Nitric oxide: A possible new biomarker in heart failure? Relationship with pulmonary hypertension secondary to left heart failure

Author(s):  
Vicente Lahera
Author(s):  
Roberto Jorge Bonafede ◽  
Juan Pablo Calvo ◽  
Julia María Valeria Fausti ◽  
Sonia Puebla ◽  
Adolfo Juan Gambarte ◽  
...  

2018 ◽  
Vol 8 (2) ◽  
pp. 204589401877304 ◽  
Author(s):  
Julio D. Duarte ◽  
Mayank Kansal ◽  
Ankit A. Desai ◽  
Katherine Riden ◽  
Meghan J. Arwood ◽  
...  

The biological mechanisms behind the development of pulmonary hypertension in the setting of left heart failure (HF-PH), including combined pre- and post-capillary pulmonary hypertension (Cpc-PH), remains unclear. This study aimed to use candidate polymorphisms in nitric oxide synthase (NOS) genes to explore the role of NOS in HF-PH. DNA samples from 118 patients with HF-PH were genotyped for the NOS3 rs1799983 and NOS2 rs3730017 polymorphisms. A multiple regression model was used to compare hemodynamic measurements between genotype groups. Patients with the T/T genotype at rs1799983 possessed a nearly 10 mmHg increased transpulmonary gradient (TPG) compared to those with other genotypes ( P = 0.006). This finding was replicated in an independent cohort of 94 HF-PH patients ( P = 0.005). However, when tested in a cohort of 162 pre-capillary pulmonary arterial hypertension patients, no association was observed. In a combined analysis of both HF-PH cohorts, mean pulmonary artery pressure (mPAP), diastolic pulmonary gradient (DPG), and CpcPH status were also associated with rs1799983 genotype ( P = 0.005, P = 0.03, and P = 0.02, respectively). In patients with HF-PH, the NOS3 rs1799983 polymorphism is associated with TPG, and potentially mPAP and DPG as well. These findings suggest that endothelial NOS (encoded by NOS3) may be involved in the pulmonary vascular remodeling observed in Cpc-PH and warrants further study.


2004 ◽  
Vol 6 (2) ◽  
pp. 181-185 ◽  
Author(s):  
Laurent Fauchier ◽  
Dominique Babuty ◽  
Alexandre Melin ◽  
Pierre Bonnet ◽  
Pierre Cosnay ◽  
...  

Author(s):  
Robert Naeije ◽  
Mario Gerges ◽  
Jean-Luc Vachiery ◽  
Sergio Caravita ◽  
Christian Gerges ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Shunsuke Tatebe ◽  
Koichiro Sugimura ◽  
Kotaro Nochioka ◽  
Tatsuo Aoki ◽  
Masanobu Miura ◽  
...  

Background: Pulmonary hypertension (PH) due to left heart disease (LHD) is a major category of the disorder. We have recently reported that elevated pulmonary vascular resistance (PVR) in patients with post-capillary PH (pc-PH: defined as mean pulmonary arterial pressure (mPAP)≥25mmHg and pulmonary capillary wedge pressure (PCWP)>15mmHg) is associated with poor prognosis compared with those with no PH or pc-PH without elevated PVR. Although new treatment is required for targeting pulmonary vascular disease (PVD), thereis a concern about raising PCWP. In this study, we thus examined acute hemodynamic effects of inhaled nitric oxide (iNO) in patients with PH due to LHD and whether optimal heart failure (HF) treatment ameliorates pc-PH. Methods: We examined 60 consecutive pc-PH patients with chronic heart failure (63±14[SD] years, M/F 38/22, NYHA≥2) who underwent acute vasoreactivity test by iNO (40 ppm for 10 min) under right heart catheterization at our hospital from June 2011 to May 2014. Among them, 25 had valvular heart disease (VHD) and 35 had non-VHD. PVD (defined as PVR> 240dynes/s/cm -5 ) was noted in 18. We also evaluated right ventricular systolic pressure (RVSP) by echocardiography after optimization of HF treatment such as medications and valvular surgery. Results: iNO significantly decreased mPAP (-1.7±0.5 mmHg; P<0.01) and PVR (-66 ±14dyne/s/cm -5 , P<0.01) without altering cardiac output. iNO significantly increased PCWP (1.3±0.5 mmHg, P=0.01) only in non-VHD patients, while it significantly increased mean arterial pressure and systemic vascular resistance in VHD patients than in non-VHD patients (both P<0.05). Pc-PH patients with PVD were re-classified as having pc-PH without PVD in 9 and no PH in 1. Eight patients remained pc-PH with PVD. After the optimal medical treatment for 7.6 months, RVSP was significantly decreased in both non-VHD and VHD patient (-8±3mmHg, P=0.04, -19±8mmHg, P=0.01, respectively). However, in non-VHD group, significant reduction in RVSP was noted only in pc-PH patients without PVD (-8±3mmHg, P=0.03). Conclusions: These results indicate that elevated PVR in patients with pc-PH and non-VHD could be a novel therapeutic indication for NO-related pulmonary vasodilators in the current practice of HF.


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