Evaluating suspected pulmonary hypertension: A structured approach

Bhatnagar, Akshay; Wiesen, Jonathan; Dweik, Raed A.; Chaisson, Neal F.

doi:10.3949/ccjm.85a.17065

Cited by 6 publications

(4 citation statements)

References 49 publications

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“…This could be explained by 2 mechanisms: first, when PH progresses to advanced stages, the RV can no longer compensate and its stroke volume declines, leading to lower PA pressures and higher Ea. 10 Second, pulsatile RV loading (LAP) increases PASP more than mPAP and therefore leads to higher Ea and mildly elevated mPAP. 21 It is also important to note that all patients with moderate/severe PH had Ea ≥0.6, which further validates our patient stratification.…”

Section: Discussionmentioning

confidence: 99%

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Prognostic Value of Right Ventricular Afterload in Patients Undergoing Mitral Transcatheter Edge‐to‐Edge Repair

Bou Chaaya,

Hatab,

Samimi

et al. 2024

JAHA

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Background Pulmonary hypertension (PH) and secondary mitral regurgitation (MR) are associated with adverse outcomes after mitral transcatheter edge‐to‐edge repair. We aim to study the prognostic value of invasively measured right ventricular afterload in patients undergoing mitral transcatheter edge‐to‐edge repair. Methods and Results We identified patients who underwent right heart catheterization ≤1 month before transcatheter edge‐to‐edge repair. The end points were all‐cause mortality and a composite of mortality and heart failure hospitalization at 2 years. Using the receiver operating characteristic curve–derived threshold of 0.6 for pulmonary effective arterial elastance ([Ea], pulmonary artery systolic pressure/stroke volume), patients were stratified into 3 profiles based on PH severity (low elastance [HE]: Ea <0.6/mean pulmonary artery pressure (mPAP)) <35; High Elastance with No/Mild PH (HE−): Ea ≥0.6/mPAP <35; and HE with Moderate/Severe PH (HE+): Ea ≥0.6/mPAP ≥35) and MR pathogenesis (Primary MR [PMR])/low elastance, PMR/HE, and secondary MR). The association between this classification and clinical outcomes was examined using Cox regression. Among 114 patients included, 50.9% had PMR. Mean±SD age was 74.7±10.6 years. Patients with Ea ≥0.6 were more likely to have diabetes, atrial fibrillation, New York Heart Association III/IV status, and secondary MR (all P <0.05). Overall, 2‐year cumulative survival was 71.1% and was lower in patients with secondary MR and mPAP ≥35. Compared with patients with low elastance, cumulative 2‐year event‐free survival was significantly lower in HE− and HE+ patients (85.5% versus 50.4% versus 41.0%, respectively, P =0.001). Also, cumulative 2‐year event‐free survival was significantly higher in patients with PMR/low elastance when compared with PMR/HE and patients with secondary mitral regurgitation (85.5% versus 55.5% versus 46.1%, respectively, P =0.005). Conclusions Assessment of the preprocedural cardiopulmonary profile based on mPAP, MR pathogenesis, and Ea guides patient selection by identifying hemodynamic features that indicate likely benefit from mitral‐transcatheter edge‐to‐edge repair in PH or lack thereof.

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Section: Discussionmentioning

confidence: 99%

“… 9 However, when PH progresses to advanced stages, the RV can no longer compensate and its stroke volume declines, leading to lower PA pressures. 10 Therefore, this study was designed to examine the prognostic value of invasively measured Ea, a parameter that measures PASP and indexes it to the ventricular function, in patients undergoing M‐TEER.…”

mentioning

confidence: 99%

Prognostic Value of Right Ventricular Afterload in Patients Undergoing Mitral Transcatheter Edge‐to‐Edge Repair

Bou Chaaya,

Hatab,

Samimi

et al. 2024

JAHA

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“…Chan Hong Jeon Division of Rheumatology, Department of Internal Medicine, Soonchunhyang University Bucheon Hospital, Bucheon, Korea Pulmonary hypertension (PH) is a hemodynamic and pathophysiologic state that is defined by an increase in mean pulmonary arterial pressure ≥25 mmHg at rest measured with right heart catheterization (RHC) [1]. PH can be classified into 5 main subgroups by the clinical and pathophysiological characteristics: group 1 -pulmonary arterial hypertension (PAH); group 2 -PH due to left heart disease; group 3 -PH due to chronic lung disease and/or hypoxemia; group 4 -PH due to chronic thromboembolism or other pulmonary artery obstruction; and group 5 -PH due to uncertain or multifactorial mechanisms [2]. Group 1 PH, PAH, is characterized by a pre-capillary PH in the absence of other causes, such as lung disease, left heart disease, chronic thromboembolism, etc.…”

Section: Early Detection Of Pulmonary Hypertension In Connective Tiss...mentioning

confidence: 99%

Early Detection of Pulmonary Hypertension in Connective Tissue Disease

Jeon

2019

J Rheum Dis

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“…The healthy right ventricular (RV) myocardium exhibits high compliance and only generates about 20% of the cardiac energy output. In response to pathologically elevated pulmonary vascular resistance (PVR) [5,7], the RV undergoes rapid dilation to compensate [8]. Both isovolumetric contraction and relaxation of the dilated RV are increased, elevating the basal oxygen consumption; however, it has limited adaptation potential compared to the LV [9].…”

Section: Introductionmentioning

confidence: 99%

Pulmonary Hypertension-Associated Right Ventricular Cardiomyocyte Remodelling Reduces Treprostinil Function

Judina,

Niglas,

Leonov

et al. 2023

Cells

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(1) Pulmonary hypertension (PH)-associated right ventricular (RV) failure is linked to a reduction in pulmonary vasodilators. Treprostinil has shown effectiveness in PAH patients with cardiac decompensation, hinting at potential cardiac benefits. We investigated treprostinil’s synergy with isoprenaline in RV and LV cardiomyocytes. We hypothesised that disease-related RV structural changes in cardiomyocytes would reduce contractile responses and cAMP/PKA signalling activity. (2) We induced PH in male Sprague Dawley rats using monocrotaline and isolated their ventricular cardiomyocytes. The effect of in vitro treprostinil and isoprenaline stimulation on contraction was assessed. FRET microscopy was used to study PKA activity associated with treprostinil stimulation in AKAR3-NES FRET-based biosensor-expressing cells. (3) RV cells exhibited maladaptive remodelling with hypertrophy, impaired contractility, and calcium transients compared to control and LV cardiomyocytes. Combining treprostinil and isoprenaline failed to enhance inotropy in PH RV cardiomyocytes. PH RV cardiomyocytes displayed an aberrant contractile behaviour, which the combination treatment could not rectify. Finally, we observed decreased PKA activity in treprostinil-treated PH RV cardiomyocytes. (4) PH-associated RV cardiomyocyte remodelling reduced treprostinil sensitivity, inotropic support, and impaired relaxation. Overall, this study highlights the complexity of RV dysfunction in advanced PH and suggests the need for alternative therapeutic strategies.

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Evaluating suspected pulmonary hypertension: A structured approach

Cited by 6 publications

References 49 publications

Prognostic Value of Right Ventricular Afterload in Patients Undergoing Mitral Transcatheter Edge‐to‐Edge Repair

Prognostic Value of Right Ventricular Afterload in Patients Undergoing Mitral Transcatheter Edge‐to‐Edge Repair

Early Detection of Pulmonary Hypertension in Connective Tissue Disease

Pulmonary Hypertension-Associated Right Ventricular Cardiomyocyte Remodelling Reduces Treprostinil Function

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