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  • Ovid Technologies (Wolters Kluwer Health)  (11)
  • 1
    Online Resource
    Online Resource
    Distribution of coronary artery disease. Prediction by echocardiography.
    Ovid Technologies (Wolters Kluwer Health) ; 1976
    In:  Circulation Vol. 54, No. 5 ( 1976-11), p. 724-729
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 54, No. 5 ( 1976-11), p. 724-729
    Abstract: To assess the sensitivity of standard echocardiography in detecting ventricular motion abnormalities in patients with coronary artery disease (CAD) without prior myocardial infarction, 56 consecutive patients with a history of angina pectoris were studied during an angina-free period. In the 48 patients with adequate echocardiograms, the amplitude of septal and posterior wall motion in the high, mid, and low left ventricle was determined and used to predict prospectively in a blinded fashion the sites of angiographically-determined CAD. Twenty-eight of 35 patients (80%) with disease of the left anterior descending artery (LAD) had diminished interventricular septal motion (P less than 0.001) and 14 of 27 patients (52%) with disease of posterior vessels had diminished posterior wall motion on echocardiogram. When abnormalties of echocardiographic wall motion were compared with left ventriculography, the results were similar. Echocardiography may aid in predicting the presence and distribution of CAD, especially LAD disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.54.5.724
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1976
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
    Online Resource
    PB2012: A PHASE 2 MULTIARM STUDY OF MAGROLIMAB COMBINATIONS IN PATIENTS WITH RELAPSED/REFRACTORY MULTIPLE MYELOMA
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  HemaSphere Vol. 6 ( 2022-06), p. 1883-1884
    Details
    In: HemaSphere, Ovid Technologies (Wolters Kluwer Health), Vol. 6 ( 2022-06), p. 1883-1884
    Type of Medium: Online Resource
    ISSN: 2572-9241
    URL: Article
    DOI: 10.1097/01.HS9.0000850880.23639.66
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2922183-3
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  • 3
    Online Resource
    Online Resource
    Congenital absence of the left circumflex coronary artery in the systolic click syndrome.
    Ovid Technologies (Wolters Kluwer Health) ; 1975
    In:  Circulation Vol. 52, No. 3 ( 1975-09), p. 490-496
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 52, No. 3 ( 1975-09), p. 490-496
    Abstract: The anatomy of the coronary artery circulation was examined by means of selective coronary arteriography in 19 patients, evaluated because of disabling chest pain and ECG abnormalities, with typical clinical findings of the systolic click syndrome (SCS). In 17 (89.5%), the elft circumflex coronary artery (LCCA) was absent; a single marginal branch arose from the left main vessel, but no vessel was present in or near the atrioventricular (A-V) groove. In contrast, the LCCA was identified in 74 of 78 control patients (94.9%) considered to have representative normal distribution of coronary artery branches, All but two patients with SCS exhibited reduced contraction of the segment of left ventricular (LV) myocardium surrounding the mitral valve ring (extent of systolic diameter decrease 1.4 +/- 3.1% vs normal 31.8 +/- 3.4%, P lwss than 0.001), as well as of the LV inflow tract (diameter decreasce 16.2 +/- 2.5% vs normal 38.6 +/- 1.8% P less than 0.001); both of these regions of the left ventricle derive their vascular supply from the LCCA, An identical segmental LV contraction disorder was observed in seven patients with functionally single vessel occlusive coronary artery disease involving the LCCA, An identical finding in this study was a relatively high incidence of absent LCCA (42%) in 19 patients with atypical angina and normal coronary arteriograms. It is concluded that a congenital anomaly of the coronary circulation, with absent LCCA, may be responsible for segmental myocardial dysfunction in some patients with SCS. In turn, this segmental contraction disorder may determine functional abnormality of the mitral valve apparatus.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.52.3.490
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1975
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Diffuse coronary artery disease in diabetic patients: fact or fiction?
    Ovid Technologies (Wolters Kluwer Health) ; 1978
    In:  Circulation Vol. 57, No. 1 ( 1978-01), p. 133-136
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 57, No. 1 ( 1978-01), p. 133-136
    Abstract: To compare angiographically-determined coronary artery disease in diabetic patients with controls, 1,653 patients coming to cardiac catheterization were reviewed retrospectively to find 37 diabetic and 79 control patients matched for sex, age (+/- 3 years), and risk factors (hypertension, hyperlipidemia, and smoking). The severity of coronary artery disease was assessed using an angiographic grading system. The following results were obtained: 16 of 37 diabetic patients (43%) had three-vessel disease compared to 20 of 79 controls (25%). Seventy-six of 111 (68%) diabetic vessels were diseased compared to 110 of 237 control vessels (46%) (P less than 0.005). The total coronary score reflecting total extent of disease for diabetic patients was 371 (mean 10.0 +/- (SEM) compared to 594 for controls (mean 7.5 +/- 0.7, (P less than 0.01). Diabetic patients had a statistically similar number of diffusely diseased vessels as controls (28% vs 22%). There were only three of 76 diabetic vessels (4%) considered inoperable compared to seven of 110 (6%) control vessels. We conclude that diabetic patients with chest pain have more coronary artery disease than nondiabetics, but no more diffuse or inoperable disease.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.57.1.133
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1978
    detail.hit.zdb_id: 1466401-X
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  • 5
    Online Resource
    Online Resource
    Effects of treatment with pyruvate and tromethamine in experimental myocardial ischemia.
    Ovid Technologies (Wolters Kluwer Health) ; 1976
    In:  Circulation Research Vol. 39, No. 3 ( 1976-09), p. 378-387
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 39, No. 3 ( 1976-09), p. 378-387
    Abstract: Failure of glycolysis to increase sufficiently to supply optimal levels of energy production in ischemic heart muscle is due in part to the cummulative restrainst of acidosis on rate-limiting enzymes, particularly glyceraldehyde-3-phosphate dehydrogenase. In an effort to modify this inhibition and salvage jeopardized myocardium, treatment with excess levels of pyruvate and tromethamine (Tris), designed to buffer intracellular hydrogen ion accumulations and improve the oxidation-reduction ratio, NAD+/NADH, was tested in 59 swine hearts in two separate preparations of global and regional ischemia. Global ischemia, per se, caused hemodynamic deterioration and shortened survival time (44.3 +/- 3.1 minutes). Myocardial oxygen consumption, fatty acid oxidation, and glucose uptake were all significantly (P less than 0.001) reduced as were estimates of glycolysis and tissue stores of creatine phosphate and ATP (P less than 0.01). Although treatment with Tris alone was inconclusive, administrations of pyruvate (40-50 mM) buffered with Tris (added directly into the coronary perfusate) effected an improvement in mechanical function and a significant prolongation in survival time (56.9 +/- 2.6 minutes. P less than 0.01). Glycogenolysis was enhanced and levels of key glycolytic intermediates were reduced, suggesting an acceleration of glycolytic flux. Excess levels of pyruvate (1.52 +/- 0.48 mumol/ml of coronary perfusate) provided added substrate for oxidation and led to a greater than 5-fold incrase in rates of pyruvate decarboxylation as compared to untreated ischemic hearts...
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.39.3.378
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1976
    detail.hit.zdb_id: 1467838-X
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  • 6
    Online Resource
    Online Resource
    Negative-Feedback Loop Attenuates Hydrostatic Lung Edema via a cGMP-Dependent Regulation of Transient Receptor Potential Vanilloid 4
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Circulation Research Vol. 102, No. 8 ( 2008-04-25), p. 966-974
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 8 ( 2008-04-25), p. 966-974
    Abstract: Although the formation of hydrostatic lung edema is generally attributed to imbalanced Starling forces, recent data show that lung endothelial cells respond to increased vascular pressure and may thus regulate vascular permeability and edema formation. In combining real-time optical imaging of the endothelial Ca 2+ concentration ([Ca 2+ ] i ) and NO production with filtration coefficient ( K f ) measurements in the isolated perfused lung, we identified a series of endothelial responses that constitute a negative-feedback loop to protect the microvascular barrier. Elevation of lung microvascular pressure was shown to increase endothelial [Ca 2+ ] i via activation of transient receptor potential vanilloid 4 (TRPV4) channels. The endothelial [Ca 2+ ] i transient increased K f via activation of myosin light-chain kinase and simultaneously stimulated NO synthesis. In TRPV4 deficient mice, pressure-induced increases in endothelial [Ca 2+ ] i , NO synthesis, and lung wet/dry weight ratio were largely blocked. Endothelial NO formation limited the permeability increase by a cGMP-dependent attenuation of the pressure-induced [Ca 2+ ] i response. Inactivation of TRPV4 channels by cGMP was confirmed by whole-cell patch-clamp of pulmonary microvascular endothelial cells and intravital imaging of endothelial [Ca 2+ ] i . Hence, pressure-induced endothelial Ca 2+ influx via TRPV4 channels increases lung vascular permeability yet concomitantly activates an NO-mediated negative-feedback loop that protects the vascular barrier by a cGMP-dependent attenuation of the endothelial [Ca 2+ ] i response. The identification of this novel regulatory pathway gives rise to new treatment strategies, as demonstrated in vivo in rats with acute myocardial infarction in which inhibition of cGMP degradation by the phosphodiesterase 5 inhibitor sildenafil reduced hydrostatic lung edema.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.107.168724
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 7
    Online Resource
    Online Resource
    Local Peroxynitrite Impairs Endothelial Transient Receptor Potential Vanilloid 4 Channels and Elevates Blood Pressure in Obesity
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Circulation Vol. 141, No. 16 ( 2020-04-21), p. 1318-1333
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 141, No. 16 ( 2020-04-21), p. 1318-1333
    Abstract: Impaired endothelium-dependent vasodilation is a hallmark of obesity-induced hypertension. The recognition that Ca 2+ signaling in endothelial cells promotes vasodilation has led to the hypothesis that endothelial Ca 2+ signaling is compromised during obesity, but the underlying abnormality is unknown. In this regard, transient receptor potential vanilloid 4 (TRPV4) ion channels are a major Ca 2+ influx pathway in endothelial cells, and regulatory protein AKAP150 (A-kinase anchoring protein 150) enhances the activity of TRPV4 channels. Methods: We used endothelium-specific knockout mice and high-fat diet–fed mice to assess the role of endothelial AKAP150-TRPV4 signaling in blood pressure regulation under normal and obese conditions. We further determined the role of peroxynitrite, an oxidant molecule generated from the reaction between nitric oxide and superoxide radicals, in impairing endothelial AKAP150-TRPV4 signaling in obesity and assessed the effectiveness of peroxynitrite inhibition in rescuing endothelial AKAP150-TRPV4 signaling in obesity. The clinical relevance of our findings was evaluated in arteries from nonobese and obese individuals. Results: We show that Ca 2+ influx through TRPV4 channels at myoendothelial projections to smooth muscle cells decreases resting blood pressure in nonobese mice, a response that is diminished in obese mice. Counterintuitively, release of the vasodilator molecule nitric oxide attenuated endothelial TRPV4 channel activity and vasodilation in obese animals. Increased activities of inducible nitric oxide synthase and NADPH oxidase 1 enzymes at myoendothelial projections in obese mice generated higher levels of nitric oxide and superoxide radicals, resulting in increased local peroxynitrite formation and subsequent oxidation of the regulatory protein AKAP150 at cysteine 36, to impair AKAP150-TRPV4 channel signaling at myoendothelial projections. Strategies that lowered peroxynitrite levels prevented cysteine 36 oxidation of AKAP150 and rescued endothelial AKAP150-TRPV4 signaling, vasodilation, and blood pressure in obesity. Peroxynitrite-dependent impairment of endothelial TRPV4 channel activity and vasodilation was also observed in the arteries from obese patients. Conclusions: These data suggest that a spatially restricted impairment of endothelial TRPV4 channels contributes to obesity-induced hypertension and imply that inhibiting peroxynitrite might represent a strategy for normalizing endothelial TRPV4 channel activity, vasodilation, and blood pressure in obesity.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.119.043385
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 1466401-X
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  • 8
    Online Resource
    Online Resource
    Acute Effects of Strength and Plyometric Training on Performance and Cardiorespiratory Responses During Endurance Exercise : 927 Board #342 May 28, 2
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Medicine & Science in Sports & Exercise Vol. 46 ( 2014-05), p. 254-
    Details
    In: Medicine & Science in Sports & Exercise, Ovid Technologies (Wolters Kluwer Health), Vol. 46 ( 2014-05), p. 254-
    Type of Medium: Online Resource
    ISSN: 0195-9131
    URL: Article
    DOI: 10.1249/01.mss.0000493946.20544.13
    RVK:
    ZX 1000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2031167-9
    SSG: 31
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  • 9
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    Abstract 750: Gene Signatures to Distinguish Amyloid Cardiomyopathy Risk in Multiple Myeloma Patients
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Circulation Research Vol. 125, No. Suppl_1 ( 2019-08-02)
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 125, No. Suppl_1 ( 2019-08-02)
    Abstract: Amyloid light chain (AL) amyloidosis results from tissue deposition of clonal light chains, most commonly produced by clonal plasma cells. AL amyloidosis is closely associated with multiple myeloma (MM), another disease which arises from clonal plasma cell proliferation. Here we aim to identify gene signatures to distinguish AL cardiomyopathy (AL-CM) risk in MM patients. We utilized publicly available data sets and applied Graph Cluster Perturbation approach to cluster the co-expression networks based on pathways in MM and AL-CM utilizing 225 samples from four datasets: GSE42955 study (12 dilated CM, 12 ischemic CM and 5 control LV human heart tissues), GSE95077 study (16 amiloride drug treated/untreated myeloma cell line samples), GSE24128 study (16 newly diagnosed AL with monoclonal plasma cell samples over- or under-expressing cyclin D1), and GSE6477 study (76 primary bone marrow samples from hyper-diploid myeloma patients and 80 non-hyperdiploid MM patients). From these data sets, the networks for extracellular matrix organization, immune system, innate immune system, metabolism, and neutrophil degranulation pathways for MM and amyloid CM were extracted. Summary: Ranking of the perturbed genes based on pathways similarity index in MM and AL resulted in a panel of genes: CD44, NRAS, GRAP2, CTLA4, GSN, CCND1, NFKB1, and IRF1 (p= 〈 0.01). As shown in Figure , the high hazard ratio of this gene cluster in MM with AL-CM (3.76; p=0.021) compared to MM without CM (0.96; p=0.032) suggests the potential of this gene panel to distinguish high or low risk groups in MM based on survival.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/res.125.suppl_1.750
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 1467838-X
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  • 10
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    Online Resource
    Effects of excess free fatty acids on mechanical and metabolic function in normal and ischemic myocardium in swine.
    Ovid Technologies (Wolters Kluwer Health) ; 1978
    In:  Circulation Research Vol. 43, No. 4 ( 1978-10), p. 652-661
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 4 ( 1978-10), p. 652-661
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/01.RES.43.4.652
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1978
    detail.hit.zdb_id: 1467838-X
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