Right Ventricular End-diastolic Pressure Research Articles

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

Does cardiac resynchronization therapy benefit patients with right bundle branch block: cardiac resynchronization therapy has a role in patients with right bundle branch block.

Sildenafil treatment in established right ventricular dysfunction improves diastolic function and attenuates interstitial fibrosis independent from afterload.

Right ventricular (RV) function is an important determinant of prognosis in congenital heart diseases, pulmonary hypertension, and heart failure. Preventive sildenafil treatment has been shown to enhance systolic RV function and improve exercise capacity in a model of fixed RV pressure load. However, it is unknown whether sildenafil has beneficial effects when treatment is started in established RV dysfunction, which is clinically more relevant. Our aim was to assess the effects of sildenafil treatment on RV function and fibrosis in a model of established RV dysfunction due to fixed afterload. Rats were subjected to pulmonary artery banding (PAB), which induced RV dysfunction after 4 wk, characterized by reduced exercise capacity, decreased tricuspid annular plane systolic excursion, and RV dilatation. From week 4 onward, 50% of rats were treated with sildenafil (100 mg·kg(-1)·day(-1), n = 9; PAB-SIL group) or vehicle (n = 9; PAB-VEH group). At 8 wk, exercise capacity was assessed using cage wheels, and RV function was assessed using invasive RV pressure-volume measurements under anesthesia. Sildenafil treatment, compared with vehicle, improved RV ejection fraction (44 ± 2% vs. 34 ± 2%, P < 0.05, PAB-SIL vs. PAB-VEH groups), reduced RV end-diastolic pressure (2.3 ± 0.5 vs. 5.1 ± 0.9 mmHg, P < 0.05), and RV dilatation (end-systolic volume: 468 ± 45 vs. 643 ± 71 μl, P = 0.05). Sildenafil treatment also attenuated RV fibrosis (30 ± 6 vs. 17 ± 3‰, P < 0.05) but did not affect end-systolic elastance, exercise capacity, or PKG or PKA activity. In conclusion, sildenafil improves RV diastolic function and attenuates interstitial fibrosis in rats with established RV dysfunction, independent from afterload. These results indicate that sildenafil treatment has therapeutic potential for established RV dysfunction.

Spontaneous hypertension induced pulmonar and diaphragm disorders in rats (856.11)

Hypertension induces modifications of standard rhythm breathing. However, the interaction of these effects with the cardiopulmonary and diaphragm morphological changes is not well known. We evaluated the influence of high blood pressure (BP) on cardiovascular modulation, chemoreflex sensitivity, right ventricle (RV) function, arterial blood gases and pulmonary morphometric parameters in rats. We also evaluated the diaphragm muscle profile in response to possible ventilator alterations. Hypertension adversely changed arterial blood gases patterns (pH, pO2, HCO3, SpO2) and the autonomic cardiovascular modulation (systolic BP variance, low frequency band and pulse interval variance), as well exacerbated chemoreflex pressor response and increased RV end diastolic pressure. We observed that SHRs present higher lung to body weight index, arterial lumen to wall ratio (lung arteries), and collagen deposition compared to aged matched Wistar rats. The SHR diaphragm muscle showed increase in type I cross‐sectional fiber (CSA) (16%) and reduction in type II CSA area (41%), increased activity of the ubiquitin proteasome system and lipid peroxidation, with no differences between groups in the analysis of ubiquitinated proteins and misfolded proteins. In conclusion, hypertension induced cardiopulmonary morphometric and functional compensatory/adverse alterations associated with diaphragm fiber type changes and protein degradation. These data suggest a possible adaptation in ventilatory pattern as an attempt to improve ventilatory endurance and prevent the development of fatigue and muscle weakness.

Segmental Analysis of Right Ventricular Longitudinal Deformation in Children before and after Percutaneous Closure of Atrial Septal Defect.

BackgroundThe aim of study is to identify the dependence of right ventricular (RV) free wall longitudinal deformation on ventricular loading through segmental approach in relatively large number of patients with atrial septal defect (ASD).MethodsPatients with ASD (n = 114) and age matched healthy children (n = 60) were echocardiographically examined the day before percutaneous device closure and within 24 hours afterwards. RV free wall deformation parameters, strain (є) and strain rate (SR), were analyzed in the apical (єA, SRA) and basal (єB, SRB) segments. Measured deformation parameters were adjusted for RV size (єAL, SRAL, єBL, SRBL) by multiplying by body surface area indexed RV longitudinal dimension. Regression analyses determined the relationships of these deformation parameters with RV loading parameters that were measured by catheterization.ResultsєBL and SRBL were not different between pre-closure patients and controls (p = 0.245, p = 0.866), and were decreased post-closure (p = 0.001, p = 0.018). Post-closure єBL was lower than in controls (p = 0.001). Pre-closure єAL and SRAL were higher than in controls (p = 0.001, p < 0.001), but decreased after closure (all p < 0.001). The pulmonary to systemic flow ratio was related to procedural differences of єBL (p = 0.017) and of SRBL (p = 0.019). RV end diastolic pressure was negatively related to post-closure єBL (p = 0.020) and post-closure SRBL (p = 0.012), and the procedural SRBL difference (p = 0.027).ConclusionThe longitudinal deformation of the RV basal segment is dependent and its remodeling is also dependent on volume loading in children with ASD.

Abstract 18046: miR-21 is a Biomarker for Fibrosis and the Progression to Right Ventricular Systolic Failure in a Model of Pulmonary Volume and Pressure Overload

Introduction: Severe pulmonary insufficiency (PI) in combination with moderate pulmonary stenosis (PS) is a common long-term complication after repair of congenital heart diseases such as tetralogy of Fallot, causing progressive right ventricular (RV) dilation and failure. We characterize the physiologic and molecular characteristics of the first murine model of combined RV volume and pressure overload (PI/PS). Methods: Physiologic data was compared between sham controls and PI/PS at 1 and 3 mos. Histopathology and gene, microRNA (miR) and protein expression were assessed in the RV free wall. Plasma miR expression was assessed in children with severe PI/moderate PS vs controls (n=4). Results: Data are presented as sham vs. PI/PS at 1 and 3 mos (*p&lt;0.05). Mice developed diastolic heart failure at 1 mo progressing to systolic heart failure by 3 mos: restrictive RV filling (E/A ratio) (0.7±0.1 vs. 2.1±0.9 and 1.9±0.4*) and elevated RV end-diastolic pressure (2.7±0.3 vs. 7.8±2, and 8.5±2 mmHg*); followed by decreased RV outflow tract shortening (44±2 vs. 39±6 and 29±6%*) and exercise capacity (32±1.1 vs. 28±1.6 and 22±1.9 min*). RV fibrosis increased over time (0 vs. 4.0±2, 3.9±0.2%* sham vs 1 and 3 mos) along with pSMAD/total SMAD expression (0.2±0.1 vs. 0.4±0.1 and 0.6±0.1*), ANP expression (25±15 and 60±27* fold at 1 and 3 mos) and tissue miR-21 expression (2.7±0.3 and 2.9±0.6 fold). However, plasma miR-21 was upregulated with diastolic heart failure and switched to being downregulated with the development of systolic heart failure (2.6±1 and -1.8 ±0.2 fold). Finally, plasma miR-21 expression from children with severe PI/moderate PS at the time of pulmonary valve replacement was downregulated compared to controls (FC -3.6±1.2). Conclusion: We describe a novel murine model of chronic RV volume and pressure overload which recapitulates many aspects of the clinical disease. Gene and protein expression changes suggest enhanced miR-21 and TGF-β signaling as a mediator of RV fibrosis. miR-21 may serve as a novel biomarker of RV fibrosis, with a decline in expression heralding the need for valve replacement. This model provides investigators with a new tool for further evaluation of a form of RV failure unique to children with repaired congenital heart disease.

A cornerstone of heart failure treatment is not effective in experimental right ventricular failure

BackgroundRight ventricular (RV) failure due to increased pressure load causes significant morbidity and mortality in patients with congenital heart diseases and pulmonary arterial hypertension. It is unknown whether renin–angiotensin–aldosterone-system (RAAS) inhibition (the cornerstone of left ventricular failure treatment) is effective in RV failure. We investigated the effects of combination treatment of aldosterone-blocker eplerenone+angiotensin II receptor blocker losartan (Ep/Lo) on RV remodeling and function in a model of RV failure due to increased pressure load. Methods and resultsRats (n=48) were randomized for pulmonary artery banding (PAB) or sham surgery and for losartan (20mg/kg/d)+eplerenone (100mg/kg/d) treatment (Ep/Lo) or vehicle (VEH). RV function was assessed by echocardiography and pressure–volume analysis at 5 and 11weeks, or at the occurrence of clinical RV failure symptoms necessitating termination.PAB resulted in RV failure in all rats, as defined by reduced cardiac output, RV stroke volume, increased RV end diastolic pressure and liver congestion as well as RV fibrosis, hypertrophy and reduced capillary density. Clinical RV failure necessitated termination in 5/12 PAB–VEH rats. Angiotensin II type 1-receptor expression in the RV was reduced in PAB rats indicating local RAAS activation. Treatment of PAB rats with Ep/Lo significantly lowered arterial pressures, but had no significant effect on RV function, remodeling or survival compared to PAB–VEH rats. ConclusionsRAAS inhibition does not beneficially affect experimental RV failure due to chronic pressure load. This is of high clinical relevance, because it indicates that the RV response to RAAS inhibition might fundamentally differ from that of the LV.

Abstract 609: Potential Role Of Adipose Derived Stem Cells In Attenuating Pulmonary Hypertension

Pulmonary hypertension (PH) is a devastating cardiopulmonary disorder, which often results in right heart failure. In spite of recent advancements in the pharmacotherapy of pulmonary hypertension, the mortality rate has not been significantly reduced. Recently stem cell therapy has gained more attention for the treatment of cardiopulmonary diseases. Despite the promising results shown by bone marrow derived stem cells in attenuating right heart failure in PH, it remains a highly invasive and laborious procedure. On the contrary, adipose derived stem cell (ADSC) presents a less complicated option. Therefore, we proposed to use ADSC in attenuating the progression of PH. Monocrotaline (MCT) at a 50 mg/kg dose was injected to eight-week old male Sprague-Dawley rats to induce PH. Four weeks post MCT injection; animals developed PH with elevated right ventricular systolic pressure (RVSP, Control: 28.65±0.40; MCT: 78.06±6.4 mmHg; n=6-8), and right ventricular hypertrophy (RVH, Control; 0.22±0.005; MCT: 0.48±0.054 [ratio, AU]; n=6-8). ADSC (isolated from inguinal fat of healthy male rat) were characterized using flow cytometry (CD44 + , CD90 + , CD34 - and CD45 - ) and their differentiation to adipocyte was confirmed by Oil Red O staining. ADSCs (1x10 6 ; passage 2-4) were injected through the jugular vein, 14 days post MCT injection. After 2 weeks following ADSC therapy, RVSP (MCT+ADSC: 55.67±8.99 mmHg; n=6-8) and RVH (MCT+ADSC: 0.32±0.062 [AU]; n=6-8) was significantly reduced. Moreover, the elevated right ventricular end diastolic pressure (RVEDP) and ±dP/dT associated with PH were attenuated significantly in ADSC treated MCT animals. An additional group of animals received only the ADSC conditioned media (CM) from 1x10 6 cells. After 2 weeks of CM administration, RVSP (MCT+CM: 42.11±4.66 mmHg; n=5) and RVH (MCT+CM: 0.29±0.020 [AU]; n=5) was significantly reduced. Further, the RVEDP and ± dP/dT were also significantly reduced in CM treated MCT animals. Collectively, either ADSC or conditioned media alone can attenuate the progression of PH, which suggest that paracrine-like substances may be responsible for the beneficial effects observed and may be considered as a potential therapeutic alternative for the treatment of right heart failure.

Noninvasive Predictors of Diastolic Dysfunction in Children after Cardiac Transplant

Purpose Current noninvasive methods of screening for diastolic dysfunction such as two-dimensional echocardiography (ECHO) and brain natriuretic peptide (BNP) levels were used to predict cardiac catheterization (CC) derived hemodynamic data. Methods and Materials Cardiac transplant patients were prospectively enrolled to undergo concurrent ECHOs at the time of CC. Prior IRB approval and informed consent was obtained. CC data included right ventricular end diastolic pressure (RVEDP), and pulmonary capillary wedge pressure (PCWP). A BNP was also drawn. ECHO parameters included left ventricular ejection fraction (EF), mitral inflow E and A waves, deceleration time, isovolumic relaxation time, and lateral and septal Doppler tissue imaging. E/A, lateral mitral E/e' and septal E/e' (E s /e') were calculated. Descriptive analysis was performed with comparisons made using chi-square and ANOVA. Regression analysis was performed to determine associations with PCWP and RVEDP. Results We enrolled 72 subjects, ages 0.8-21 years (median 12.9). The majority, 66/69 (96%), had an EF >50% (3 inadequate images). Acute rejection was present in 9/72 (13%). Evidence of cardiac allograft vasculopathy was found in 10/53 (19%) of subjects who had angiography performed. No single ECHO parameter was associated with both elevated PCWP and RVEDP. However, BNP >100 pg/ml was associated with abnormal PCWP (p=0.016) and RVEDP (p=0.040). E s /e'>10 was associated with abnormal PCWP (p=0.039). Mitral E/A >3 was associated with an abnormal RVEDP (p=0.021). Conclusions This is the largest pediatric study to evaluate diastolic ECHO parameters and BNP in association with elevations in RVEDP and PCWP after transplant. Most ECHO parameters were not associated. Conversely, elevation in BNP was consistently associated with elevation in RVEDP and PCWP. This study suggests mitral E/A and E s /e' may be useful as an adjunct to routine BNP for predicting diastolic dysfunction following cardiac transplant.

Right Ventricular Distension in Donor Hearts Following Cardiocirculatory Death: Implications for Post-Transplant Function

<h3>Purpose</h3> Donation after cardiocirculatory death (DCD) may expand the donor pool for heart transplantation; however, right ventricular (RV) dysfunction has been observed in resuscitated DCD hearts and the cause of this is not well understood. We sought to characterize changes in RV pressure and volume following withdrawal of life-sustaining therapy (WLST) in a large animal model of DCD. <h3>Methods and Materials</h3> Thirteen pigs were anesthetized and mechanically ventilated with room air. Mechanical ventilation was discontinued, hypoxic cardiac arrest ensued, and a 10-minute standoff period was observed. Changes in RV pressure and volume were monitored using a conductance catheter and magnetic resonance imaging (MRI). <h3>Results</h3> The arterial partial pressure of oxygen decreased rapidly and reached its nadir after 2 minutes (Figure 1). This corresponded with an increase in RV systolic pressure (baseline RVSP 24.1±0.9 vs. 35±2 mmHg, p<0.01), diastolic function (baseline dPdt_min −172±24 vs. −267±24 mmHg/s, p<0.01), and systolic function (baseline dPdt_max 254±32 vs. 378±32 mmHg/s, p=0.01) compared to baseline. Subsequent RV function progressively declined leading to an 18±6% (p<0.01) increase in RV end-diastolic volume and an increase in RV end diastolic pressure (baseline 4.2±0.5 vs. 7.3±0.4 mmHg, p<0.01). MRI confirmed an 18±12% increase in RV end diastolic volume compared to baseline. <h3>Conclusions</h3> Following WLST the RV experiences significant distension that may exacerbate myocardial injury. Assessment of RV function prior to transplantation of the DCD heart is essential, highlighting the need for an <i>ex vivo</i> perfusion device capable of biventricular functional assessment.

Pulmonary Hypertension is Associated With Right Ventricular Diastolic Dysfunction

Purpose: The effect of chronic pressure overload on right ventricular (RV) diastolic function is unknown. We examined invasive measures of RV diastolic function in patients with a range of pulmonary pressures. Methods: Twenty-five patients (seven male, mean age 57.6) underwent right heart catheterisation for investigation of dyspnoea and/or suspected pulmonary hypertension (PH). These included nine patients with left ventricular diastolic dysfunction (LVDD), seven patients with scleroderma, two patients with scleroderma and LVDD, one patient with IPAH, one patient with severe mitral stenosis, one patient with interstitial lung disease and four ostensibly healthy subjects. RV pressure was sampled by a Radi PressureWire. RV systolic pressure (RVSP), RV minimum diastolic pressure (RVDP), RV dP/dt max and RV dP/dt min were obtained. RV end diastolic pressure (RVEDP) was defined as the pressure at 10% RV dP/dt max. RV isovolumic relaxation time (IVRT) was defined as the time between RV dP/dt min and the time at RVEDP during initial pressure decay. RV tau was determined using the method of Weiss. Patients were divided into a PH group (mPAP > 25 mmHg) and a non-PH group. Results: Eleven patients had mPAP > 25 mmHg. This group had higher RVSP, RVDP, RVEDP and longer RV tau. There was a trend to a longer IVRT. RV dP/dt min was greater in the PH group, reflecting the after load dependence of this measure. In contrast, RV dP/dt max (a surrogate of contractility) was similar.Tabled 1RVSP (mmHg)RVDP (mmHg)RV EDP (mmHg)dP/dt min (mmHg/s)dP/dt max (mmHg/s)RV tau (ms)IVRT (ms)PH56.0 ± 21.55.1 ± 6.611.0 ± 6.3−530 ± 219521 ± 20953 ± 3252 ± 25Non−PH30.0 ± 5.2−0.1 ± 3.33.8 ± 3.7−304 ± 78436 ± 14631 ± 1338 ± 16p0.0020.030.0040.0060.270.040.13 Open table in a new tab Conclusion: Pulmonary hypertension is associated with abnormal measures of RV active relaxation and increased RVEDP.

Effects of exercise on monocrotaline-induced changes in right heart function and pulmonary artery remodeling in rats

Pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT) is an experimental protocol of right heart failure. We analyzed the role of exercise training on the right ventricle structure and function, pulmonary artery remodeling, and GSK-3β expression. Rats were divided among the following groups: sedentary control (SC), sedentary monocrotaline (SM), trained control (TC), and trained monocrotaline (TM). Rats underwent exercise training for a period of 5 weeks, with 3 weeks post-MCT injection. Rats in the SM and TM groups presented with an increase in right ventricle hypertrophy indexes and lung congestion. The right ventricular end diastolic pressure (RVEDP), right ventricular systolic pressure (RVSP), and its minimum and maximal pressure derivates were increased in the SM and TM groups. The right ventricle interstitial volume pulmonary artery thickness and p-GSK-3β/GSK-3β were increased in the MCT groups as compared with the control groups. The TM group had a reduction in interstitial volume, p-GSK-3β/GSK-3β ratio, pulmonary artery thickness, RVEDP, and an increase in intramyocardial vessels volume as compared with the SM group. The overall results have shown that the exercise protocol used promoted positive changes in right ventricle and pulmonary artery remodeling. These observations also suggest that structural remodeling may be influenced by signaling proteins, such as GSK-3β.

Mechanisms of right heart failure-A work in progress and a plea for failure prevention.

Mechanisms of right heart failure-A work in progress and a plea for failure prevention.

Right Ventricular End-Diastolic Wall Stress: Does It Impact on Right Atrial Size, and Does It Differ in Right Ventricular Pressure vs Volume Loading Conditions?

BackgroundRight ventricular (RV) diastolic dysfunction precedes RV systolic dysfunction. Improvement in noninvasive assessment of RV diastolic function may enable earlier detection of RV dysfunction, especially important in the assessment of patients with congenital heart disease. We investigated a new parameter we call RV end-diastolic wall stress (RVEDWS) in an effort to better characterize RV diastolic function. MethodsWe retrospectively studied consecutive adults with right-sided congenital heart disease between January 2005 and November 2006. RVEDWS was calculated with the Laplace law: r × p/λ, where r = basal RV dimension at end-diastole, p = RV end-diastolic pressure obtained from catheterization of the right side of the heart, and λ = thickness of RV free wall at end-diastole in the subcostal view. Calculated RVEDWS was correlated to echocardiographically derived right atrial (RA) measurements by means of the Pearson correlation. ResultsTwenty-four patients, aged 41 ± 15 years, were included in the study. Mean RVEDWS was 20 ± 11 g/cm2 (range, 3-46 g/cm2). RVEDWS correlated significantly with RA area and volume (r = 0.71, P < 0.0001; r = 0.69, P < 0.001, respectively). An RVEDWS > 17 g/cm2 had a sensitivity of 91% and specificity of 85% in predicting significant RA enlargement. RVEDWS was significantly higher in patients with RV volume overload compared with those with pressure or normal loading conditions (28 g/cm2 vs 17 g/cm2, P = 0.01). ConclusionsRVEDWS correlates significantly with RA size and differs considerably between RV volume and pressure overload states. Further work is needed to determine whether this RV diastolic parameter can be predictive of clinical outcomes in patients with RV loading lesions.

Abstract 335: Murine Model of Chronic Right Ventricular Diastolic Heart Failure Is Associated with Energetic Alterations and Extracellular Matrix Remodeling

Introduction: Pulmonary insufficiency (PI) is a common long-term complication after repair of congenital heart diseases such as tetralogy of Fallot, causing progressive right ventricular (RV) dilation and eventual RV failure. We characterize the physiologic and molecular characteristics of the first murine model of RV volume overload Methods: PI was created by entrapping the pulmonary valve leaflets with 2 sutures. Echo, MRI, catheterization and exercise testing were compared to sham controls at 1, 3 and 6 mos. RNA from RV free wall was hybridized to Agilent whole-genome microarrays. Results: Data is presented as sham vs. PI at 1, 3 and 6 mos (*p&lt;0.05). PI resulted in increased RV end-diastolic volume (5.6±1.4 vs. 8.7±2.5, 9.8±1.3, 10.5±1.1μ l*) and diastolic heart failure: early reversal of E/A ratio followed by pseudonormalization (1.04±0.07 vs. 0.87±0.15, 0.82±0.17 and 0.96±0.16*), elevated RV end-diastolic pressure (2.7±0.5 vs. 7.6±1.3, 6.9±1.6 and 7±1mmHg*) and decreased exercise capacity (30±2.3 vs. 26±0.8, 26±2 and 22±2.6min*). Systolic function (RV outflow tract shortening) was relatively preserved (49±6 vs. 39±4, 44±3 and 41±3%, p=NS). At 1 mo, 372 genes were downregulated, with metabolic pathways, including Complex I, III and V, and G protein-coupled receptor signaling being the most enriched. At 3 mos, 434 genes were upregulated featuring numerous collagen genes, while 307 were downregulated, including fatty acid transport and Ca2+ signaling. During this time course, pathways involving TGFβ signaling, extracellular matrix and p53 signaling transitioned from down- to up-regulated. Key hubs in upregulated gene networks were TGFβ1, thrombospondin1, VEGFa, TNFα and GSK3β while NFκB1 was a downregulated hub. RV Fibrosis increased over time (0 vs. 0.6±0.5, 5.9±2.9, 3.92±0.2%*). Conclusion: We describe a novel murine model of chronic RV volume overload which recapitulates many aspects of clinical disease including RV dilation, impaired relaxation and decreased exercise capacity but preserved RV systolic function. Gene expression changes suggest mitochondrial bioenergetic dysfunction, ECM remodeling, enhanced TGF-β signaling and apoptosis. Many of these processes of RV diastolic heart failure are also known mechanisms of LV failure.

Demographic Characteristics and Estimated Prevalence of Fontan-Associated Plastic Bronchitis

Plastic bronchitis (PB) is a poorly understood disease that can complicate any underlying pulmonary disease. However, it appears to most often occur in patients with surgically palliated congenital heart disease, particularly after the Fontan procedure. Few data exist about the prevalence and etiology of PB in this population. In an effort to establish data about prevalence, we conducted a retrospective study of an existing Fontan surgery database (n = 654) comprised of data, including sex, age at date of surgery, alive/dead status, New York Heart Association classification at last follow-up, right-ventricular end-diastolic pressure and pulmonary artery pressure before Fontan surgery, and the presence of a Fontan fenestration. An initial medical record review of 173 patients in the database who were followed at the University of Michigan identified seven patients with PB resulting in an estimated prevalence of 4 %. Subsequently, 14 % of 211 surveyed patients reported that they presently expectorate mucus or fibrin plugs (casts). Demographic and clinical variables did not differ between patients with or without possible PB. Collectively, these findings suggest that Fontan patients presently with PB may range from 4 to 14 %, indicating potential under-diagnosis of the disease. There were no remarkable physical or hemodynamic indicators that differentiated patients with or without possible PB. These data also highlight the need for more elaborate, prospective studies to improve our understanding of PB pathogenesis so that more definitive diagnostic criteria for this devastating disease can be established and its prevalence more accurately determined.

Hemodynamic findings in severe tricuspid regurgitation

Tricuspid regurgitation (TR) most commonly occurs in response to right ventricular (RV) dilation with structural abnormalities in the tricuspid valve being rarer. In addition to RV size and valvular integrity, the amount of TR is influenced by RV preload and afterload, the respiratory cycle, left heart function and atrial fibrillation. Hemodynamic changes in right atrial (RA) pressures in severe TR include elevated mean pressures, a large systolic wave called an "s" wave, a prominent 'Y' descent and a blunted 'X' descent. In addition, RV end diastolic pressure is elevated and cardiac output is reduced, especially with exercise. "Ventricularization" of the RA pressure tracing, in which the contour of the RA pressure is similar to, but of lower amplitude than, the contour of the RV pressure is the most specific finding but is found in a minority of patients with severe TR. In summary, alterations in the RA pressure tracing are common in patients with severe TR but specific hemodynamic findings lack sensitivity, which may in part be due to the large effects of RV preload, RV afterload and RA compliance on the amount of TR.

Percutaneous Circulatory Support in Cardiogenic Shock

Over the past 2 decades, innovation in the realm of mechanical ventricular assist devices (VADs) has altered the management of cardiogenic shock (CS). Percutaneous VADs (PVADs) allow emergent and effective ventricular unloading while providing sufficient systemic perfusion pressure to reverse end-organ dysfunction. Despite relatively few randomized trials evaluating these devices, some cardiovascular society guidelines recommend the use of PVADs in patients not responding to standard treatments for CS, including intra-aortic balloon pump (IABP) counterpulsation (Class IIa, Level of Evidence C).1 The purpose of this review is to highlight the spectrum of CS, to review modern PVADs as an interventional bridge to recovery, to discuss unique clinical issues related to PVAD support, and finally to offer a perspective on the future directions of acute mechanical circulatory support research. CS is a state of end-organ hypoperfusion caused by left ventricular (LV), right ventricular (RV), or biventricular myocardial injury resulting in systolic and/or diastolic myocardial pump failure. Myocardial infarction (MI) with LV failure remains the most common cause of CS. In general, CS complicates 8.6% of ST-segment elevation MIs (STEMI)2 and 2.5% of non–ST segment elevation MIs.3 Common causes of CS are listed in Table 1. View this table: Table 1. Common Causes of Cardiogenic Shock Clinically, CS is defined by both hemodynamic parameters (persistent hypotension [systolic blood pressure 18 mm Hg or RV end-diastolic pressure >10–15 mm Hg]) and clinical signs/symptoms of hypoperfusion (cool extremities, decreased urine output, and/or altered mental status). Inadequate systemic perfusion results in secondary lactic acidosis, catecholamine and neurohormone release, and activation of …

Right Ventricular Tau is an Important Determinant of Right Ventricular End Diastolic Pressure

Purpose: The effect of chronic pressure overload on the diastolic function of the right ventricle (RV) has not been well studied in humans. We explored the relationship between invasive measures of RV diastolic function and RV pressure across a range of patients with and without pulmonary hypertension. Methods: Eighteen patients undergoing diagnostic right heart catheterisation were studied. Six patients had left ventricular diastolic dysfunction (LVDD), six had scleroderma, two had LVDD and scleroderma, two had idiopathic pulmonary arterial hypertension and two patients were found to be normal after investigation. RV pressure was measured invasively by a Radi PressureWire sampling at 100 Hz. Afterload was measured by peak RV systolic pressure (RVSP). Diastolic function parameters of minimum RV diastolic pressure (minRVDP) and RV (dP/dt)min and RV end diastolic pressure (RVEDP) were derived. RV tau was calculated using the method of Weiss. All measurements were averaged over five cardiac cycles. Results:Tabled 1Parameter (range)RVSP (18.4–69.3 mmHg)minRVDP (−5.9 to 10.2 mmHg)RVEDP (−2.5 to 15.2 mmHg)RV tau (9–80 ms)r = 0.32p = nsr = 0.91p < 0.0001r = 0.94p < 0.0001RV (dP/dt)min (−200 to −856 mmHg/s)r = −0.89p < 0.0001r = −0.15p = nsr = −0.12p = ns Open table in a new tab RV tau was strongly associated with minRVDP and RVEDP but not with RVSP. RV (dP/dt)min was strongly correlated with RVSP but not minRVDP or RVEDP. Conclusion: RV tau is an afterload independent measure of RV relaxation, while RV (dP/dt)min is strongly inversely associated with peak RV systolic pressure. Early RV relaxation as measured by RV tau is an important determinant of RVEDP as well as minimum RV diastolic pressure.

Relation of Left Ventricular End Diastolic Pressure to Right Ventricular End Diastolic Volume After Operative Treatment of Tetralogy of Fallot

Left ventricular (LV) diastolic dysfunction is associated with poor outcomes after tetralogy of Fallot (TOF) repair, although its cause is not known, and its relation to right ventricular (RV) performance has never been examined. The aim of this study was to test the hypothesis that RV dilation leads to LV diastolic dysfunction after TOF repair. Patients with repaired TOF who underwent cardiac catheterization and cardiac magnetic resonance imaging within 6 months from January 2003 and April 2011 were reviewed to assess the relation of LV end-diastolic pressure (LVEDP) and indexed RV end-diastolic volume (RVEDVi). Thirty-eight patients were included at a median age of 10.1 years (range 0.6 to 54.7). There was a significant linear association between RVEDVi and LVEDP (p = 0.05). RV end-diastolic pressure (p <0.001), right pulmonary artery systolic pressure (p = 0.009), left pulmonary artery systolic pressure (p = 0.02), and total cardiopulmonary support time (p = 0.04) during TOF repair were also significantly associated with LVEDP. Compared to patients with LVEDP <12 mm Hg, those with LVEDP ≥12 mm Hg had significantly higher mean RVEDVi (135.2 ± 47.8 vs 98.6 ± 28 ml/m(2), p = 0.007) and mean RV end-diastolic pressure (11.7 ± 1.6 vs 8.5 ± 2.8 mm Hg, p = 0.0003). In conclusion, after TOF repair, LVEDP is significantly associated with RVEDVi. Furthermore, mean RVEDVi is significantly higher in patients with LVEDP ≥12 mm Hg. These findings support the theory that RV dilation may impair LV diastolic function and that LV parameters may also be important to consider in determining timing of pulmonary valve replacement.

ACE2 Improves Right Ventricular Function in a Pressure Overload Model

BackgroundRight ventricular (RV) dysfunction is a complication of pulmonary hypertension and portends a poor prognosis. Pharmacological therapies targeting RV function in pulmonary hypertension may reduce symptoms, improve hemodynamics, and potentially increase survival. We hypothesize that recombinant human angiotensin-converting enzyme 2 (rhACE2) will improve RV function in a pressure overload model.ResultsrhACE2 administered at 1.8 mg/kg/day improved RV systolic and diastolic function in pulmonary artery banded mice as measured by in vivo hemodynamics. Specifically, rhACE2 increased RV ejection fraction and decreased RV end diastolic pressure and diastolic time constant (p<0.05). In addition, rhACE2 decreased RV hypertrophy as measured by RV/LV+S ratio (p<0.05). There were no significant negative effects of rhACE2 administration on LV function. rhACE2 had no significant effect on fibrosis as measured by trichrome staining and collagen1α1 expression. In pulmonary artery banded mice, rhACE2 increased Mas receptor expression and normalized connexin 37 expression.ConclusionIn a mouse RV load-stress model of early heart failure, rhACE2 diminished RV hypertrophy and improved RV systolic and diastolic function in association with a marker of intercellular communication. rhACE2 may be a novel treatment for RV failure.