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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 through percutaneous cardiovascular interventions.
Improving the quality of life and reducing sudden cardiac death by limiting the impact of heart rhythm disturbances.
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.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Several novel issues from basic science were highlighted in depth in the presentation “Pathophysiology and diagnosis” by Prof. C J M Vrints (Edegem,BE). The traditional concept regarding the pathophysiology of APE is based on Starling forces and imbalance between the pressure of pulmonary capillaries and plasma oncotic pressure. As pulmonary capillary wedge pressure increases, a passive fluid filtration from blood circulation to the alveolar space occurs. Many of the regulatory pathways are activated only when left atrial pressure (LAP) is elevated, typically over 25 mmHg. The NO-dependent inhibition of alveolar fluid re-absorption in high LAP states has been observed using inhibitors of the NO pathway, which improve the fluid re-absorption. In addition, chloride(Cl-) transport-driven alveolar fluid secretion increases while LAP is elevated. Thirdly, Na-K-Cl cotransporter1 (NKCC1) is involved in alveolar fluid secretion. Interestingly, several structural changes have been shown in the bronchi to underlie the classic clinical symptom of cardiac asthma. First, vascular engorgement of the mucosal plexus occurs, then interstitial oedema compresses the airway wall, and in prolonged situations, squamous metaplasia of airway epithelium as well fibrosis and smooth muscle cell proliferation lead to more chronic impairment of airflow.In conclusion, these findings might be novel targets for therapy in the future.
Prof. P Ponikowski (Wroclaw, PL) discussed the potential role of lung impedance and lung ultrasound in the early diagnosis of APE in his talk “Diagnostic advances, why we should look to the lungs”. In addition, he suggested procalcitonin as a potential marker to identify pneumonia in these patients with pulmonary infiltrates of uncertain origin.
The strategies and novel options of positive pressure ventilation (CPAP and non-invasive positive pressure ventilation (NIPPV)) in APE were presented by Prof J Masip (Barcelona, ES). Of essence is the careful initiation of the therapy with fairly low positive end-expiratory pressure (PEEP) of 4-5 cmH20 and low inspiratory positive airway pressure in NIPPV. Some new modalities like high flow nasal cannula seem to be a new option for subacutely dyspneic patients.
Advances in therapy were presented by Prof P Pang (Chicago, US). Actually, little has changed since the 1970s concerning the first-line medical management. Thus, it still consists of diuretics, oxygen, nitrates, positive pressure ventilation, morphine, as well as digoxin. However, there are some new data regarding the use of these therapies. Only some new modalities like levosimendan and nesiritide have become available. Mortality benefit has not been proven with any of these therapies in a randomized fashion. Prof Pang emphasized the need for very early intervention in the emergency department or even pre-hospital. Most of the recent RCTs have now started to recruit patients within 4-16 hours. At the end of the session, the chairman emphasized that indeed, the need for vasodilators or pressure support ventilation is an exclusion criteria in these recent trials, which thus leaves open questions concerning the use of novel therapies in APE.
Session Title: New insights into acute pulmonary oedema
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