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Coronary Vessels (coronary + vessel)
Selected AbstractsA search for cyclophilin-A gene (PPIA) variation and its contribution to the risk of atherosclerosis and myocardial infarctionINTERNATIONAL JOURNAL OF IMMUNOGENETICS, Issue 2 2008M. Palacín Summary Cyclophilin A is secreted by vascular smooth muscle cells in response to inflammatory stimuli, and could thus contribute to atherosclerosis. We hypothesized that the genetic variation at the cyclophilin A gene (PPIA) could affect the risk for developing atherosclerosis and myocardial infarction. This study included 250 myocardial infarction patients (all male and < 60 years; 95% are smokers). All these cases had at least one atherosclerotic diseased coronary vessel. DNA was obtained from patients and from 250 healthy controls. The variation at the PPIA gene was determined in the patients through single-strand conformation analysis and direct sequencing of seven polymerase chain reaction fragments. Allele and genotype frequencies were compared between patients and controls. The effect of a promoter polymorphism (,11 G/C) on gene expression was in vitro analysed with luciferase-reporter assays. We found two common polymorphisms in the PPIA promoter (,11 G/C) and the 5, non-translated (+36 G/A) regions. Cells transfected with luciferase-plasmids containing the ,11 G had significantly higher luciferase activity. Genotype frequencies for these polymorphisms did not differ between patients and controls. In conclusion, we reported a functional variant in the PPIA promoter. However, the PPIA variation did not significantly contribute to the risk of suffering from myocardial infarction among patients with atherosclerotic diseased vessels. [source] Differential growth and multicellular villi direct proepicardial translocation to the developing mouse heartDEVELOPMENTAL DYNAMICS, Issue 1 2008Laurel S. Rodgers Abstract In the mammalian system the proepicardium (PE) arises from mesothelium of the septum transversum before translocation to the heart where it forms the epicardium and progenitor cells of the coronary vessels. Despite its importance, the process in which PE cells translocate to the myocardium in mammals is not well defined. The current paradigm states that cellular cysts of PE float across the pericardial space and contact the outer surface of the myocardium. This mechanism does not provide a satisfactory explanation for the directionality or localization of PE migration. To better define PE migration, we performed a detailed study of mouse PE development. We provide thorough documentation that redefines the size of the PE migratory field and the mechanism of migration. Our new model incorporates differential growth and direct contact between multicellular PE villi and the myocardium as mechanisms in formation of the epicardium. Developmental Dynamics 237:145,152, 2008. © 2007 Wiley-Liss, Inc. [source] Differential levels of tissue hypoxia in the developing chicken heartDEVELOPMENTAL DYNAMICS, Issue 1 2006Jamie Wikenheiser Abstract Tissue hypoxia plays a critical role in normal development, including cardiogenesis. Previously, we showed that oxygen concentration, as assessed by the hypoxia indicator EF5, is lowest in the outflow tract (OFT) myocardium of the developing chicken heart and may be regulating events in OFT morphogenesis. In this study, we identified additional areas of the embryonic chicken heart that were intensely positive for EF5 within the myocardium in discrete regions of the atrial wall and the interventricular septum (IVS). The region of the IVS that is EF5-positive includes a portion of the developing central conduction system identified by HNK-1 co-immunostaining. The EF5 positive tissues were also specifically positive for nuclear-localized hypoxia inducible factor 1, (HIF-1,), the oxygen-sensitive component of the hypoxia inducible factor 1 (HIF-1) heterodimer. The pattern of the most intensely EF5-stained myocardial regions of the atria and IVS resemble the pattern of the major coronary vessels that form in later stages within or immediately adjacent to these particular regions. These vessels include the sinoatrial nodal artery that is a branch of the right coronary artery within the atrial wall and the anterior/posterior interventricular vessels of the IVS. These findings indicate that a portion of the developing central conduction system and the patterning of coronary vessels may be subject to a level of regulation that is dependent on differential oxygen concentration within cardiac tissues and subsequent HIF-1 regulation of gene expression. Developmental Dynamics 235:115,123, 2006. © 2005 Wiley-Liss, Inc. [source] MAP kinase activation in avian cardiovascular developmentDEVELOPMENTAL DYNAMICS, Issue 4 2004Christine M. Liberatore Abstract Signaling pathways mediated by receptor tyrosine kinases (RTK) and mitogen-activated protein kinase (MAPK) activation have multiple functions in the developing cardiovascular system. The localization of diphosphorylated extracellular signal regulated kinase (dp-ERK) was monitored as an indicator of MAPK activation in the forming heart and vasculature of avian embryos. Sustained dp-ERK expression was observed in vascular endothelial cells of embryonic and extraembryonic origins. Although dp-ERK was not detected during early cardiac lineage induction, MAPK activation was observed in the epicardial, endocardial, and myocardial compartments during heart chamber formation. Endocardial expression of dp-ERK in the valve primordia and heart chambers may reflect differential cell growth associated with RTK signaling in the heart. dp-ERK localization in the epicardium, subepicardial fibroblasts, myocardial fibroblasts, and coronary vessels is consistent with MAPK activation in epicardial-derived cell lineages. The complex temporal,spatial regulation of dp-ERK in the heart supports diverse regulatory functions for RTK signaling in different cell populations, including the endocardium, myocardium, and epicardial-derived cells during cardiac organogenesis. Developmental Dynamics 230:773,780, 2004. © 2004 Wiley-Liss, Inc. [source] Impact of genetic defects on coronary atherosclerosis in patients suspected of having familial hypercholesterolaemiaEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2003O. S. Descamps Abstract Background In the present study we assessed whether the presence of genetic mutations typical of familial hypercholesterolaemia (FH) was associated with greater atherosclerosis in the coronary vessels in patients with severe hypercholesterolaemia and a family history of early cardiovascular disease. Materials and methods Two hundred and thirty-five patients selected for having severe hypercholesterolaemia and a family history of cardiovascular disease were classified as FH (57 men and 38 women) or non-FH (84 men and 56 women) according to a genetic analysis of the LDL-R or ApoB genes. Coronary atherosclerosis was evaluated by performing a thoracic CT scan and exercise stress testing. Results Familial hypercholesterolaemia individuals had a significantly higher prevalence of coronary calcification than the non-FH patients from among both the men (OR = 3·90; 95% CI 1·86,8·19; P < 0·001) and the women (OR = 2·34; 95% CI 1·01,5·48; P = 0·05). In exercise stress testing, ECG abnormalities suggestive of cardiac ischaemia were found with a higher prevalence in the FH patients than the non-FH patients from among both the men (OR 6·15; 95% CI 2·16,17·5; P < 0·001) and the women (OR 4·76; 95% CI 0·91,24·6; P = 0·06). All differences were statistically significant after adjusting for age and cholesterol and for most classical risk factors that differed between the FH and non-FH groups. Conclusion Among patients with severe hypercholesterolaemia and a family history of early cardiovascular disease, the presence of a genetically ascertained FH is associated with a higher prevalence of coronary artery calcifications and a positive exercise stress test. These results suggest that despite a similar phenotype, patients carrying mutations suggestive of FH may have a greater cardiovascular risk than patients without these mutations. [source] Migraine and Raynaud Phenomenon: Possible Late Complications of Kawasaki DiseaseHEADACHE, Issue 3 2002Cris S. Constantinescu MD Migraine and Raynaud phenomenon often coexist and may reflect similar vascular reactions. Both have been associated with vascular endothelial cell dysfunction. Kawasaki disease is a systemic vasculitis of unknown etiology that affects children and may lead to the formation of coronary artery aneurysms. Endothelial cell dysfunction has been demonstrated late in Kawasaki disease and is not restricted to coronary vessels. We report the case of a patient who developed typical migraine with aura and Raynaud phenomenon at the age of 14, 12 years after onset of Kawasaki disease. His migraine responded well to pizotifen, and both migraine and Raynaud phenomenon improved after initiation of treatment with valproic acid. We postulate that both migraine and Raynaud phenomenon in this case represent late consequences of Kawasaki disease and result from extracoronary endothelial dysfunction. [source] Coronary Artery Bypass Surgery Versus Percutaneous Coronary Artery Intervention in Patients on Chronic Hemodialysis: Does a Drug-Eluting Stent Have an Impact on Clinical Outcome?JOURNAL OF CARDIAC SURGERY, Issue 3 2009Susumu Manabe M.D. For chronic hemodialysis (HD) patients, however, the impact of DES on clinical outcome is yet to be determined. Forty-six consecutive chronic HD patients who underwent myocardial revascularization in our institute were retrospectively reviewed. Twenty-eight patients underwent coronary artery bypass surgery (CABG) and 18 patients underwent percutaneous coronary artery intervention (PCI). Patient characteristics were similar between the two groups. In the CABG group, bilateral internal thoracic artery (ITA) bypass grafting was performed in 27 patients and off-pump CABG was performed in 20 patients. In the PCI group, a DES was used in 12 patients. The number of coronary vessels treated per patient was higher in the CABG group (CABG: 4.25 ± 1.32 vs. PCI: 1.44 ± 0.78; p < 0.001). Two-year survival rates were similar between the two groups (CABG: 94.1% vs. PCI: 73.9%; p = 0.41), but major adverse cardiac event-free survival (CABG: 85.9% vs. PCI: 37.1%; p = 0.001) and angina-free survival (CABG: 84.9% vs. PCI: 28.9%; p < 0.001) rates were significantly higher in the CABG group. The one-year patency rate for the CABG grafts was 93.3% (left ITA: 100%, right ITA: 84.6%, sapenous vein: 90.9%, gastro-epiploic artery: 100%), and six-month restenosis rate for PCI was 57.1% (balloon angio-plasty: 75%, bare metal stent 40%, DES: 58.3%). Even in the era of DES, clinical results favored CABG. The difference in clinical results is due to the sustainability of successful revascularization. [source] Coronary Artery Stenting in Vessels with Reference Diameter < 3 MMJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 5 2000ALFRIED GERMING M.D. The study included 220 consecutive patients with coronary artery stenting. In 128 patients (60.8 ± 10.2 years, 68% men), a total of 184 stents were placed in coronary vessels with a reference diameter < 3 mm (group S). One hundred thirty-four stents were implanted in 92 patients (62.9 ± 9.8 years, 82.6% men) in vessels > 3 mm (group L). There was no significant difference according to clinical baseline characteristics. The primary end point of this retrospective study was the rate of periinterventional complications (death, stent thrombosis, myocardial infarction, urgent angioplasty, or surgical revascularization). The, secondary end point was the clinical and angiographic follow-ups (restenosis, recurrent angina, further revascularization) after 3 months. Cardiac complications occurred in group S in two (1.6%) patients, two stent thromboses with urgent angioplasty, one Q-wave and one non-Q-wave infarction. There was one (1.1%) event in group L, a stent thrombosis with Q-wave infarction and urgent angioplasty. Angiography at 3-month follow-up was performed in 148 patients. Restenosis occurred in group S in 31.8% and in group L in 21.7% (NS). Data according recurrent angina and recommended surgical revascularization did not differ between both groups. In group S, significantly more angioplasties of the stented lesion were performed (23/60 patients) compared to group L (6/88) (P = 0,015). Coronary artery stenting in vessels with a reference diameter < 3 mm can be performed without a high rate of periinterventional complications. Restenosis tends to be more frequent in the small vessel group, a higher rate of reangioplasties have to be expected. The clinical follow-up is comparable to a control group. [source] Bone marrow stem cells regenerate infarcted myocardiumPEDIATRIC TRANSPLANTATION, Issue 2003Donald Orlic Abstract: Heart disease is the leading cause of death in the United States for both men and women. Nearly 50% of all cardiovascular deaths result from coronary artery disease. Occlusion of the left coronary artery leads to ischemia, infarction, necrosis of the affected myocardial tissue followed by scar formation and loss of function. Although myocytes in the surviving myocardium undergo hypertrophy and cell division occurs in the border area of the dead tissue, myocardial infarcts do not regenerate and eventually result in the death of the individual. Numerous attempts have been made to repair damaged myocardium in animal models and in humans. Bone marrow stem cells (BMSC) retain the ability throughout adult life to self-renew and differentiate into cells of all blood lineages. These adult BMSC have recently been shown to have the capacity to differentiate into multiple specific cell types in tissues other than bone marrow. Our research is focused on the capacity of BMSC to form new cardiac myocytes and coronary vessels following an induced myocardial infarct in adult mice. In this paper we will review the data we have previously published from studies on the regenerative capacity of BMSC in acute ischemic myocardial injury. In one experiment donor BMSC were injected directly into the healthy myocardium adjacent to the injured area of the left ventricle. In the second experiment, mice were treated with cytokines to mobilize their BMSC into the circulation on the theory that the stem cells would traffic to the myocardial infarct. In both experimental protocols, the BMSC gave rise to new cardiac myocytes and coronary blood vessels. This BMSC-derived myocardial regeneration resulted in improved cardiac function and survival. [source] Vasculogenesis of the embryonic heart: Origin of blood island-like structuresTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2006Anna Ratajska Abstract The earliest vascular structures (blood island-like) in the embryonic heart are clusters of angioblasts and nucleated red blood cells (NRBCs), which differentiate into endothelial cells and erythrocytes, respectively. Our purpose was to define the area and chronology of NRBC appearance in the mouse embryonic heart at the stages before a patency between coronary vessels and peripheral circulation is established (10.5,13.5 dpc). Before and at the onset of vascularization, NBCs were not present within the proepicardium; however, Ter/119+ differentiating erythroblasts and single scattered CD45+ were found in the heart beginning from 10.5 dpc. The Ter/119+ cells were in close apposition to angioblasts (PECAM1+) and were recognized as components of blood island-like structures or vascular vesicles in transmission electron microscope and were located mostly in the subepicardium. Some of the NRBCs were not accompanied by angioblasts and located close to the endocardial endothelium or at the border of the endocardial endothelium or in the subepicardium. These erythroblasts were beginning to assemble with angioblasts. CD34+ NBCs as well as progenitor cells of erythroid lineage were not detected in the heart at these stages of development. The state of differentiation of NRBCs of blood islands was similar/the same as the morphology of circulating blood cells at the respective stages of embryo development. The presence of mature NRBCs in the subendocardial area and lack of progenitor cells of erythroid lineage within the heart indicate that erythroid commitment occurs outside the heart. We suggest that NRBCs enter the heart from the blood stream at 10.5,12 dpc independently from angioblasts. © 2006 Wiley-Liss, Inc. [source] Ex vivo hypothermic recirculatory adenoviral gene transfer to the transplanted pig heartTHE JOURNAL OF GENE MEDICINE, Issue 7 2006Keiji Oi Abstract Background To facilitate the application of adenoviral gene therapy in clinical heart transplantation, we developed an ex vivo hypothermic recirculatory adenoviral gene transfer method to the transplanted pig heart. Methods Experimental animals were assigned into three groups; controls, 1 × 108 plaque-forming units (pfu)/ml group and 1 × 109 pfu/ml group. During the 30 min gene transfer perfusion, 200 ml of University of Wisconsin solution containing the adenoviral vector was recirculated through the coronary vessels. The myocardial temperature was maintained below 4 °C and the perfusion pressure was adjusted at 50 mmHg. Results Cardiac myocyte transduction efficiencies in the 1 × 108 pfu/ml group were 0.04% and 0.07%, whereas transduction efficiencies in the 1 × 109 pfu/ml group were widely distributed from 0.45% to 22.62%. The gene transduction efficiency increased with the virus titer. Additionally, no difference in the transduction efficiency was observed between different segments of the left ventricle. The current gene transfer method at 1 × 109 pfu/ml of adenovirus titer enabled homogeneous gene transduction into the transplanted pig heart up to a maximum of 22.62%. Conclusions This model can be applied to a large isolated heart and will greatly facilitate the investigation of gene therapy in large animal models of heart transplantation. Copyright © 2006 John Wiley & Sons, Ltd. [source] An everolimus-eluting stent versus a paclitaxel-eluting stent in small vessel coronary artery disease: A pooled analysis from the SPIRIT II and SPIRIT III trials,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 1 2010Antonio L. Bartorelli MD Abstract Objectives: To evaluate the safety and efficacy of the XIENCE V everolimus-eluting stent compared to the TAXUS paclitaxel-eluting stent in small vessels. Backgroud: The XIENCE V everolimus-eluting stent (EES) has been shown to improve angiographic and clinical outcomes after percutaneous myocardial revascularization, but its performance in small coronary arteries has not been investigated. Methods: In this pooled analysis, we studied a cohort of 541 patients with small coronary vessels (reference diameter <2.765 mm) by using patient and lesion level data from the SPIRIT II and SPIRIT III studies. TAXUS Express (73% of lesions) and TAXUS Liberté (27% of lesions) paclitaxel-eluting stents (PES) were used as controls in SPIRIT II. In SPIRIT III, Taxus Express2 PES was the control. Results: Mean angiographic in-stent and in-segment late loss was significantly less in the EES group compared with the PES group, (0.15 ± 0.37 mm vs. 0.30 ± 0.44 mm; P = 0.011 for in-stent; 0.10 ± 0.38 mm vs. 0.21 ± 0.34 mm; P = 0.034 for in-segment). EES also resulted in a significant reduction in composite major adverse cardiac events at 1 year (19/366 [5.2%] vs. 17/159 [10.7%]; P = 0.037), due to fewer non-Q-wave myocardial infarctions and target lesion revascularizations. At 1 year, the rate of non-Q-wave myocardial infarction was significantly lower in the EES group compared with that of the PES group (6/366 [1.6%] vs. 8/159 [5.0%]; P = 0.037). Conclusions: In patients with small vessel coronary arteries, the XIENCE V EES was superior to the TAXUS PES. © 2010 Wiley-Liss, Inc. [source] A randomised controlled study comparing conventional and magnetic guidewires in a two-dimensional branching tortuous phantom simulating angulated coronary vesselsCATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 5 2007DPHIL, Steve Ramcharitar MRCP Objectives: To directly compare the magnetic navigation system (MNS) guidewires with conventional guidewires in branching tortuous phantoms with operators of varying MNS and percutaneous coronary intervention experience. Background: Vessel tortuosity, angulation, and side branches remain limiting factors in coronary interventions. The MNS addresses these limitations by precisely directing the tip of a magnetised guidewire in vivo aided by two permanent adjustable external magnets. Methods: Crossing and fluoroscopy times of six operators were evaluated in five tortuous Perspex® phantom vessels in three consecutive attempts. Standard guidewire (SG) usage was unrestricted. Two 2nd generation magnetic guidewires (MG) were used. Failure was noted if the cross was unsuccessful within 5 min. Results: The magnetic navigation was vastly superior to SG techniques with increasingly tortuous phantoms. It dramatically decreased both the crossing and fluoroscopy times with maximal reduction from 201.7 ± 111 to 36.4 ± 13 sec, P < 0.001 and 204.7 ± 24 to 47.2 ± 19 sec, P < 0.001, respectively. The MNS had a 98.8% procedural success rate compared to 68% with SG techniques. Moreover it considerably limited the amount of wire usage from 5.5 to 1.3. Operators with prior MG experience performed significantly better than those without, except in the simplest phantom where the difference was nonsignificant (33.8 ± 13 sec vs. 41.7 ± 17 sec, P = 0.2). Conclusion: MNS significantly reduces both the crossing and fluoroscopy times in tortuous coronary phantom models achieving excellent success rates with dramatic reductions in guidewire usage. Operators with prior MNS experience had an advantage over the inexperienced. © 2007 Wiley-Liss, Inc. [source] Risk of Heart Failure Due to a Combination of Mild Mitral Regurgitation and Impaired Distensibility of the Left Ventricle in Patients with Old Myocardial InfarctionCLINICAL CARDIOLOGY, Issue 12 2008Shu Inami MD Abstract Background Ischemic mitral regurgitation (MR) is a serious complication after myocardial infarction, and the incidence of heart failure (HF) increases as the severity of MR increases. However, little is known about the relationship between mild MR and HF in the patients with old myocardial infarction (OMI) and a normal ejection fraction (EF). Hypothesis We hypothesized that a combination of mild MR and impaired distensibility of the left ventricle may increase the risk of diastolic HF in the patients with OMI and a normal EF. Methods The relationship between HF and mild MR was retrospectively investigated in 62 patients with OMI and EF of > 50% on echocardiography. Results Of the 62 patients, 47 (76%) did not have HF and 15 (24%) had HF. There was a significant difference in the incidence of mild MR between the patients with and without HF (p < 0.0001): of the 47 patients without HF, mild MR was detected in 19, but all 15 patients with HF had mild MR. However, there were no significant differences in age, gender, infarct sites, diseased coronary vessels, peak CK level, and observation period between the 2 groups. An increased E-wave and the ratio of the E-wave to the A-wave (E/A), a reduction of the E-wave deceleration time, and an increased brain natriuretic peptide (BNP) level were significantly noted in HF patients with mild MR compared with patients without HF. Conclusions Even a mild MR may cause diastolic HF in patients with impaired distensibility of the left ventricle due to ischemic heart disease. 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