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  • 1
    Online-Ressource
    Online-Ressource
    Noninvasive Diagnosis of Ischemia-Induced Wall Motion Abnormalities With the Use of High-Dose Dobutamine Stress MRI : Comparison With Dobutamine Stress Echocardiography
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Vol. 99, No. 6 ( 1999-02-16), p. 763-770
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 99, No. 6 ( 1999-02-16), p. 763-770
    Kurzfassung: Background —The analysis of wall motion abnormalities with dobutamine stress echocardiography (DSE) is an established method for the detection of myocardial ischemia. With ultrafast magnetic resonance tomography, identical stress protocols as used for echocardiography can be applied. Methods and Results —In 208 consecutive patients (147 men, 61 women) with suspected coronary artery disease, DSE with harmonic imaging and dobutamine stress magnetic resonance (DSMR) (1.5 T) were performed before cardiac catheterization. DSMR images were acquired during short breath-holds in 3 short-axis views and a 4- and a 2-chamber view (gradient echo technique). Patients were examined at rest and during a standard dobutamine-atropine scheme until submaximal heart rate was reached. Regional wall motion was assessed in a 16-segment model. Significant coronary heart disease was defined as ≥50% diameter stenosis. Eighteen patients could not be examined by DSMR (claustrophobia 11 and adipositas 6) and 18 patients by DSE (poor image quality). Four patients did not reach target heart rate. In 107 patients, coronary artery disease was found. With DSMR, sensitivity was increased from 74.3% to 86.2% and specificity from 69.8% to 85.7% (both P 〈 0.05) compared with DSE. Analysis for women yielded similar results. Conclusions —High-dose dobutamine magnetic resonance tomography can be performed with a standard dobutamine/atropine stress protocol. Detection of wall motion abnormalities by DSMR yields a significantly higher diagnostic accuracy in comparison to DSE.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.99.6.763
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 1999
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 2
    Online-Ressource
    Online-Ressource
    Spectrum of clinical phenotypes and gene variants in cardiac myosin-binding protein C mutation carriers with hypertrophic cardiomyopathy
    Elsevier BV ; 2001
    In:  Journal of the American College of Cardiology Vol. 38, No. 2 ( 2001-08), p. 322-330
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 38, No. 2 ( 2001-08), p. 322-330
    Materialart: Online-Ressource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(01)01387-0
    RVK:
    XA 17760
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 2001
    ZDB Id: 1468327-1
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 3
    Online-Ressource
    Online-Ressource
    Is the medical literature an accurate source for estimating the survival of patients with recurrent ischemia after coronary artery bypass grafting?
    Elsevier BV ; 1996
    In:  Journal of the American College of Cardiology Vol. 27, No. 2 ( 1996-02), p. 263-
    Details
    In: Journal of the American College of Cardiology, Elsevier BV, Vol. 27, No. 2 ( 1996-02), p. 263-
    Materialart: Online-Ressource
    ISSN: 0735-1097
    URL: Article
    DOI: 10.1016/S0735-1097(96)81941-3
    RVK:
    XA 17760
    Sprache: Englisch
    Verlag: Elsevier BV
    Publikationsdatum: 1996
    ZDB Id: 1468327-1
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    Abstract 2468: Chronic Treatment Of Hypertensive Patients With The At1 Receptor Blocker Losartan Results In Sufficient Serum Levels Of The Metabolite Exp3179 Exhibiting Pparγ-stimulating Properties
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Vol. 118, No. suppl_18 ( 2008-10-28)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 118, No. suppl_18 ( 2008-10-28)
    Kurzfassung: The losartan metabolite EXP3174 exhibits angiotensin II receptor 1 (AT1R)-blocking properties, whereas the metabolite EXP3179 potently induces the activity of the insulin-sensititzing peroxisome proliferator-activated receptor γ (PPARγ) as a partial agonist in vitro.. We investigated, whether hypertensive patients chronically treated with losartan exhibit sufficient plasma levels of EXP3179 to activate PPARγ in monocytes derived from losartan-treated patients. Hypertensive patients (n=9) treated with losartan (100mg/daily during at least the past two months), and control patients (n=7) with no chronic AT1R-blocking therapy were included. Blood was taken from all individuals and serum was prepared. Monocytes were extracted by negative isolation using a Dynal Monocyte Kit, followed by RNA-isolation and measurement of PPARγ target gene expression (CD36, ABC transporter G1 (ABCG1)) by quantitative real-time RT-PCR. Losartan-treated patients received 100mg orally, and serum was prepared 2, 4, and 6h after drug ingestion for HPLC-based determination of losartan and losartan metabolites (EXP3174/ EXP3179) in serum. Serum levels were standardized to measurements of purified compounds. Chronic treatment with losartan resulted in basal levels (24h after drug intake) of losartan, EXP3174 and EXP3179 of 382,5ng/ml, 97,0ng/ml and 164,2ng/ml, respectively. Levels of both, EXP3174 and EXP3179 were time-dependently enhanced in serum with a maximum 2h after drug intake (2619,6ng/ml, 980,9ng/ml, respectively). In order to evaluate the possible agonistic property of chronic EXP3179 serum levels on PPARγ, we determined the transcript levels of CD36 and ABCG1 as known PPARγ target genes. Gene expression was significantly upregulated in patients chronically treated with losartan by 5.26±1.55- and 188.54±56.92-fold for CD36 and ABCG1 (p=0.039, p=0.023 vs. control patients, respectively). This is the first clinical description of monocytic PPARγ-target gene regulation by chronic treatment with losartan, which likely is mediated by its metabolite EXP3179. Our data show that sufficient serum levels of EXP3179 are present under losartan treatment. PPARγ activation by AT1R-blockers may translate into synergistic beneficial actions in monocytes.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.118.suppl_18.S_731-c
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2008
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
  • 5
    Online-Ressource
    Online-Ressource
    Regulation and Differential Expression of Neutral Endopeptidase 24.11 in Human Endothelial Cells
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Hypertension Vol. 26, No. 2 ( 1995-08), p. 230-235
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 26, No. 2 ( 1995-08), p. 230-235
    Kurzfassung: Abstract Neutral endopeptidase 24.11, a membrane-bound metallopeptidase, cleaves and degrades vasoactive peptides such as atrial natriuretic peptide, endothelin, angiotensin I, substance P, and bradykinin. Therefore, the presence of this metallopeptidase may contribute to the regulation of vascular tone and local inflammatory responses in the vascular endothelium and elsewhere. We determined neutral endopeptidase in cultured human endothelial cells from different vascular beds and studied its regulation by protein kinase C. Neutral endopeptidase was detected in all cultured endothelial cell types. Lowest concentrations were measured in human endothelial cells from umbilical veins (360±14 pg/mg protein), followed by pulmonary and coronary arteries; higher concentrations were found in endothelial cells from the cardiac microcirculation (1099±73 pg/mg protein). Neutral endopeptidase content increased during cell growth but was not affected by endothelial cell growth factor or modifications of the growth medium. Stimulation of protein kinase C with 1-oleoyl-2-acetyl-rac-glycerol (0.1 to 1 μmol/L) and phorbol 12-myristate 13-acetate (0.01 to 0.1 μmol/L) induced a time- and concentration-dependent increase of endothelial cells that was inhibited by cycloheximide (5 μmol/L), an inhibitor of protein synthesis. Incubation with phospholipase C (1 μmol/L) and thrombin (10 IU/mL) induced upregulation of neutral endopeptidase, resulting in 158±26% and 150±22% increases, respectively, compared with controls. The thrombin effect was inhibited by calphostin C (1 μmol/L), an inhibitor of protein kinase C. Endothelial neutral endopeptidase is constitutively expressed in endothelial cells from different origins and is inducible by thrombin via activation of the protein kinase C pathway.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.26.2.230
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 1995
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    Magnetic Resonance Perfusion Measurements for the Noninvasive Detection of Coronary Artery Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Circulation Vol. 108, No. 4 ( 2003-07-29), p. 432-437
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 108, No. 4 ( 2003-07-29), p. 432-437
    Kurzfassung: Background— With MRI, an index of myocardial perfusion reserve (MPRI) can be determined. We assessed the value of this technique for the noninvasive detection of coronary artery disease (CAD) in patients with suspected CAD. Methods and Results— Eighty-four patients referred for a primary diagnostic coronary angiography were examined with a 1.5 T MRI tomograph (Philips-ACS). For each heartbeat, 5 slices were acquired during the first pass of 0.025 mmol gadolinium-diethylenetriamine pentaacetic acid/kg body weight before and during adenosine vasodilation by using a turbo-gradient echo/echo-planar imaging-hybrid sequence. MPRI was determined from the alteration of the upslope of the myocardial signal intensity curves for 6 equiangular segments per slice. Receiver operating characteristics were performed for different criteria to differentiate ischemic and nonischemic segments. Prevalence of CAD was 51%. Best results were achieved when only the 3 inner slices were assessed and a threshold value of 1.1 was used for the second smallest value as a marker for significant CAD. This approach yielded a sensitivity of 88%, specificity of 90%, and accuracy of 89%. Conclusion— The determination of MPRI with MRI yields a high diagnostic accuracy in patients with suspected CAD.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000080915.35024.A9
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2003
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    Abstract 17314: Impact of Mild Therapeutic Hypothermia on Platelet Inhibition in Acute Coronary Syndrome
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Circulation Vol. 130, No. suppl_2 ( 2014-11-25)
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 130, No. suppl_2 ( 2014-11-25)
    Kurzfassung: Background: Mild therapeutic hypothermia (MTH) improves outcome for patients with acute coronary syndrome (ACS) after cardiac arrest (CA). Previous data point to an interaction between hypothermia and drug metabolism, thus potentially impacting on platelet function under antiplatelet therapy. Purpose: The aim of the study is to determine clopidogrel metabolism and platelet function in clopidogrel naïve ACS patients treated with mild hypothermia (33°C, n=12) compared with ACS patients (troponin positive) with normal body temperature (n=14). Methods: Platelet function was measured by light transmittance aggregometry (LTA), multiple electrode platelet aggregometry (MEA) and VASP phosphorylation analysis before, 2h, 4h and 24h after administration of a 600 mg clopidogrel loading dose. Furthermore, plasma concentrations of clopidogrel, the active thiol metabolite and the inactive carboxyl metabolite were determined. All patients were screened for CYP2C19*2 polymorphism and scheduled for PCI. Mild hypothermia was carried out according to current guidelines for 24 hours at a target temperature of 33°C. Results: Plasma concentration of clopidogrel and metabolites were lower in the MTH group after 2h and 4h, respectively (all p 〈 0.005). All platelet function tests showed an attenuated response to clopidogrel with respect to baseline platelet activity in the MTH group. This was significant for VASP analysis and LTA (p 〈 0.05). Moreover, there was no difference in genotype and platelet function determined ex vivo with 33°C and 37°C, respectively. Conclusion: Inhibition of platelet function is decreased under MTH, presumably due to a diminished clopidogrel absorption and metabolization. Thus, these patients might have a higher risk for cardiovascular events despite antiplatelet therapy.
    Materialart: Online-Ressource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/circ.130.suppl_2.17314
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2014
    ZDB Id: 1466401-X
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
    Online-Ressource
    Online-Ressource
    Angiotensin II Induces Migration and Pyk2/Paxillin Phosphorylation of Human Monocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Hypertension Vol. 37, No. 2 ( 2001-02), p. 587-593
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 37, No. 2 ( 2001-02), p. 587-593
    Kurzfassung: Angiotensin (Ang) II has been shown to enhance the development of atherosclerotic lesions. Migration of monocytes is an early critical step in the atherosclerotic process. To elucidate mechanisms by which Ang II promotes atherogenesis, we investigated its effects on human monocyte migration. Ang II induced migration of human peripheral blood monocytes (HPBM) and human THP-1 monocytes at concentrations between 0.01 and 1 μmol/L, with a 3.6±0.6-fold induction in HPBM and a 4.8±0.9-fold induction in THP-1 cells at 1 μmol/L Ang II (both P 〈 0.01 versus unstimulated cells). Addition of the Ang II receptor type 1 (AT1-R) antagonist losartan (1 to 100 μmol/L) suppressed Ang II–induced migration of HPBM and THP-1 monocytes in a dose-dependent manner, demonstrating an AT1-R–mediated mechanism. Ang II–directed migration was also blocked by the Src kinase inhibitor PP2 (10 μmol/L), by the extracellular-regulated protein kinase (ERK 1/2) inhibitor PD98059 (30 μmol/L), and by the p38-MAPK inhibitor SB203580 (10 μmol/L), indicating that Src, ERK 1/2, and p38 are all involved in Ang II–induced migration of HPBM and human THP-1 monocytes. The proline-rich tyrosine kinase 2 (Pyk2) and paxillin are 2 cytoskeleton-associated proteins involved in cell movement, phosphorylated by Ang II in other cell types, and abundantly expressed in monocytes. Ang II (1 μmol/L) induced Pyk2 and paxillin phosphorylation in human THP-1 monocytes, peaking after 10 minutes for Pyk2 with a 6.7±0.9-fold induction and after 2 minutes for paxillin with a 3.2±0.4-fold induction. Ang II–induced phosphorylation of both proteins was suppressed by losartan and the Src inhibitor PP2, whereas no effect was observed with PD98059 and SB203580. This study demonstrates a novel proatherogenic action of Ang II on human monocytes by stimulating their migration, through an AT1-R–dependent process, involving signaling through Src, ERK 1/2, and p38. Furthermore, the promigratory actions of Ang II in human monocytes are associated with the phosphorylation of 2 cytoskeleton-associated proteins, Pyk2 and paxillin.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.37.2.587
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2001
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
    Online-Ressource
    Online-Ressource
    Angiotensin II and α v β 3 Integrin Expression in Rat Neonatal Cardiac Fibroblasts
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Hypertension Vol. 35, No. 4 ( 2000-04), p. 978-984
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 35, No. 4 ( 2000-04), p. 978-984
    Kurzfassung: Abstract —We recently demonstrated that α v β 3 integrins are involved in the mechanisms of angiotensin II (Ang II)–induced DNA synthesis and collagen gel contractions in rat cardiac fibroblasts (CFBs), cellular mechanisms that are relevant for cardiac remodeling. The aim of the present study was to elucidate the effect of Ang II and other growth factors on the regulation of the α v β 3 integrins in fibroblasts from neonatal rat hearts. The α v β 3 integrin receptor expression was significantly increased ( P 〈 0.05) at the mRNA level after treatment with Ang II, transforming growth factor-β 1 (TGF-β 1 ), and platelet-derived growth factor (PDGF) for 8 and 16 hours. The surface expression of the α v and β 3 integrin subunits was elevated after 32 and 48 hours ( P 〈 0.05) as determined with flow cytometry. To investigate fibroblast motility, we performed chemotaxis experiments with transwell chambers. Ang II was chemotactic for CFBs, as tested with checkerboard experiments. The chemotactic effect was concentration dependent and was completely blocked by Ang II type 1 receptor blockers but not by Ang II type 2 receptor blocker PD 123319. Ang II– and PDGF-BB–mediated chemotaxis could be significantly inhibited by RGD peptides and the blocking antibodies against α v β 3 integrin (both P 〈 0.01). Adhesion of CFBs to vitronectin was partially inhibited by an antibody to α v β 3 integrin but was mainly mediated by an α v β 5 integrin. Relevant in vivo expression of α v β 3 integrin by CFBs was confirmed with in situ hybridization with probes for α v and β 3 mRNA in rat hearts. The present study demonstrates that the expression of α v β 3 integrin is augmented by Ang II, PDGF, and TGF-β 1 in neonatal CFBs. Furthermore, this integrin is involved in the chemotaxis, motility, and adhesion of CFBs. The present findings support the current concept that integrins participate in the control of fibroblast behavior during cardiac remodeling mechanisms.
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.35.4.978
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2000
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
    Online-Ressource
    Online-Ressource
    Aortic Stiffness, Impaired Fasting Glucose, and Aging
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Hypertension Vol. 55, No. 1 ( 2010-01), p. 18-20
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 55, No. 1 ( 2010-01), p. 18-20
    Materialart: Online-Ressource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.109.135897
    Sprache: Englisch
    Verlag: Ovid Technologies (Wolters Kluwer Health)
    Publikationsdatum: 2010
    ZDB Id: 2094210-2
    Standort Signatur Einschränkungen Verfügbarkeit
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    Online-Ressource
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