Comparing the Risk Factors of Plaque Rupture and Failed Plaque Healing in Acute Coronary Syndrome

Brezinski, Mark E.

doi:10.1001/jamacardio.2019.0312

Cited by 9 publications

(4 citation statements)

References 10 publications

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“…These distinct features between NSTEMI and STEMI might reflect different pathophysiological mechanisms leading to these ACS entities, which could not be picked up based on neutrophil count or NLR only. Noteworthy, it has recently been recognized that beside differences in ECG and troponin levels, plaque composition as well as mechanisms of atherogenesis influence CAD patient outcome [28][29][30]. MPO, stored in neutrophil azurophilic granules, is released upon neutrophil activation.…”

Section: Soluble Neutrophil Markers In Acsmentioning

confidence: 99%

Neutrophil Phenotypes in Coronary Artery Disease

Maréchal

Tridetti

Nguyen

et al. 2020

JCM

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Clinical evidence indicates that innate immune cells may contribute to acute coronary syndrome (ACS). Our prospective study aimed at investigating the association of neutrophil phenotypes with ACS. 108 patients were categorized into chronic stable coronary artery disease (n = 37), unstable angina (UA) (n = 19), Non-ST-Elevation Myocardial Infarction (NSTEMI) (n = 25), and ST-Elevation Myocardial Infarction (STEMI) (n = 27). At the time of inclusion, blood neutrophil subpopulations were analysed by flow cytometry. Differential blood cell count and plasma levels of neutrophilic soluble markers were recorded at admission and, for half of patients, at six-month follow-up. STEMI and NSTEMI patients displayed higher neutrophil count and neutrophil-to-lymphocyte ratio than stable and UA patients (p < 0.0001), which normalized at six-month post-MI. Atypical low-density neutrophils were detected in the blood of the four patient groups. STEMI patients were characterized by elevated percentages of band cells compared to the other patients (p = 0.019). Multivariable logistic regression analysis revealed that plasma levels of total myeloperoxidase was associated with STEMI compared to stable (OR: 1.434; 95% CI: 1.119–1.837; P < 0.0001), UA (1.47; 1.146–1.886; p = 0.002), and NSTEMI (1.213; 1.1–1.134; p = 0.0001) patients, while increased neutrophil side scatter (SSC) signal intensity was associated with NSTEMI compared to stable patients (3.828; 1.033–14.184; p = 0.045). Hence, changes in neutrophil phenotype are concomitant to ACS.

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Section: Soluble Neutrophil Markers In Acsmentioning

confidence: 99%

Neutrophil Phenotypes in Coronary Artery Disease

Maréchal

Tridetti

Nguyen

et al. 2020

JCM

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“…Conversely, it has been postulated that angiogenesis is necessary for healing and stabilization after plaque rupture, and that defective angiogenesis in plaques with a long necrotic core is the pathological correlate of acute coronary syndromes (ACS) 39 . Indeed, the frequency of lipid‐rich, thin‐cap coronary plaques is similar in patients with recurrent ACS and in those with a single unheralded MI, but healed coronary plaques are rare among subjects with recurrent ACS and prevalent among those who suffered from a single MI or have long‐standing stable angina 40,41 . According to this view, suppression of VEGF signalling, such as that achieved with nintedanib, may result in atheroma instability and rupture 39 (Figure 2).…”

Section: Effects Of Nintedanib On Coronary Atherosclerotic Plaquesmentioning

confidence: 99%

Cardiovascular safety of the tyrosine kinase inhibitor nintedanib

Ameri

Tini

Spallarossa

et al. 2021

Brit J Clinical Pharma

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The intracellular tyrosine kinase inhibitor nintedanib has shown great efficacy for the treatment of idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases. However, the incidence rate of myocardial infarction (MI) among participants in landmark IPF trials was remarkable, peaking at 3/100 patient‐years. Although subjects with IPF often have a high cardiovascular (CV) risk profile, the occurrence of MI in nintedanib‐treated patients may not be fully explained by clustering of CV risk factors. Nintedanib inhibits the vascular endothelial growth factor, platelet‐derived growth factor and fibroblast growth factor pathways, which play important roles in the biology of the atherosclerotic plaque and in the response of the heart to ischaemia. Hence, unwanted CV effects may partly account for nintedanib‐related MI. We review the evidence supporting this hypothesis and discuss possible actions for a safe implementation of nintedanib in clinical practice, building on the experience with tyrosine kinase inhibitors acquired in cardio‐oncology.

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“…These distinct features between NSTEMI and STEMI might reflect different pathophysiological mechanisms leading to these ACS entities, which could not be picked up based on neutrophil count or NLR only. Noteworthy, it has recently been recognized that beside differences in ECG and troponin levels, plaque composition as well as mechanisms of atherogenesis influence CAD patient outcome [28][29][30] . MPO, stored in neutrophil azurophilic granules, is released upon neutrophil activation.…”

Section: Soluble Neutrophil Markers In Acsmentioning

confidence: 99%

Neutrophil Dynamics in Acute Coronary Syndrome

Maréchal¹,

Tridetti²,

Nguyen³

et al. 2020

Preprint

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Aims: Clinical evidence indicates that innate immune cells may contribute to the onset and outcome of acute coronary syndrome (ACS). Our prospective study aimed at analysing neutrophil phenotypes in ACS and their role in predicting 1-year major cardiovascular events.Methods: Blood neutrophil phenotypes were analysed by flow cytometry. Differential blood cell count and plasma levels of soluble markers were recorded at admission and at 6-month follow-up.

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Comparing the Risk Factors of Plaque Rupture and Failed Plaque Healing in Acute Coronary Syndrome

Cited by 9 publications

References 10 publications

Neutrophil Phenotypes in Coronary Artery Disease

Neutrophil Phenotypes in Coronary Artery Disease

Cardiovascular safety of the tyrosine kinase inhibitor nintedanib

Neutrophil Dynamics in Acute Coronary Syndrome

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