ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Ventricular thrombus formation is a frequent and potentially dangerous complication in patients with ischemic heart disease. Although transthoracic echocardiography (TTE) is generally used as diagnostic technique, we explored the role of contrast-enhanced (CE)-MRI to detect ventricular thrombi.Methods and Results—In 57 patients with acute myocardial infarction, chronic myocardial infarction, or ischemic cardiomyopathy, MRI was performed to evaluate ventricular function (CINE-MRI) and to depict presence of myocardial necrosis and/or scarring and no-reflow areas (CE-MRI). All studies were analyzed for concomitant ventricular thrombi. CE-MRI depicted 12 mural thrombi (3.1±2.9 cm3), located in left ventricular (LV) apex or adherent to anteroseptum, presenting as black, well-defined structures surrounded by bright contrast-enhanced blood. Thrombus formation on CE-MRI was related to larger end-diastolic volumes; lower ejection fractions; the region of delayed enhancement and lowest wall motion score, especially in left anterior descending coronary artery territory; and LV aneurysm formation. On CINE-MRI, thrombi were found in 6 patients. Nonvisualized thrombi were usually small (mean size 1.2±0.7 cm3). TTE depicted thrombi in 5. Nonvisualized lesions were most frequently located in LV apex and had a larger size than nonvisualized lesions on CINE-MRI (3.0±3.2 cm3). In 3 patients with suspected apical thrombus on TTE, MRI was normal.Conclusions—CE-MRI is not only an excellent technique to depict myocardial necrosis and scar tissue in patients with ischemic heart disease, but this study also suggests a better identification of LV thrombi than with presently used clinical imaging modalities, such as TTE.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Human urotensin II (UTN) has potent vasoactive and cardiostimulatory effects, acting on the G protein–linked receptor GPR14. Myocardial UTN expression is upregulated in heart failure, and UTN stimulates myocardial expression of the natriuretic peptides. We investigated plasma UTN levels in heart failure (HF; left ventricular systolic dysfunction) in comparison with plasma N-terminal pro-brain natriuretic peptide (N-BNP) levels.Methods and Results—N-BNP and UTN were measured in plasma from 126 patients with HF and 220 age- and sex-matched controls. Both peptides were elevated in plasma of HF patients and were correlated (rs=0.35,P<0.001). In contrast to N-BNP, there was no relationship of plasma UTN with New York Heart Association (NYHA) class. Although plasma N-BNP showed a positive relationship with age and female sex, there was no such age-dependent change in plasma UTN, and control women had lower levels compared with control men. Receiver operating characteristic curves for the diagnosis of HF had areas of 0.90 and 0.86 for N-BNP and UTN, respectively (P<0.001 for both). Receiver operating characteristic curve area for diagnosis of NYHA class I HF with UTN was better than that with N-BNP.Conclusions—Plasma UTN is elevated in HF, which suggests a pathophysiological role for this peptide. Plasma UTN may be a useful alternative to N-BNP in the diagnosis of HF, inasmuch as its levels are elevated irrespective of age, sex, or NYHA class.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Ischemic preconditioning reduces local tissue injury caused by subsequent ischemia-reperfusion (IR), but may also have a salutary effect on IR injury of tissues remote from those undergoing preconditioning. We tested the hypothesis that limb ischemia induces remote preconditioning, reduces endothelial IR injury in humans, and reduces experimental myocardial infarct size.Methods and Results—Endothelial IR injury of the human forearm was induced by 20 minutes of upper limb ischemia (inflation of a blood pressure cuff to 200 mm Hg) followed by reperfusion. Remote preconditioning was induced by three 5-minute cycles of ischemia of the contralateral limb. Venous occlusion plethysmography was used to assess forearm blood flow in response to acetylcholine at baseline and 15 minutes after reperfusion. Experimental myocardial infarction was achieved by 40 minutes of balloon occlusion of the left anterior descending artery in 15-kg pigs. Remote preconditioning was induced by four 5-minute cycles of lower limb ischemia. Triphenyltetrazolium staining was used to assess the extent of myocardial infarction. In the human study, the response to acetylcholine was significantly attenuated in the control group after 15 minutes’ reperfusion, but remote preconditioning prevented this reduction. Limb ischemia caused a significant reduction in the extent of myocardial infarction relative to the area at risk compared with control (26±9% versus 53±8%,P<0.05).Conclusion—Remote ischemic preconditioning prevents IR-induced endothelial dysfunction in humans and reduces the extent of myocardial infarction in experimental animals. Transient limb ischemia is a simple preconditioning stimulus with important potential clinical applications.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Statins are widely used to treat hypercholesterolemia and atherosclerotic disease. Noninvasive MRI allows serial monitoring of atherosclerotic plaque size changes. Our aim was to investigate the effects of lipid lowering with simvastatin on atherosclerotic lesions.Methods and Results—A total of 44 aortic and 32 carotid artery plaques were detected in 21 asymptomatic hypercholesterolemic patients at baseline. The effects of statin on these atherosclerotic lesions were evaluated as changes versus baseline in lumen area (LA), vessel wall thickness (VWT), and vessel wall area (VWA) by MRI. Maximal reduction of plasma total and LDL cholesterol by simvastatin (23% and 38% respectively;P<0.01 versus baseline) was achieved after ≈6 weeks of therapy and maintained thereafter throughout the study. Significant (P<0.01) reductions in maximal VWT and VWA at 12 months (10% and 11% for aortic and 8% and 11% for carotid plaques, respectively), without changes in LA, have been reported. Further decreases in VWT and VWA ranging from 12% to 20% were observed at 18 and 24 months. A slight but significant increase (ranging from 4% to 6%) in LA was seen in both carotid and aortic lesions at these later time points.Conclusion—The present study demonstrates that maintained lipid-lowering therapy with simvastatin is associated with significant regression of established atherosclerotic lesions in humans. Our observations indicate that lipid-lowering therapy is associated with sustained vascular remodeling and emphasize the need for longer-term treatment.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Although CD40 signaling participates in atherosclerosis, links between lipid risk factors and this inflammatory pathway remain obscure. Cardiovascular risk reduction by 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) may involve actions beyond lipid lowering, including reduced inflammation. Therefore, this study analyzed whether oxidized low-density lipoprotein (oxLDL) induces CD40/CD40L expression on cells implicated in atherogenesis and whether statins affect their expression in vitro as well as the expression of soluble CD40L (sCD40L) in vivo.Methods and Results—Treatment of human vascular endothelial and smooth muscle cells and mononuclear phagocytes with oxLDL augmented the basal expression of CD40 and CD40L mRNA and protein. In contrast, cerivastatin, atorvastatin, or simvastatin concentration-dependently diminished the constitutive as well as oxLDL- or cytokine-induced expression of the receptor/ligand dyad, an effect reversed by mevalonate. Patients treated with statins had diminished sCD40L plasma levels compared with untreated control patients (8.3±3.1 ng/mL [n=11] versus 13.1±2.5 ng/mL [n=16],P<0.05), supporting the clinical relevance of the in vitro observations. Platelet-enriched plasma of mice deficient in CD40L showed markedly delayed fibrin clot formation, suggesting a role for the ligand in blood coagulation and supporting the hypothesis that statin-mediated reduction in CD40/CD40L expression might limit thrombosis.Conclusions—OxLDL may promote expression of CD40 and CD40L in human atheroma. Statins may limit the expression of the CD40 receptor/ligand dyad in two ways, directly as well as through diminished lipoprotein levels. Thus, reduced CD40 signaling may account for some of the statins’ antiinflammatory action.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID

摘要:

Background—Neutrophils in unstable atherosclerotic lesions have not received much consideration, despite accumulating evidence suggesting a link between systemic inflammation and acute coronary syndromes.Methods and Results—Coronary artery segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI); 8 had a ruptured and 5 an eroded plaque. Patients (n=45) who had died of noncardiovascular diseases served as reference. Atherectomy specimens were obtained from 35 patients with stable angina pectoris (SAP) and from 32 patients with unstable angina pectoris (UAP). Antibodies against CD66b, elastase, myeloperoxidase, and CD11b identified neutrophils; CD10 identified neutral endopeptidase (NEP). CD66b-positive and NEP-positive neutrophils were counted and expressed as a number per square millimeter of tissue. All specimens with plaque rupture or erosion showed distinct neutrophil infiltration; the number did not differ between ruptured and eroded plaques. However, the number of NEP-positive neutrophils was significantly higher (P<0.0001) in ruptured plaques than in eroded plaques. UAP patients showed neutrophils in 14 of 32 culprit lesions; in SAP only 2 of 35 lesions contained neutrophils. The number of neutrophils and NEP-positive cells in patients with UAP was significantly higher (neutrophils,P<0.0005; NEP-positive cells,P<0.005) than in patients with SAP.Conclusions—The observations suggest that neutrophil infiltration is actively associated with acute coronary events. The high number of NEP-positive neutrophils in ruptured plaques, compared with eroded plaques, may reflect differences in the underlying pathophysiological mechanisms.

ISSN:0009-7322    

出版商:OVID    

年代:2002

数据来源: OVID