Change In Right Ventricular Mass Research Articles

Collagen 18A1/Endostatin Expression in the Progression of Right Ventricular Remodeling and Dysfunction in Pulmonary Arterial Hypertension.

Numerous studies have demonstrated that endostatin (ES), a potent angiostatic peptide derived from collagen type XVIII α 1 chain and encoded by COL18A1, is elevated in pulmonary arterial hypertension (PAH). It is important to note that elevated ES has consistently been associated with altered hemodynamics, poor functional status, and adverse outcomes in adult and pediatric PAH. This study used serum samples from patients with Group I PAH and plasma and tissue samples derived from the Sugen/hypoxia rat pulmonary hypertension model to define associations between COL18A1/ES and disease development, including hemodynamics, right ventricle (RV) remodeling, and RV dysfunction. Using cardiac magnetic resonance imaging and advanced hemodynamic assessments with pressure-volume loops in patients with PAH to assess RV-pulmonary arterial coupling, we observed a strong relationship between circulating ES levels and metrics of RV structure and function. Specifically, RV mass and the ventricular mass index were positively associated with ES, whereas RV ejection fraction and RV-pulmonary arterial coupling were inversely associated with ES levels. Our animal data demonstrate that the development of pulmonary hypertension is associated with increased COL18A1/ES in the heart as well as the lungs. Disease-associated increases in COL18A1 mRNA and protein were most pronounced in the RV compared with the left ventricle and lung. COL18A1 expression in the RV was strongly associated with disease-associated changes in RV mass, fibrosis, and myocardial capillary density. These findings indicate that COL18A1/ES increases early in disease development in the RV and implicates COL18A1/ES in pathologic RV dysfunction in PAH.

Cardiac MRI assessment of the right ventricle pre-and post-kidney transplant.

Worsening renal function in chronic kidney disease correlates with worsening right ventricular (RV) systolic function. We evaluated the association between kidney transplantation (KT) and RV structure and systolic function, and the relationships between RV and left ventricular (LV) changes, blood pressure, and specific cardiac biomarkers, in patients with end-stage kidney disease using cardiac magnetic resonance imaging (CMR).In this prospective, multi-centre, cohort study, 39 adult patients on dialysis receiving KT and 42 patients eligible for, but not yet receiving KT, were recruited. CMR was performed at baseline, and repeated at 12 months.Among 81 patients (mean age 51 years, 30% female), RV end-diastolic volume index (RVEDVi), end-systolic volume index (RVESVi), mass index (RVMi), and ejection fraction (RVEF) did not change significantly within either the dialysis or KT group over 12months (all p ≥ 0.10). There were no significant differences in the 12-month changes of these parameters between the dialysis and KT groups (all p ≥ 0.10). RVMI demonstrated positive correlations with NT-proBNP and systolic blood pressure, but not GDF-15, at baseline and at 12months. Changes in RVEDVi, RVESVi, and RVEF were positively correlated with changes in LVEDVi, LVESVi, and LVEF, respectively over 12months (Spearman r = 0.72, 0.52, and 0.41; all p < 0.001), but not mass index (Spearman r = 0.20, p = 0.078).In conclusion,there were no significant changes in RV mass, volumes, or systolic function 12 months after KT, as compared with continuation of dialysis. The associations between RV and LV remodeling may suggest similar underlying pathophysiologic mechanisms.

Prognostic impact of right ventricular mass change in patients with idiopathic pulmonary arterial hypertension

BackgroundCompensatory remodelling i.e. increased right ventricular (RV) mass frequently occurs as an adaptive response to the chronic pressure overload to maintain contractile function. The prognostic value of the serial change in RV mass is unclear. AimThe aim of our study was to examine the longitudinal changes in RV mass and survival in patients with idiopathic pulmonary arterial hypertension (IPAH). MethodsConsecutive newly diagnosed IPAH patients >18 years old were prospectively recruited from a tertiary referral center. All recruited patients were maintained on guideline-based therapy and were followed up with echocardiography and cardiac magnetic resonance for 2 years. ResultsSerial measures of RV mass revealed that survivors appeared to have had a compensatory increase in RV mass, which constituted adaptive RV remodelling early in the disease process, which was not seen in those who died. (Hazard ratio of 0.932, 95% confidence interval 0.893–0.973, p = 0.001). ConclusionThis study shows that serial measurement of RV mass in IPAH patients provides prognostic information. RV mass regression is an ominous prognostic sign, which may predict early mortality in these patients.

Association between conversion to in-center nocturnal hemodialysis and right ventricular remodeling.

In-center nocturnal hemodialysis (INHD) is associated with favorable left ventricular (LV) remodeling. Although right ventricular (RV) structure and function carry prognostic significance, the impact of dialysis intensification on RV is unknown. Our objectives were to evaluate changes in RV mass index (MI), end-diastolic volume index (EDVI), end-systolic volume index (ESVI) and ejection fraction (EF) after conversion to INHD and their relationship with LV remodeling. Of 67 conventional hemodialysis (CHD, 4 h/session, three times/week) patients, 30 continued on CHD and 37 converted to INHD (7-8 h/session, three times/week). Cardiac magnetic resonance imaging was performed at baseline and 1 year using a standardized protocol; an experienced and blinded reader performed RV measurements. At 1 year there were significant reductions in RVMI {-2.1 g/m2 [95% confidence interval (CI) -3.8 to - 0.4], P = 0.017}, RVEDVI [-9.5 mL/m2 (95% CI - 16.3 to - 2.6), P = 0.008] and RVESVI [-6.2 mL/m2 (95% CI - 10.9 to - 1.6), P = 0.011] in the INHD group; no significant changes were observed in the CHD group. Between-group comparisons showed significantly greater reduction of RVESVI [-7.9 mL/m2 (95% CI - 14.9 to - 0.9), P = 0.03] in the INHD group, a nonsignificant trend toward greater reduction in RVEDVI and no significant difference in RVMI and RVEF changes. There was significant correlation between LV and RV in terms of changes in mass index (MI) (r = 0.46), EDVI (r = 0.73), ESVI (r = 0.7) and EF (r = 0.38) over 1 year (all P < 0.01). Conversion to INHD was associated with a significant reduction of RVESVI. Temporal changes in RV mass, volume and function paralleled those of LV. Our findings support the need for larger, longer-term studies to confirm favorable RV remodeling and determine its impact on clinical outcomes.

Geometric and functional change of both ventricles after atrial ventricular septal defect closure.

REFER TO THE PAGE 182-188 The secundum type atrial septal defect (ASD) is a relatively common congenital heart defect. The long-standing left to right shunt causes right ventricular (RV) volume overload and pulmonary vascular changes resulting in later RV pressure overload. Also it causes and results in reduced left ventricular (LV) preload, leading to a decrease in cardiac output. Therefore, in patients with significant ASD shunts, the RV chamber distends and the septum deviates toward the LV, resulting in a compressed LV. Transcatheter or surgical closure of the defect causes reverse remodeling of the both ventricles. However, such adaptation may take long time and can be in completion in adult patients. Standard echocardiographic studies in ASD patients showed higher RV dimensions with lower LV dimensions.1) Also higher global RV systolic function indices such as tricuspid annular plane systolic excursion (TAPSE) and RV ejection fraction (EF) were reported in ASD patients. After ASD closure, the RV shrink and the LV expand dramatically in 24 hours and show further change slowly after that time. Neither show further significant diameter change after 1 month.2) All of the RV systolic functional parameters including TAPSE, RVEF RV fractional area change and RV myocardial performance index were worsened immediately after the closure, and improved again at first month follow-up. This biphasic change by time may be due to a delayed change in RV mass in the face of acute volume reduction. Assessment of the RV function in ASD patients remained difficult as conventional echocardiographic parameters such as EF, which may not represent the contractility of a dilated, volume and pressure overloaded RV. Myocardial deformation parameters such as strain and strain rate are closely related to the intrinsic myocardial contractility and allow regional function analysis.3) Interestingly, previous studies shows that there are some regional differences regarding the extent and the time course of deformational changes.2) The regional heterogeneity in RV wall thickness and curvature may explain some of the variance in RV regional deformation. In ASD patients, RV lateral longitudinal strain is higher and RV septal strain is similar (or slightly higher) compared with healthy controls.2),4),5) The difference between the septal and lateral wall deformation can be explained with the fact that 2 dimensional speckle tracking could not distinguish between right sided and left sided component of the septum. However, there is no difference of strain rate in ASD patients compared with healthy controls and this finding has demonstrated in some studies,3),6),7) that systolic strain rate is mainly related to the change in contractility, whereas systolic strain primarily determined by the stroke volume and more dependent on volume overload. After the closure, strain and strain rate of most segments excluding apical lateral segment decrease immediately. Transcatheter device closure, an attractive alternative to cardiac surgery, has been increasingly performed and offered as a primary therapy for the secundum ASD. Also it is good for evaluation the pure effect excluding cardiopulmonary bypass effect regarding to volume unloading after ASD closure. Lower apical strain values shows strong correlation with systolic pulmonary arterial pressure and global RV systolic function indices. The prognostic value of changes in systolic strain over time was notable especially in patients with severe pulmonary arterial hypertension.8) An individual improvement > 5% in RV strain at follow-up was correlated with better pulmonary hemodynamics, improved clinical status, and less evidence of right heart failures, and it also predicted greater long-term survival that was incremental over clinical factors and choice of therapy. Rare data are available on the impact of ASD closure on LV deformation. LV systolic twist was significantly reduced in patients with ASD mainly due to the heterogonous basal rotation. LV basal rotation improved significantly while apical rotation remained unchanged after transcatheter ASD closure.9) Since the LV twist is defined as the LV apical rotation relative to the basal rotation, and the basal rotation was improved, it is observed a significant increased LV twist after ASD closure. This study also showed similar findings that the lateral longitudinal strain of RV was higher in ASD patients and decreased after ASD closure.10) However, in terms of regional difference, there were somewhat different compared with previous studies.

Simvastatin as a Treatment for Pulmonary Hypertension Trial

In animal models of pulmonary hypertension, simvastatin has been shown to reduce pulmonary artery pressure and induce regression of associated right ventricular (RV) hypertrophy. To assess the therapeutic value of simvastatin in patients with pulmonary arterial hypertension (PAH). Forty-two patients with PAH were randomized to receive either simvastatin (80 mg/d) or placebo in addition to current care for 6 months, and thereafter offered open-label simvastatin. The primary outcome was change in RV mass, assessed by cardiac magnetic resonance (CMR). At 6 months, RV mass decreased by 5.2 +/- 11 g in the statin group (P = 0.045) and increased 3.9 +/- 14 g in the placebo group. The treatment effect was -9.1 g (P = 0.028). N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels decreased significantly in the statin group (-75 +/- 167 fmol/ml; P = 0.02) but not the placebo group (49 +/- 224 fmol/ml; P = 0.43; overall treatment effect -124 fmol/ml; P = 0.041). There were no significant changes in other outcome measures (including 6-minute walk test, cardiac index, and circulating cytokines). From 6 to 12 months, both RV mass and NT-proBNP increased toward baseline values in 16 patients on active treatment who continued with simvastatin but remained stable in 18 patients who switched from placebo to simvastatin. Two patients required a reduction in dose but not cessation of simvastatin. Simvastatin added to conventional therapy produces a small and transient early reduction in RV mass and NT-proBNP levels in patients with PAH, but this is not sustained over 12 months.

P3379 Response to therapy of patients with primary pulmonary hypertension assessed by 6-minute walk test performance correlates with changes in right-ventricular mass

P3379 Response to therapy of patients with primary pulmonary hypertension assessed by 6-minute walk test performance correlates with changes in right-ventricular mass

MRI complements standard assessment of right ventricular function after lung transplantation

Changes in right ventricular mass and ejection fraction after single-lung transplantation for pulmonary hypertension are poorly understood. To complement functional data provided by echocardiography, radionuclide ventriculography, and right heart catheterization, magnetic resonance imaging was used to assess right ventricular function in 5 single-lung transplant recipients with preoperative pulmonary hypertension and right ventricular dysfunction (right ventricular ejection fraction, 0.21 +/- 0.09). The right and left ventricular mass, ejection fraction, and mass ratio (left ventricular mass/right ventricular mass) were calculated from the magnetic resonance images. The mean pulmonary artery pressure fell from 72 +/- 18 to 21 +/- 8 mm Hg after transplantation. At 3 months after transplantation both the left ventricular and right ventricular ejection fractions approached normal values, as shown by both radionuclide ventriculography and magnetic resonance imaging, but the right ventricular mass remained abnormally high with slightly low mass ratios. By 1 year both the left ventricular and right ventricular masses had regressed to normal with near-normal mass ratios. Right ventricular performance returns to nearly normal early after transplantation, but the right ventricular mass regresses over a more prolonged time. Cine magnetic resonance imaging provides a noninvasive means of assessing changes in right ventricular function and mass after lung transplantation.

Right ventricular coronary flow in arterial hypertension

Right ventricular (RV) coronary circulation in systemic hypertension offers an opportunity to assess the effects of marked increases in coronary perfusion pressure in vivo without appreciable increases in workload or marked hypertrophy of the cardiac chamber. This study investigates RV coronary circulation in renal hypertensive rats (RHR). Mean arterial pressure rose by 50% to 60% in RHR as compared to control groups and RV mass increased by 15% (7.15 vs 6.19 mg/gm body weight, p < 0.01). Coronary blood flow, which was measured by left atrial injection of microspheres in conscious rats, was not signficantly different between study groups both at rest and after maximal coronary vasodilation with carbochrome (6 mg/kg). However, minimal RV coronary resistance level per gram were significantly elevated ( p < 0.05) in RHR. A second study was designed to further dissociate the effects of arterial hypertension from the effects of changes in RV mass in RHR. In one group, blood pressure was acutely reduced by 1 week of captopril therapy, while RV mass remained high. In the second group, captopril was discontinued after 14 weeks of treatment, allowing arterial pressure to rise, while RV mass, which had regressed with treatment, remained normal. After treatment, RV minimal coronary resistance levels remained high in the short-term-treated hypertensive rats, but returned to normal levels in the long-term-treated RHR. These results suggest the following possibilities: (1) the RV is not immune to the effects of systemic hypertension, (2) coronary structural changes are probably the main factor that accounts for the increase in RV coronary resistance levels, and (3) coronary alterations are amenable to long-term antihypertensive therapy.