Mean platelet volume (MPV) is a strong predictor of impaired angiographic reperfusion and 6-month mortality in ST-elevation myocardial infarction (MI) treated with primary percutaneous coronary intervention (PCI). No data is available for other platelet volume indices: platelet distribution width (PDW) and platelet large cell ratio (P-LCR). The aim was to assess the impact of 3 platelet volume indices on long-term prognosis in patients treated with primary PCI in acute MI. This prospective study enrolled 538 patients who underwent primary PCI in acute MI. Admission blood samples were measured for MPV, PDW, and P-LCR. The patients were followed-up a mean period of 26 ± 11 months with regard to cardiac death, non-fatal reinfarction, re-PCI or coronary artery bypass grafting. Kaplan-Meier survival analysis showed a significantly higher 26-month mortalityrate in patients with high MPV (≥ 11.7 fL) than in those with low MPV (< 11.7 fL) (14.6% vs. 5.5%, p = 0.0008). Similar findings were related to high P-LCR (≥ 38.1%) vs. low P-LCR (< 38.1%) - mortality 13.8% vs. 5.8%, p = 0.0025. Higher PDW values (≥ 16 fL) correlated with higher mortality rate as compared to PDW < 16 fL (17.4% vs. 6.3%, p = 0.0012). PDW was found to be an independent prognostic factor for cardiac mortality and composite endpoint. Mean platelet volume, platelet distribution width and platelet large cell ratio measured on admission are strong, independent prognostic factors in PCI-treated acute MI.

Classic atherosclerosis risk factors do not explain all cases of chronic heart disease. There is significant evidence that gut microbiota may influence the development of atherosclerosis. The widespread prevalence of chronic Helicobacter pylori (H. pylori, HP) infections suggests that HP can be the source of components that stimulate local and systemic inflammatory responses. Elevated production of reactive oxygen species during HP infection leads to cholesterol oxidation, which drives atherogenesis. The aim of this study is to explore the link between persistent HP infection and a high-fat diet in the development of proinflammatory conditions that are potentially proatherogenic. An in vivo model of Caviae porcellus infected with HP and exposed to an experimental diet was investigated for the occurrence of a proinflammatory and proatherogenic endothelial environment. Vascular endothelial primary cells exposed to HP components were tested in vitro for oxidative stress, cell activation and apoptosis. The infiltration of inflammatory cells into the vascular endothelium of animals infected with HP and exposed to a high-fat diet was observed in conjunction with an increased level of inflammatory markers systemically. The arteries of such animals were the least elastic, suggesting the role of HP in arterial stiffness. Soluble HP components induced transformation of macrophages to foam cells in vitro and influenced the endothelial life span, which was correlated with Collagen I upregulation. These preliminary results support the hypothesis that HP antigens act synergistically with a high-fat diet in the development of proatherogenic conditions.

Objectives: Atmospheric pressure is the most objective weather factor because regardless of if outdoors or indoors it affects all objects in the same way. The majority of previous studies have used the average daily values of atmospheric pressure in a bioclimatic analysis and have found no...

Introduction : Pathogens, including Helicobacter pylori (Hp), have been suggested to contribute to the development of coronary heart disease (CHD), although the evidence still remains insufficient. The study was focused on the exposure of CHD patients to Hp and resulting anti-Hp heat shock...