The Right Ventricle Under Pressure

Abstract

Abbreviations: ACE ϭ angiotensin converting enzyme; ATII ϭ angiotensin II; ECM ϭ extracellular matrix; ET-1 ϭ endothelin-1; HO-1 ϭ heme oxygenase 1; IL ϭ interleukin; LV ϭ left ventricle/ventricular; MHC ϭ myosin heavy chain; MMP ϭ matrix metalloproteinase; NO ϭ nitric oxide; PAH ϭ pulmonary arterial hypertension; PDE-5 ϭ phosphodiesterase type 5; RNS ϭ reactive nitrogen species; ROS ϭ reactive oxygen species; RV ϭ right ventricle/ventricular; sST2 ϭ interleukin-1 receptor-like protein soluble isoform; ST2L ϭ interleukin-1 receptor-like protein transmembrane isoform; TGF ϭ transforming growth factor; TNF ϭ tumor necrosis factor; VEGF ϭ vascular endothelial growth factor

Nebivolol has a beneficial effect in monocrotaline-induced pulmonary hypertension

“…These results may suggest that selective β 1 receptor blockade along with β 3 receptor agonism and NO release may provide a beneficial effect in the treatment of pulmonary hypertensive disorders and are consistent with results showing that nebivolol has beneficial effects on pulmonary vascular remodeling not seen with metoprolol (Perros et al 2015;Rubin 2015). β adrenergic receptor blocking agents are used in the treatment of congestive heart failure and most patients with pulmonary hypertension succumb as a consequence of right heart failure (Bogaard et al 2009;Voelkel et al 2013). Treatment with β receptor blocking agents reduces mortality by about 30% in patients with left-D r a f t sided heart failure, but β blocking agents are not used in the treatment of pulmonary hypertension and cor pulmonale (Doughty et al 1997;McLaughlin et al 2009).…”

Right atrial emptying fraction non-invasively predicts mortality in pulmonary hypertension

“…RA areas were measured from the apical four chamber view only, by tracing the endocardial contour at the time of maximum distension [RA end-diastolic (ED) area], which occurs at LV end-systole, and at the time of smallest RA area [RA end-systolic (ES) area]. Measurements were made in accordance with published recommendations on four chamber measurements of ventricular (RV) structure, function, and remodeling in PH [7][8][9][10][11]. I nterestingly, the main clinical endpoints used in trials might generally be considered as surrogate markers of right heart function and reserve: World Health Organization (WHO) functional classification, 6-minute walk distance (6MWD), exercise testing, cardiac biomarkers, and anatomic/functional echocardiographic parameters [5,[12][13][14][15][16][17][18][19].…”

The Right Ventricle in Health and Disease: Insights into Physiology, Pathophysiology and Diagnostic Management

“…The increase in ventricular mass induced by an increase in afterload is predominantly the result of protein synthesis and an increase in cell size through the addition of sarcomeres in parallel. Protein synthesis in the cardiomyocytes is directly induced by stretch and enhanced by autocrine, paracrine and neurohormonal signals including activation of the renin-angiotensin and enhanced sympathetic activity [17,18]. However, the RV is not capable of sustaining pressure overload over the long term.…”

“…Phosphorylation of troponin T by protein kinase C inhibits troponin T binding to tropomyosin, which may contribute to the inhibition of maximal myofibrillar adenosine triphosphatase and contractile performance [26,27]. Finally, abnormalities in enzymes and ion channels involved in myocyte stimulation/contraction, mitochondrial defects, depletion of myocardial adenosine triphosphate and modifications of myocardial substrate use (from fatty acids to glucose) have been implicated in maladaptive remodeling [18]. …”