Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction

Mahaffey, K. W.; Puma, Joseph A.; Barbagelata, N.Alejandro; Dicarli, M; Leesar, Massoud A.; Browne, Kevin F.; Eisenberg, Paul R.; Bolli, Roberto; Casas, AC; Molina-Viamonte, Victor; Orlandi, Cesare; Blevins, Roger D.; Gibbons, Raymond J.; Califf, Robert M.; Granger, CB

doi:10.1016/s0735-1097(99)00418-0

Cited by 473 publications

(67 citation statements)

References 52 publications

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“…Gibbons et al used radioimaging techniques to document that the anticipated benefit from improved reperfusion therapy is much greater and easier to detect in individual patients with an anterior AMI than in those with an inferior wall lesion, 22 which is mainly because of the greater size of the risk area in an anterior AMI. The results of the AMISTAD trial documented that the reduction in MI size by adenosine infusion in conjunction with thrombolysis is detected only in patients with an anterior lesion, 6 and our results concur with that observation. Among the present patients with an anterior AMI, improvement in LV function was significantly better and the frequency of LV dilation was significantly lower in the nicorandil group than in the control group.…”

Section: Impact Of the Site Of Ami On Prognosissupporting

confidence: 90%

Intravenous Nicorandil in Conjunction With Coronary Reperfusion Therapy is Associated With Better Clinical and Functional Outcomes in Patients With Acute Myocardial Infarction.

Sugimoto

Ito

Iwakura

et al. 2003

Circ J

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Section: Impact Of the Site Of Ami On Prognosissupporting

confidence: 90%

Intravenous Nicorandil in Conjunction With Coronary Reperfusion Therapy is Associated With Better Clinical and Functional Outcomes in Patients With Acute Myocardial Infarction.

Sugimoto

Ito

Iwakura

et al. 2003

Circ J

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“…508 For RIC, even an improved clinical outcome has been reported. 36 In contrast to the positive clinical studies with mechanical conditioning strategies, studies attempting to recruit cardioprotective signals pharmacologically have largely failed, including those on adenosine, [495][496][497][498] on PKCδ inhibition, 188 and on intravenous nitrite which is bio-converted to NO. 499 Erythropoietin failed to reduce IS in 2 trials, 501,502 but there was no evidence before that erythropoietin participated in the conditioning phenomena.…”

Section: Recruitment Of Cardioprotective Signaling In Patients With Amimentioning

confidence: 99%

Molecular Basis of Cardioprotection

Heusch

2015

Circulation Research

687

409

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Abstract:Reperfusion is mandatory to salvage ischemic myocardium from infarction, but reperfusion per se contributes to injury and ultimate infarct size. Therefore, cardioprotection beyond that by timely reperfusion is needed to reduce infarct size and improve the prognosis of patients with acute myocardial infarction. The conditioning phenomena provide such cardioprotection, insofar as brief episodes of coronary occlusion/ reperfusion preceding (ischemic preconditioning) or following (ischemic postconditioning) sustained myocardial ischemia with reperfusion reduce infarct size. Even ischemia/reperfusion in organs remote from the heart provides cardioprotection (remote ischemic conditioning). The present review characterizes the signal transduction underlying the conditioning phenomena, including their physical and chemical triggers, intracellular signal transduction, and effector mechanisms, notably in the mitochondria. Cardioprotective signal transduction appears as a highly concerted spatiotemporal program. Although the translation of ischemic postconditioning and remote ischemic conditioning protocols to patients with acute myocardial infarction has been fairly successful, the pharmacological recruitment of cardioprotective signaling has been largely disappointing to date.

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“…Perhaps not surprisingly, the trial did not document a protective effect of the purine. 10 A subsequent subgroup analysis suggested that protection occurred only in patients with lesions of the left anterior descending (LAD) coronary artery. 11 The larger AMISTAD II trial accordingly limited the study group to only those with anterior infarcts, but there was still no significant difference in infarct size between the treated and untreated groups.…”

Section: Have We Been Testing the Wrong Drugs?mentioning

confidence: 99%

Why Do We Still Not Have Cardioprotective Drugs?

Downey

Cohen

2009

Circ J

125

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Despite thousands of publications describing agents that limit infarct size in animals, all we have available today is reperfusion therapy. In this review, we examine why these drugs have not been translated into clinical practice.Many of the first interventions tested in clinical trials were very controversial in animal trials and their actual efficacy is still in question. Interventions based on the preconditioning mechanism have been very reproducible in animals, but clinical testing of them has just begun. Only approximately 25% of reperfused patients have infarcts large enough to put them at risk of heart failure and would require additional treatment. Inclusion of the 75% of patients with small infarcts in treatment groups has greatly diluted the significance of data in past clinical trials. Size of the risk zone has emerged as a reliable way to identify the vulnerable 25%. Recent small-scale clinical trials using risk stratification algorithms have shown clear infarct size limitation using ischemic and pharmacological postconditioning, confirming that the human heart responds like hearts of animal models. Most cardioprotectants have been studied in healthy animals, but recent studies indicate that aging and diabetes, common in coronary patients, do interfere with preconditioning-based interventions in animals. Clearly more study is needed to identify which interventions are adversely affected by comorbidities. (Circ J 2009; 73: 1171 -1177

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Adenosine as an adjunct to thrombolytic therapy for acute myocardial infarction

Abstract: Many agents thought to attenuate reperfusion injury have been unsuccessful in clinical investigation. In this study, adenosine resulted in a significant reduction in infarct size. These data support the need for a large clinical outcome trial.

Cited by 473 publications

References 52 publications

Intravenous Nicorandil in Conjunction With Coronary Reperfusion Therapy is Associated With Better Clinical and Functional Outcomes in Patients With Acute Myocardial Infarction.

Intravenous Nicorandil in Conjunction With Coronary Reperfusion Therapy is Associated With Better Clinical and Functional Outcomes in Patients With Acute Myocardial Infarction.

Molecular Basis of Cardioprotection

Why Do We Still Not Have Cardioprotective Drugs?

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