Cardioprotective Effects of Intracoronary Morphine in ST‐Segment Elevation Myocardial Infarction Patients Undergoing Primary Percutaneous Coronary Intervention: A Prospective, Randomized Trial

Abstract

BackgroundA cardioprotective role of morphine acting via opioid receptors has been demonstrated, and previous preclinical studies have reported that morphine could reduce reperfusion injury and myocardial infarct size in a way similar to that of ischemic periconditioning. This study aimed to evaluate the effect of intracoronary morphine on myocardial infarct size in patients with ST‐elevation myocardial infarction undergoing primary percutaneous coronary intervention.Methods and ResultsThis study was designed as a 2‐center, prospective, randomized, open‐label, blinded end point trial. A total of 91 ST‐elevation myocardial infarction patients with thrombolysis in myocardial infarction flow grade of 0 to 1 undergoing primary percutaneous coronary intervention were randomly assigned to a morphine or control group at a 1:1 ratio. The morphine group received 3 mg of morphine sulfate diluted with 3 mL of normal saline, and the control group received 3 mL of normal saline into a coronary artery immediately after restoration of coronary flow. The primary end point was myocardial infarct size assessed by cardiac magnetic resonance imaging The cardiac magnetic resonance images were evaluated for 42 and 38 patients in the morphine and control groups, respectively. Myocardial infarct size was not different between the 2 groups (25.6±11.2% versus 24.6±10.5%, P=0.77), nor was the extent of microvascular obstruction or myocardial salvage index (6.0±6.3% versus 5.1±4.6%, P=0.91; 31.1±15.2% versus 30.3±10.9%, P=0.75, respectively). There was no difference in peak creatine kinase‐MB level, final thrombolysis in myocardial infarction flow, myocardial brush grade, or complete resolution of ST‐segment.ConclusionsIntracoronary morphine administration could not reduce myocardial infarct size in ST‐elevation myocardial infarction patients undergoing primary percutaneous coronary intervention.Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT01738100.

Análise da interação farmacológica e eficácia da morfina perante pacientes com síndrome coronariana aguda: revisão sistemática / Analysis of pharmacological interaction and morphine efficacy in patients with acute coronary syndrome: systematic review

“…Gwag et al, 2017 (28) Amostragem: 91 pacientes. Metodologia: pacientes com infarto do miocárdio com supradesnivelamento do segmento ST no ECG foram divididos em grupo controle (solução salina) e morfina, ambos pós intervenção coronária percutânea, proporção 1:1.…”

“…Além deste cenário importante frente a inibição da agregação, o resultado de pesquisas deste campo tem mostrado que o efeito isolado da morfina, em aplicação durante terapia de intervenção coronariana percutânea, não apresenta melhora no padrão do infarto, tendo um mesmo espectro de musculatura cardíaca isquemiada, associado à ausência de mudanças nos picos de CK-MB, bem como semelhança de tempo de resolução do supra desnivelamento do segmento ST para grupos que utilizam ou não a morfina. Isso demonstra que o potencial de sobrevida para esse paciente não melhora com a analgesia (28) .…”

Mechanical and Pharmacological Revascularization Strategies for Prevention of Microvascular Dysfunction in ST-Segment Elevation Myocardial Infarction: Analysis from Index of Microcirculatory Resistance Registry Data

“…However, another randomized controlled trial demonstrated that morphine did not show the preventive effect of myocardial salvage. They suggested that morphine use is associated with a slower uptake, delayed onset of action, and diminished effects of oral antiplatelet agents [ 33 ]. We demonstrated that intravenous morphine use during primary PCI did not differ between the two groups.…”

Overexpression of miR‑200a‑3p promoted inflammation in�sepsis‑induced brain injury through ROS‑induced NLRP3

“…In the case of sepsis, miRNAs can upregulate the expression of miRNA-155, enhance the release of inflammatory factors and inhibit the synthesis of anti-inflammatory factors (15). In the pathophysiological process of sepsis, miRNAs can promote the synthesis of inflammatory factors, enhance immune function, induce the apoptosis of immune cells and induce immunosuppression (16). miRNAs are involved in the precise regulation of the genesis, development and outcome of sepsis at various levels, such as the inflammatory response, immune cell differentiation and apoptosis.…”

“…miRNAs are involved in the precise regulation of the genesis, development and outcome of sepsis at various levels, such as the inflammatory response, immune cell differentiation and apoptosis. It is speculated that these miRNAs may possess regulatory effects on the differentiation of the effector T-cell (16). Thus, the present study next determined that overexpression of miRNA-200a-3p promoted the levels of IL-1β and IL-18 in vitro .…”