Our mission is to become a worldwide reference for education in the field for all professionals involved in the process to disseminate 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 mission is to promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our mission is to reduce the burden of cardiovascular disease in Europe through percutaneous cardiovascular interventions.
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.
Our mission is to improve quality of life and longevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
The ESC Councils' goal is to share knowledge among medical professionals practising in specific cardiology domains.
OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
De Angelis A, Piegari E, Cappetta D, Marino L, Filippelli A, Berrino L, Ferreira-Martins J, Zheng H, Hosoda T, Rota M, Urbanek K, Kajstura J, Leri A, Rossi F, Anversa P. Circulation 2010;121:276-292.
Cardiac progenitor cells (CPCs) from rats were exposed to anthracycline, which increased the formation of reactive oxygen species and caused increases in DNA damage, expression of p53, telomere attrition, and apoptosis, and finally a cell-cycle arrest at the G2/M transition, and a decrease in CPC growth. Delivery of syngeneic progenitor cells into the failing myocardium opposed the progression of doxorubicin cardiotoxicity and stimulated the regeneration of cardiomyocytes and vascular structures, which improved ventricular performance and rate of animal survival.
Anthracyclines are commonly used in several types of cancers. Their effectiveness is opposed to toxicity against myocardium resulting in resistant heart failure. The study provides experimental evidence that the critical pathomechanism is dysfunction of cardiac progenitor cells (CPCs). It is suggested that autologous CPCs obtained before antineoplastic drugs when administered to individuals after an expose to cardiotoxic drugs may inhibit the development of heart failure.
Chen HH, Cataliotti A, Schirger JA, Martin FL, Harstad LK, Burnett JC Jr.
J Am Coll Cardiol. 2009 Apr 14;53(15):1302-8.
In dogs with pacing-induced subacute overt heart failure accompanied by renal dysfunction (cardiorenal syndrome), the authors demonstrated that the systemic infusion of B-type natriuretic peptide (BNP) increased only urine flow (with only a trend for an increase in urinary sodium excretion and glomerular filtration rate), whereas local renal delivery of BNP (related to greater direct exposition of renal tubules to BNP) resulted in a significant dieresis, natriuresis and an increase in glomerular filtration rate, overcoming renal resistance to BNP.
The management of cardiorenal syndrome remains a difficult clinical task. Among the diverse pathophysiological mechanisms leading to combined heart and kidney dysfunction, the phenomenon of resistance to natriuretic peptides is of a particular importance. However, the interventions counteracting this pathomechanisms are lacking. The experimental study provides the argument that such a therapy (local renal delivery of natriuretic peptide) might be advantageous for patients with acute heart failure and renal dysfunction, but this promising therapeutic approach needs to be further tested in clinical trials.
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