Improved contractile performance of right ventricle in response to increased RV afterload in newborn lamb

2000 ◽  
Vol 278 (1) ◽  
pp. H100-H105 ◽  
Author(s):  
Maartje de Vroomen ◽  
Robbert H. Lopes Cardozo ◽  
Paul Steendijk ◽  
Frank van Bel ◽  
Jan Baan
Keyword(s):  
Right Ventricle ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Balloon Occlusion ◽  
Newborn Lamb ◽  
End Diastolic Volume ◽  
Volume Relation ◽  
The Right ◽  
Homeometric Autoregulation ◽  
Contractile Performance

Pulmonary hypertension results in an increased afterload for the right ventricle (RV). To determine the effects of this increased afterload on RV contractile performance, we examined RV performance before and during 4 h of partial balloon occlusion of the pulmonary artery and again after releasing the occlusion in nine newborn lambs. RV contractile performance was quantified by indexes derived from systolic RV pressure-volume relations obtained by a combined pressure-conductance catheter during inflow reduction. An almost twofold increase of end-systolic RV pressure (from 22 to 38 mmHg) was maintained during 4 h. Cardiac output (CO) (0.74 ± 0.08 l/min) and stroke volume (4.3 ± 0.4 ml) were maintained, whereas end-diastolic volume (7.9 ± 1.3 ml) did not change significantly during this period. RV systolic function improved substantially; the end-systolic pressure-volume relation shifted leftward indicated by a significantly decreased volume intercept (up to 70%), together with a slightly increased slope. In this newborn lamb model, maintenance of CO during increased RV afterload is not obtained by an increased end-diastolic volume (Frank-Starling mechanism). Instead, the RV maintains its output by improving contractile performance through homeometric autoregulation.

Differential negative effects of acute exhaustive swim exercise on the right ventricle is associated with disproportionate hemodynamic loading

2021 ◽  
Author(s):  
Robert Lakin ◽  
Ryan Debi ◽  
Sibao Yang ◽  
Nazari Polidovitch ◽  
Jack M. Goodman ◽  
...  
Keyword(s):  
Right Ventricle ◽  
Negative Impact ◽  
Systolic Function ◽  
Systolic Pressure ◽  
Exhaustive Exercise ◽  
Lv Function ◽  
Time To Exhaustion ◽  
Negative Effects ◽  
Post Exercise ◽  
The Right

Acute exhaustive endurance exercise can differentially impact the right ventricle (RV) versus the left (LV). However, the hemodynamic basis for these differences and its impact on post-exercise recovery remains unclear. Therefore, we assessed cardiac structure and function along with hemodynamic properties of mice subjected to single bouts (216±8min) of exhaustive swimming (ES). One-hour after ES, LVs displayed mild diastolic impairment compared to sedentary (SED) mice. Following dobutamine administration to assess functional reserve, diastolic and systolic function were slightly impaired. Twenty-four hours after ES, LV function was largely indistinguishable from SED. By contrast, one-hour post-swim, RVs showed pronounced impairment of diastolic and systolic function with and without dobutamine, which persisted twenty-four hours later. The degree of RV impairment correlated with time-to-exhaustion. To identify hemodynamic factors mediating chamber-specific responses to ES, LV pressure was recorded during swimming. Swimming initiated immediate increases in heart rates (HRs), systolic pressure, dP/dtmax and -dP/dtmin, which remained stable for ~45min. LV end-diastolic pressures (LVEDP) increased to ≥45mmHg during the first 10min and subsequently declined. After 45 mins, HR and -dP/dtmin declined, which correlated with gradual elevations in LVEDP (to ~45mmHg) as mice approached exhaustion. All parameters rapidly normalized post-exercise. Consistent with human studies, our findings demonstrate a disproportionate negative impact of acute exhaustive exercise on RVs that persisted for at least 24-hours. We speculate that the differential effects of exhaustive exercise on the ventricles arise from a ~2-fold greater hemodynamic load in the RV versus LV originating from profound elevations in LVEDPs as mice approach exhaustion.

Biventricular systolic function in young lambs subject to chronic systemic right ventricular pressure overload

2001 ◽  
Vol 281 (6) ◽  
pp. H2697-H2704 ◽  
Author(s):  
Boudewijn P. J. Leeuwenburgh ◽  
Willem A. Helbing ◽  
Paul Steendijk ◽  
Paul H. Schoof ◽  
Jan Baan
Keyword(s):  
Systolic Function ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Left Ventricular ◽  
Biventricular Function ◽  
Pressure Volume Relationship ◽  
Lv Volume ◽  
The Right ◽  
Contractile Performance ◽  
Biventricular Systolic Function

In various clinical situations of congenital heart disease, the right ventricle (RV) is subject to a chronic systemic pressure overload which affects biventricular function and may progress to the development of RV failure. Young lambs (2–3 wk old) underwent adjustable pulmonary artery banding (PAB) at systemic (aortic) level for 8 wk. Biventricular function was determined by using load-independent indexes of global ventricular contractile performance by the end-systolic pressure-volume relationship (ESPVR) using the conductance catheter at baseline and during dobutamine infusion. PAB resulted in a significant fivefold increase in RV end-systolic pressure (12–64 mmHg) and a doubling of the RV-to-left ventricular (LV) wall thickness ratio ( P < 0.01). RV global contractile performance increased significantly, as indicated by an increased slope of the ESPVR. Compared with age-matched control lambs, cardiac output decreased from 2.6 to 1.6 l/min ( P < 0.05) whereas heart rates were equal. In contrast with RV volume, LV volume decreased significantly after PAB ( P < 0.01), whereas the LV-ESPVR slope was unchanged. In the PAB group, the RV, but not the LV, showed a reduced response to dobutamine. We concluded that chronic RV pressure overload for 8 wk results in diminished pump function despite compensatory increased RV global contractile performance.

Ventricular systolic interdependence: volume elastance model in isolated canine hearts

1987 ◽  
Vol 253 (6) ◽  
pp. H1381-H1390 ◽  
Author(s):  
W. L. Maughan ◽  
K. Sunagawa ◽  
K. Sagawa
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Cross Talk ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Ventricular Free Wall ◽  
Free Wall ◽  
Right Ventricular Free Wall ◽  
Systolic Volume ◽  
The Right

To analyze the interaction between the right and left ventricle, we developed a model that consists of three functional elastic compartments (left ventricular free wall, septal, and right ventricular free wall compartments). Using 10 isolated blood-perfused canine hearts, we determined the end-systolic volume elastance of each of these three compartments. The functional septum was by far stiffer for either direction [47.2 +/- 7.2 (SE) mmHg/ml when pushed from left ventricle and 44.6 +/- 6.8 when pushed from right ventricle] than ventricular free walls [6.8 +/- 0.9 mmHg/ml for left ventricle and 2.9 +/- 0.2 for right ventricle]. The model prediction that right-to-left ventricular interaction (GRL) would be about twice as large as left-to-right interaction (GLR) was tested by direct measurement of changes in isovolumic peak pressure in one ventricle while the systolic pressure of the contralateral ventricle was varied. GRL thus measured was about twice GLR (0.146 +/- 0.003 vs. 0.08 +/- 0.001). In a separate protocol the end-systolic pressure-volume relationship (ESPVR) of each ventricle was measured while the contralateral ventricle was alternatively empty and while systolic pressure was maintained at a fixed value. The cross-talk gain was derived by dividing the amount of upward shift of the ESPVR by the systolic pressure difference in the other ventricle. Again GRL measured about twice GLR (0.126 +/- 0.002 vs. 0.065 +/- 0.008). There was no statistical difference between the gains determined by each of the three methods (predicted from the compartment elastances, measured directly, or calculated from shifts in the ESPVR). We conclude that systolic cross-talk gain was twice as large from right to left as from left to right and that the three-compartment volume elastance model is a powerful concept in interpreting ventricular cross talk.

P3527Echocardiographic assessment of the right ventricle in chronic heart failure with focus on patients with atrial fibrillation

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
E Majos ◽  
A Kraska ◽  
I Kowalik ◽  
E Smolis-Bak ◽  
H Szwed ◽  
...  
Keyword(s):  
Heart Failure ◽  
Atrial Fibrillation ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Systolic Function ◽  
Pressure Overload ◽  
Ventricular Ejection Fraction ◽  
Rv Pacing ◽  
The Right ◽  
Rv Function

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.

Early and late outcomes of surgical repair of double-chambered right ventricle: a single-centre experience

2020 ◽  
Vol 30 (3) ◽  
pp. 409-412
Author(s):  
Murat Surucu ◽  
İlkay Erdoğan ◽  
Birgül Varan ◽  
Murat Özkan ◽  
N. Kürşad Tokel ◽  
...  
Keyword(s):  
Ventricular Septal Defect ◽  
Right Ventricle ◽  
Septal Defect ◽  
Surgical Intervention ◽  
Systolic Pressure ◽  
Presenting Symptoms ◽  
Long Term Follow Up ◽  
The Right

AbstractObjective:Double-chambered right ventricle is characterised by division of the outlet portion of the right ventricle by hypertrophy of the septoparietal trabeculations into two parts. We aim to report our experiences regarding the presenting symptoms of double-chambered right ventricle, long-term prognosis, including the recurrence rate and incidence of arrhythmias after surgery.Methods:We retrospectively investigated 89 consecutive patients who were diagnosed to have double-chambered right ventricle and underwent a surgical intervention from 1995 to 2016. The data obtained by echocardiography, cardiac catheterisation, and surgical findings as well as post-operative follow-up, surgical approaches, post-operative morbidity, mortality, and cardiac events were evaluated.Results:Median age at the time of diagnosis was 2 months and mean age at the time of operation was 5.3 years. Concomitant cardiac anomalies were as follows: perimembranous ventricular septal defect (78 patients), atrial septal defect (9 patients), discrete subaortic membrane (32 patients), right aortic arch (3 patients), aortic valve prolapse and/or mild aortic regurgitation (14 patients), and left superior caval vein (2 patients). The mean follow-up period was 4.86 ± 4.6 years. In these patients, mean systolic pressure gradient in the right ventricle by echocardiography before, immediately, and long-term after surgical intervention was 66.3, 11.8, and 10.4 mmHg, respectively. There were no deaths during the long-term follow-up period. Surgical reinterventions were performed for residual ventricular septal defect (2), residual pulmonary stenosis (1), and severe tricuspid insufficiency (1).Conclusion:The surgical outcomes and prognosis of double-chambered right ventricle are favourable, recurrence and fatal arrhythmias are unlikely in long-term follow-up.

Pressure segment length analysis of right ventricular function: influence of loading conditions

1991 ◽  
Vol 260 (4) ◽  
pp. H1087-H1097
Author(s):  
J. E. Calvin
Keyword(s):  
Right Ventricle ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Systolic Pressure ◽  
Pressure Overload ◽  
Outflow Tract ◽  
Segment Length ◽  
Stroke Work ◽  
Volume Changes ◽  
The Right

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.

Long-term results after palliative intra-cardiac repair for tetralogy of Fallot and diminutive pulmonary arteries

2019 ◽  
Vol 29 (8) ◽  
pp. 1036-1039
Author(s):  
Yoichi Kawahira ◽  
Kyoichi Nishigaki ◽  
Koji Kagisaki ◽  
Takuji Watanabe ◽  
Kazuki Tanimoto
Keyword(s):  
Right Ventricle ◽  
Tetralogy Of Fallot ◽  
Arterial Oxygen Saturation ◽  
Pulmonary Arteries ◽  
Systolic Pressure ◽  
Cardiac Repair ◽  
Long Term Results ◽  
Arterial Oxygen ◽  
The Right

AbstractBackground:In patients with tetralogy of Fallot with the diminutive pulmonary arteries, we sometimes have to give up the complete intra-cardiac repair due to insufficient growth of the pulmonary arteries. We have carried out palliative intra-cardiac repair using a fenestrated patch.Methods:Of all 202 patients with tetralogy of Fallot in our centre since 1996, five patients (2.5%) with the diminutive pulmonary arteries underwent palliative intra-cardiac repair using a fenestrated patch. Mean operative age was 1.8 years. Previous operation was Blalock–Taussig shunt in 4. At operation, the ventricular septal defect was closed using a fenestrated patch and the right ventricular outflow tract was enlarged. Follow-up period was 9.8 ± 2.6 years.Results:There were no operative and late deaths. Fenestration closed spontaneously on its own in four patients 2.7 ± 2.1 years after the intra-cardiac repair with a stable haemodynamics; however, the last patient with the smallest pulmonary artery index had supra-systemic pressure of the right ventricle post-operatively. The fenestration was emergently enlarged. Systemic arterial oxygen saturation was significantly and dramatically increased from 83.5 to 94% after the palliative intra-cardiac repair, and to 98% at the long term. A ratio of systolic pressure of the right ventricle to the left was significantly decreased to 0.76 ± 0.12 at the long term. Now all five patients were Ross classification class I.Conclusion:Although frequent catheter and surgical interventions were needed after the palliative intra-cardiac repair, this repair might be a choice improving quality of life with good results in patients with tetralogy of Fallot associated with the diminutive pulmonary arteries.

scholarly journals Cardiac matrix metalloproteinase-2 expression independently induces marked ventricular remodeling and systolic dysfunction

2007 ◽  
Vol 292 (4) ◽  
pp. H1847-H1860 ◽  
Author(s):  
Marina R. Bergman ◽  
John R. Teerlink ◽  
Rajeev Mahimkar ◽  
Luyi Li ◽  
Bo-Qing Zhu ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Matrix Metalloproteinase ◽  
Ventricular Remodeling ◽  
Systolic Function ◽  
Systolic Dysfunction ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Matrix Metalloproteinase 2 ◽  
Membrane Type ◽  
Volume Relation

Although enhanced cardiac matrix metalloproteinase (MMP)-2 synthesis has been associated with ventricular remodeling and failure, whether MMP-2 expression is a direct mediator of this process is unknown. We generated transgenic mice expressing active MMP-2 driven by the α-myosin heavy chain promoter. At 4 mo MMP-2 transgenic hearts demonstrated expression of the MMP-2 transgene, myocyte hypertrophy, breakdown of Z-band registration, lysis of myofilaments, disruption of sarcomere and mitochondrial architecture, and cardiac fibroblast proliferation. Hearts from 8-mo-old transgenic mice displayed extensive myocyte disorganization and dropout with replacement fibrosis and perivascular fibrosis. Older transgenic mice also exhibited a massive increase in cardiac MMP-2 expression, representing recruitment of endogenous MMP-2 synthesis, with associated expression of MMP-9 and membrane type 1 MMP. Increases in diastolic [control (C) 33 ± 3 vs. MMP 51 ± 12 μl; P = 0.003] and systolic (C 7 ± 2 vs. MMP 28 ± 14 μl; P = 0.003) left ventricular (LV) volumes and relatively preserved stroke volume (C 26 ± 4 vs. MMP 23 ± 3 μl; P = 0.16) resulted in markedly decreased LV ejection fraction (C 78 ± 7% vs. MMP 48 ± 16%; P = 0.0006). Markedly impaired systolic function in the MMP transgenic mice was demonstrated in the reduced preload-adjusted maximal power (C 240 ± 84 vs. MMP 78 ± 49 mW/μl2; P = 0.0003) and decreased end-systolic pressure-volume relation (C 7.5 ± 1.5 vs. MMP 4.7 ± 2.0; P = 0.016). Expression of active MMP-2 is sufficient to induce severe ventricular remodeling and systolic dysfunction in the absence of superimposed injury.

scholarly journals MicroRNA-140 is elevated and mitofusin-1 is downregulated in the right ventricle of the Sugen5416/hypoxia/normoxia model of pulmonary arterial hypertension.

2016 ◽  
Vol 311 (3) ◽  
pp. H689-H698 ◽  
Author(s):  
Sachindra Raj Joshi ◽  
Vidhi Dhagia ◽  
Salina Gairhe ◽  
John G. Edwards ◽  
Ivan F. McMurtry ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Right Ventricle ◽  
Arterial Hypertension ◽  
Systolic Pressure ◽  
Right Heart ◽  
Biochemical Processes ◽  
Pulmonary Arterial ◽  
Direct Target ◽  
The Right ◽  
Mitofusin 1

Heart failure, a major cause of morbidity and mortality in patients with pulmonary arterial hypertension (PAH), is an outcome of complex biochemical processes. In this study, we determined changes in microRNAs (miRs) in the right and left ventricles of normal and PAH rats. Using an unbiased quantitative miR microarray analysis, we found 1) miR-21-5p, miR-31-5 and 3p, miR-140-5 and 3p, miR-208b-3p, miR-221-3p, miR-222-3p, miR-702-3p, and miR-1298 were upregulated (>2-fold; P < 0.05) in the right ventricle (RV) of PAH compared with normal rats; 2) miR-31-5 and 3p, and miR-208b-3p were upregulated (>2-fold; P < 0.05) in the left ventricle plus septum (LV+S) of PAH compared with normal rats; 3) miR-187-5p, miR-208a-3p, and miR-877 were downregulated (>2-fold; P < 0.05) in the RV of PAH compared with normal rats; and 4) no miRs were up- or downregulated with >2-fold in LV+S compared with RV of PAH and normal. Upregulation of miR-140 and miR-31 in the hypertrophic RV was further confirmed by quantitative PCR. Interestingly, compared with control rats, expression of mitofusin-1 (MFN1), a mitochondrial fusion protein that regulates apoptosis, and which is a direct target of miR-140, was reduced in the RV relative to LV+S of PAH rats. We found a correlation between increased miR-140 and decreased MFN1 expression in the hypertrophic RV. Our results also demonstrated that upregulation of miR-140 and downregulation of MFN1 correlated with increased RV systolic pressure and hypertrophy. These results suggest that miR-140 and MFN1 play a role in the pathogenesis of PAH-associated RV dysfunction. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/mir140-and-right-heart-hypertrophy/ .

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