Impact of active smoking on the immature platelet fraction and its relationship with the extent of coronary artery disease

Abstract

Introduction:Smoking represents a major cardiovascular risk factor, due to the induction of oxidative stress and low-grade, continuous, inflammation that contribute to promote atherothrombosis. However, the mechanisms leading to increased platelet aggregability associated with smoking are only partially defined. A potential role has been hypothesized for immature platelets, a younger and potentially more reactive fraction, previously associated with the main determinants of coronary artery disease (CAD). Therefore, the aim of our study was to define the impact of smoking on the immature platelet fraction (IPF) and its relationship with prevalence and extent of coronary artery disease. Methods: We enrolled a cohort of consecutive patients undergoing coronary angiography in a single centre. Significant CAD was defined as at least 1 vessel stenosis >50%, while severe CAD was defined as left main and/or three-vessel disease. IPF was measured at admission by routine blood cell count (Sysmex XE-2100). Results: We included in our study 2553 patients who were divided according to smoking status (active smokers: 512; nonactive smokers: 2041). Smokers were younger, more frequent males, with lower rate of diabetes mellitus, previous PCI and previous CABG (P < .001, respectively) and were in treatment less often with ARB, BB, nitrates, statins, ASA, clopidogrel, CCB and diuretics (P < .001, respectively) as compared to nonactive smokers. Higher percentage of smokers was observed in patients with higher IPF values, and at multivariate analysis, active smoking resulted as an independent predictor of higher IPF (adjusted OR [95% CI] = 1.59[1.03-2.45], P = .035). Among smokers, higher IPF was associated with lower ejection fraction (P = .034), percentage of acute coronary syndrome (P = .002) and platelet count (P < .001) compared to ones with lower IPF. However, the IPF (according to quartiles values) was not associated with the prevalence and extent of CAD (82.5%, 80.4%, 86.1% and 80.9%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 0.98[0.79-1.23], P = .89) and severe CAD (31%, 31.1%, 39.1% and 35.2%, from 1st to 4th quartile, respectively, adjusted OR[95% CI] = 1.03[0.86-1.23], P = .76).

Platelets and renal failure in the SARS-CoV-2 syndrome

“…Interestingly, we found increased immature platelet fraction IPF (IPF>7) in COVID-19-infected subjects, who had evidence of elevated D-dimers and AKI. Immature platelets usually have larger size and are considered to be more reactive and increased IPF has been associated with smokingrelated cardiovascular disease and inflammation [28,29]. Day to day variation in MVP can be related to various factors, including misinterpretation of the true platelet size due to platelets clumps, and some more activated platelets will be consumed in clot formation and not counted by automatic reader.…”

The role of traditional obesity parameters in predicting the number of stenosed coronary arteries (≥ 60%) among patients undergoing cardiac catheterization

“…Meanwhile, Nardin et al 31 held that smoking was not a contributing factor of CAD, and Akyüz et al 32 found that nonsmokers had a higher tendency than smokers to develop severe CAD. Akyüz et al 32 explained this finding by highlighting that non-smoker CAD patients have higher tumor necrosis factor (cytokine 1A (TL1A)).…”

Epigenetic Biomarkers Screening of Non-Coding RNA and DNA Methylation Based on Peripheral Blood Monocytes in Smokers

“…Platelet activation is commonly seen in the blood of smokers. Platelets isolated from smokers exhibit spontaneous aggregation ( Nardin et al, 2020 ). After exposure to smoker serum, platelets isolated from non-smokers exhibit a high degree of aggregation ( Pamukcu et al, 2011 ).…”