Open-Label, Randomized, Placebo-Controlled Evaluation of Intracoronary Adenosine or Nitroprusside After Thrombus Aspiration During Primary Percutaneous Coronary Intervention for the Prevention of Microvascular Obstruction in Acute Myocardial Infarction

Niccoli, Giampaolo; Rigattieri, Stefano; Vita, Maria Rosaria De; Valgimigli, Marco; Corvo, Pierfrancesco; Fabbiocchi, Franco; Romagnoli, Enrico; Caterina, Alberto Ranieri De; Torre, Giuseppe La; Schiavo, Paolo Lo; Tarantino, Fabio; Ferrari, Roberto; Tomai, Fabrizio; Olivares, Paolo; Cosentino, Nicola; D’Amario, Domenico; Leone, Antonio Maria; Porto, Italo; Burzotta, Francesco; Trani, Carlo; Crea, Filippo

doi:10.1016/j.jcin.2013.02.009

Cited by 112 publications

(99 citation statements)

References 39 publications

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“…Intracoronary abciximab as compared with intravenous abciximab reduced infarct size (creatine kinase and MRI) and microvascular obstruction (MRI). 228 For intracoronary adenosine, concordantly reduced infarct size (creatine kinase and MRI) and less microvascular obstruction (TIMI flow on angiography) were reported in patients undergoing interventional reperfusion for acute myocardial infarction in 2 229,230 but not in 3 other studies. 31,231,232 Intravenous nitrite in patients with ST-segment elevation myocardial infarction and interventional reperfusion failed to reduce infarct size (biomarker and MRI) or to affect TIMI flow (angiography).…”

Section: Clinical Studiesmentioning

confidence: 89%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

209

160

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Abstract:The atherosclerotic coronary vasculature is not only the culprit but also a victim of myocardial ischemia/ reperfusion injury. Manifestations of such injury are increased vascular permeability and edema, endothelial dysfunction and impaired vasomotion, microembolization of atherothrombotic debris, stasis with intravascular cell aggregates, and finally, in its most severe form, capillary destruction with hemorrhage. In animal experiments, local and remote ischemic pre-and postconditioning not only reduce infarct size but also these manifestations of coronary vascular injury, as do drugs which recruit signal transduction steps of conditioning. Clinically, no-reflow is frequently seen after interventional reperfusion, and it carries an adverse prognosis. The translation of cardioprotective interventions to clinical practice has been difficult to date. Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged to date in reducing infarct size in patients with reperfused acute myocardial infarction; unfortunately, for these drugs, no information on their impact on the ischemic/reperfused coronary circulation is available. (Circ Res.

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Section: Clinical Studiesmentioning

confidence: 89%

The Coronary Circulation as a Target of Cardioprotection

Heusch

2016

Circulation Research

209

160

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“…However, a later study provided evidence for contrasting beneficial effects of adenosine under similar conditions [639]. Intracoronary administration of adenosine, but not of nitroprusside, resulted in a significant improvement following acute MI [640].…”

Section: Myocardial Infarctionmentioning

confidence: 99%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

120

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This review is a historical account about purinergic signalling in the heart, for readers to see how ideas and understanding have changed as new experimental results were published. Initially, the focus is on the nervous control of the heart by ATP as a cotransmitter in sympathetic, parasympathetic, and sensory nerves, as well as in intracardiac neurons. Control of the heart by centers in the brain and vagal cardiovascular reflexes involving purines are also discussed. The actions of adenine nucleotides and nucleosides on cardiomyocytes, atrioventricular and sinoatrial nodes, cardiac fibroblasts, and coronary blood vessels are described. Cardiac release and degradation of ATP are also described. Finally, the involvement of purinergic signalling and its therapeutic potential in cardiac pathophysiology is reviewed, including acute and chronic heart failure, ischemia, infarction, arrhythmias, cardiomyopathy, syncope, hypertrophy, coronary artery disease, angina, diabetic cardiomyopathy, as well as heart transplantation and coronary bypass grafts.

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“…When looking at the post hoc analysis of the AMISTAD II trial, in the subgroup with successful reperfusion within 3 h, the adjunct of adenosine infusion enhanced early and late survival and reduced the composite clinical endpoint of death or congestive heart failure at 6 months [26]. In addition, during reperfusion, the addition of intracoronary adenosine after thromboaspiration, through the thrombectomy catheter, showed a significant improvement in STR, with better 1-year left ventricular remodelling and reduction in clinical events compared with saline and nitroprusside [27,28].…”

Section: Adenosinementioning

confidence: 96%

A Handbook of Primary PCI: No-Reflow Management

Adjedj

Müller

Eeckhout

2018

Primary Angioplasty

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Although substantial progress has been made in recent decades in reducing mortality and performing optimal revascularization in patients with acute coronary syndrome (ACS) and stable coronary artery disease (CAD), one of the remaining challenges is to better prevent and treat extended myocardial damage despite "apparent" angiographic optimal percutaneous coronary intervention (PCI). The presence of no-reflow is related to higher risk of major adverse cardiac events (MACE) due to the poor healing of the infarct, adverse left ventricular remodelling, congestive heart failure occurrence and death. Despite optimal epicardial coronary artery reperfusion performed by PCI, distal microembolization into the coronary microcirculation limits myocardial salvage especially during ACS. No-reflow represents the ultimate stage of extended myocardial damage after PCI with absence of contrast medium progression in the coronary artery. This complication occurs mainly during ACS or during PCI of rotational atherectomy and venous graft in stable patients. The objective of this chapter is to describe how to manage a noreflow phenomenon from the pathophysiology to the management in order to help physician to prevent this complication and if no-reflow occurs adapt therapeutics to limit myocardial damage and reduce poor outcomes. DefinitionThe no-reflow phenomenon is defined as inadequate myocardial perfusion through a given segment of the coronary circulation without angiographic evidence of mechanical obstruction [1].

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Open-Label, Randomized, Placebo-Controlled Evaluation of Intracoronary Adenosine or Nitroprusside After Thrombus Aspiration During Primary Percutaneous Coronary Intervention for the Prevention of Microvascular Obstruction in Acute Myocardial Infarction

Abstract: In STEMI patients treated by PCI and TA, the additional intracoronary administration of adenosine, but not that of nitroprusside, results in a significant improvement of MVO, as assessed by STR.

Cited by 112 publications

References 39 publications

The Coronary Circulation as a Target of Cardioprotection

The Coronary Circulation as a Target of Cardioprotection

Cardiac purinergic signalling in health and disease

A Handbook of Primary PCI: No-Reflow Management

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