Exogenous adenosine triphosphate disodium administration during primary percutaneous coronary intervention reduces no-reflow and preserves left ventricular function in patients with acute anterior myocardial infarction: A study using myocardial contrast echocardiography

Sakuma, Tadamichi; Motoda, Chikaaki; Tokuyama, Takehito; Oka, Takahiro; Tamekiyo, Hiromichi; Okada, Takenori; Otsuka, Masaya; Okimoto, Tomokazu; Toyofuku, Mamoru; Hirao, Hidekazu; Muraoka, Yuji; Ueda, Hiroyuki; Masaoka, Yoshiko; Hayashi, Yasuhiko

doi:10.1016/j.ijcard.2008.11.041

Cited by 16 publications

(13 citation statements)

References 20 publications

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“…Intravenous administration of high doses of ATP during primary PCI reduced left ventricular improved wall motion within an area at risk for MI suggesting that ATP can prevent reperfusion injury [645]. In addition, intravenous ATP administration significantly extended ST-segment resolution, reduced the no-reflow ratio, preserved left ventricular systolic function and prevented left ventricular remodelling [646]. An association of the P2Y2R gene with MI in Japanese men has been reported [647].…”

Section: Myocardial Infarctionmentioning

confidence: 97%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

119

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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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Section: Myocardial Infarctionmentioning

confidence: 97%

Cardiac purinergic signalling in health and disease

Burnstock

Pelleg

2014

Purinergic Signalling

119

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“…Intracoronary adenosine accelerated ST segment resolution and recovery of microvascular perfusion assessed by TIMI frame count and MBG. Also, Sakuma et al [31] in a group of patients with first anterior myocardial infarction, after intravenous administration of a high dose of adenosine (150 ug/kg/min started 5 min before the beginning of the primary PCI and continued for up to 1 h) observed enhanced ST segment resolution 90 min after recanalization, reduced no-reflow ratio, preserved left ventricular systolic function and prevented left ventricular remodeling at 6 months after primary PCI. Wang et al [32], after intravenous adenosine infusion (50 μg/kg/min for 3 h) in patients with acute ST segment elevation noted improved myocardial perfusion, segmental wall motion and global contractile function.…”

Section: Discussionmentioning

confidence: 99%

Effect of New Method of Intracoronary Adenosine Injection during Primary Percutaneous Coronary Intervention on Microvascular Reperfusion Injury - Clinical Outcome and 1-Year Follow-Up

Grygier¹,

Araszkiewicz²,

Lesiak³

et al. 2013

Cardiology

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Objectives: The aim of this single-center, randomized placebo-controlled trial in 70 consecutive patients (64 ± 14 years) with acute myocardial infarction was to examine the role of a new protocol of adenosine administration during primary angioplasty on immediate electrocardiographic and angiographic results, clinical outcome and 1-year follow-up. Methods: Group A (n = 35) twice received intracoronary adenosine through the guiding catheter: immediately after crossing the lesion of the infarct-related artery with guidewire and then after first balloon inflation. Group B (n = 35) received placebo. Results: Resolution of ST segment elevation was more frequently observed in the adenosine than in the placebo group (p < 0.01). Percutaneous coronary intervention (PCI) resulted in borderline better TIMI 3 flow after the procedure in the adenosine group than in the placebo group. Myocardial blush grade 3 at the end of the procedure was significantly improved in the adenosine compared to the placebo group (p < 0.05). At 1-year the composite end-point of death, recurrent myocardial infarction, heart failure and clinically driven target vessel revascularization was present in 8 patients in the adenosine group and 16 patients in placebo group (p < 0.05). Conclusions: Intracoronary adenosine improved electrocardiographic and angiographic results in patients undergoing primary PCI and seemed to be associated with more favorable clinical course.

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“…This hypothesis is supported by the evidence that microembolization of coronary thrombus or fragments of atheromatous plaques is frequent in cases of no-reflow [19] and by the fact that in most cases no reflow occurs immediately after balloon inflation or stent implantation, suggesting a direct link with plaque damage. Many trials have assessed the role of different drugs and treatments (including intracoronary adenosine, intracoronary verapamil, ATP, use of abciximab, thrombus aspiration, and statins) [8][9][10][11][12][13]20,21] to prevent no-reflow during AMI. This is the first randomized study to assess the effects of dipyridamole on already established no-reflow.…”

Section: Discussionmentioning

confidence: 99%