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Cardiovascular News |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1-2
Ruth SoRelle,
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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2. |
C-Reactive ProteinA Simple Test to Help Predict Risk of Heart Attack and Stroke |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 81-85
Paul Ridker,
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PDF (104KB)
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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3. |
Fetal Progression of Ebstein’s Anomaly |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 86-87
Marcy Schwartz,
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PDF (252KB)
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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4. |
Circulation Announcement PageSeptember 23, 2003 |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1419-1419
James Willerson,
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PDF (6KB)
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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5. |
A Novel Mechanism for Pulmonary Arterial Hypertension? |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1420-1421
John Cooke,
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PDF (41KB)
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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6. |
The Metabolic SyndromePractical Guide to Origins and Treatment: Part I |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1422-1424
Peter Wilson,
Scott Grundy,
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PDF (55KB)
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ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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7. |
Polymorphism in Glutamate-Cysteine Ligase Modifier Subunit Gene Is Associated With Impairment of Nitric Oxide–Mediated Coronary Vasomotor Function |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1425-1427
Shin-ichi Nakamura,
Seigo Sugiyama,
Daisuke Fujioka,
Ken-ichi Kawabata,
Hisao Ogawa,
Kiyotaka Kugiyama,
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摘要:
Background—The minor −588T allele of polymorphism −588C/T of a modifier subunit gene in glutamate-cysteine ligase (GCLM), a rate-limiting enzyme for glutathione (GSH) synthesis, was associated with lower plasma GSH levels and was a risk factor for myocardial infarction.Methods and Results—We examined effects of the −588C/T polymorphism on coronary arterial diameter and blood flow responses to intracoronary infusion of acetylcholine in 157 consecutive subjects who had normal coronary angiograms. In multivariate linear regression analysis with covariates including traditional risk factors, the minor −588T allele had an independent association with impaired dilation or enhanced constriction of epicardial coronary arteries in response to acetylcholine, and it was independently associated with blunted increase in coronary flow response to acetylcholine. In a subgroup of 59 consecutive subjects, constrictor responses of epicardial coronary diameter to intracoronary infusion ofNG-monomethyl-l-arginine, reflecting the presence of coronary nitric oxide (NO) bioactivity, had an inverse and independent association with the −588T allele in multivariate analysis.Conclusions—The −588T polymorphism of the GCLM gene causes a decrease in endothelial NO bioactivity, leading to impairment of endothelium-dependent vasomotor function in large and resistance coronary arteries. The GCL–GSH–NO axis may play a role in the defense system against coronary artery disease.
ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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8. |
Local Generation of C-Reactive Protein in Diseased Coronary Artery Venous Bypass Grafts and Normal Vascular Tissue |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1428-1431
Wolfram Jabs,
Elisabeth Theissing,
Martin Nitschke,
J.F. Bechtel,
Michael Duchrow,
Salah Mohamed,
Bernhard Jahrbeck,
Hans-Hinrich Sievers,
Jürgen Steinhoff,
Claus Bartels,
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摘要:
Background—Venous coronary artery bypass grafts (CABGs) are prone to accelerated atherosclerosis. In atherosclerotic diseases, serum C-reactive protein (CRP) levels have become an important diagnostic and prognostic marker. The origin of CRP in this setting remains to be elucidated.Methods and Results—Monoclonal anti-CRP identified CRP expression in medial and intimal &agr;-actin–positive smooth muscle cells (SMCs) of diseased CABGs with type V and VI lesions and also of native saphenous veins of atherosclerotic individuals. In addition, patent coronary arteries with type IV and V but not with type I through III lesions exhibited intense SMC staining for CRP. Calcified desobliterates of occluded coronary arteries with end-stage disease did not show SMC staining for CRP and were consistently negative for CRP mRNA, as detected by means of real-time polymerase chain reaction. However, CRP mRNA was expressed in 11 of 15 diseased CABGs and also in 10 of 15 native veins. By contrast, only 3 of 18 internal mammary and 4 of 12 radial arteries with virtually no atherosclerosis were positive for CRP mRNA.Conclusions—CRP is produced by SMCs of atherosclerotic lesions with active disease but not in end-stage plaques. The role of CRP constitutively expressed by normal vascular tissue in vein graft disease has yet to be elucidated.
ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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9. |
Novel Role for the Potent Endogenous Inotrope Apelin in Human Cardiac Dysfunction |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1432-1439
Mary Chen,
Euan Ashley,
David Deng,
Anya Tsalenko,
Alicia Deng,
Raymond Tabibiazar,
Amir Ben-Dor,
Brett Fenster,
Eugene Yang,
Jennifer King,
Michael Fowler,
Robert Robbins,
Frances Johnson,
Laurakay Bruhn,
Theresa McDonagh,
Henry Dargie,
Zohar Yakhini,
Philip Tsao,
Thomas Quertermous,
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摘要:
Background—Apelin is among the most potent stimulators of cardiac contractility known. However, no physiological or pathological role for apelin–angiotensin receptor-like 1 (APJ) signaling has ever been described.Methods and Results—We performed transcriptional profiling using a spotted cDNA microarray with 12 814 unique clones on paired samples of left ventricle obtained before and after placement of a left ventricular assist device in 11 patients. The significance analysis of microarrays and a novel rank consistency score designed to exploit the paired structure of the data confirmed that natriuretic peptides were among the most significantly downregulated genes after offloading. The most significantly upregulated gene was the G-protein–coupled receptor APJ, the specific receptor for apelin. We demonstrate here using immunoassay and immunohistochemical techniques that apelin is localized primarily in the endothelium of the coronary arteries and is found at a higher concentration in cardiac tissue after mechanical offloading. These findings imply an important paracrine signaling pathway in the heart. We additionally extend the clinical significance of this work by reporting for the first time circulating human apelin levels and demonstrating increases in the plasma level of apelin in patients with left ventricular dysfunction.Conclusions—The apelin-APJ signaling pathway emerges as an important novel mediator of cardiovascular control.
ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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10. |
Myeloperoxidase Serum Levels Predict Risk in Patients With Acute Coronary Syndromes |
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Circulation: Journal of the American Heart Association,
Volume 108,
Issue 12,
2003,
Page 1440-1445
Stephan Baldus,
Christopher Heeschen,
Thomas Meinertz,
Andreas Zeiher,
Jason Eiserich,
Thomas Münzel,
Maarten Simoons,
Christian Hamm,
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摘要:
Background—Polymorphonuclear neutrophils (PMNs) have gained attention as critical mediators of acute coronary syndromes (ACS). Myeloperoxidase (MPO), a hemoprotein abundantly expressed by PMNs and secreted during activation, possesses potent proinflammatory properties and may contribute directly to tissue injury. However, whether MPO also provides prognostic information in patients with ACS remains unknown.Methods and Results—MPO serum levels were assessed in 1090 patients with ACS. We recorded death and myocardial infarctions during 6 months of follow-up. MPO levels did not correlate with troponin T, soluble CD40 ligand, or C-reactive protein levels or with ST-segment changes. However, patients with elevated MPO levels (>350 &mgr;g/L; 31.3%) experienced a markedly increased cardiac risk (adjusted hazard ratio [HR] 2.25 [1.32 to 3.82];P=0.003). In particular, MPO serum levels identified patients at risk who had troponin T levels below 0.01 &mgr;g/L (adjusted HR 7.48 [95% CI 1.98 to 28.29];P=0.001). In a multivariate model that included other biochemical markers, troponin T (HR 1.99;P=0.023), C-reactive protein (1.25;P=0.044), vascular endothelial growth factor (HR 1.87;P=0.041), soluble CD40 ligand (HR 2.78;P<0.001), and MPO (HR 2.11;P=0.008) were all independent predictors of the patient’s 6-month outcome.Conclusions—In patients with ACS, MPO serum levels powerfully predict an increased risk for subsequent cardiovascular events and extend the prognostic information gained from traditional biochemical markers. Given its proinflammatory properties, MPO may serve as both a marker and mediator of vascular inflammation and further points toward the significance of PMN activation in the pathophysiology of ACS.
ISSN:0009-7322
出版商:OVID
年代:2003
数据来源: OVID
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