Pulmonary Vascular Versus Right Ventricular Function Changes During Targeted Therapies of Pulmonary Hypertension – An Argument for Upfront Combination Therapy?

2012 ◽  
Vol 8 (3) ◽  
pp. 209
Author(s):  
Wouter Jacobs ◽  
Anton Vonk-Noordegraaf ◽  
◽  
Keyword(s):  
Combination Therapy ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Meta Analysis ◽  
Right Heart Failure ◽  
Functional Class ◽  
Pulmonary Vasculature ◽  
The Right

Pulmonary arterial hypertension is a progressive disease of the pulmonary vasculature, ultimately leading to right heart failure and death. Current treatment is aimed at targeting three different pathways: the prostacyclin, endothelin and nitric oxide pathways. These therapies improve functional class, increase exercise capacity and improve haemodynamics. In addition, data from a meta-analysis provide compelling evidence of improved survival. Despite these treatments, the outcome is still grim and the cause of death is inevitable – right ventricular failure. One explanation for this paradox of haemodynamic benefit and still worse outcome is that the right ventricle does not benefit from a modest reduction in pulmonary vascular resistance. This article describes the physiological concepts that might underlie this paradox. Based on these concepts, we argue that not only a significant reduction in pulmonary vascular resistance, but also a significant reduction in pulmonary artery pressure is required to save the right ventricle. Haemodynamic data from clinical trials hold the promise that these haemodynamic requirements might be met if upfront combination therapy is used.

scholarly journals Metastatic adenocarcinoma involving the right ventricle and pulmonary artery leading to right heart failure: case report

2017 ◽  
Vol 136 (3) ◽  
pp. 262-265 ◽  
Author(s):  
Turgut Karabag ◽  
Caner Arslan ◽  
Turab Yakisan ◽  
Aziz Vatan ◽  
Duygu Sak
Keyword(s):  
Heart Failure ◽  
Case Report ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Ventricular Outflow Tract ◽  
Right Heart Failure ◽  
Ventricular Outflow Tract ◽  
Right Heart ◽  
The Right

ABSTRACT CONTEXT: Obstruction of the right ventricular outflow tract due to metastatic disease is rare. Clinical recognition of cardiac metastatic tumors is rare and continues to present a diagnostic and therapeutic challenge. CASE REPORT: We present the case of a patient who had severe respiratory insufficiency and whose clinical examinations revealed a giant tumor mass extending from the right ventricle to the pulmonary artery. We discuss the diagnostic and therapeutic options. CONCLUSION: In patients presenting with acute right heart failure, right ventricular masses should be kept in mind. Transthoracic echocardiography appears to be the most easily available, noninvasive, cost-effective and useful technique in making the differential diagnosis.

The Hemodynamic Characteristics of Right Ventricle After Gradient Pulmonary Artery Banding in Rats

2020 ◽  
Author(s):  
Song Jiyang ◽  
Wan Nan ◽  
Shen Shutong ◽  
Wei Ying ◽  
Cao Yunshan
Keyword(s):  
Heart Failure ◽  
Pulmonary Artery ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Right Heart Failure ◽  
Therapeutic Strategies ◽  
Pulmonary Artery Banding ◽  
Right Heart ◽  
Pulmonary Arterial ◽  
The Right

Abstract Background: Right ventricular (RV) failure induced by sustained pressure overload is a major contributor to morbidity and mortality in several cardiopulmonary disorders. Reliable and reproducible animal models of RV failure are important in order to investigate disease mechanisms and effects of potential therapeutic strategies. To establish a rat model of RV failure perfectly, we observed the right ventricle and carotid artery hemodynamics characteristics in different degrees of pulmonary artery banding of rats of different body weights. Methods: Rats were subjected to 6 groups：control(0%, n=5)(pulmonary arterial banding 0%), PAB(1-30%, n=4)(pulmonary arterial banding1-30%), PAB(31-60%, n=6)(pulmonary arterial banding31-60%),PAB(61-70%, n=5)(pulmonary arterial bandin61-70%), PAB(71-80%,n=4)(pulmonary arterial banding71-80%), PAB(100%, n=3)(pulmonary arterial banding 100%). We measured the right ventricular pressure(RVP) by right heart catheterization when the pulmonary arterial was ligated. Results: The RVP gradually increased with increasing degree of banding, but when occlusion level exceeding 70%, high pressure state can be only maintained for a few minutes or seconds, and then the RVP drops rapidly until it falls below the normal pressure, which in Group F particularly evident.Conclusions: RVP have different reactions when the occlusion level is not the same, and the extent of more than 70% ligation is a successful model of acute right heart failure. These results may have important consequences for therapeutic strategies to prevent acute right heart failure.

scholarly journals Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension

2017 ◽  
Vol 7 (3) ◽  
pp. 572-587 ◽  
Author(s):  
Nolwenn Samson ◽  
Roxane Paulin
Keyword(s):  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Pressure Overload ◽  
Right Heart Failure ◽  
Left Ventricular ◽  
Ventricular Failure ◽  
Pulmonary Arterial ◽  
Ventricle Hypertrophy ◽  
The Right

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.

Effect of increased pulmonary vascular resistance on right ventricular systolic performance in dogs

1984 ◽  
Vol 246 (3) ◽  
pp. H339-H343 ◽  
Author(s):  
M. Ghignone ◽  
L. Girling ◽  
R. M. Prewitt
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Glass Beads ◽  
Ventricular Systolic Pressure ◽  
Bead Injection ◽  
The Right

We tested the possibility that for a given contractile state and right ventricular systolic pressure (RVSP), rate and extent of ventricular shortening would be reduced as resistance to ejection increased. In eight anesthetized, ventilated dogs, we measured RV and pulmonary artery pressure (Ppa), blood pressure, heart rate, cardiac output (CO), and RV dP/dt before (condition 1) and after (condition 2) pulmonary vascular resistance (PVR) was increased by injection of small (80 micron) glass beads. Glass beads caused a large increase (P less than 0.001) in Ppa and in RVSP and, despite increased RV end-diastolic pressure (EDP), CO and stroke volume (SV) were reduced. A third set of measurements was obtained following a further increase in resistance (condition 3). A comparison of condition 2 with condition 3, despite constant RVSP, constant mean Ppa, and increased EDP, showed a marked fall in CO and SV (P less than 0.001) when glass bead injection increased calculated resistance from 21 (condition 2) to 34 (condition 3) mmHg X 1(-1) X min. RV contractility, as assessed by Vmax and peak dP/dt was similar in both conditions. In five additional dogs, we measured the same parameters as before plus instantaneous pulmonary artery flow in all conditions. In a comparison of conditions 2 and 3, despite constant RVSP and increased EDP, peak and total flow (P less than 0.05) were reduced as resistance to RV ejection increased. We conclude that the right ventricle shortens more slowly and to a smaller extent against the same systolic pressure when its resistive afterload increases.

Ultrastructural and functional features of the developing mammalian heart: a brief overview

1995 ◽  
Vol 7 (3) ◽  
pp. 451 ◽  
Author(s):  
JJ Smolich
Keyword(s):  
Blood Flow ◽  
Sarcoplasmic Reticulum ◽  
Left Ventricle ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Postnatal Development ◽  
Vascular Resistance ◽  
Ventricular Myocytes ◽  
Left Ventricular ◽  
The Right

The heart undergoes marked ultrastructural alterations during fetal and postnatal development. Early in fetal development, cardiac myocytes contain abundant pools of glycogen, scattered mitochondria and sparse, peripheral myofibrils. Transverse tubules are absent, and sarcoplasmic reticulum and intercalated discs are poorly developed. During late fetal and early postnatal development, myofibrils extend into the myocyte interior and attain a mature appearance, and the glycogen pools are reduced in size. In addition, transverse tubules develop and the morphological appearance of the sarcoplasmic reticulum and intercalated disc becomes increasingly complex. Experimental studies in sheep, corroborated by clinical studies in humans, also point to marked functional changes during development. In the fetus, the right ventricle is the dominant pumping chamber because right ventricular output exceeds left ventricular output, while pulmonary arterial and aortic pressures are similar. This functional difference is reflected in myocardial blood flow patterns, with blood flow to the right ventricle exceeding that to the left ventricle. The ventricular outputs equalize after birth, but a functional left ventricular dominance rapidly emerges following a postnatal increase in systemic vascular resistance and a decrease in pulmonary vascular resistance. This postnatal switchover in functional dominance is accompanied by a corresponding alteration in the relative level of ventricular myocardial blood flows. Consistent with right ventricular dominance in utero, myocytes in the right ventricle of the fetal sheep are larger and contain more myofibrillar material than those in the left ventricle. Left ventricular myocytes become larger than right ventricular myocytes after birth, but this adaptation to altered postnatal haemodynamics requires some weeks to become fully established.

CMR markers for early right ventricular dysfunction in precapillary pulmonary hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J Vos ◽  
T Leiner ◽  
A.P.J Van Dijk ◽  
F.J Meijboom ◽  
G.T Sieswerda ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Right Ventricle ◽  
Right Ventricular ◽  
Circumferential Strain ◽  
Peak Strain ◽  
Healthy Controls ◽  
Free Wall ◽  
Global Circumferential Strain ◽  
The Right ◽  
Rv Function

Abstract Introduction Precapillary pulmonary hypertension (pPH) causes right ventricular (RV) pressure overload inducing RV remodeling, often resulting in dysfunction and dilatation, heart failure, and ultimately death. The ability of the right ventricle to adequately adapt to increased pressure loading is key for patients' prognosis. RV ejection fraction (RVEF) by cardiac magnetic resonance (CMR) is related to outcome in pPH patients, but this global measurement is not ideal for detecting early changes in RV function. Strain analysis on CMR using feature tracking (FT) software provides a more detailed assessment, and might therefore detect early changes in RV function. Aim 1) To compare RV strain parameters in pPH patients and healthy controls, and 2) to compare strain parameters in a subgroup of pPH patients with preserved RVEF (pRVEF) and healthy controls. Methods In this prospective study, a CMR was performed in pPH patients and healthy controls. Using FT-software on standard cine images, the following RV strain parameters were analyzed: global, septal, and free wall longitudinal strain (GLS, sept-LS, free wall-LS), time to peak strain (TTP, as a % of the whole cardiac cycle), the fractional area change (FAC), global circumferential strain (GCS), global longitudinal and global circumferential strain rate (GLSR and GCSR, respectively). A pRVEF is defined as a RVEF >50%. To compare RV strain parameters in pPH patients to healthy controls, the Mann-Whitney U test was used. Results 33 pPH-patients (55 [45–63] yrs; 10 (30%) male) and 22 healthy controls (40 [36–48] yrs; 15 (68%) male) were included. All RV strain parameters were significantly reduced in pPH patients compared to healthy controls (see table), except for GCS and GCSR. Most importantly, in pPH patients with pRVEF (n=8) GLS (−26.6% [−22.6 to −27.3] vs. −28.1% [−26.2 to −30.6], p=0.04), sept-LS (−21.2% [−19.8 to −23.2] vs. −26.0% [−24.0 to −27.9], p=0.005), and FAC (39% [35–44] vs. 44% [42–47], p=0.02) were still significantly impaired compared to healthy controls. The RV TTP was significantly increased in pPH patients compared to healthy controls (47% [44–57] vs. 40% [33–43], p≤0.001). Conclusions Several CMR-FT strain parameters of the right ventricle are impaired in pPH patients when compared to healthy controls. Moreover, even in pPH patients with a preserved RVEF multiple RV strain parameters (GLS, sept-LS, and FAC) remained significantly impaired, and TTP significantly prolonged, in comparison to healthy controls. This suggests that RV strain parameters may be used as an early marker of RV dysfunction in pPH patients. Funding Acknowledgement Type of funding source: None

scholarly journals Importance of Preserved Tricuspid Valve Function for Effective Soft Robotic Augmentation of the Right Ventricle in Cases of Elevated Pulmonary Artery Pressure

2021 ◽  
Author(s):  
Isaac Wamala ◽  
Christopher J. Payne ◽  
Mossab Y. Saeed ◽  
Daniel Bautista-Salinas ◽  
David Van Story ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Right Ventricle ◽  
Tricuspid Regurgitation ◽  
Diastolic Pressure ◽  
Right Heart Failure ◽  
Lower Grade ◽  
Ventricular Assist ◽  
Valve Function ◽  
Right Ventricular Assist Device ◽  
The Right

Abstract Purpose In clinical practice, many patients with right heart failure (RHF) have elevated pulmonary artery pressures and increased afterload on the right ventricle (RV). In this study, we evaluated the feasibility of RV augmentation using a soft robotic right ventricular assist device (SRVAD), in cases of increased RV afterload. Methods In nine Yorkshire swine of 65–80 kg, a pulmonary artery band was placed to cause RHF and maintained in place to simulate an ongoing elevated afterload on the RV. The SRVAD was actuated in synchrony with the ventricle to augment native RV output for up to one hour. Hemodynamic parameters during SRVAD actuation were compared to baseline and RHF levels. Results Median RV cardiac index (CI) was 1.43 (IQR, 1.37–1.80) L/min/m2 and 1.26 (IQR 1.05–1.57) L/min/m2 at first and second baseline. Upon PA banding RV CI fell to a median of 0.79 (IQR 0.63–1.04) L/min/m2. Device actuation improved RV CI to a median of 0.87 (IQR 0.78–1.01), 0.85 (IQR 0.64–1.59) and 1.11 (IQR 0.67–1.48) L/min/m2 at 5 min (p = 0.114), 30 min (p = 0.013) and 60 (p = 0.033) minutes respectively. Statistical GEE analysis showed that lower grade of tricuspid regurgitation at time of RHF (p = 0.046), a lower diastolic pressure at RHF (p = 0.019) and lower mean arterial pressure at RHF (p = 0.024) were significantly associated with higher SRVAD effectiveness. Conclusions Short-term augmentation of RV function using SRVAD is feasible even in cases of elevated RV afterload. Moderate or severe tricuspid regurgitation were associated with reduced device effectiveness.

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