Prasugrel compared to ticagrelor in primary PCI

Abstract Background Prasugrel and ticagrelor have similar recommendations in the setting of primary PCI by current guidelines. Data comparing both in daily clinical practice of primary PCI for ST-elevation myocardial infarction is limited. Purpose To compare the effect of prasugrel and ticagrelor on in-hospital outcomes after primary PCI. Methods and results We prospectively enrolled 5365 patients treated with prasugrel (n=2785, 51.9%) or ticagrelor (n=2580; 48.1%) in the setting of primary PCI from January 2011 to December 2018 in a nationwide registry. In-hospital outcomes were compared and multiple logistic regression analysis was performed. Prasugrel treated patients were younger, less often in cardiogenic shock, with lower rates of previous stroke and had shorter ischemic time. Both groups showed similar rates of previous MI, diabetes and current resuscitation. In the univariate analysis mortality was lower in patients with prasugrel (2.5% vs. 4.4% p&amp;lt;0.01). Similarly, MACE (3.3% vs. 5.3%, p&amp;lt;0.01) and NACE (4.0% vs. 5.7% p&amp;lt;0.01) were lower in prasugrel treated patients, whereas major bleeding events did not differ (0.4% vs. 0.6% p=0.24). After adjustment in multivariable analysis mortality (0.99 95% CI 0.57 to 1.72), MACE (OR 0.99 95% CI 0.65 to 1.52) as well as NACE (0.86 95% CI 0.61 to 1.22) did not differ in patients treated with prasugrel compared to ticagrelor. Conclusion Patients treated with prasugrel showed improved outcomes compared to ticagrelor in a large cohort of primary PCI. However, after adjustment for confounders the Advantage of prasugrel in primary PCI did not persist. Funding Acknowledgement Type of funding source: Other. Main funding source(s): Austrian Society of Cardiology </jats:sec

Peripheral blood monocyte Sirt1 expression is reduced in patients with coronary artery disease

BACKGROUND: Inflammation plays a key role in atherosclerosis. Sirt1 regulates transcription factors involved in inflammatory processes and blunts atherosclerosis in mice. However, its role in humans remains to be defined. This study was therefore designed to investigate the role of Sirt1 in the development of atherosclerosis. METHODS AND RESULTS: 48 male subjects admitted for cardiac catheterization were subdivided into healthy subjects, patients with stable coronary artery disease (CAD), and with acute coronary syndromes (ACS). Monocytes were isolated and Sirt1 mRNA levels were determined. Sirt1 gene expression was higher in healthy subjects as compared to patients with CAD or ACS (P<0.05), respectively. Interestingly, HDL levels correlated positively with Sirt1 expression. Thus, HDL from the three groups was isolated and incubated with THP-1 monocytes to determine the effects of HDL on Sirt1 protein in controlled experimental conditions. HDL from healthy subjects stimulated Sirt1 expression in THP-1 monocytes to a higher degree than HDL from CAD and ACS patients (P<0.05). Paraoxonase-1 (PON-1), a HDL-associated enzyme, showed a reduced activity in HDL isolated from CAD and ACS patients as compared to the controls (P<0.001). CONCLUSIONS: Monocytic Sirt1 expression is reduced in patients with stable CAD and ACS. Experiments on THP-1 monocytes suggest that this effect is HDL-dependent and is mediated by a reduced activity of HDL-associated enzyme PON1