Page 63 - Assessing right ventricular function and the pulmonary circulation in pulmonary hypertension Onno Anthonius Spruijt
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Introduction
Pulmonary hypertension (PH) is a hemodynamic condition caused by a variety of underlying etiologies leading to a progressive increase in pulmonary vascular resistance (PVR) and pulmonary artery pressure (PAP). The diagnosis of PH is based on a right heart catheterization (RHC) showing a mean PAP (mPAP) > 25 mmHg. Coping of the RV to increases in afterload is through mechanisms of hypertrophy and dilatation and is essential in determining patient outcome: RV failure is the main cause of death in PH [1]. Established predictors of long-term outcome in PAH all represent RV function in one way or another: cardiac output (CO), mixed venous oxygen saturation, right atrial pressure, NT-proBNP, NYHA functional class and exercise capacity [2]. When performed at baseline or after initiation of treatment, cardiac imaging by means of echocardiography (ECHO) and cardiac magnetic resonance imaging (cMRI) provides additional prognostic information [3]. The mechanisms of RV adaptation to increases in load are not fully understood and have only recently become an important research topic. The importance of the RV, ‘the forgotten chamber’ in PH, was long unrecognized and very few investigators studied RV responses to PH therapy [4]. The possibility to treat the RV directly – i.e. not by decreasing afterload- was addressed in a few preclinical studies [5, 6], but never in PH patients. While there is an urgent need to study the RV response to PH therapy, there is no universally accepted consensus on the optimal method of assessing RV function and structure [2]. This short review will give an overview of, in our opinion, the most suitable functional parameters to assess the RV response to therapy in PH patients.
RV function and structure after initiation of treatment
While treatment of PH with specific therapy leads to a reduction in PVR in the majority of patients, this is not necessarily accompanied by an improvement in RV function [7]. The poor correlation between treatment associated changes in PVR and changes in RV function may be explained by a persistently elevated PVR (in most patients, drug treatment partially normalizes afterload at best), or by a load-independent deterioration of RV function over time. In addition, vasodilators may have direct pharmacological effects on the heart. Such direct effects have been suggested of all classes of PH treatment in preclinical studies [8-10], but were never evaluated in humans. Accurate assessment of cardio-specific effects of treatment requires a load-independent description of the function of the RV, which is not routinely provided by RHC or cardiac imaging (see table 1). Commonly studied load-dependent RV functional parameters are stroke volume (SV) and CO (calculated as SV times heart rate). SV and CO can be assessed during RHC using the thermodilution
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