Abstract
The aim of this review article is to summarize current knowledge of the pathophysiology underlying right ventricular failure (RVF), focusing, in particular, on right ventricular assessment and prognosis. The right ventricle (RV) can tolerate volume overload well, but is not able to sustain pressure overload. Right ventricular hypertrophy (RVH), as a response to increased afterload, can be adaptive or maladaptive. The easiest and most common way to assess the RV is by two-dimensional (2D) trans-thoracic echocardiography measuring surrogate indexes, such as tricuspid annular plane systolic excursion (TAPSE), fractional area change (FAC), and tissue Doppler velocity of the lateral aspect of the tricuspid valvular plane. However, both volumes and function are better estimated by 3D echocardiography and cardiac magnetic resonance (CMR). The prognostic role of the RV in heart failure (HF), pulmonary hypertension (PH), acute myocardial infarction (AMI), and cardiac surgery has been overlooked for many years. However, several recent studies have placed much greater importance on the RV in prognostic assessments. In conclusion, RV dimensions and function should be routinely assessed in cardiovascular disease, as RVF has a significant impact on disease prognosis. In the presence of RVF, different therapeutic approaches, either pharmacological or surgical, may be beneficial.
Highlights
The right ventricle (RV) encompasses two myocardial bands: the ventriculo-infundibular band; a muscular fold between the pulmonary valve and the tricuspid valve (TV) that extends to the subpulmonary infundibulum of the RV outlet, and the septomarginal band, extending from the septum to the anterior wall and supporting a papillary muscle
There are several known causes of right ventricular failure (RVF), but this condition is generally attributed to PAH, T4.VCdaiuseseaseo, fleRftV-sFide heart failure with secondary pulmonary hypertension, chronic pulmonary disease, left vTenhterriecualraer saesvsiesrtadl ekvniocew(nLVcAauDse) simopf lRaVntFa,tibount, tohriscocnognednititioalnhiesagrtendeisreaallsyesa.ttributed to PAH, TV disease, left-side heart failure with secondary pulmonary hypertension, chronic pulmonary disease, left ventricular assist device (LVAD) implantation, or congenital heart diseases
According to World Health Organization (WHO), the majority of cases of pulmonary hypertension (PH) and RVF are those associated with chronic lung diseases; such as chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD), and sleep disordered breathing (SDB) [42]
Summary
The RV has a unique crescent shape which influences its physiological properties. The normal range of right ventricular end-diastolic volume (RVESV) is 49–101 mL/m2 (55–105 mL/m2 in men and 48–87 mL/m2 in women), whereas the normal range of left ventricular end-diastolic volume (LVESV) is 44–89 mL/m2 (men, 47–92 mL/m2; women, 41–81 mL/m2), assessed by MRI. The RV is composed of superficial (circumferential) and deep muscle layers (longitudinal) [5,6]. This arrangement contributes to the more complex movement of the, which includes torsion, translation, rotation, and thickening [5,6]. The ventricles share the visceral cavity (pericardium) and myofibres, in their superficial layers, and the interventricular septum, which contributes to the ejection of both cavities. The LV positively influences RV performance, contributing significantly to its pressure generation, both as a whole and through septal contraction. When there is RV enlargement and reduction of RV free wall contractility, there is a progressive reduction in both RV and LV mechanical work; LV pressure development and stroke work dcrease. Danton et al showed that acute RV ischaemia due to coronary artery ligation, induced LV dysfunction [11]
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