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  • 1
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    Online Resource
    Icosapent Ethyl Reduces Ischemic Events in Patients With a History of Previous Coronary Artery Bypass Grafting: REDUCE-IT CABG
    Ovid Technologies (Wolters Kluwer Health) ; 2021
    In:  Circulation Vol. 144, No. 23 ( 2021-12-07), p. 1845-1855
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 144, No. 23 ( 2021-12-07), p. 1845-1855
    Abstract: Despite advances in surgery and pharmacotherapy, there remains significant residual ischemic risk after coronary artery bypass grafting surgery. Methods: In REDUCE-IT (Reduction of Cardiovascular Events With Icosapent Ethyl–Intervention Trial), a multicenter, placebo-controlled, double-blind trial, statin-treated patients with controlled low-density lipoprotein cholesterol and mild to moderate hypertriglyceridemia were randomized to 4 g daily of icosapent ethyl or placebo. They experienced a 25% reduction in risk of a primary efficacy end point (composite of cardiovascular death, myocardial infarction, stroke, coronary revascularization, or hospitalization for unstable angina) and a 26% reduction in risk of a key secondary efficacy end point (composite of cardiovascular death, myocardial infarction, or stroke) when compared with placebo. The current analysis reports on the subgroup of patients from the trial with a history of coronary artery bypass grafting. Results: Of the 8179 patients randomized in REDUCE-IT, a total of 1837 (22.5%) had a history of coronary artery bypass grafting, with 897 patients randomized to icosapent ethyl and 940 to placebo. Baseline characteristics were similar between treatment groups. Randomization to icosapent ethyl was associated with a significant reduction in the primary end point (hazard ratio [HR], 0.76 [95% CI, 0.63–0.92] ; P =0.004), in the key secondary end point (HR, 0.69 [95% CI, 0.56–0.87]; P =0.001), and in total (first plus subsequent or recurrent) ischemic events (rate ratio, 0.64 [95% CI, 0.50–0.81]; P =0.0002) compared with placebo. This yielded an absolute risk reduction of 6.2% (95% CI, 2.3%–10.2%) in first events, with a number needed to treat of 16 (95% CI, 10–44) during a median follow-up time of 4.8 years. Safety findings were similar to the overall study: beyond an increased rate of atrial fibrillation/flutter requiring hospitalization for at least 24 hours (5.0% vs 3.1%; P =0.03) and a nonsignificant increase in bleeding, occurrences of adverse events were comparable between groups. Conclusions: In REDUCE-IT patients with a history of coronary artery bypass grafting, treatment with icosapent ethyl was associated with significant reductions in first and recurrent ischemic events. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT01492361.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/CIRCULATIONAHA.121.056290
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2021
    detail.hit.zdb_id: 1466401-X
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  • 2
    Online Resource
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    Inhibition of the Na + /H + Exchanger Confers Greater Cardioprotection Against 90 Minutes of Myocardial Ischemia Than Ischemic Preconditioning in Dogs
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Circulation Vol. 100, No. 25 ( 1999-12-21), p. 2519-2526
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 25 ( 1999-12-21), p. 2519-2526
    Abstract: Background —This study compared the efficacy of ischemic preconditioning (IPC) and sodium-hydrogen exchanger (NHE)-1 inhibition to reduce infarct size (IS) induced by a 90-minute ischemic insult and examined the interaction between NHE-1 inhibition and IPC. Methods and Results —In a canine infarct model, either IPC, produced by 1 or four 5-minute coronary artery occlusions, or the specific NHE-1 inhibitor BIIB 513, 0.75 or 3.0 mg/kg, was administered 15 minutes before either a 60- or 90-minute coronary artery occlusion followed by 3 hours of reperfusion. IS was determined by TTC staining and expressed as a percentage of the area at risk (IS/AAR). Although both IPC and BIIB 513 at 0.75 mg/kg produced comparable and significant reductions in IS/AAR in the 60-minute occlusion model, insignificant reductions in IS/AAR were observed in the 90-minute occlusion model. However, BIIB 513 at 3.0 mg/kg markedly reduced IS in both models ( P 〈 0.05). Next, to examine the interaction between NHE-1 blockade and IPC, BIIB 0.75 mg/kg was administered either before IPC or during the washout phase of IPC before 90 minutes of coronary artery occlusion. Both combinations resulted in a greater-than-additive reduction in IS/AAR ( P 〈 0.05). Conclusions —These data demonstrate that although IPC and NHE-1 inhibition provide comparable protection against 60 minutes of myocardial ischemia, NHE-1 inhibition is more efficacious than IPC at protecting against a 90-minute ischemic insult. Furthermore, the combination of NHE-1 inhibition and IPC produces a greater-than-additive reduction in IS/AAR, suggesting either that NHE activity limits the efficacy of IPC or that different mechanisms are involved in the cardioprotective effect of IPC and NHE-1 inhibition.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.100.25.2519
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 1466401-X
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  • 3
    Online Resource
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    Effect of COX-1/COX-2 Inhibition versus Selective COX-2 Inhibition on Coronary Vasodilator Responses to Arachidonic Acid and Acetylcholine
    S. Karger AG ; 2004
    In:  Pharmacology Vol. 71, No. 3 ( 2004), p. 135-142
    Details
    In: Pharmacology, S. Karger AG, Vol. 71, No. 3 ( 2004), p. 135-142
    Abstract: The effect of a nonselective COX-1/COX-2 inhibitor, naproxen, was compared with a COX-2-selective inhibitor (SC-58236) on coronary vasodilatory responses in the anesthetized dog. Coronary vasodilation was induced by direct intracoronary injection of acetylcholine (ACH) and arachidonic acid (AA) in control animals and in those treated with either naproxen (1, 3, or 10 mg/kg p.o. 24 h prior to the experiment) or SC-58236 (1, 5, or 15 mg/kg p.o. 24 h prior to the experiment). Naproxen, at 10 mg/kg, significantly attenuated the AA-induced vasodilation (prostacyclin dependent) with no effect on ACH-induced vasodilation (nitric oxide dependent). SC-58236 failed to attenuate either AA- or ACH-induced vasodilation. Ex vivo assays were utilized to establish inhibition of COX-2 (lipopolysaccharide-stimulated prostaglandin E 〈 sub 〉 2 〈 /sub 〉 formation) and COX-1 (serum thromboxane B 〈 sub 〉 2 〈 /sub 〉 ) in blood taken from dogs administered 1, 3, or 10 mg/kg naproxen or 15 mg/kg SC-58236. Naproxen (3 and10 mg/kg) and SC-58236 (15 mg/kg) markedly reduced the lipopolysaccharide-induced prostaglandin E 〈 sub 〉 2 〈 /sub 〉 formation, whereas SC- 58236 (15 mg/kg) had no effect on serum thromboxane B 〈 sub 〉 2 〈 /sub 〉 . Naproxen significantly reduced thromboxane B 〈 sub 〉 2 〈 /sub 〉 at all three doses studied. Furthermore, naproxen (10 mg/kg p.o.) significantly inhibited the AA-induced platelet aggregation (thromboxane B 〈 sub 〉 2 〈 /sub 〉 dependent), whereas SC-58236 had no effect. Collectively, these results demonstrate that SC-58236 is selective for COX-2, while naproxen is a nonselective inhibitor. These data also suggest that vasodilatory responses to AA in the dog are primarily COX-1 dependent. Selective COX-2 inhibition does not affect either prostacyclin or nitric oxide mediated vasodilation in the canine coronary circulation.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000077447
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2004
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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  • 4
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    Abdominal Surgical Incision Induces Remote Preconditioning of Trauma (RPCT) via Activation of Bradykinin Receptors (BK2R) and the Cytochrome P450 Epoxygenase Pathway in Canine Hearts
    Springer Science and Business Media LLC ; 2011
    In:  Cardiovascular Drugs and Therapy Vol. 25, No. 6 ( 2011-12), p. 517-522
    Details
    In: Cardiovascular Drugs and Therapy, Springer Science and Business Media LLC, Vol. 25, No. 6 ( 2011-12), p. 517-522
    Type of Medium: Online Resource
    ISSN: 0920-3206 , 1573-7241
    URL: Article
    DOI: 10.1007/s10557-011-6321-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2011
    detail.hit.zdb_id: 2003553-6
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  • 5
    Online Resource
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    Na + /H + exchange inhibition-induced cardioprotection in dogs: effects on neutrophils versus cardiomyocytes
    American Physiological Society ; 2000
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 279, No. 4 ( 2000-10-01), p. H1563-H1570
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 279, No. 4 ( 2000-10-01), p. H1563-H1570
    Abstract: Numerous studies have examined the effect of Na + /H + exchanger (NHE) inhibition on the myocardium; however, the effect of NHE-1 inhibition on neutrophil function has not been adequately examined. An in vivo canine model of myocardial ischemia-reperfusion injury in which 60 min of left anterior descending coronary artery occlusion followed by 3 h of reperfusion was used to examine the effect of NHE-1 inhibition on infarct size (IS) and neutrophil function. BIIB-513, a selective inhibitor of NHE-1, was infused before ischemia. IS was expressed as a percentage of area at risk (IS/AAR). NHE-1 inhibition significantly reduced IS/AAR and reduced neutrophil accumulation in the ischemic myocardium. NHE-1 inhibition attenuated both phorbol 12-myristate 13-acetate- and platelet-activating factor-induced neutrophil respiratory burst but not CD18 upregulation. Furthermore, NHE-1 inhibition directly protected cardiomyocytes against metabolic inhibition-induced lactate dehydrogenase release and hypercontracture. This study provides evidence that the cardioprotection induced by NHE-1 inhibition is likely due to specific protection of cardiomyocytes and attenuation of neutrophil activity.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.2000.279.4.H1563
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2000
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    IN VIVO 31P NMR SPECTROSCOPY FOR EVALUATION OF OSTEOPOROSIS
    Elsevier BV ; 1987
    In:  The Lancet Vol. 330, No. 8549 ( 1987-7), p. 37-38
    Details
    In: The Lancet, Elsevier BV, Vol. 330, No. 8549 ( 1987-7), p. 37-38
    Type of Medium: Online Resource
    ISSN: 0140-6736
    URL: Article
    DOI: 10.1016/S0140-6736(87)93066-2
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1987
    detail.hit.zdb_id: 2067452-1
    detail.hit.zdb_id: 3306-6
    detail.hit.zdb_id: 1476593-7
    SSG: 5,21
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  • 7
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    Comparison of Three Different A 1 Adenosine Receptor Antagonists on Infarct Size and Multiple Cycle Ischemic Preconditioning in Anesthetized Dogs
    American Society for Pharmacology & Experimental Therapeutics (ASPET) ; 2004
    In:  Journal of Pharmacology and Experimental Therapeutics Vol. 308, No. 3 ( 2004-03), p. 846-856
    Details
    In: Journal of Pharmacology and Experimental Therapeutics, American Society for Pharmacology & Experimental Therapeutics (ASPET), Vol. 308, No. 3 ( 2004-03), p. 846-856
    Type of Medium: Online Resource
    ISSN: 0022-3565 , 1521-0103
    URL: Article
    DOI: 10.1124/jpet.103.057943
    Language: English
    Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
    Publication Date: 2004
    detail.hit.zdb_id: 1475023-5
    SSG: 15,3
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  • 8
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    Effects of the selective EET antagonist, 14,15-EEZE, on cardioprotection produced by exogenous or endogenous EETs in the canine heart
    American Physiological Society ; 2008
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 294, No. 6 ( 2008-06), p. H2838-H2844
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 294, No. 6 ( 2008-06), p. H2838-H2844
    Abstract: Previously, we demonstrated ( 17 ) that 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) produce marked reductions in myocardial infarct size. Although it is assumed that this cardioprotective effect of the EETs is due to a specific interaction with a membrane-bound receptor, no evidence has indicated that novel EET antagonists selectively block the EET actions in dogs. Our goals were to investigate the effects of 11,12- and 14,15-EET, the soluble epoxide hydrolase inhibitor, 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA), and the putative selective EET antagonist, 14,15-epoxyeicosa-5( Z)-enoic acid (14,15-EEZE), on infarct size of barbital anesthetized dogs subjected to 60 min of coronary artery occlusion and 3 h of reperfusion. Furthermore, the effect of 14,15-EEZE on the cardioprotective actions of the selective mitochondrial ATP-sensitive potassium channel opener diazoxide was investigated. Both 11,12- and 14,15-EET markedly reduced infarct size [expressed as a percentage of the area at risk (IS/AAR)] from 21.8 ± 1.6% (vehicle) to 8.7 ± 2.2 and 9.4 ± 1.3%, respectively. Similarly, AUDA significantly reduced IS/AAR from 21.8 ± 1.6 to 14.4 ± 1.2% (low dose) and 9.4 ± 1.8% (high dose), respectively. Interestingly, the combination of the low dose of AUDA with 14,15-EET reduced IS/AAR to 5.8 ± 1.6% ( P 〈 0.05), further than either drug alone. Diazoxide also reduced IS/AAR significantly (10.2 ± 1.9%). In contrast, 14,15-EEZE had no effect on IS/AAR by itself (21.0 ± 3.6%), but completely abolished the effect of 11,12-EET (17.8 ± 1.4%) and 14,15-EET (19.2 ± 2.4%) and AUDA (19.3 ± 1.6%), but not that of diazoxide (10.4 ± 1.4%). These results suggest that activation of the EET pathway, acting on a putative receptor, by exogenous EETs or indirectly by blocking EET metabolism, produced marked cardioprotection, and the combination of these two approaches resulted in a synergistic effect. These data also suggest that 14,15-EEZE is not blocking the mitochondrial ATP-sensitive potassium channel as a mechanism for antagonizing the cardioprotective effects of the EETs.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00186.2008
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
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    Postischemic Administration of CGX-1051, a Peptide from Cone Snail Venom, Reduces Infarct Size in Both Rat and Dog Models of Myocardial Ischemia and Reperfusion
    Ovid Technologies (Wolters Kluwer Health) ; 2005
    In:  Journal of Cardiovascular Pharmacology Vol. 46, No. 2 ( 2005-08), p. 141-146
    Details
    In: Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 46, No. 2 ( 2005-08), p. 141-146
    Type of Medium: Online Resource
    ISSN: 0160-2446
    URL: Article
    DOI: 10.1097/01.fjc.0000167015.84715.27
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2005
    detail.hit.zdb_id: 2049700-3
    SSG: 15,3
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  • 10
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    A 3 adenosine receptor agonist IB-MECA reduces myocardial ischemia-reperfusion injury in dogs
    American Physiological Society ; 2003
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 285, No. 2 ( 2003-08), p. H607-H613
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 285, No. 2 ( 2003-08), p. H607-H613
    Abstract: We examined the effect of the A 3 adenosine receptor (AR) agonist IB-MECA on infarct size in an open-chest anesthetized dog model of myocardial ischemia-reperfusion injury. Dogs were subjected to 60 min of left anterior descending (LAD) coronary artery occlusion and 3 h of reperfusion. Infarct size and regional myocardial blood flow were assessed by macrohistochemical staining with triphenyltetrazolium chloride and radioactive microspheres, respectively. Four experimental groups were studied: vehicle control (50% DMSO in normal saline), IB-MECA (100 μg/kg iv bolus) given 10 min before the coronary occlusion, IB-MECA (100 μg/kg iv bolus) given 5 min before initiation of reperfusion, and IB-MECA (100 μg/kg iv bolus) given 10 min before coronary occlusion in dogs pretreated 15 min earlier with the ATP-dependent potassium channel antagonist glibenclamide (0.3 mg/kg iv bolus). Administration of IB-MECA had no effect on any hemodynamic parameter measured including heart rate, first derivative of left ventricular pressure, aortic pressure, LAD coronary blood flow, or coronary collateral blood flow. Nevertheless, pretreatment with IB-MECA before coronary occlusion produced a marked reduction in infarct size (∼40% reduction) compared with the control group (13.0 ± 3.2% vs. 25.2 ± 3.7% of the area at risk, respectively). This effect of IB-MECA was blocked completely in dogs pretreated with glibenclamide. An equivalent reduction in infarct size was observed when IB-MECA was administered immediately before reperfusion (13.1 ± 3.9%). These results are the first to demonstrate efficacy of an A 3 AR agonist in a large animal model of myocardial infarction by mechanisms that are unrelated to changes in hemodynamic parameters and coronary blood flow. These data also demonstrate in an in vivo model that IB-MECA is effective as a cardioprotective agent when administered at the time of reperfusion.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.01001.2002
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2003
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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