Reduction of myocardial ischemic injury following coronary intervention (The MC-1 to eliminate necrosis and damage trial)

Kandzari, David E.; Labinaz, Marino; Cantor, Warren J.; Madan, Mina; Gallup, Dianne; Hasselblad, Vic; Joseph, Diane; Allen, Andrew S.; Green, Cindy; Hidinger, Karl G; Krucoff, Mitchell W.; Christenson, Robert H.; Harrington, Robert A.; Tcheng, James E.

doi:10.1016/s0002-9149(03)00818-x

Cited by 17 publications

(14 citation statements)

References 24 publications

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“…A reduction of the ischemia-reperfusion (I/R) injury and infarct size was also seen in isolated rat hearts [ 9 , 37 ]. A phase II clinical trial, in which PLP was given to patients undergoing percutaneous coronary intervention, showed a decrease in infarct size 24 h after angioplasty [ 39 ]. In 901 high-risk patients undergoing coronary artery bypass graft (CABG) surgery, PLP resulted in a significant decrease in preoperative myocardial infarction but did not affect the prespecified primary end point [ 40 ].…”

Section: Cardioprotective Effects Of Vitamin B6 and Plp In Ischemic Hmentioning

confidence: 99%

“…However, in another study, in which 3023 intermediate-to high-risk patients undergoing CABG were used as subjects, PLP did not show any significant effect on cardiovascular death or non-fatal myocardial infarction [ 42 , 43 ]. Although the exact reason for the negative results of this study using intermediate-to high-risk patients for CABG [ 42 , 43 ] is not clear, the clinical studies using high-risk patients for CABG [ 40 , 41 ] as well as in patients following angioplasty [ 39 ] show a high potential for PLP therapy in ischemic heart disease.…”

Section: Cardioprotective Effects Of Vitamin B6 and Plp In Ischemic Hmentioning

confidence: 99%

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Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Dhalla

Takeda²,

Elimban

2013

Clinical Chemistry and Laboratory Medicine

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Although vitamin B6 and its metabolite, pyridoxal 5 ′ -phosphate (PLP), have been shown to exert bene ficial effects in ischemic heart disease, the mechanisms of their action are not fully understood. Some studies have shown that ventricular arrhythmias and mortality upon the occlusion of coronary artery were attenuated by pretreatment of animals with PLP. Furthermore, ischemia-reperfusion-induced abnormalities in cardiac performance and defects in sarcoplasmic reticular Ca 2 + -transport activities were decreased by PLP. The increase in cardiac contractile activity of isolated heart by ATP was reduced by PLP, unlike propranolol, whereas that by isoproterenol was not depressed by PLP. ATP-induced increase in [Ca ] i in cardiomyocytes was depressed by PLP. Both high-and low-affinity sites for ATP binding in sarcolemmal membranes were also decreased by PLP. These observations support the view that PLP may produce cardioprotective effects in ischemic heart disease by attenuating the occurrence of intracellular Ca 2 + overload due to the blockade of purinergic receptors.

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Section: Cardioprotective Effects Of Vitamin B6 and Plp In Ischemic Hmentioning

confidence: 99%

Section: Cardioprotective Effects Of Vitamin B6 and Plp In Ischemic Hmentioning

confidence: 99%

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Dhalla

Takeda²,

Elimban

2013

Clinical Chemistry and Laboratory Medicine

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“…MC-1 inhibits calcium influx in ischemic cardiomyocytes via adenosine triphosphate receptor antagonism [123].…”

Section: Othersmentioning

confidence: 99%

Myocardial ischemia/reperfusion-injury, a clinical view on a complex pathophysiological process

Moens

Claeys

Timmermans

et al. 2005

International Journal of Cardiology

381

321

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“…In ARMYDA, atorvastatin reduced the release of CK-MB, troponin, and myoglobin compared with placebo. 15 Intracoronary propranolol, 21 celecoxib, 20 glycoprotein IIb/IIIa inhibitors, 18 and pyridoxal-5Ј-phosphate monohydrate 17 all reduced myocardial damage after PCI.…”

Section: Discussionmentioning

confidence: 99%

“…The sample size of previous studies 15,[17][18][19][20][21] testing interventions to reduce markers after elective PCI has ranged from 50 to 153 (mean, 105). The sample size used in ARMYDA was 153.…”

Section: Sample Size Considerationsmentioning

confidence: 99%

The sPLA ₂ Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) Trial

Džavík

Lavi²,

Thorpe³

et al. 2010

Circulation

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Background— Secretory phospholipase A 2 (sPLA 2 ) may play a role in myonecrosis after elective percutaneous coronary intervention (PCI). Inhibition of this enzyme may have a beneficial effect. The central hypothesis of this study was that treatment with varespladib, a small-molecule inhibitor of sPLA 2 would reduce postprocedural release of cardiac biomarkers after elective percutaneous coronary intervention. Methods and Results— Between October 2007 and June 2009, 144 stable patients were randomized in a phase II trial to receive varespladib 500 mg PO BID or placebo 3 to 5 days before and for 5 days after elective percutaneous coronary intervention. The primary end point was elevation of troponin I or creatine kinase-MB above the upper limit of normal at 6 to 8 or 18 to 24 hours after percutaneous coronary intervention. Mean age was 63±10 and 64±10 years, with 38% and 42% with diabetes mellitus and 29% and 28% with prior myocardial infarction for the varespladib and placebo groups, respectively. The primary end point occurred in 75% of varespladib and 63% of placebo patients ( P =0.14). Troponin I 3 times the upper limit of normal was observed in 57% and 50% ( P =0.39) and creatine kinase-MB 2 times the upper limit of normal in 14% and 3% ( P =0.018). Median (first and third quartiles) change in high-sensitivity C-reactive protein in these 2 groups was 0.65 mg/L (−0.18 and 1.48) and 0.70 mg/L (0.00 and 1.50) at 18 to 24 hours ( P =0.81) and 0.20 mg/L (−0.70 and 1.40) and 0.60 mg/L (−0.12 and 1.72) at 3 to 5 days ( P =0.23), whereas change in sPLA 2 activity at 3 to 5 days in a subset was −2.85 ng/ml (−3.40 and −1.85) and 0.25 ng/ml (−0.20 and 0.85) ( P <0.001). Conclusions— Inhibition of sPLA 2 by varespladib administered for 3 to 5 days before the procedure does not reduce periprocedural myonecrosis associated with elective percutaneous coronary intervention. Clinical Trial Registration— URL: http://www.clinicaltrials.gov . Unique identifier: NCT00533039.

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Reduction of myocardial ischemic injury following coronary intervention (The MC-1 to eliminate necrosis and damage trial)

Cited by 17 publications

References 24 publications

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Myocardial ischemia/reperfusion-injury, a clinical view on a complex pathophysiological process

The sPLA ₂ Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) Trial

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Reduction of myocardial ischemic injury following coronary intervention (The MC-1 to eliminate necrosis and damage trial)

Cited by 17 publications

References 24 publications

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Myocardial ischemia/reperfusion-injury, a clinical view on a complex pathophysiological process

The sPLA 2 Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) Trial

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The sPLA ₂ Inhibition to Decrease Enzyme Release After Percutaneous Coronary Intervention (SPIDER-PCI) Trial