronary arteriography, a 90% stenosis of the left main coronary artery (LMCA). The mechanism involved appears to be a transient failure of the anterior wall to generate adequate depolarization forces for the genesis of Q-waves in the inferior leads and R-waves in the anterior leads. This electrocardiogram sign is diagnostic of severe anterior wall ischemia due to left anterior descending or LMCA stenosis. [source] Hemodynamic Changes in a Model of Chronic Heart Failure Induced by Multiple Sequential Coronary Microembolization in SheepARTIFICIAL ORGANS, Issue 11 2009Jan Dieter Schmitto Abstract Although a large variety of animal models for acute ischemia and acute heart failure exist, valuable models for studies on the effect of ventricular assist devices in chronic heart failure are scarce. We established a stable and reproducible animal model of chronic heart failure in sheep and aimed to investigate the hemodynamic changes of this animal model of chronic heart failure in sheep. In five sheep (n = 5, 77 ± 2 kg), chronic heart failure was induced under flouroscopic guidance by multiple sequential microembolization through bolus injection of polysterol microspheres (90 µm, n = 25.000) into the left main coronary artery. Coronary microembolization (CME) was repeated up to three times in 2 to 3-week intervals until animals started to develop stable signs of heart failure. During each operation, hemodynamic monitoring was performed through implantation of central venous catheter (central venous pressure [CVP]), arterial pressure line (mean arterial pressure [MAP]), implantation of a right heart catheter {Swan-Ganz catheter (mean pulmonary arterial pressure [PAPmean])}, pulmonary capillary wedge pressure (PCWP), and cardiac output [CO]) as well as pre- and postoperative clinical investigations. All animals were followed for 3 months after first microembolization and then sacrificed for histological examination. All animals developed clinical signs of heart failure as indicated by increased heart rate (HR) at rest (68 ± 4 bpm [base] to 93 ± 5 bpm [3 mo][P < 0.05]), increased respiratory rate (RR) at rest (28 ± 5 [base] to 38 ± 7 [3 mo][P < 0.05]), and increased body weight 77 ± 2 kg to 81 ± 2 kg (P < 0.05) due to pleural effusion, peripheral edema, and ascites. Hemodynamic signs of heart failure were revealed as indicated by increase of HR, RR, CVP, PAP, and PCWP as well as a decrease of CO, stroke volume, and MAP 3 months after the first CME. Multiple sequential intracoronary microembolization can effectively induce myocardial dysfunction with clinical and hemodynamic signs of chronic ischemic cardiomyopathy. The present model may be suitable in experimental work on heart failure and left ventricular assist devices, for example, for studying the impact of mechanical unloading, mechanisms of recovery, and reverse remodeling. [source] Left main coronary artery compression from pulmonary artery enlargement due to pulmonary hypertension: A contemporary review and argument for percutaneous revascularization,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 4 2010Michael S. Lee MD Abstract Extrinsic compression of the left main coronary artery by an enlarged pulmonary artery is an increasingly recognized and potentially reversible cause of angina and left ventricular dysfunction in patients with pulmonary hypertension. The diagnosis of extrinsic left main coronary artery compression requires a high index of suspicion and should be considered in patients with severe pulmonary hypertension who experience angina. Coronary angiography with intravascular ultrasound is the gold standard for diagnosis of this condition, though cardiac computed tomography and magnetic resonance angiography allow for noninvasive means of screening. The optimal treatment is debatable, but percutaneous coronary intervention appears to be a feasible, safe, and effective treatment option for patients with extrinsic compression of the left main coronary artery from pulmonary artery enlargement. Given the high risk of postoperative right ventricular failure and mortality observed with surgical revascularization in these patients, we recommend that physicians recognize percutaneous coronary intervention as the preferred revascularization strategy for selected patients with extrinsic compression of the left main coronary artery due to pulmonary hypertension. © 2010 Wiley-Liss, Inc. [source] Coronary compression caused by stenting a right pulmonary artery conduit,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 1 2009Marc Gewillig PhD Abstract Extrinsic compression of the left main coronary artery is a rare and life-threatening complication of endovascular stenting of pulmonary artery conduits. This case report describes fatal myocardial infarction caused by compression of the left main coronary artery due to stent placement in a stenosed right pulmonary artery conduit. © 2009 Wiley-Liss, Inc. [source] Postpartum dissection of the left main coronary arteryCLINICAL CARDIOLOGY, Issue 4 2006Ian S. Rogers M.D., M.B.A. Abstract Peripartum coronary artery dissection is rare, but it is an increasingly recognized risk to women of childbearing age. Literature reviews reveal that about 80% of the population with spontaneous coronary artery dissections (SCAD) are female, and approximately 25,33% of cases occurred while the woman was pregnant or in the peripartum phase. Most cases have presented within 2 weeks of delivery. The left anterior descending is the most commonly affected vessel. The etiology is poorly understood, but many reports suggest that SCAD occurs as a result of protease release secondary to an eosinophilic vasculitis resulting in vessel lysis. Many investigators have examined the correlation between peripartum SCAD and estrogen levels; however, case studies have shown conflicting results regarding estrogen levels as the putative causative factor. Optimal treatment remains controversial. Presently, stenting appears to be best employed in the patients who have single-vessel dissection not involving the left main coronary artery (LMCA). Surgical revascularization via coronary artery bypass graft remains the optimal therapy in patients whose dissection involves the LMCA, in patients with concurrent multi-vessel dissection, and in patients with disease refractory to medical management. It is important to consider coronary artery dissection in the differential of any young woman who presents with signs or symptoms consistent with acute coronary syndrome, particularly if she is peripartum. Furthermore, once suspected, it is imperative that a definitive diagnostic study, that is, coronary angiography, be completed prior to the initiation of treatment whenever possible. [source] | ||||||||||