Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to dissemintate knowledge & skills of Acute Cardiovascular Care
Our mission is to promote excellence in clinical diagnosis, research, technical development, and education in cardiovascular imaging in Europe.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Promoting excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
Working Groups goals is to stimulate and disseminate scientific knowledge in different fields of cardiology.
ESC Councils goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Dr. Manuel Mayr
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List of Authors: Anna Zampetaki*, Peter Willeit*, Lindsey Tilling, Ignat Drozdov, Agnes Mayr, Siegfried Weger, Ajay Shah, Chantal Boulanger, Johann Willeit, Philip J. Chowienczyk, Stefan Kiechl, Manuel Mayr(* equal contribution)
ObjectivesWe sought to explore the association between baseline levels of microRNAs (miRNAs) (1995) and incident myocardial infarction (1995-2005) in the Bruneck cohort and determine their cellular origin.
BackgroundCirculating miRNAs are emerging as potential biomarkers. We have previously identified a miRNA signature for type 2 diabetes in the general population.
MethodsA total of nineteen candidate miRNAs were quantified by real time polymerase chain reactions in 820 participants.
ResultsIn multivariable Cox regression analysis, three miRNAs were consistently and significantly related with incident myocardial infarction: miR-126 showed a positive association (multivariable hazard ratio 2.69 [95%CI 1.45-5.01], P=0.002) while miR-223 and miR-197 were inversely associated with disease risk (multivariable hazard ratio 0.47 [95% CI 0.29-0.75], P=0.002, and 0.56 [95% CI 0.32-0.96], P=0.036). Upon addition of the three miRNAs to a base model of the Framingham Risk Score for hard coronary heart disease as an endpoint, the net reclassification improvement (NRI) was 16.86 [-1.99 – 35.71] % (P=0.080). The integrated discrimination improvement (IDI) was 0.047 [0.005 – 0.089] (P=0.029). To determine the cellular origin of these miRNAs associated with cardiovascular risk, healthy volunteers were subject to limb ischaemia-reperfusion generated by thigh cuff inflation and plasma miRNA changes were analysed at baseline, at 10 min, 1h, 5h, 2 days and 7 days. Computational analysis using the temporal clustering by affinity propagation algorithm identified six distinct miRNA clusters. One cluster included all miRNAs associated with risk of future myocardial infarction. It was characterized by early (1h) and sustained activation (7 days) post ischaemia-reperfusion injury and consisted of miRNAs predominantly expressed in platelets.
ConclusionsIn subjects with subsequent myocardial infarction differential co-expression patterns of circulating miRNAs occur around endothelial-enriched miR-126 with platelets being a major contributor to this miRNA signature.
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