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Our mission is to reduce the burden of cardiovascular disease through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
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The ESC Working Groups' goal is to stimulate and disseminate scientific knowledge in different fields of cardiology.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Ms Elisabetta Cerbai,
The famous Mona Lisa painting is celebrated for the enigmatic feminine portrait; however, the vast landscape receding to icy mountains behind her is likewise a powerful synthesis of Leonardo’s imagination. The four excellent speakers of the symposium succeeded in widening our view of the complex substrate underlying cardiac arrhythmogenesis.
Professor Ravens (Dresden, DE) reviewed ion channel changes in atrial fibrillation as a consequence of electrophysiological remodeling. Given the huge numbers of channels involved, she focused on sodium and potassium channels likely representing suitable pharmacological targets for atrial fibrillation treatment and prevention of recurrence. To some extent, expectations on specific blockers of ultrarapid delayed rectifier current – although effective in preclinical studies - were disappointed once translated to the clinical arena. However, novel targets seem to emerge from Dr. Ravens studies, such as the acetylcholine activated potassium current. This current, which contributes to shortening action potential duration and refractory period thus favoring AF substrate, is blocked by flecainaide but not by other antiarrhythmics. Hopefully, research in this field will increase our therapeutic armamentarium.
The role of ancillary subunits of sodium and potassium channels is a hot line of investigation for both clinical electrophysiology and genetics. Dr. Watanabe (Nijigata, JP) focused on the emerging role of beta subunits in human arrhythmias, from Brugada to Long QT syndrome to lone atrial fibrillation. As an example, probands with Brugada syndrome (none with SCN5A mutations) may have mutations of the β1 subunit, able to alter sodium channel function and expression. Likely the situation is complicated by the temporal and spatial heterogeneity of channels in terms of subunit composition. Thus, in the future, genetics of arrhythmogenesis will likely switch from gene identification and single pathway understanding to genomic medicine by integrating complex gene and environmental information.
Dr Iribe (Okayama, JP) reported on the contribution of two different mechanisms to calcium-related arrhythmogenic mechanisms. In particular, they noticed that stretching myocytes induces a local immediate and short lasting (about 60-second) increase in resting Ca2+ spark production. Ca2+ sparks are subcellular events, temporally and spatially confined, due to transient opening of sarcoplasmic reticulum ryanodine receptor. They are unable to trigger contraction, but provide a substrate that favors electrical abnormalities and lately arrhythmias. Interestingly, they proved that microtubules represent the intracellular structure mediating stretch-induced calcium release, thus uncovering a novel signal transduction mechanism in cardiac myocytes.
Dr. Fleischmann moved to a larger (multicellular) scale of complexity, involving cellular electrical coupling and cell-matrix interaction. By combining superior biomolecular and electrophysiological approaches, they demonstrated not only the critical role of matrix and gap junctions for intact electrical signal propagation, but also the possibility of reducing life-threatening post-infarct arrhythmias by engraftment of engineered myocyte progenitors expressing connexin-43.
Molecular characteristics of arrhythmogenic substrates
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