'The Joint Symposium with the ESC: The pulmonary circulation in heart failure syndrome', focused on the development of pulmonary hypertension (PH) and right ventricular dysfunction in patients with left ventricular heart failure, which by far represents the most common form of PH.
The first talk by Prof Dr Marco Guazzi (University of Milano, Italy) focused on three main keynotes – (1) the burden of right heart disease (RHD); (2) the evolving stages of RHD: Right heart catheterization (RHC) vs. Imaging; and (3) therapeutic perspectives for the treatment of RHD in patients with left ventricular heart failure in the future. In this regard, aspects of disease pathogenesis as well as mechanisms and long-term changes in RV function in patients with PH-HFpEF were discussed. Prof Dr Guazzi highlighted that RHD in patients with HFpEF matters due to its rapid evolution and high prognostic impact. In addition, the talk described strengths and weaknesses of RHC and other imaging modalities in PH-HFpEF and concluded that both are integrated and synergic sources of knowledge. The outlook for therapeutic approaches included potential benefits with PDE5-inhibition in these patients as well as promising perspectives by levosimendan and beta3-stimulators.
In the second talk, Dr Mark Toshner (Cambridge, UK) reported on genetic aspects in group 2 PH. Dr Toshner highlighted that we are looking for smaller effects in more common variants in this group of patients and that leveraging genetic studies is important to interrogate therapy targets.
The third talk by Prof Dr Gabor Kovacs (Graz, Austria) looked at the definition of „abnormal exercise hemodynamics“ as well as the prognostic relevance of exercise hemodynamics in clinical practice. In addition, differential diagnostic considerations of pulmonary exercise hemodynamics were presented.
The fourth talk by Prof Stephan Rosenkranz (Cologne, Germany) focused on systemic consequences and interorgan cross-talk in heart failure and PH. The talk described cardio-pulmonary-renal interactions in heart failure, driven by hemodynamics and other mechanisms such as neurohormonal activation and circulation mediators. It was discussed that the combination of congestion and low output triggers a systemic inflammatory disease that affects multiple organ systems. In addition, Prof Rosenkranz reported on the deterioration in RV structure and function over time in patients with HFpEF, which is associated with limited survival, and concluded that these patients at present may be underrecognized in clinical practice. Finally, the talk looked at the left versus right ventricular phenotype in heart failure and the increased mortality associated with a shift from the LV to the RV phenotype over time.
As part of the best abstract talks, Dr Vineet Agrawal (Nashville, USA) presented his findings on a selective NPRC ligand, ANP-4-23, which causes selective RV remodelling in a mouse model of obesity induced PH-HFpEF. Dr Agrawal demonstrated that in vitro overexpression of NPRC causes decreased mitochondrial density and respiration in vitro and hypothesized that inhibiting or knocking down NRPC as a diagnostic target may prevent or reverse the PH-HFpEF phenotype. Finally, Dr Swathi Veeroju (Gießen, Germany) discussed her data on Smyd2 mediated HIF 1A stabilization, that was shown to induce pro-angiogenic signalling and to improve cardiac function.
Summary by Christopher Hohmann, University of Cologne, Germany
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