|
1. |
CirculationElectronic PagesJuly 2, 2002 |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 1-1
James Willerson,
Preview
|
PDF (6KB)
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
2. |
Cardiac Chimerism as a Mechanism for Self-RepairDoes It Happen and If So to What Degree? |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 2-4
Doris Taylor,
Ralph Hruban,
E. Rodriguez,
Pascal Goldschmidt-Clermont,
Preview
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
3. |
Health Status and Clinical PracticeWhen Will They Meet? |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 5-7
John Rumsfeld,
Preview
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
4. |
Clinical Implications of Cardiac Ryanodine Receptor/Calcium Release Channel Mutations Linked to Sudden Cardiac Death |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 8-10
Andrew Marks,
Preview
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
5. |
And the Answer Is, It Doesn’t Much Matter |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 11-13
David Holmes,
Bernard Gersh,
Preview
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
6. |
Atrial Fibrillation |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 14-16
Johan Waktare,
Preview
|
PDF (65KB)
|
|
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
7. |
Smooth Muscle Cells, But Not Myocytes, of Host Origin in Transplanted Human Hearts |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 17-19
Ruchira Glaser,
Min Lu,
Navneet Narula,
Jonathan Epstein,
Preview
|
PDF (265KB)
|
|
摘要:
Background—There is increasing evidence to support a role for stem cells in the regeneration and repair of the human cardiovascular system. However, significant controversy still remains about the extent of chimerism present in blood vessels and myocytes of transplanted human hearts.Methods and Results—We investigated the contribution of infiltrating host cells to human cardiac allografts by evaluating the origin of vascular smooth muscle cells and cardiac myocytes in hearts after orthotopic cardiac transplantation. Smooth muscle cells were identified in pathological human coronary artery specimens with antibodies against smooth muscle &agr;-actin. DNA in situ hybridization for the human Y chromosome was then performed on the same samples to identify cells of male origin. Both myocytes and vascular smooth muscle cells were examined for the presence of the Y chromosome in sex-mismatched specimens. In positive control samples, 34.7% of nuclei contained a detectable Y chromosome; in sex-mismatched samples, 2.6% of the smooth muscle cells examined were of host origin. The Y chromosome in myocyte nuclei in male positive controls was detected; however, despite examination of >6000 myocyte nuclei in sex-mismatched specimens, we were unable to detect any nuclei with the clear presence of the Y chromosome.Conclusions—Vascular smooth muscle cells of infiltrating host cell origin can be found in human cardiac allografts. However, unlike prior reports, we found no evidence that chimerism is present in cardiac myocytes.
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
8. |
Simvastatin Reduces Neointimal Thickening in Low-Density Lipoprotein Receptor–Deficient Mice After Experimental Angioplasty Without Changing Plasma Lipids |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 20-23
Zhiping Chen,
Tatsuya Fukutomi,
Alexandre Zago,
Raila Ehlers,
Patricia Detmers,
Samuel Wright,
Campbell Rogers,
Daniel Simon,
Preview
|
PDF (168KB)
|
|
摘要:
Background—Statins exert antiinflammatory and antiproliferative actions independent of cholesterol lowering. To determine whether these actions might affect neointimal formation, we investigated the effect of simvastatin on the response to experimental angioplasty in LDL receptor–deficient (LDLR−/−) mice, a model of hypercholesterolemia in which changes in plasma lipids are not observed in response to simvastatin.Methods and Results—Carotid artery dilation (2.5 atm) and complete endothelial denudation were performed in male C57BL/6J LDLR−/−mice treated with low-dose (2 mg/kg) or high-dose (20 mg/kg) simvastatin or vehicle subcutaneously 72 hours before and then daily after injury. After 7 and 28 days, intimal and medial sizes were measured and the intima to media area ratio (I:M) was calculated. Total plasma cholesterol and triglyceride levels were similar in simvastatin- and vehicle-treated mice. Intimal thickening and I:M were reduced significantly by low- and high-dose simvastatin compared with vehicle alone. Simvastatin treatment was associated with reduced cellular proliferation (BrdU), leukocyte accumulation (CD45), and platelet-derived growth factor–induced phosphorylation of the survival factor Akt and increased apoptosis after injury.Conclusions—Simvastatin modulates vascular repair after injury in the absence of lipid-lowering effects. Although the mechanisms are not yet established, additional research may lead to new understanding of the actions of statins and novel therapeutic interventions for preventing restenosis.
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
9. |
Interleukin-18 Is a Strong Predictor of Cardiovascular Death in Stable and Unstable Angina |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 24-30
Stefan Blankenberg,
Laurence Tiret,
Christoph Bickel,
Dirk Peetz,
François Cambien,
Jürgen Meyer,
Hans Rupprecht,
Preview
|
PDF (145KB)
|
|
摘要:
Background—Interleukin (IL)-18 plays a central role in orchestrating the cytokine cascade and accelerates atherosclerosis and plaque vulnerability in animal models. However, epidemiological data evaluating the role of IL-18 levels in atherosclerosis are lacking.Methods and Results—In a prospective study of 1229 patients with documented coronary artery disease, we measured baseline serum concentrations of IL-18 and other markers of inflammation. During the follow-up period (median, 3.9 years), 95 patients died of cardiovascular causes. Median serum concentrations of IL-18 were significantly higher among patients who had a fatal cardiovascular event than among those who did not (68.4 versus 58.7 pg/mL;P<0.0001). The hazard risk ratio of future cardiovascular death increased with increasing quartiles of IL-18 (hazard risk ratio, 1.46; 95% CI 1.21 to 1.76;Pfor trend <0.0001). After adjustment for most potential confounders, including the strong predictor ejection fraction as well as the inflammatory variables IL-6, high-sensitive C-reactive protein, and fibrinogen, this relation remained almost unchanged, such that patients within the highest quartile of IL-18 had a 3.3-fold increase in hazard risk compared with those in the first quartile (95% CI, 1.3 to 8.4,P=0.01). This relation was observed in patients with stable angina and patients with unstable angina at baseline.Conclusions—Serum IL-18 level was identified as a strong independent predictor of death from cardiovascular causes in patients with coronary artery disease regardless of the clinical status at admission. This result strongly supports recent experimental evidence of IL-18–mediated inflammation leading to acceleration and vulnerability of atherosclerotic plaques.
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
10. |
Cardiomyocytes of Noncardiac Origin in Myocardial Biopsies of Human Transplanted Hearts |
|
Circulation: Journal of the American Heart Association,
Volume 106,
Issue 1,
2002,
Page 31-35
Patrick Müller,
Peter Pfeiffer,
Jörg Koglin,
Hans-Joachim Schäfers,
Ute Seeland,
Ingrid Janzen,
Steffi Urbschat,
Michael Böhm,
Preview
|
PDF (486KB)
|
|
摘要:
Background—Cell replacement therapy with stem cells able to differentiate into cardiomyocytes has been discussed as a method for remodeling damaged myocardium. A physiological or pathophysiological situation in which this phenomenon might be relevant is not known. We studied the origin of cardiomyocytes in myocardial biopsies of male patients that had undergone sex-mismatched cardiac transplantation to determine whether cells containing a Y chromosome (and therefore being of recipient origin) are able to differentiate into cardiomyocytes.Methods and Results—Myocardial biopsies (n=21) were obtained from the right ventricles of male patients (n=13) who had undergone sex-mismatched heart transplantation. Tissue from 1 nontransplanted male and myocardial biopsies from sex-matched heart–transplanted patients served as controls. Cells from donor and recipient origins were identified by fluorescence in situ hybridization with the use of specific probes for X and Y chromosomes on paraffin sections of the biopsies. Cell types were identified by using immunostaining procedures on the same tissue sections. Cardiomyocytes of recipient origin were detected in 8 of 13 male recipients of female hearts. They were connected by gap junctions with adjacent myocytes. Of the cardiomyocyte nuclei, 0.16±0.04% (mean±SEM, median 0.09%) contained the Y-chromosomal marker. There was no detectable correlation with the extent or number of rejection episodes, time of transplantation, or medical treatment regimen.Conclusions—These results show that regeneration by cells of noncardiac origin (differentiated into cardiomyocytes and physiologically linked to neighboring myocytes) can be detected even in small myocardial biopsies. This may lead to new diagnostic and therapeutic strategies in the treatment of myocardial infarction, inflammatory heart disease, and/or heart failure.
ISSN:0009-7322
出版商:OVID
年代:2002
数据来源: OVID
|
|