Journal of cardiovascular pharmacology
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J. Cardiovasc. Pharmacol. · Mar 2014
Review Comparative StudyRevascularization versus medical treatments in stable coronary artery disease: predicting the future of novel drug therapies for stable angina.
Over the past 2 decades, drug therapy of patients with stable angina pectoris has improved, with a marked impact on the hard clinical outcomes of mortality and myocardial infarction. In contrast, recent trials have not demonstrated beneficial effects of revascularization on mortality. However, in the large trials that compared medical treatment with percutaneous coronary intervention (PCI) or surgery, high-risk patients, such as those with severe 3-vessel disease with or without left ventricular dysfunction, were excluded. ⋯ These include new lipid-lowering drugs acting in concert with statins (cholesteryl ester transfer protein inhibitors, proprotein convertase subtilisin/kexin type 9 inhibitors), aldosterone antagonists, colchicine, methotrexate, and interleukin-1 inhibitors. In conclusion, from the available data, PCI and coronary surgery have not been shown to improve hard end points and routine use of invasive revascularization should be avoided in patients with chronic stable angina. Evidence-based secondary prevention remains the most important approach.
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J. Cardiovasc. Pharmacol. · Feb 2014
Review Meta AnalysisPerioperative levosimendan therapy is associated with a lower incidence of acute kidney injury after cardiac surgery: a meta-analysis.
Levosimendan is a calcium sensitizer that enhances myocardial contractility without increasing myocardial oxygen use. Limited data are available on its renal-protective effect, and no statistically significant effects have been found. A meta-analysis was conducted for randomized studies to show whether perioperative levosimendan use could reduce acute kidney injury (AKI) in patients undergoing cardiac surgery. ⋯ This analysis suggests that levosimendan might reduce renal injury in adult patients undergoing cardiac surgery. More prospective randomized studies are needed to further demonstrate the benefits of levosimendan on renal protection in cardiac surgery.
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J. Cardiovasc. Pharmacol. · Nov 2013
(-)-Epigallocatechin gallate inhibits TNF-α-induced PAI-1 production in vascular endothelial cells.
: (-)-Epigallocatechin gallate (EGCG), the major catechin derived from green tea, reduces the incidence of cardiovascular diseases such as atherosclerosis. Plasminogen activator inhibitor-1 (PAI-1) accelerates thrombus formation upon ruptured atherosclerotic plaques. However, it is not known whether or not EGCG inhibits PAI-1 production induced by tumor necrosis factor-α (TNF-α) in endothelial cells. ⋯ The ERK1/2 inhibitor, PD98059 (20 μmol/L), downregulated TNF-α-induced PAI-1 expression 57.69 ± 2.46% (P < 0.01), but had no effect in cells pretreated with EGCG. TNF-α stimulation resulted in a significant decrease in TNFR1, an effect that was abolished by pretreatment with EGCG. These results suggest that EGCG could provide vascular benefits in inflammatory cardiovascular diseases such as decreased thrombus formation associated with ruptured atherosclerotic plaques.
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J. Cardiovasc. Pharmacol. · Aug 2013
Globular adiponectin attenuates myocardial ischemia/reperfusion injury by upregulating endoplasmic reticulum Ca²⁺-ATPase activity and inhibiting endoplasmic reticulum stress.
The aim of this study was to explore the mechanisms underlying the effects of globular adiponectin (gAd) on myocardial ischemia/reperfusion (I/R) injury. ⋯ The protective effects of gAd during I/R are mediated, at least in part, by modulating SERCA activity and consequently suppressing ER stress via the activation of PI3K/Akt signaling.
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J. Cardiovasc. Pharmacol. · Jul 2013
Continuous inhibition of poly(ADP-ribose) polymerase does not reduce reperfusion injury in isolated rat heart.
Poly(ADP-ribose) polymerase (PARP), an enzyme that is important to the regulation of nuclear function, is activated by DNA strand breakage. In massive DNA damage, PARP is overactivated, exhausting nicotinamide adenine dinucleotide and leading to cell death. Recent studies have succeeded in reducing cellular damage in ischemia/reperfusion by inhibiting PARP. ⋯ In the 3-AB continuous group, these advantages were not apparent. At the end of reperfusion, PARP cleavage had significantly proceeded in the 3-AB continuous group, indicating initiation of the apoptotic cascade. Thus, continuous PARP inhibition by 3-AB does not reduce reperfusion injury in the isolated rat heart, which may be because of acceleration of apoptosis.