201 Stage-dependent activation of cell cycle and apoptosis mechanisms in the right ventricle by pressure overload

2003 ◽  
Vol 2 (1) ◽  
pp. 41
Author(s):  
A ECARNOT ◽  
L ROCHETTE ◽  
J TEYSSIER
Author(s):  
A. Ecarnot-Laubriet ◽  
M. Assem ◽  
F. Poirson-Bichat ◽  
M. Moisant ◽  
C. Bernard ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Majos ◽  
A Kraska ◽  
I Kowalik ◽  
E Smolis-Bak ◽  
H Szwed ◽  
...  

Abstract Background Assessment of the right ventricle (RV) in heart failure (HF) is challenging and requires applicable methods and parameters. Atrial fibrillation (AF) is a common and clinically significant arrhythmia in 30–50% of HF patients. Assessment of the RV function in patients with AF is problematic. Still little is known about RV function in HF and AF patients. The aim of the study was to assess RV function in HF with focus on AF patients. Methods Patients with HF of ischemic etiology, NYHA II-III, LVEF ≤40%, with AF and sinus rhythm (SR), underwent two- and three- dimensional echocardiography (2DE and 3DE) for assessment of the RV with use of multiple parameters. The RV was examined for: linear dimensions, end-diastolic and end-systolic areas adjusted to body surface area (RV EDA and RV ESA/BSA) and end-diastolic and end-systolic volumes adjusted to lean body mass (RV EDV and RV ESV/LBM) to reflect volume overload and in terms of right ventricular pressure (RVSP) as an index of pressure overload. RV systolic function was assessed with 2DE: tricuspid annular plane systolic excursion (TAPSE), right ventricular fractional area change (RV FAC), tricuspid lateral annular systolic velocity (s') and 3DE parameters: right ventricular ejection fraction (RVEF) and free wall right ventricular longitudinal strain (FW RVLS). Also, TAPSE/RVSP parameter was included. Results The study included 126 patients: 94 with AF and 32 with SR. Within the AF group 28 patients were treated medically, 41 had RV pacing (pacemaker or an implantable cardioverter-defibrillator, ICD) and 25 had cardiac resynchronisation therapy (CRT). In comparison with SR group AF patients had: larger RV inflow tract dimension (4.49±0.85 vs. 3.95±0.72 cm; p=0.0017), RV EDA/BSA (12.7±3.9 vs. 11.1±3.0 cm2/m2; p=0.0358) and RV ESA/BSA (8.0±3.0 vs. 6.7±2.4 cm2/m2; p=0.0226). Similarly, patients with AF had greater RV volumes in 3DE than patients with SR: RV EDV/LBM (1.82±0.60 vs. 1.61±0.38ml/kg, p=0.0267) and RV ESV/LBM (1.11±0.40 ml/kg vs. 0.81±0.28, p<0,0001). Also, in patients with AF right ventricular systolic pressure (RVSP) was higher (40.8±10.2 vs. 34.0±8.1 mmHg, p=0,0010). No differences in TAPSE and RVFAC were found but the relation TAPSE/RVSP was higher in AF than in SR group (0.51±0.21 vs. 0.65±0.24 cm/mmHg; p=0.0046). Also, in AF patients in comparison to SR group some parameters had worse values: s' (9.7±2.31 vs. 12.1±3.83, p=0.014), RVEF (37.2±7.3 vs. 48.2±7.5, p<0.0001 and FW RVLS (−18.3±4.6 vs. −23.9±4.23%, p<0,0001). Within the AF group no significant differences in studied variables depending on RV pacing or CRT were found. Conclusions Larger volumes and higher pressure overload of the RV were observed in patients with AF in comparison to SR. Systolic function of the RV seems to be more depressed in AF compared to SR patients with systolic heart failure. Further research in larger groups is required to identify the most applicable and valuable methods of RV evaluation.


1991 ◽  
Vol 260 (4) ◽  
pp. H1087-H1097
Author(s):  
J. E. Calvin

The purpose of this study was to determine whether segment lengths measured from the right ventricular inflow and outflow tract regions of the right ventricle would accurately reflect true volume changes of the right ventricle and to determine the response of the right ventricle to afterload increases induced by both constricting the pulmonary artery (PAC) and embolizing the pulmonary circulation with glass beads (GBE). Three excised hearts were instrumented with segment-length crystals attached to the inflow and outflow tract regions, and saline was instilled into a balloon implanted inside the right ventricular cavity. The experiments showed a high correlation (r greater than or equal to 0.90 in all cases) between static segment lengths and volume instilled. In open chest, open pericardial canine experiments, vena caval occlusion reduced end-diastolic segments lengths and right ventricular systolic pressure consistent with a reduction in right ventricular end-diastolic volume. In a separate group of animals, volume loading with dextran increased inflow and outflow end-diastolic segment lengths and increased cardiac output. In two further groups of animals, one of which was pretreated intravenously with propranolol (Inderal), both forms of pressure overload increased end-diastolic lengths in both regions. However, GBE increased right ventricular stroke work compared with PAC. We conclude that end-diastolic segment lengths reflect true volume changes of the right ventricle. Furthermore, during acute pressure overload, the right ventricle dilates to compensate for the afterload change. However, ventricular function is better maintained after GBE.


2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.


Heart Disease ◽  
2003 ◽  
Vol 5 (5) ◽  
pp. 308-312 ◽  
Author(s):  
Aline Ecarnot-Laubriet ◽  
Luc Rochette ◽  
Catherine Vergely ◽  
Pierre Sicard ◽  
Jean-Raymond Teyssier

2013 ◽  
Vol 98 (8) ◽  
pp. 1274-1278 ◽  
Author(s):  
Wiebke Janssen ◽  
Ralph Theo Schermuly ◽  
Baktybek Kojonazarov

1988 ◽  
Vol 255 (2) ◽  
pp. H325-H328 ◽  
Author(s):  
R. Nagai ◽  
R. B. Low ◽  
W. S. Stirewalt ◽  
N. R. Alpert ◽  
R. Z. Litten

We measured the rate of protein synthesis and total RNA content in the right ventricle (RV) at day 2 and day 4 after pulmonary artery constriction to determine the contributions of changes in capacity and efficiency of in vivo protein synthesis to pressure overload (PO) cardiac hypertrophy. A significant increase in the proportion of RV weight to total heart weight was observed at day 2 and day 4 when compared with untreated controls. The rate of protein synthesis was significantly higher at day 2 post-PO (0.31 +/- 0.06 day-1 or 30 +/- 5 mg.g RV-1.day-1, means +/- SD, P less than 0.05) as well as at day 4 (0.25 +/- 0.05 day-1 or 28 +/- 9 mg.g RV-1.day-1, P less than 0.05) than for untreated rabbits (0.15 +/- 0.03 day-1 or 17 +/- 4 mg.g RV-1.day-1). RNA content was significantly higher at day 2 (1.47 +/- 0.17 mg/g RV, P less than 0.05) than in controls (1.16 +/- 0.14 mg/g RV), whereas there was a slight but nonsignificant increase at day 4 (1.36 +/- 0.21 mg/g RV, P less than 0.1). The efficiency of protein synthesis (synthesis/RNA) per gram RV was significantly increased both at day 2 (20.5 +/- 2.2 g protein.g RNA-1.day-1, P less than 0.05) and day 4 (19.8 +/- 3.5 g protein.g RNA-1.day-1, P less than 0.05) compared with control (14.6 +/- 2.3 g protein.g RNA-1.day-1). The increase in efficiency appeared to be caused by pressure overload itself based on a comparison of 0-4 day data vs. data obtained from sham animals (P less than 0.05).


1982 ◽  
Vol 243 (2) ◽  
pp. H175-H180 ◽  
Author(s):  
P. G. Schmid ◽  
D. D. Lund ◽  
J. A. Davis ◽  
C. A. Whiteis ◽  
R. K. Bhatnagar ◽  
...  

Selective pressure overload of the right ventricle in guinea pigs resulted in early and sustained reductions in tyrosine hydroxylase and dopamine-beta-hydroxylase activities in the right ventricle. No changes in tyrosine hydroxylase activity were detected in stellate ganglia sinoatrial (SA) nodal region, atrioventricular (AV) nodal region, or left ventricle. Reductions in tyrosine hydroxylase activity in stressed right ventricle were similar regardless of duration of pulmonary artery constriction, extent of hypertrophy, presence or absence of hepatic congestion, and preservation or depletion of catecholamines. The changes may represent localized loss of sympathetic nerve fibers; factors involved directly in the process of pressure-overload-induced hypertrophy may be responsible. However, sympathetic nerves remaining in hypertrophied ventricle respond normally to cold-induced sympathetic activation. The reduction in tyrosine hydroxylase activity and the maintenance of norepinephrine turnover in residual innervation to hypertrophied right ventricle support the concept that sympathetic neural regulation of hypertrophied cardiac tissue is altered but not lost.


CHEST Journal ◽  
1980 ◽  
Vol 78 (1) ◽  
pp. 10-15 ◽  
Author(s):  
Paul D. Stein ◽  
Hani N. Sabbah ◽  
Mario Mazilli ◽  
Daniel T. Anbe

Sign in / Sign up

Export Citation Format

Share Document