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      Effect of intravenous application of nicorandil on area of myocardial infarction in patients with STEMI during the perioperative stage of PCI

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          Abstract

          OBJECTIVE: The aim of the present study was to evaluate the effectiveness and safety of nicorandil in improving the area of myocardial infarction in patients with acute myocardial infarction (AMI). METHODS: One hundred and twenty patients with acute ST-segment elevation myocardial infarction (STEMI) admitted to our hospital between December 1, 2018 and December 31, 2019 were selected and randomly allocated to the experimental group (group A, n = 60) and the control group (group B, n = 60). In the experimental group, an infusion of nicorandil was given intravenously before the first balloon dilation or 1 minute before the stent placement, and with the completion of the infusion, nicorandil maintenance infusion was given. In the control group, only balloon dilation and stent placement were undertaken. RESULTS: The postoperative peak levels of myoglobin, creatine kinase isoform and hypersensitive troponin T were significantly lower in group A than in group B (p < 0.05). Moreover, the left ventricular ejection fraction (LVEF) on the 180th day post operation was substantially greater in group A than in group B (p < 0.01), and the area of myocardial infarction was significantly smaller in patients in group A than those in group B on the 180th day post operation (p < 0.01). In terms of the safety, there were no statistically significant differences in the incidence of slow flow/no reflow, malignant arrhythmias, and hypotension within 24 hours post operation between the two groups (p > 0.05), and no major adverse cardiovascular event (MACE) occurred in either group during the postoperative follow-up period of 180 days (p > 0.05). CONCLUSION: Intravenous administration of nicorandil in patients with STEMI during the perioperative percutaneous coronary intervention (PCI) period was effective in reducing the area of myocardial infarction and myocardial injury without increasing the incidence of malignant arrhythmias, hypotension, or composite cardiovascular events during the drug administration period.

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          Does reperfusion injury exist in humans?

          Robert Kloner (1993)
          Timely coronary reperfusion as treatment for acute myocardial infarction reduces myocardial infarct size, improves left ventricular function and survival. There is still concern that at the time of reperfusion, a further injury occurs to the myocardium. Theoretically, if this "reperfusion injury" could be treated and eliminated, the outcome for patients with myocardial infarction might further improve. The concept of reperfusion injury is closely tied to the concept that oxygen radicals generated at the time of reperfusion cause tissue damage. There are four basic forms of reperfusion injury. Lethal reperfusion injury is described as myocyte cell death due to reperfusion itself rather than to the preceding ischemia. This concept continues to be controversial in both experimental animal and clinical studies. Vascular reperfusion injury refers to progressive damage to the vasculature over time during the phase of reperfusion. Manifestations of vascular reperfusion injury include an expanding zone of no reflow and a deterioration of coronary flow reserve. This form of reperfusion injury has been documented in animal models and probably occurs in humans. Stunned myocardium refers to postischemic ventricular dysfunction of viable myocytes and probably represents a form of "functional reperfusion injury." This phenomenon is well documented in both animal models and humans. Reperfusion arrhythmias represent the fourth form of reperfusion injury. They include ventricular tachycardia and fibrillation that occur within seconds to minutes of restoration of coronary flow after brief (5 to 15 min) episodes of myocardial ischemia. True reperfusion arrhythmias occur in only a small percentage of patients receiving thrombolytic therapy for acute myocardial infarction and are not a sensitive indicator for successful reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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            Myocardial protection from ischemia-reperfusion injury post coronary revascularization

            Andrew Binder, Asghar Ali, Raveen Chawla … (2015)
            Effective primary and secondary prevention and advances in cardiac surgery have significantly improved the care and outcomes of patients with myocardial ischemia. While timely reperfusion has proved to be an invaluable tool, ischemia-reperfusion injury represents a mechanism that may limit its effectiveness. Numerous experimental studies have shown effective protection from ischemia-reperfusion injury in animal models, but translation into clinical practice has been less successful. This article summarizes the role of ischemia-reperfusion injury in the pathophysiology of ischemic heart disease and gives an overview of the various modalities that have been developed in order to provide myocardial protection from reperfusion injury in clinical practice.
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              Intracoronary versus intravenous bolus abciximab during primary percutaneous coronary intervention in patients with acute ST-elevation myocardial infarction: a randomised trial.

              Holger Thiele, Jochen Wöhrle, Rainer Hambrecht … (2012)
              Intracoronary administration of an abciximab bolus during a primary percutaneous coronary intervention results in a high local drug concentration, improved perfusion, and reduction of infarct size compared with intravenous bolus application. However, the safety and efficacy of intracoronary versus standard intravenous bolus application in patients with ST-elevation myocardial infarction (STEMI) undergoing this intervention has not been tested in a large-scale clinical trial. The AIDA STEMI trial was a randomised, open-label, multicentre trial. Patients presenting with STEMI in the previous 12 h with no contraindications for abciximab were randomly assigned in a 1:1 ratio by a central web-based randomisation system to intracoronary versus intravenous abciximab bolus (0·25 mg/kg bodyweight) during percutaneous coronary intervention with a subsequent 12 h intravenous infusion 0·125 μg/kg per min (maximum 10 μg/min). The primary endpoint was a composite of all-cause mortality, recurrent infarction, or new congestive heart failure within 90 days of randomisation. Secondary endpoints were the time to occurrence of the primary endpoint, each individual component of that endpoint, early ST-segment resolution, thrombolysis in myocardial infarction (TIMI) flow grade, and enzymatic infarct size. A masked central committee adjudicated the primary outcome and its components. Treatment allocation was not concealed from patients and investigators. This trial is registered with ClinicalTrials.gov, NCT00712101. Between July, 2008, and April, 2011, 2065 patients were randomly assigned intracoronary abciximab (n=1032) or intravenous abciximab (n=1033). Intracoronary, as compared with intravenous abciximab, resulted in a similar rate of the primary composite clinical endpoint at 90 days in 1876 analysable patients (7·0%vs 7·6%; odds ratio [OR] 0·91; 95% CI 0·64-1·28; p=0·58). The incidence of death (4·5%vs 3·6%; 1·24; 0·78-1·97; p=0·36) and reinfarction (1·8%vs 1·8%; 1·0; 0·51-1·96; p=0·99) did not differ between the treatment groups, whereas less patients in the intracoronary group had new congestive heart failure (2·4%vs 4·1%; 0·57; 0·33-0·97; p=0·04). None of the secondary endpoints or safety measures differed significantly between groups. In patients with STEMI undergoing primary percutaneous coronary intervention, intracoronary as compared to intravenous abciximab did not result in a difference in the combined endpoint of death, reinfarction, or congestive heart failure. Since intracoronary abciximab bolus administration is safe and might be related to reduced rates of congestive heart failure the intracoronary route might be preferred if abciximab is indicated. Lilly, Germany. University of Leipzig-Heart Centre. University of Leipzig, Clinical Trial Centre Leipzig, supported by the Federal Ministry of Education and Research (BMBF). Copyright © 2012 Elsevier Ltd. All rights reserved.
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                Author and article information

                Journal
                Title: Clinical Hemorheology and Microcirculation
                Abbreviated Title: CH
                Publisher: IOS Press
                ISSN (Print): 13860291
                ISSN (Electronic): 18758622
                Publication date Created: May 06 2021
                Publication date (Print): May 06 2021
                Volume: 77
                Issue: 4
                Pages: 411-423
                Affiliations
                [1 ]Department of Cardiology, Yulin First People’s Hospital, The Sixth Affiliated Hospital of Guangxi Medical University, Yulin, Guangxi, China
                Article
                DOI: 10.3233/CH-200998
                PubMed ID: 33386796
                SO-VID: d5e4396c-e194-464c-a9ae-1a29ffde5ac8
                Copyright © © 2021
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