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 mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in 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"
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. Philippe Charron,
Dr Van Tintelen (Netherlands) reviewed the recent molecular genetic data available in ARVC (Arrhythmogenic right ventricular cardiomyopathy), a monogenic disorder mostly related to mutations in desmosomal genes. He underlined the genetic heterogeneity as well as the variable cardiac expression and the reduced penetration of the disease. Although genetic testing is already translated into the clinical practice, he acknowledges the difficulties of interpreting some mutations that should be considered rather as genetic variants of unknown significance. He also reported unpublished data from his group about mutations in phospholamban gene identified in ARVC patients, expanding the complexity of the genetic background.
Dr Delmar (USA) emphasized how important is the insight provided by desmosomal mutations into the pathophysiology of ARVC. He nicely explained the major component of the disease that appears to be related to structural modifications of the mechanical junctions (desmosomes), electrical coupling abnormalities (gap junction) and also possibly to abnormal sodium channel current, with new data he provided today.
Dr Lambiase (UK) provided interesting data from a mouse model of ARVC (heterozygous desmoplakine gene knock out) with in vivo electrophysiology that demonstrated ventricular tachycardia in this model but not in the wild type mouse. Conduction abnormalities (coupling interval) could be also demonstrated. In human, refined voltage mapping in patients with ARVC also demonstrated abnormalities in both conduction and repolarization kinetics.
Dr Corrado (Italy) reviewed data about the natural history of ARVC that represents a major cause of sudden death in the young and in athletes. Progressive loss of right or left myocardium occurs usually late in life whereas ventricular electrical instability leading to sudden death can occur at any time during the course of the disease. He underlined the major role for ICD as an efficient treatment to prevent sudden death. The predictors of sudden death or appropriated defibrillator therapy were also recently re-evaluated through the DARVIN II study and emphasised the role of syncope as a very strong predictor after multivariate analyses, in addition to aborted sudden death and haemodynamically unstable VT that were previously reported.
Advances in arrhythmogenic right ventricular cardiomyopathy