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. Per Anton Sirnes,
This was the theme for a Sunday morning session proposed by the Council of Cardiology Practice. The interest in this conduction defect has increased the last 10 years with the evolution of Cardiac Resynchronization Therapy (CRT)
Prof. Silvia Prioi (Pavia, IT) gave an overview of the genetics related to cardiac conduction disorders. Is there a genetic predisposition to LBBB? Sodium channel mutations have been linked to progressive cardiac conduction disorders, but in many studies hemiblocks and RBBB are much more frequent then LBBB. Lamin A/C mutations have though been linked to atrial fibrillation, ventricular arrhythmias, dilated CMP and LBBB. She referred to studies of transcriptom (what types of RNA are transcribed) showing that the remodelling induced by LBBB causes the cardiac myocytes to downregulate energy deriving processes and upregulate processes related to signalling pathways and extracellular matrix. Prof Juan Cinca, (Bareclona, SP) referred to animal studies showing how induction of LBBB causes remodelling, dyssychrony, increase in LV mass and dimensions and reduced EF. Furthermore, measurements with flow catheter in LAD showed that when LBBB was induced, the flow in LAD was reduced; possible mechanisms are shorter diastolic filling, increased septal pressure and possible compression of septal vessels. In patients with mitral regurgitation LBBB is associated with reduced LV filling time and increased MR duration. There is a dual relation between heart failure and LBBB; LBBB can cause HF and increasing HF is associated with more frequent LBBB. LBBB is a primary cause of LV remodelling and aggravates LV dysfunction in patients with HF. There are several studies showing that LBBB is related to a poorer prognosis both in normal patients and in patients with HF. But in several registries of HF patients, the occurrence of RBBB has been shown to be associated with an even poorer prognosis than those with LBBB. This was evident in a so far unpublished Spanish HF registry study, where he also showed that RBBB was more associated with LVH and right sided HF whereas LBBB was more correlated with LV dilatation and lower EF.
The ESC newly elected president-elect Fausto Pinto (Lisbon, PT) continued with an inspiring lecture on prognosis and imaging in LBBB. LBBB is related to sudden and coronary deaths in large registries, but in registries of heart failure patients the prognosis is even worse for RBBB patients than LBBB patients. In LBBB, he showed how dyssynchrony can be demonstrated by deformation imaging, MRI and nuclear studies. The recent publication by Hara et al (EHJ 2012) showed how radial dyssynchrony assessed by short axis 2D-strain is associated with improved outcome following CRT even in non-LBBB patients. Nuclear studies have shown decreased septal uptake in LBBB, this septal hypoperfusion may be related to less septal work and /or reduced LAD flow. However, this may limit SPECT to diagnose CAD in LBBB patients. Prof Pinto suggested using coronary CT in patients with low/middle risk, but go directly to coronary angiography when there is moderate to high suspicion of CAD in patients with LBBB. A good imaging (echo and or MRI) is necessary as a basal assessment. As regards follow-up of otherwise asymptomatic LBBB patients, there are no clear recommendations in guidelines, but he felt that a yearly visit would be reasonable. In asymptomatic patients above 50 years with LBBB, an increasing proportion will experience future problems with heart failure and could be candidates for CRT
Prof. Cecila Linde (Stockholm, SE) is one of the pioneers in CRT treatment and reviewed the relevant studies showing the success of CRT treatment in patients with HF and LBBB (CARE HF, COMPANION,MADIT CRT, RAFT,REVERSE). The RAFT study showed an effect on mortality after several years follow-up even in NYHA II patients. The wider the QRS, the greater the benefit, but the recent ESC guideline has a IA indication for CRT in NYHA III patients and LBBB even from a QRS ≥ 120ms. Women derive a greater effect than men , possibly related to a greater proportion of DCM as the improvement in reverse remodelling is greater in DCM than in CAD. The extent of reverse remodelling is linked to the mortality benefit. She concluded that in patients with HF and LBBB, the sooner CRT is added to pharmacological therapy, the greater the benefit.
Left bundle branch block - benign or a harbinger of heart failure?