scholarly journals Right ventricular-vascular coupling in heart failure with preserved ejection fraction and pre- vs. post-capillary pulmonary hypertension

2017 ◽  
Vol 19 (4) ◽  
pp. 425-432 ◽  
Author(s):  
Thomas M Gorter ◽  
Dirk J van Veldhuisen ◽  
Adriaan A Voors ◽  
Yoran M Hummel ◽  
Carolyn S P Lam ◽  
...  
2020 ◽  
Vol 9 (4) ◽  
pp. 1110 ◽  
Author(s):  
Antoni Bayes-Genis ◽  
Felipe Bisbal ◽  
Julio Núñez ◽  
Enrique Santas ◽  
Josep Lupón ◽  
...  

To better understand heart failure with preserved ejection fraction (HFpEF), we need to better characterize the transition from asymptomatic pre-HFpEF to symptomatic HFpEF. The current emphasis on left ventricular diastolic dysfunction must be redirected to microvascular inflammation and endothelial dysfunction that leads to cardiomyocyte remodeling and enhanced interstitial collagen deposition. A pre-HFpEF patient lacks signs or symptoms of heart failure (HF), has preserved left ventricular ejection fraction (LVEF) with incipient structural changes similar to HFpEF, and possesses elevated biomarkers of cardiac dysfunction. The transition from pre-HFpEF to symptomatic HFpEF also involves left atrial failure, pulmonary hypertension and right ventricular dysfunction, and renal failure. This review focuses on the non-left ventricular mechanisms in this transition, involving the atria, right heart cavities, kidneys, and ultimately the currently accepted driver—systemic inflammation. Impaired atrial function may decrease ventricular hemodynamics and significantly increase left atrial and pulmonary pressure, leading to HF symptoms, irrespective of left ventricle (LV) systolic function. Pulmonary hypertension and low right-ventricular function are associated with the incidence of HF. Interstitial fibrosis in the heart, large arteries, and kidneys is key to the pathophysiology of the cardiorenal syndrome continuum. By understanding each of these processes, we may be able to halt disease progression and eventually extend the time a patient remains in the asymptomatic pre-HFpEF stage.


2019 ◽  
Vol 9 (4) ◽  
pp. 204589401987859 ◽  
Author(s):  
Vineet Agrawal ◽  
Niki Fortune ◽  
Sheeline Yu ◽  
Julio Fuentes ◽  
Fubiao Shi ◽  
...  

Heart failure with preserved ejection fraction (HFpEF) currently has no therapies that improve mortality. Right ventricular dysfunction and pulmonary hypertension are common in HFpEF, and thought to be driven by obesity and metabolic syndrome. Thus, we hypothesized that an animal model of obesity-induced HFpEF with pulmonary hypertension would provide insight into the pathogenesis of right ventricular failure in HFpEF. Two strains of mice, one susceptible (AKR) and one resistant (C3H) to obesity-induced HFpEF, were fed high fat (60% fat) or control diet for 0, 2, or 20 weeks and evaluated by cardiac catheterization and echocardiography for development of right ventricular dysfunction, pulmonary hypertension, and HFpEF. AKR, but not C3H, mice developed right ventricular dysfunction, pulmonary hypertension, and HFpEF. NPRC, which antagonizes beneficial natriuretic peptide signaling, was found in RNA sequencing to be the most differentially upregulated gene in the right ventricle, but not left ventricle or lung, of AKR mice that developed pulmonary hypertension and HFpEF. Overexpression of NPRC in H9C2 cells increased basal cell size and increased expression of hypertrophic genes, MYH7 and NPPA. In conclusion, we have shown that NPRC contributes to right ventricular modeling in obesity-induced pulmonary hypertension-HFpEF by increasing cardiomyocyte hypertrophy. NPRC may represent a promising therapeutic target for right ventricular dysfunction in pulmonary hypertension-HFpEF.


Author(s):  
Pankaj Garg ◽  
Robert A. Lewis ◽  
Christopher S. Johns ◽  
Andrew J. Swift ◽  
David Capener ◽  
...  

AbstractThis study aimed to determine the prognostic value of cardiovascular magnetic resonance (CMR) in patients with heart failure with preserved ejection fraction and associated pulmonary hypertension (pulmonary hypertension-HFpEF). Patients with pulmonary hypertension-HFpEF were recruited from the ASPIRE registry and underwent right heart catheterisation (RHC) and CMR. On RHC, the inclusion criteria was a mean pulmonary artery pressure (MPAP) ≥ 25 mmHg and pulmonary arterial wedge pressure > 15 mmHg and, on CMR, a left atrial volume > 41 ml/m2 with left ventricular ejection fraction > 50%. Cox regression was performed to evaluate CMR against all-cause mortality. In this study, 116 patients with pulmonary hypertension-HFpEF were identified. Over a mean follow-up period of 3 ± 2 years, 61 patients with pulmonary hypertension-HFpEF died (53%). In univariate regression, 11 variables demonstrated association to mortality: indexed right ventricular (RV) volumes and stroke volume, right ventricular ejection fraction (RVEF), indexed RV mass, septal angle, pulmonary artery systolic/diastolic area and its relative area change. In multivariate regression, only three variables were independently associated with mortality: RVEF (HR 0.64, P < 0.001), indexed RV mass (HR 1.46, P < 0.001) and IV septal angle (HR 1.48, P < 0.001). Our CMR model had 0.76 area under the curve (P < 0.001) to predict mortality. This study confirms that pulmonary hypertension in patients with HFpEF is associated with a poor prognosis and we observe that CMR can risk stratify these patients and predict all-cause mortality. When patients with HFpEF develop pulmonary hypertension, CMR measures that reflect right ventricular afterload and function predict all-cause mortality.


2020 ◽  
Vol 7 (1) ◽  
pp. 254-264 ◽  
Author(s):  
Ravi B. Patel ◽  
Emily Li ◽  
Brandon C. Benefield ◽  
Stanley A. Swat ◽  
Vincenzo B. Polsinelli ◽  
...  

2021 ◽  
Vol 23 (Supplement_G) ◽  
Author(s):  
Francesco Chietera ◽  
Fabio Dardi ◽  
Mariangela Rotunno ◽  
Massimiliano Palazzini ◽  
Daniele Guarino ◽  
...  

Abstract Aims One of the most challenging differential diagnoses in pulmonary hypertension clinical practice, is the discrimination between idiopathic pulmonary arterial hypertension (IPAH) and pulmonary hypertension due to heart failure with preserved ejection fraction (PH-HFpEF). We elaborate a score (considering patient clinical history, demographics, and echocardiographic characteristics) that can predict, noninvasively, PH-HFpEF vs. IPAH diagnosis. Methods and results Data were prospectively collected on 466 consecutive patients with a final diagnosis of IPAH or PH-HFpEF referred to a single tertiary pulmonary vascular disease centre. Data included clinical history, demographics, and parameters of an electrocardiogram and a transthoracic echocardiogram. A multivariate regression model was developed to predict a PH-HFpEF diagnosis, and an integer risk score was generated using adjusted regression coefficients of the multivariate logistic regression analysis. At the multivariate logistic regression a high ratio between left and right ventricular dimensions, a history of atrial fibrillation (AF), a high body mass index (BMI), a reduced mitral deceleration time and a high E-wave at trans-mitral Doppler, an advanced age and a high right ventricular fractional area change (FAC) were predictors of PH-HFpEF. The derived PH-HFPEF score (Figure), with a cut-point ≥11, yielded a specificity/sensitivity, respectively, for the diagnosis of PH-HFpEF, of 100%/49% with an AUC of 0.987. ED, end-diastolic; LV, left ventricle; RV, right ventricle. Conclusions The PH-HFPEF score can predict PH-HFpEF vs. IPAH. The PH-HFPEF score may be used to potentially avoid an invasive diagnostic testing in almost half of PH-HFpEF patients.


2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Evgeny Belyavskiy ◽  
Artem Ovchinnikov ◽  
Alexandra Potekhina ◽  
Fail Ageev ◽  
Frank Edelmann

Abstract Background Heart failure with preserved ejection fraction (HFpEF) is frequently complicated by pulmonary hypertension (PH). A pulmonary vascular contribution could be considered as a substantial therapeutic target in HFpEF and PH and combined pre- and postcapillary PH (Cpc-PH). Methods We enrolled 50 patients with HFpEF and Cpc-PH who were determined by echocardiography to have pulmonary artery systolic pressure (PASP) > 40 mmHg, pulmonary vascular resistance > 3 Wood units, and/or transpulmonary gradient > 15 mmHg. Results The patients were assigned to the phosphodiesterase 5 (PDE5) inhibitor sildenafil group (25 mg TID for 3 months followed by 50 mg TID for 3 months; n = 30) or the control group (n = 20). In the sildenafil group after 6 months, the 6-min walk distance increased by 50 m (95% CI, 36 to 64 m); substantial improvement in NYHA functional class and exercise capacity during diastolic stress test were revealed; decreases in early mitral inflow to mitral annulus relaxation velocities ratio by 2.4 (95% CI, − 3.3 to − 1.4) and PASP by 17.0 mmHg (95% CI, 20.4 to 13.5) were observed; right ventricular systolic function (M-mode tricuspid annular plane systolic excursion) increased by 0.42 cm (95% CI, 0.32 to 0.52 cm; P < 0.01 for all). No changes occurred in the control group. Conclusions In a subset of patients with HFpEF and Cpc-PH assessed by echocardiography, PDE5 inhibition was associated with an improvement in exercise capacity, pulmonary haemodynamic parameters, and right ventricular function. The role of sildenafil needs to be considered in randomized trials in selected patients with HFpEF with invasively confirmed Cpc-PH. Trial registration Russian National Information System of Research, Development and Technology Data of Civilian Usage (NIS, https://rosrid.ru), registration number 01201257849. Registered 20 April 2012. This manuscript adheres to the CONSORT guidelines.


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