Right Ventricular Anterior Wall Thickness Research Articles

Prognostic value of soluble ST2 biomarker in heart failure patients with obstructive sleep apnea syndrome

Abstract Funding Acknowledgements Type of funding sources: None. Objective. To analyze the relationships between soluble ST2 (sST2) levels, apnea/hypopnea index (AHI) and echocardiographic parameters in heart failure patients with preserved ejection fraction (HFpEF) and to evaluate prognostic values of sST2 in the development of adverse cardiac events (ASE) during the 12-month follow-up period. Methods. A total of 86 men, median age of 62.0 (41.0; 78.0) years with obstructive sleep apnea syndrome (OSAS) and HF of NYHA class I-III with baseline LVEF of 60% [52; 65]% were enrolled in the study. The severity of obstructive breathing disorders during sleep was assessed by AHI. Serum levels of NT-proBNP and sST2 were measured using ELISA at baseline. Two-dimensional transthoracic echocardiography with assessment of right ventricular (RV) function and 6-minute walk test (6MWT) were performed at baseline. Results. The values of AHI significantly correlated with body mass index (r = 0.362), left atrial volume (r = 0.570), fractional change in the area of the RV (r=-0.527), RV myocardial function index (r=-0.377), NT-proBNP (r = 0.611), 6MWT (r=-0.511), RV anterior wall thickness (r = 0,472), while the levels of sST2 significantly correlated with LV remodeling parameters: LVEF (r =-0.301), end-systolic volume (r =0.453), end-diastolic volume (r =0.396), end-systolic dimension (r = 0.373), end-diastolic dimension (r =0.288). Based on ROC-analysis, sST2 ≥29.67 ng/mL (sensitivity 63.6%, specificity 73.6%, AUC = 0.645; p < 0.0001) were identified as a cut-off values predicting the development of ACE. At 12 months of follow-up period all patients were divided into 2 groups according to cut-off values of sST2: group 1 (n = 29) comprised patients with sST2 ≥29.67 ng/mL, group 2 (n = 42) comprised patients with sST2 <29.67 ng/mL. The median baseline values of sST2 were 41.39 [33.31; 50.99] ng/mL in group 1, and 22.18 [20.64; 25.5] ng/mL in group 2. The concentrations of NT-proBNP did not differ between the groups. During the 12-month follow-up period in group 1 the rate of ACE was 29.7% cases, and 5.2% in group 2, respectively. According to Kaplan-Meier analysis, a higher sST2 levels was associated with a higher frequency of ACE during 12 months of follow-up (р<0.0001). Univariable and multivariable Cox regression analyses showed sST2 concentrations were significantly associated with ACE (odds ratio 2.25, 95%CI: 2.06 to 3.29, p < 0.001), when adding AHI and LV myocardial mass index improved reclassification of risk stratification (odds ratio 3,28, 95%CI: 3,09 to 4,49, p < 0.001, AUC of 0.945, percent of cases correctly classified of 90.14 %). However, NT-proBNP addition had a limited effect on risk stratification. Conclusion. Our data suggest that sST2 may be used as a diagnostic biomarker for prediction of ACE in patients with HFpEF and OSAS during the 12-month follow-up period. The combined evaluation of sST2, AHI and LV myocardial mass index values demonstrated higher diagnostic sensitivity and specificity for prediction of ACE.

Right Ventricular Growth and Function After Balloon Valvuloplasty for Critical Pulmonary Valve Stenosis in Infants and Neonates.

Little data are published about right ventricular (RV) growth and function in infants and neonates after balloon pulmonary valvuloplasty (BPV) for critical valvular pulmonary stenosis (PS). We aimed to assess the RV growth and function during 1year after BPV for critical valvular PS in neonates and infants. A total of 41 infants and neonates with isolatedcriticalvalvular PSwho underwent BPV from August 2016 to Sep 2018 were enrolled in the study. Complete Echocardiographic examination was performed to all infants before, 1week, 1month, 3months, 6months, and 1year after BPV. The RV systolic pressure and transvalvular pulmonary pressure gradient significantly decreased 1week after BPV and continue to decrease more slowly during the period of follow-up. During follow-up, RV end-diastolic dimension increased significantly, whereas RV anterior wall thickness significantly decreased. The mean diameters of pulmonary valve annulus and tricuspid valve annulus significantly increased after BPV over the period of follow-up. RV systolic and diastolic dysfunction improved significantly as reported by reduced RV Tei index and tricuspid annular systolic velocity and increased RV E/A ratio. RV growth and function were significantly improved after BPV for critical PS in infants and neonates and catch-up growth of right ventricular structures occurred after 6months of BPV.

Genetic ablation of interleukin-18 does not attenuate hypobaric hypoxia-induced right ventricular hypertrophy.

Interleukin-18 (IL-18), a proinflammatory cytokine, has been implicated in pathologic left ventricular hypertrophy and is elevated in plasma of heart failure patients. However, IL-18 blockade strategies have been conflicting. The purpose of these experiments was to determine whether genetic ablation of IL-18 would protect mice against hypobaric hypoxia (HH)-induced right ventricular (RV) hypertrophy, a condition in which chamber-specific inflammation is prominent. We hypothesized that IL-18 knockout (KO) mice would be protected while wild-type (WT) mice would demonstrate RV hypertrophy in response to HH exposure. KO and WT mice were exposed to HH for 7 wk, and control mice were exposed to normoxic ambient air. Following echocardiography, the RV was dissected and flash-frozen for biochemical analyses. HH exposure increased IL-18 mRNA (P = 0.08) in RV from WT mice. Genetic ablation of IL-18 mildly attenuated RV hypertrophy as assessed by myocyte size. However, IL-18 KO mice were not protected against HH-induced organ-level remodeling, as evidenced by higher RV weights, elevated RV systolic pressure, and increased RV anterior wall thickness compared with normoxic KO mice. These RV changes were similar to those seen in HH-exposed WT mice. Compensatory upregulation of other proinflammatory cytokines IL-2 and stromal cell-derived factor-1 was seen in the HH-KO animals, suggesting that activation of parallel inflammatory pathways might mitigate the effect of IL-18 KO. These data suggest targeted blockade of IL-18 alone is not a viable therapeutic strategy in this model.

Abstract 202: Genetic Ablation of Interleukin-18 Does Not Attenuate Hypobaric Hypoxia-Induced Right Ventricular Dysfunction

Interleukin-18 (IL-18), a pro-inflammatory cytokine, has been implicated in pathogenic left ventricular hypertrophy and is elevated in plasma of heart failure patients. However, IL-18 blockade strategies in animal models of heart disease have been conflicting. Accordingly, the purpose of these experiments was to determine whether genetic ablation of IL-18 would protect male and female mice against hypobaric hypoxia-induced right ventricular (RV) dysfunction. We hypothesized that IL-18 knockout mice (KO) would be protected while wild type (WT) mice would show significant right ventricular dysfunction in response to exposure to hypobaric hypoxia (HH). KO and WT mice were exposed to HH for 7 weeks, and control (CO) mice were exposed to normoxic, ambient air. Following echocardiography, the RV was dissected and flash frozen for biochemical analyses. 7 week HH exposure trended toward an increase in IL-18 mRNA (p=0.08) in RV from WT mice. However, contrary to our hypothesis, IL-18 KO mice were not protected against HH-induced RV dysfunction, as evidenced by higher RV weights, elevated RV systolic pressure, and increased RV anterior wall thickness compared to normoxic KO mice. Importantly, these measurements were not significantly different from WT HH mice. Biochemical analyses suggest HH RV underwent early remodeling, as no changes were observed at the molecular level in the RV of HH mice compared to CO in either KO or WT animals. Compensatory upregulation of the other pro-inflammatory cytokines IL-2 and SDF-1 may have contributed to the lack of protection in IL-18 KO animals. These data suggest IL-18 signaling is not necessary for hypobaric hypoxia induced RV dysfunction, and blockade of IL-18 is not a viable therapeutic strategy in this model.

Right ventricular myocardial motion and deformation in adolescents and young adults after repair of coarctation of the aorta.

Alteration of right ventricular (RV) function has been found in patients with pressure-loaded left ventricles due to systemic hypertension and aortic stenosis. We tested the hypothesis that RV mechanics are altered in adolescents and adults with repaired coarctation of the aorta (CoA). Twenty-eight (15 male) patients, aged 23.7 ± 6.5 years, and 28 (14 male) controls were studied. M-mode, tissue Doppler imaging, and speckle tracking echocardiography were performed to assess, respectively, LV mass and RV wall thickness, RV myocardial tissue velocities, and deformation. Systolic (P = 0.14) and diastolic (P = 0.32) blood pressures were similar between patients and controls. Compared with controls, patients had significantly greater LV mass (P = 0.016) and RV anterior wall thickness (P = 0.012). Tricuspid annular systolic (P < 0.001) and early diastolic (P < 0.001) velocities, isovolumic acceleration (P = 0.004), global RV systolic longitudinal strain (P = 0.03), systolic strain rate (P = 0.012), and early (P = 0.021) and late (P = 0.012) diastolic strain rates were significantly lower in patients than controls. Patients with an associated ventricular septal defect (n = 6) requiring closure compared to those without had even lower tricuspid annular systolic (P = 0.01) and early diastolic (P = 0.041) velocities. Left ventricular mass correlated negatively with RV systolic strain rate (r = -0.27, P = 0.045) and tricuspid annular early diastolic velocity (r = -0.40, P = 0.002), while RV anterior wall thickness correlated negatively with tricuspid annular systolic (r = -0.42, P = 0.002) and late diastolic (r = -0.40, P = 0.003) velocities, and positively with e/a ratio (r = 0.31, P = 0.024). RV systolic and diastolic mechanics are impaired in patients late after repair of CoA and related to increased LV mass and RV thickness.

Right ventricular wall hypertrophy predicts functional capacity in pulmonary hypertension. A cardiac magnetic resonance study

Purpose: Right ventricular (RV) dilatation and wall hypertrophy is a compensatory mechanism to pressure and volume overload occurring in patients with pulmonary arterial hypertension (PAH). The aim of our study is to investigate the relationship between RV dimensions and wall thickness as accessed with cardiac magnetic resonance (CMR) and distance walked in 6-minute walking test (6MWD) in adult patients with PAH. Methods: All patients underwent 6 minute walking test (6MWT) and CMR on the same day. RV end diastolic (RVEDa) and end systolic area (RVESa) was obtained in short axis at the level of the papillary muscles at end diastole and end systole respectively and RV anterior wall thickness (RVWT) was measured at the same level at end diastole. Results: Our study included 14 patients with PAH (12 women, mean age 46.64±13.4 years), that walked 485.1±108.0 m in 6MWT. After controlling for confounding parameters as age, sex and body surface index, a negative correlation between distance walked in 6 minutes and RVWT (r=-0.671, p<0.001), RVESa (r=-0.660, p<0.01) and RVEDa (r=-0.704, p<0.005) was observed. Multivariate regression analysis showed that only RVWT is an independent predictor of 6MWD (B=-0.267, p<0.05) in the studied population (Table). View this table: Conclusions: The degree of RV hypertrophy may be used as a predictor of functional capacity of patients with PAH.

Computed tomographic pulmonary angiography in the assessment of severity of chronic thromboembolic pulmonary hypertension and right ventricular dysfunction

The aim was to investigate the role of computed tomographic pulmonary angiography (CTPA) in the assessment of severity and right ventricular function in chronic thromboembolic pulmonary hypertension (CTEPH). Clinical and radiological data of 56 patients with CTEPH January 2006-October 2009 were retrospectively reviewed in the present study. All patients received CTPA with a 64-row CT using the retrospective ECG-Gated mode before digital subtraction pulmonary angiography and right-heart catheterization. CTPA findings including Right Ventricular diameter (RVd) and left ventricular diameter (LVd) were measured at the end diastole. CT Pulmonary Artery Obstruction Indexes including Qanadli Index and Mastora Index were used in the assessment of severity of pulmonary arterial obstruction. Hemodynamic parameters and pulmonary hypertension classification were evaluated by right-heart catheterization in all patients. Right ventricular function was measured with echocardiography in 49 patients. Qanadli Index and Mastora Index respectively were (37.93±14.74)% and (30.92±16.91)%, which showed a significant difference (Z=-5.983, P=0.000) and a good correlation (r=0.881, P=0.000). Neither Qanadli nor Mastora Index correlated with pulmonary hypertension classification (r=-0.009, P=0.920) or New York Heart Association heart function classification (r=-0.031, P=0.756). Neither Qanadli nor Mastora Index correlated with any echocardiographic right ventricular parameters (P>0.05), while RVd/LVd by CTPA correlated with echocardiographic right ventricular functional parameters (P<0.05). Both Qanadli (r=-0.288, P=0.006) and Mastora Index (r=-0.203, P=0.032) demonstrated a weakly negative correlation with SPO2. CTPA findings correlated with hemodynamic variables. Backward linear regression analysis revealed that the RVd/LVd, Right Ventricular Anterior Wall Thickness (RVAWT), Main Pulmonary Artery trunk diameter (MPAd) were shown to be independently associated with mean Pulmonary Artery Pressure (mPAP) levels (model: r2=0.351, P=0.025; RVd/LVd: beta=11.812, P=0.000; RVAWT: beta=2.426, P=0.000; MPAd: beta=0.677, P=0.003). Computed tomographic pulmonary angiography is a valuable tool to evaluate hemodynamics, right ventricular function of CTEPH, but neither Qanadli Index nor Mastora Index can reflect pulmonary arterial obstruction in CTEPH accurately.

Noninvasive Assessment of Pulmonary Arterial Capacitance by Echocardiography

Pulmonary arterial capacitance (PAC) has been associated with right ventricular (RV) workload and mortality in pulmonary hypertension, but is not routinely evaluated in children. We investigated whether PAC can be estimated noninvasively by echocardiography. We retrospectively determined PAC in 31 children with pulmonary hypertension, using echocardiography, and compared the results with those obtained at cardiac catheterization. PAC derived from echocardiography was similar to that derived from catheterization (mean +/- SD 1.16 +/- 1.0 vs 1.10 +/- 0.95 mL(3) x mm Hg(-1), P = not significant) and the two correlated well (r = 0.74, P < .0001). There was a highly significant polynomial relationship between PAC and RV anterior wall thickness indexed to body surface area (R(2) = 0.54, P < .0001), but not between pulmonary vascular resistance and RV wall thickness. Pulmonary vascular resistance and PAC did not correlate. Echocardiography can reliably estimate PAC, which strongly correlates with RV hypertrophy, a surrogate for RV work.

Changes in right ventricular geometry and heart rate early after hemi-Fontan procedure

To document and quantitate changes in right ventricular (RV) geometry and heart rate, we prospectively examined 35 consecutive patients with hypoplastic left heart syndrome under steady-state conditions (chloral hydrate sedation) before and after a bidirectional cavopulmonary anastomosis (hemi-Fontan) procedure. Right ventricular end-diastolic volume (RVEDV) was calculated as the product of RV cavity areas in two orthogonal planes divided by RV maximal length in either plane. After the hemi-Fontan procedure, RVEDV decreased by 33% from 33 ± 13 to 22 ± 11 mL (mean ± standard deviation). Indexed RVEDV decreased from 86 ± 37 to 57 ± 28 mL/m2. The RV wall thickness at the diaphragm in subcostal frontal view (RVWD) increased by only 11% from 8 ± 0.2 to 9 ± 0.2 mm (p = not significant), but RVWD/RVEDV increased by 111% from 0.36 ± 0.22 to 0.76 ± 0.69 mm/ml (p = 0.002). The RV anterior wall thickness in subcostal sagittal view (RVWA) increased by only 13% from 7 ± 0.2 to 8 ± 0.2 mm (p = not significant), but RVWA/RVEDV increased by 103% from 0.31 ± 0.20 to 0.63 ± 0.54 mm/mL (p = 0.002). In 11 of 35 patients (31%), resting heart rate did not change (118 ± 14 versus 108 ± 9 beats/min; p = not significant); however, in 24 of 35 patients (69%), heart rate increased significantly (108 ± 9 versus 127 ± 10 beats/min; p = 0.05). In conclusion, RV wall thickness is high before the hemi-Fontan procedure and increases slightly in the first post-operative week. A concomitant decrease in RVEDV results in a marked change in RV geometry. There is usually a significant increase in resting heart rate as well. Thus, early postoperative chances in RV geometry may have a hemodynamically important impact on stroke volume.

Echocardiographic and hemodynamic assessment of right heart impairment in chronic obstructive lung disease.

42 patients with chronic obstructive lung disease underwent right heart hemodynamics (Swan-Ganz catheter) and M mode echocardiography. Echocardiographic study showed that right ventricular index (RVI) and right ventricular anterior wall thickness (RVAWT) were increased in most patients, while septal thickness and motion were nearly always normal. The finding of impaired RVI and normal RVAWT in several patients, while no one showed normal RVI and increased RVAWT, suggests that arterial pulmonary hypertension results in initial dilatation and only later in hypertrophy of the right ventricle. Echocardiographic parameters were well correlated with hemodynamic and pulmonary function parameters. The good correlations between echocardiographic and hemodynamic data suggest that echocardiography may be a useful technique in the noninvasive assessment of the effects of pulmonary hypertension on the right heart in COLD.