Right Ventricular Echo Assessment in Mitral Valve Replacement

In 1994, it was estimated that 12 million individuals had RF and RHD worldwide , and at least 3 million had congestive heart failure (CHF) that required repeated hospital admissions. A large section of the individuals with CHF required cardiac valve surgery within 5-10 years . The mortality rate for RHD varied from 0.5 per 100 000 population in Denmark, to 8.2 per 100 000 population in China , and the estimated annual number of deaths from RHD for 2000 was 332000 worldwide . The mortality rate per 100 000 population varied from 1.8 in the WHO Region of the Americas, to 7.6 in WHO South-East Asia Region. The disability-adjusted life years (DALYs)1 lost to RHD ranged from 27.4 DALYs per 100 000 population in the WHO Region of the Americas, to 173.4 per 100 000 population in the WHO South-East Asia Region. An estimated 6.6 million DALYs are lost per year worldwide. THE PATHOLOGY OF RHEUMATIC MITRAL VALVE DISEASE Rheumatic mitral valves shows a different set of lesions by comparison with degenerative valves, because of the characteristic inflammatory process, which results in thickening of the leaflets and other components of the mitral valve apparatus, of variable degrees, and distorts and impairs the movements of the valve. So, the disease appears here in two forms - stenosis and regurgitation, or a combination of both. In the case of valve regurge, the most frequent lesion is prolapse of the anterior leaflet, which is present in more than 90% of young patients and is most often caused by elongated chordae to its central and medial areas (A2 and A3). In contrast to degenerative disease, posterior leaflet prolapse is practically not found, except in cases with ruptured chordae due to infective endocarditis. On the contrary, this leaflet is often shortened in its width, sometimes resumed to a very narrow and thick strip of tissue. In more complicated cases, the chordae may be thick and retracted, as may also be the papillary muscles, and the commissures may be fused in varying degrees. Often, the leaflets and subvalvular apparatus are a continuous mass of fibrous tissue. Lastly, the annulus is dilated in 95% of the patients. It is widely accepted that dilatation occurs essentially in the posterior segment of the annulus, although there is some evidence that it may also occur in the anterior segment, especially in dilated cardiomyopathy. Pulmonary hypertension and valvular heart disease Valvular Heart Disease VHD is a common etiology of pulmonary hypertension, which may result from many mechanisms as an increase in pulmonary vascular resistance, pulmonary blood flow, or pulmonary venous pressure. The chronic rise in pulmonary arterial pressure (PAP) often leads to right ventricular (RV) pressure overload and subsequent RV failure. When present, PH is a marker of poor outcome in VHD. Assessment of the presence and severity of Pulmonary hypertension thus has an important role in the risk stratification and therapeutic management of VHD. The sure diagnosis of PH related to VHD is based on the following criteria: mean PAP 25 mm Hg together with an abnormally high pulmonary capillary wedge pressure (PCWP) \>15 mm Hg or left ventricular (LV) end-diastolic pressure \>18 mm Hg in the context of significant VHD. When pulmonary venous congestion is the main determinant of PH, PH is named isolated post-capillary PH or pulmonary venous hypertension. PATHOPHYSIOLOGY Increase in LV filling pressure and left atrial (LA) pressure leads to a passive rise in backward pressure of the pulmonary vein. Persistently elevated pulmonary venous pressure can favor fragmentation of the structure and result in "alveolar capillary stress failure," accompanied by capillary leakage and acute alveolar edema. This acute phase is reversible, but long-term persistence of high pulmonary venous pressure may provocate some degree of irreversible remodeling of the alveolar capillary membrane, with excessive deposition of type IV collagen. Plus, chronic elevated pulmonary venous pressure progressively and passively increases PAP and concomitantly produces pathological changes in pulmonary veins. and arteries, leading to increased pulmonary vascular resistance . The pathophysiology of PH in VHD thus involves progressive structural alteration of the pulmonary vascular bed mediated by the potent vasoconstrictor endothelin-1 . An increase in pulmonary-arterial vasoconstriction and systolic PAP results into RV dilation and hypertrophy. The RV failure is associated with tricuspid annulus dilation and an increase in tricuspid regurgitation severity, which further acerbates RV dysfunction. At the decompensated phase, systolic PAP can decrease despite the increase in pulmonary vascular resistance, due to the fall in RV stroke volume related to advanced RV failure. After treatment, the reversibility of PH depends on the type, severity, and chronicity of VHD, as well as the underlying pathophysiological adaptations. For instance, in mitral stenosis (MS), a rapid decrease in PAP is observed after relief of the stenosis, whereas a longer time could be required in other VHDs, especially when PH is linked to volume overload, as in mitral regurgitation (MR). Right ventricular function assessment The right ventricle has long been neglected, yet it is RV function that is strongly associated with clinical outcomes in many conditions. Although the left ventricle has been studied extensively, with established normal values for dimensions, volumes, mass, and function, measures of RV size and function are lacking. The relatively predictable left ventricular (LV) shape and standardized imaging planes have helped establish norms in LV assessment. There are, however, limited data regarding the normal dimensions of the right ventricle, in part because of its complex shape. The right ventricle is composed of 3 distinct portions: the smooth muscular inflow (body), the outflow region, and the trabecular apical region. Volumetric quantification of RV function is challenging because of the many assumptions required. As a result, many physicians rely on visual estimation to assess RV size and function. The basics of RV dimensions and function were included as part of the ASE and European Association of Echocardiography recommendations for chamber quantification published in 2005. This document, however, focused on the left heart, with only a small section covering the right-sided chambers. Since this publication, there have been significant advances in the echocardiographic assessment of the right heart. In addition, there is a need for greater dissemination of details regarding the standardization of the RV echocardiographic examination . PERIOPERATIVE ASSESSMENT OF THE RV In cardiac surgery, right heart catheterization and echocardiography play an essential and complementary role in the assessment of RV structure and function. Both provide useful information that may help tailor the anesthetic and surgical approach and provide guidance in the management of hemodynamically unstable patients. Hemodynamically, Right ventricular dysfunction or failure is usually recognized in the presence of a right atrial pressure (RAP) \_8-10 mm Hg or a RAP to pulmonary capillary wedge pressure \_0.8 (isolated RV failure) and/or a low cardiac index (\_2.2 L \_ min\_1 \_ m\_2). Increasing RAP may also be a sign of impeding RV failure. echocardiography also provides useful information on RV and pulmonary structure, valvular function and pericardial physiology. The echocardiographic evaluation of the RV is more challenging than that of the left ventricle. The main difficulties encountered may be explained by 1) the complex shape of the RV, 2) heavy apical trabeculations of the RV, which limits endocardial surface recognition, and 3) the marked load dependence of several indices of RV function. Despite these limitations, a comprehensive assessment of the RV may provide important data into its contractility, preload, and afterload. Lastly and as recommended by the American society of Echocardiography Endorsed by the European Association of Echocardiography, a registered branch of the European Society of Cardiology, and the Canadian Society of Echocardiography in 2010 guidelines all studies, the sonographer and physician should examine the right heart using multiple acoustic windows, and the report should represent an assessment based on qualitative and quantitative parameters. The parameters to be performed and reported should include a measure of right ventricular (RV) size, right atrial (RA) size, RV systolic function (at least one of the following: fractional area change \[FAC\], S', and tricuspid annular plane systolic excursion \[TAPSE\]; with or without RV index of myocardial performance \[RIMP\]), and systolic pulmonary artery (PA) pressure (SPAP) with estimate of RA pressure on the basis of inferior vena cava (IVC) size and collapse. So in this study we will focus on right ventricular function and performance after performing Mitral valve replacement to the rheumatic heart disease patients associated with pulmonary hypertension either mild or severe, to put a hand on the extent of benefit the patient who developed pulmonary hypertension will get from mitral valve replacement as regard function improvement and remodeling of the right ventricle and the proper timing of surgery.