Cangrelor in addition to standard therapy reduces cardiac damage and inflammatory markers in patients with ST-segment elevation myocardial infarction

Abo-Aly, Mohamed; George, Bennet; Shokri, Elica; Chelvarajan, Lakshman; El-Helw, Mohamed; Smyth, Susan S.; Abdel‐Latif, Ahmed; Ziada, Khaled M.

doi:10.1007/s11239-020-02345-8

Cited by 9 publications

(10 citation statements)

References 29 publications

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“…The structure of NETs has been detected in thrombi of ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI) ( 39 ), and the myocardial infarction score ( 18 ) and circulating markers (citrullinated histone 3; myeloperoxidase, neutrophil elastase, etc.) of NETs are significantly reduced after treatment ( 40 ). The activation of platelets and neutrophils increases the risk of major adverse cardiovascular events (MACEs) after acute myocardial infarction ( 41 ).…”

Section: The Role Of Nets In Atherosclerosis and Arterial Thrombosismentioning

confidence: 99%

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Zhou

Tao

Shen

et al. 2021

Front. Cardiovasc. Med.

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Neutrophils play a vital role in the formation of arterial, venous and cancer-related thrombosis. Recent studies have shown that in a process known as NETosis, neutrophils release proteins and enzymes complexed to DNA fibers, collectively called neutrophil extracellular traps (NETs). Although NETs were originally described as a way for the host to capture and kill bacteria, current knowledge indicates that NETs also play an important role in thrombosis. According to recent studies, the destruction of vascular microenvironmental homeostasis and excessive NET formation lead to pathological thrombosis. In vitro experiments have found that NETs provide skeletal support for platelets, red blood cells and procoagulant molecules to promote thrombosis. The protein components contained in NETs activate the endogenous coagulation pathway to promote thrombosis. Therefore, NETs play an important role in the formation of arterial thrombosis, venous thrombosis and cancer-related thrombosis. This review will systematically summarize and explain the study of NETs in thrombosis in animal models and in vivo experiments to provide new targets for thrombosis prevention and treatment.

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Section: The Role Of Nets In Atherosclerosis and Arterial Thrombosismentioning

confidence: 99%

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Zhou

Tao

Shen

et al. 2021

Front. Cardiovasc. Med.

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“…Furthermore, NET burden at the culprit site correlates positively with infarct size, assessed by cardiac enzyme elevation and cardiac MRI, and left ventricular dysfunction, assessed by wall-motion score index at a year follow-up ( 45 ). Circulating MPO and NE levels significantly decrease after MI treatment ( 46 ).…”

Section: Role Of Nets In the Complications Of Diabetesmentioning

confidence: 99%

Emerging role of neutrophil extracellular traps in the complications of diabetes mellitus

et al. 2022

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Immune dysfunction is widely regarded as one of the central tenants underpinning the pathophysiology of diabetes mellitus (DM) and its complications. When discussing immunity, the role of neutrophils must be accounted for: neutrophils are the most abundant of the circulating immune cells and are the first to be recruited to sites of inflammation, where they contribute to host defense via phagocytosis, degranulation, and extrusion of neutrophil extracellular traps (NETs). NETs are composed of DNA associated with nuclear and cytosolic neutrophil proteins. Although originally reported as an antimicrobial strategy to prevent microbial dissemination, a growing body of evidence has implicated NETs in the pathophysiology of various autoimmune and metabolic disorders. In these disorders, NETs propagate a pathologic inflammatory response with consequent tissue injury and thrombosis. Many diabetic complications—such as stroke, retinopathy, impaired wound healing, and coronary artery disease—involve these mechanisms. Therefore, in this review, we discuss laboratory and clinical data informing our understanding of the role of NETs in the development of these complications. NET markers, including myeloperoxidase, citrullinated histone H3, neutrophil elastase, and cell-free double-stranded DNA, can easily be measured in serum or be detected via immunohistochemical/immunocytochemical staining of tissue specimens. Therefore, NET constituents potentially constitute reliable biomarkers for use in the management of diabetic patients. However, no NET-targeting drug is currently approved for the treatment of diabetic complications; a candidate drug will require the outcomes of well-designed, robust clinical trials assessing whether NET inhibition can benefit patients in terms of morbidity, quality of life, health expenditures, and mortality. Therefore, much work remains to be done in translating these encouraging pieces of data into clinical trials for NET-targeting medications to be used in the clinic.

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“…Interestingly, cangrelor allows a reversible anti-platelet effect with a low bleeding risk and transition to ticagrelor may be started during infusion, thereby minimizing the risk of a newly increased platelet reactivity respect to clopidogrel and prasugrel [128,129]. Furthermore, early administration of cangrelor in STEMI patients was associated with more effective platelet inhibition during pPCI and significantly lowered the deleterious inflammatory response compared to standard anti-platelet therapy [130]. On the other hand, preloading with a glycoprotein IIb IIIa inhibitor determines a non-reversible anti-platelet effect with a higher bleeding risk [131].…”

Section: Anti-platelet Therapymentioning

confidence: 99%

Reducing Cardiac Injury during ST-Elevation Myocardial Infarction: A Reasoned Approach to a Multitarget Therapeutic Strategy

Bellis

Gioia²,

Mauro

et al. 2021

JCM

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The significant reduction in ‘ischemic time’ through capillary diffusion of primary percutaneous intervention (pPCI) has rendered myocardial-ischemia reperfusion injury (MIRI) prevention a major issue in order to improve the prognosis of ST elevation myocardial infarction (STEMI) patients. In fact, while the ischemic damage increases with the severity and the duration of blood flow reduction, reperfusion injury reaches its maximum with a moderate amount of ischemic injury. MIRI leads to the development of post-STEMI left ventricular remodeling (post-STEMI LVR), thereby increasing the risk of arrhythmias and heart failure. Single pharmacological and mechanical interventions have shown some benefits, but have not satisfactorily reduced mortality. Therefore, a multitarget therapeutic strategy is needed, but no univocal indications have come from the clinical trials performed so far. On the basis of the results of the consistent clinical studies analyzed in this review, we try to design a randomized clinical trial aimed at evaluating the effects of a reasoned multitarget therapeutic strategy on the prevention of post-STEMI LVR. In fact, we believe that the correct timing of pharmacological and mechanical intervention application, according to their specific ability to interfere with survival pathways, may significantly reduce the incidence of post-STEMI LVR and thus improve patient prognosis.

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Cangrelor in addition to standard therapy reduces cardiac damage and inflammatory markers in patients with ST-segment elevation myocardial infarction

Cited by 9 publications

References 29 publications

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

The Emerging Role of Neutrophil Extracellular Traps in Arterial, Venous and Cancer-Associated Thrombosis

Emerging role of neutrophil extracellular traps in the complications of diabetes mellitus

Reducing Cardiac Injury during ST-Elevation Myocardial Infarction: A Reasoned Approach to a Multitarget Therapeutic Strategy

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