Interplay between Oxidative Stress and Platelet Activation in Coronary Thrombus of STEMI Patients

Calvieri, Camilla; Tanzilli, Gaetano; Bartimoccia, Simona; Cangemi, Roberto; Arrivi, Alessio; Dominici, Marcello; Cammisotto, Vittoria; Viceconte, Nicola; Madon, E; Frati, Giacomo; Violi, Francesco

doi:10.3390/antiox7070083

Cited by 18 publications

(11 citation statements)

References 27 publications

(27 reference statements)

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“…Therefore, HDL has an anti-inflammatory effect and antioxidant properties that may prevent the oxidation of low-density lipoprotein (LDL). Oxidized LDL (oxLDL) increases the risk of both endothelial dysfunction and changes in vessels owing to infiltration by leukocytes and induction of inflammation [8,14,15,16].…”

Section: Introductionmentioning

confidence: 99%

Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease

et al. 2019

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(1) Background: Oxidative stress, chronic inflammation, vasoocclusion, and free iron are all features present in sickle cell disease. Paraoxonases (PON) are a family (PON-1, PON-2, PON-3) of antioxidant enzymes with anti-inflammatory action. Here, for the first time, we described PON-1 activities and PON-1, PON-2, PON-3 polymorphisms in patients with sickle cell disease, homozygous for HbSS, compared with healthy controls. (2) Methods: The groups were matched for age and gender. PON-1 activities (arylesterase and paraoxonase) were determined by enzymatic hydrolysis of phenylcetate and paraoxon, respectively. Polymorphisms were determined by Restriction Fragment Length Polymorphism- Polymerase Chain Reaction (RFLP-PCR). (3) Results: Plasma cholesterol and fractions, ApoA1 and ApoB levels were all decreased in sickle cell disease patients, while anti-oxidized low-density lipoprotein (LDL) antibodies and C-reactive protein were increased. Serum arylesterase activity was lower in sickle cell disease patients when compared with healthy controls. In patients, paraoxonase activity was higher in those with PON-1 RR Q192R polymorphism. In these patients, the increase of serum iron and ferritin levels and transferrin saturation were less pronounced than those observed in patients with QQ or QR polymorphism. No differences were observed with PON-1 L55M, and PON-2 and PON-3 polymorphisms. Multivariate regression analysis showed that transferrin and ferritin concentrations correlated with arylesterase and paraoxonase activities. (4) Conclusions: Both transferrin and ferritin were the main predictors of decreased arylesterase and paraoxonase activities in patients with sickle cell disease. LDL oxidation increased, and RR PON-1 Q192R polymorphism is likely to be a protective factor against oxidative damage in these patients.

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Section: Introductionmentioning

confidence: 99%

Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease

et al. 2019

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“…These events increase the risk of cardiac microvascular occlusion and myocardial dysfunction, a contention that is supported by findings that various biomarkers of platelet activation and neutrophil:platelet aggregates, as well as NETs and their constituents, such as histones, are major components of intravascular thrombi (134)(135)(136). In this context it is noteworthy that systemic histones, presumably derived from NETs, are associated with thrombocytopenia in critically ill patients, an association that has also been observed following experimental administration of histones to mice (137,138).…”

Section: Evidence Linking Platelet Activation To the Pathogenesis Of mentioning

confidence: 90%

Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia

Feldman

Anderson

2020

Front. Immunol.

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Community-acquired pneumonia (CAP) remains an important cause of morbidity and mortality throughout the world with much recent and ongoing research focused on the occurrence of cardiovascular events (CVEs) during the infection, which are associated with adverse short-term and long-term survival. Much of the research directed at unraveling the pathogenesis of these events has been undertaken in the settings of experimental and clinical CAP caused by the dangerous, bacterial respiratory pathogen, Streptococcus pneumoniae (pneumococcus), which remains the most common bacterial cause of CAP. Studies of this type have revealed that although platelets play an important role in host defense against infection, there is also increasing recognition that hyperactivation of these cells contributes to a pro-inflammatory, prothrombotic systemic milieu that contributes to the etiology of CVEs. In the case of the pneumococcus, platelet-driven myocardial damage and dysfunction is exacerbated by the direct cardiotoxic actions of pneumolysin, a major pore-forming toxin of this pathogen, which also acts as potent activator of platelets. This review is focused on the role of platelets in host defense against infection, including pneumococcal infection in particular, and reviews the current literature describing the potential mechanisms by which platelet activation contributes to cardiovascular complications in CAP. This is preceded by an evaluation of the burden of pneumococcal infection in CAP, the clinical features and putative pathogenic mechanisms of the CVE, and concludes with an evaluation of the potential utility of the anti-platelet activity of macrolides and various adjunctive therapies.

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“…32 Calvieri et al recently showed a correlation between platelet activation and increased oxidative stress in patients with STEMI. 33 Reactive oxygen species damage is also the main mechanism in CIN pathogenesis. 34 Increased ROS products, as a result of toxic effects of contrast agents and hypoxia, are considered to be one of the major factors in CIN development.…”

Section: Discussionmentioning

confidence: 99%

Can Thrombus Burden Predict Contrast-Induced Nephropathy in Patients With ST-Segment Elevation Myocardial Infarction?

et al. 2019

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The incidence of contrast-induced nephropathy (CIN) increases in the range from patients with unstable angina to ST-segment elevation myocardial infarction (STEMI). Platelet activation has been associated with pathophysiology of nephropathy and thrombus burden in the infarct-related arteries. We investigated the impact of thrombus burden on CIN in patients with STEMI. We enrolled 883 patients with STEMI who received primary percutaneous coronary intervention. Patients were divided into groups according to thrombus burden and CIN development. Thrombus burden was scored based on thrombolysis in myocardial infarction thrombus grades (TGs). Thrombus grade 4 was defined as large thrombus burden (LTB), while thrombus burden <TG 4 was defined as small thrombus burden. A total of 126 (14.2%) patients with STEMI had CIN, while 313 (35.4%) patients had LTB. Compared to CIN (−) patients, CIN (+) patients were older, had lower hemoglobin levels, lower ejection fraction, and higher contrast media volume administration. Multivariate logistic regression analysis demonstrated that LTB, age, hypertension, and admission glomerular filtration rate were independent predictors of CIN ( P = .016, P < .001, P = .028, P < .001, respectively). Thrombus burden, which is measurable during angiography, may be helpful in the determination of CIN risk in patients with STEMI.

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Interplay between Oxidative Stress and Platelet Activation in Coronary Thrombus of STEMI Patients

Cited by 18 publications

References 27 publications

Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease

Paraoxonases (PON) 1, 2, and 3 Polymorphisms and PON-1 Activities in Patients with Sickle Cell Disease

Platelets and Their Role in the Pathogenesis of Cardiovascular Events in Patients With Community-Acquired Pneumonia

Can Thrombus Burden Predict Contrast-Induced Nephropathy in Patients With ST-Segment Elevation Myocardial Infarction?

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