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      Comparison of continuous‐flow ventricular assist device therapy with intensive medical therapy in fixed pulmonary hypertension secondary to advanced left heart failure

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          Abstract

          Aims

          Both ventricular assist device (VAD) and pulmonary vasodilator therapy have been shown in uncontrolled studies to improve pulmonary hypertension secondary to advanced left heart failure (Group 2 PH). This study aimed to compare haemodynamic benefits and survival in patients with fixed Group 2 PH treated with continuous‐flow VAD to intensive medical therapy.

          Methods and results

          Ninety‐five patients listed for heart transplantation with sequential right heart catheters were studied, 24 patients having fixed Group 2 PH (as defined by cardiac index < 2.8 L/min/m 2, pulmonary capillary wedge pressure > 15 mmHg, and transpulmonary gradient ≥ 15 mmHg or pulmonary vascular resistance > 3.0 WU, unresponsive to vasodilator challenge). Ten patients received VAD therapy, and 14 patients received standard heart failure therapy with or without sildenafil, nitrates, or endothelin receptor antagonists.

          At repeat right heart catheterization, patients treated with VAD therapy demonstrated significant improvement in both transpulmonary gradient (19 vs. 12 mmHg, P = 0.046) and pulmonary vascular resistance (6.5 vs. 2.9 WU, P = 0.003) compared with baseline, while those treated with medical therapy did not (20.9 vs. 20.3 mmHg and 6.5 vs. 6.4 WU, P = NS for both). Patients who received VAD therapy were significantly more likely to achieve normalized transpulmonary gradient (8/10 vs. 4/14, P = 0.013) and were more likely to be listed for orthotopic heart transplantation (7/10 vs. 4/14, P < 0.05). There were no significant differences between groups in terms of all‐cause mortality.

          Conclusions

          Continuous‐flow VAD therapy more effectively reverses fixed Group 2 PH compared with medical therapy alone and may allow a higher rate of listing for orthotopic heart transplantation.

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          Most cited references26

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          Pulmonary hypertension in heart failure with preserved ejection fraction: a community-based study.

          This study sought to define the prevalence, severity, and significance of pulmonary hypertension (PH) in heart failure with preserved ejection fraction (HFpEF) in the general community. Although HFpEF is known to cause PH, its development is highly variable. Community-based data are lacking, and the relative contribution of pulmonary venous versus pulmonary arterial hypertension (HTN) to PH in HFpEF is unknown. We hypothesized that PH would be a marker of symptomatic pulmonary congestion, distinguishing HFpEF from pre-clinical hypertensive heart disease. This community-based study of 244 HFpEF patients (age 76 +/- 13 years; 45% male) was followed up using Doppler echocardiography over 3 years. Control subjects were 719 adults with HTN without HF (age 66 +/- 10 years; 44% male). Pulmonary artery systolic pressure (PASP) was derived from the tricuspid regurgitation velocity and PH defined as PASP >35 mm Hg. Pulmonary capillary wedge pressure (PCWP) was estimated from the ratio of early transmitral flow velocity to early mitral annular diastolic velocity. In HFpEF, PH was present in 83% and the median (25th, 75th percentile) PASP was 48 (37, 56) mm Hg. PASP increased with PCWP (r = 0.21; p < 0.007). Adjusting for PCWP, PASP was higher in HFpEF than HTN (p < 0.001). The PASP distinguished HFpEF from HTN with an area under the receiver-operating characteristic curve of 0.91 (p < 0.001) and strongly predicted mortality in HFpEF (hazard ratio: 1.3 per 10 mm Hg; p < 0.001). PH is highly prevalent and often severe in HFpEF. Although pulmonary venous HTN contributes to PH, it does not fully account for the severity of PH in HFpEF, suggesting that a component of pulmonary arterial HTN also contributes. The potent effect of PASP on mortality lends support for therapies aimed at pulmonary arterial HTN in HFpEF.
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            The 2016 International Society for Heart Lung Transplantation listing criteria for heart transplantation: A 10-year update

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              Independent and additive prognostic value of right ventricular systolic function and pulmonary artery pressure in patients with chronic heart failure.

              We sought a better understanding of the coupling between right ventricular ejection fraction (RVEF) and pulmonary artery pressure (PAP), as it might improve the accuracy of the prognostic stratification of patients with heart failure. Despite the long-standing view that systolic function of the right ventricle (RV) is almost exclusively dependent on the afterload that this cardiac chamber must confront, recent studies claim that RV function is an independent prognostic factor in patients with chronic heart failure. Right heart catheterization was performed in 377 consecutive patients with heart failure. During a median follow-up period of 17 +/- 9 months, 105 patients died and 35 underwent urgent heart transplantation. Pulmonary artery pressure and thermodilution-derived RVEF were inversely related (r = 0.66, p < 0.001). However, on Cox multivariate survival analysis, no interaction between such variables was found, and both turned out to be independent prognostic predictors (p < 0.001). It was found that RVEF was preserved in some patients with pulmonary hypertension, and that the prognosis of these patients was similar to that of the patients with normal PAP. In contrast, when PAP was normal, reduced RV function did not carry an additional risk. These observations emphasize the necessity of combining the right heart hemodynamic variables with a functional evaluation of the RV when trying to define the individual risk of patients with heart failure.
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                Author and article information

                Contributors
                cshayward@stvincents.com.au
                Journal
                ESC Heart Fail
                ESC Heart Fail
                10.1002/(ISSN)2055-5822
                EHF2
                ESC Heart Failure
                John Wiley and Sons Inc. (Hoboken )
                2055-5822
                24 March 2018
                August 2018
                : 5
                : 4 ( doiID: 10.1002/ehf2.v5.4 )
                : 695-702
                Affiliations
                [ 1 ] Heart and Lung Transplant Unit St. Vincent's Hospital Darlinghurst NSW Australia
                [ 2 ] University of New South Wales Sydney NSW Australia
                [ 3 ] Victor Chang Cardiac Research Institute Darlinghurst NSW Australia
                Author notes
                [*] [* ] Correspondence to: Christopher Hayward, Heart and Lung Transplant Unit, St. Vincent's Hospital, 390 Victoria Street, Darlinghurst, NSW 2010, Australia.

                Tel: + 61 2 8382 6880; Fax: + 61 2 8382 6881. Email: cshayward@ 123456stvincents.com.au

                Article
                EHF212284 ESCHF-17-00167
                10.1002/ehf2.12284
                6073035
                29573567
                fe82f15f-78e7-4c08-9dae-5a2c3473d24d
                © 2018 The Authors. ESC Heart Failure published by John Wiley & Sons Ltd on behalf of the European Society of Cardiology.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

                History
                : 19 September 2017
                : 12 February 2018
                : 20 February 2018
                Page count
                Figures: 3, Tables: 3, Pages: 8, Words: 3037
                Categories
                Original Research Article
                Original Research Articles
                Custom metadata
                2.0
                ehf212284
                August 2018
                Converter:WILEY_ML3GV2_TO_NLMPMC version:version=5.4.4 mode:remove_FC converted:03.08.2018

                lvad,pulmonary hypertension,heart transplantation,hemodynamics

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