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The diastolic pulmonary gradient does not predict survival in patients with pulmonary hypertension due to left heart disease.

ABSTRACT: OBJECTIVES:This study sought to evaluate if diastolic pulmonary gradient (DPG) can predict survival in patients with pulmonary hypertension due to left heart disease (PH-LHD). BACKGROUND:Patients with combined post- and pre-capillary PH-LHD have worse prognosis than those with passive pulmonary hypertension. The transpulmonary gradient (TPG) and pulmonary vascular resistance (PVR) have commonly been used to identify high-risk patients. However, these parameters have significant shortcomings and do not always correlate with pulmonary vasculature remodeling. Recently, it has been suggested that DPG may be better a marker, yet its prognostic ability in patients with cardiomyopathy has not been fully assessed. METHODS:A retrospective cohort of 1,236 patients evaluated for unexplained cardiomyopathy at Johns Hopkins Hospital was studied. All patients underwent right heart catheterization and were followed until death, cardiac transplantation, or the end of the study period (mean time 4.4 years). The relationships between DPG, TPG, or PVR and survival in subjects with PH-LHD (n = 469) were evaluated with Cox proportional hazards regression and Kaplan-Meier analyses. RESULTS:DPG was not significantly associated with mortality (hazard ratio [HR]: 1.02, p = 0.10) in PH-LHD whereas elevated TPG and PVR predicted death (HR: 1.02, p = 0.046; and HR: 1.11, p = 0.002, respectively). Similarly, DPG did not differentiate survivors from non-survivors at any selected cut points including a DPG of 7 mm Hg. CONCLUSIONS:In this retrospective study of patients with cardiomyopathy and PH-LHD, an elevated DPG was not associated with worse survival.

SUBMITTER: Tampakakis E

PROVIDER: S-EPMC4289416 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature

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The diastolic pulmonary gradient does not predict survival in patients with pulmonary hypertension due to left heart disease.

Tampakakis Emmanouil E Leary Peter J PJ Selby Van N VN De Marco Teresa T Cappola Thomas P TP Felker G Michael GM Russell Stuart D SD Kasper Edward K EK Tedford Ryan J RJ

JACC. Heart failure 20141112 1

<h4>Objectives</h4>This study sought to evaluate if diastolic pulmonary gradient (DPG) can predict survival in patients with pulmonary hypertension due to left heart disease (PH-LHD).<h4>Background</h4>Patients with combined post- and pre-capillary PH-LHD have worse prognosis than those with passive pulmonary hypertension. The transpulmonary gradient (TPG) and pulmonary vascular resistance (PVR) have commonly been used to identify high-risk patients. However, these parameters have significant sh ...[more]

PMID: 25453535

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Project description:BackgroundHeart failure is a severe condition often involving pulmonary hypertension (PH). Soluble low-density lipoprotein receptor with 11 ligand-binding repeats (sLR11) has been associated with pulmonary artery hypertension. We examined whether sLR11 correlates with PH in left heart disease and can be used as a predictive marker.MethodWe retrospectively analyzed patients with severe mitral regurgitation who underwent right heart catheterization before surgery for valve replacement or valvuloplasty from November 2005 to October 2012 at Juntendo University. We measured sLR11 levels before right heart catheterization and analyzed correlations with pulmonary hemodynamics. We compared prognoses between a group with normal sLR11 (≤9.4 ng/ml) and a group with high sLR11 (>9.4 ng/ml). Follow-up was continued for 5 years, with end points of hospitalization due to HF and death due to cardiovascular disease.ResultsAmong 34 patients who met the inclusion criteria, sLR11 correlated with mean pulmonary artery pressure (r = 0.54, p<0.001), transpulmonary pressure gradient (r = 0.42, p = 0.012), pulmonary vascular resistance (r = 0.36, p<0.05), and log brain natriuretic peptide (BNP). However, logBNP did not correlate with pulmonary vascular resistance (p = 0.6). Levels of sLR11 were significantly higher in the 10 patients with PH (14.4±4.3 ng/ml) than in patients without PH (9.9±3.9 ng/ml; p = 0.002). At 5 years, the event rate was higher in the high-sLR11 group than in the normal-sLR11 group. The high-sLR11 group showed 5 hospitalizations due to HF (25.0%) and 2 deaths (10.0%), whereas the normal-sLR11 group showed no hospitalizations or deaths. Analyses using receiver operating characteristic curves showed a higher area under the concentration-time curve (AUC) for sLR11 level (AUC = 0.85; 95% confidence interval (CI) = 0.72-0.98) than for BNP (AUC = 0.80, 95%CI = 0.62-0.99) in the diagnosis of PH in left heart disease.ConclusionsConcentration of sLR11 is associated with severity of PH and offers a strong predictor of severe mitral regurgitation in patients after surgery.

Project description:BackgroundThe left ventricular assist devices (LVADs) are increasingly used for advanced heart failure as a bridge to heart transplantation or as a destination therapy. The aim of this study was to investigate the changes of diastolic pulmonary gradient (DPG), pulmonary vascular resistance (PVR) and transpulmonary gradient (TPG) after LVAD implantation and their impact on survival after LVAD and heart transplantation.ResultsA total of 73 patients who underwent LVAD (HeartMate III) implantation between 2016 and 2022 were retrospectively studied. According to pre-LVAD catheterization, 49 (67.1%) patients had DPG < 7 mmHg and 24 (32.9%) patients had DPG ≥ 7 mmHg. The patients with a pre-VAD DPG ≥ 7 mmHg had higher frequencies of right ventricular (RV) failure (p < 0.001), RVAD insertion (p < 0.001), need for renal replacement therapy (p = 0.002), total mortality (p = 0.036) and on-VAD mortality (p = 0.04) with a longer ICU stay (p = 0.001) compared to the patients with DPG < 7 mmHg. During the follow-up period of 38 (12-60) months, 24 (32.9%) patients died. Pre-LVAD DPG ≥ 7 mmHg (adjusted HR 1.83, 95% CI 1.21-6.341, p = 0.039) and post-LVAD DPG ≥ 7 mmHg (adjusted HR 3.824, 95% CI 1.482-14.648, p = 0.002) were associated with increased risks of mortality. Neither pre-LVAD TPG ≥ 12 (p = 0.505) nor post-LVAD TPG ≥ 12 mmHg (p = 0.122) was associated with an increased risk of death. Pre-LVAD PVR ≥ 3 WU had a statistically insignificant risk of mortality (HR 2.35, 95% CI 0.803-6.848, p = 0.119) while post-LVAD PVR ≥ 3 WU had an increased risk of death (adjusted HR 2.37, 95% CI 1.241-7.254, p = 0.038). For post-transplantation mortality, post-LVAD DPG ≥ 7 mmHg (p = 0.55), post-LVAD TPG ≥ 12 mmHg (p = 0.85) and PVR ≥ 3 WU (p = 0.54) did not have statistically increased risks. The logistic multivariable regression showed that post-LVAD PVR ≥ 3 WU (p = 0.013), post-LVAD DPG ≥ 7 mmHg (p = 0.026) and RVF (p = 0.018) were the predictors of mortality after LVAD implantation. Pre-LVAD DPG ≥ 7 mmHg (p < 0.001) and pre-LVAD PVR ≥ 3 WU (p = 0.036) were the predictors of RVF after LVAD implantation.ConclusionsPersistently high DPG was associated with right ventricular failure and mortality after LVAD implantation rather than after heart transplantation. DPG is a better predictor of pulmonary vascular remodeling compared to TPG and PVR. Further larger prospective studies are required in this field due to the growing numbers of patients with advanced heart failure, as possible candidates for LVAD implantation, and limitations of heart transplantation.

Project description:Left heart disease (LHD) frequently causes lung vascular remodelling and pulmonary hypertension (PH). Yet, pharmacological treatment for PH in LHD is lacking and its pathophysiological basis remains obscure. We aimed to identify candidate mechanisms of PH in LHD and to test their relevance and therapeutic potential. In rats, LHD was induced by supracoronary aortic banding. Whole genome microarray analyses were performed, candidate genes were confirmed by RT-PCR and Western blots and functional relevance was tested in vivo by genetic and pharmacological strategies. In lungs of LHD rats, mast cell activation was the most prominently upregulated gene ontology cluster. Mast cell gene upregulation was confirmed at RNA and protein levels and remodelled vessels showed perivascular mast cell accumulations. In LHD rats treated with the mast cell stabiliser ketotifen, or in mast cell deficient Ws/Ws rats, PH and vascular remodelling were largely attenuated. Both strategies also reduced PH and vascular remodelling in monocrotaline-induced pulmonary arterial hypertension, suggesting that the role of mast cells extends to noncardiogenic PH. In PH of different aetiologies, mast cells accumulate around pulmonary blood vessels and contribute to vascular remodelling and PH. Mast cells and mast cell-derived mediators may present promising targets for the treatment of PH. Whole rat genome microarray analyses were performed in lung homogenates of three rats with established PH following supracoronary aortic banding and in three sham-operated controls. Out of a total of 28,000 analysed genes, differential expression defined as 2-fold change with p<0.05 was evident for 120 genes. Of these, 76 were upregulated and 44 downregulated in aortic banding compared with control lungs gene. Enrichment analysis revealed regulation of mast cell specific genes - 13 out of 20 genes were significantly upregulated in aortic banding compared with control lungs. To test for a putative functional role of mast cells in lung vascular remodelling and PH in LHD, we applied a pharmacological approach by treatment of aortic banding rats with the mast cell stabiliser ketotifen. Microarray analysis then compared rats that were treated with untreated. In brief, congestive heart failure (CHF) was induced in juvenile rats by supracoronary aortic banding and rats were analyzed 9 weeks thereafter when they had established left heart failure with preserved ejection fraction and secondary pulmonary hypertension. Three heart failure rats were untreated, and 3 received the mast cell stabilizer ketotifen (1 mg/kg-1 bodyweight/day-1) with the drinking water. Sham rats underwent the same surgical procedure but without placement of a clip on the supracoronary aorta. Microarray analyses: Lungs from banded and control rats were excised and total RNA was extracted (Stratagene Absolutely RNA Miniprep Kit; Stratagene, La Jolla, USA). Three Âµg total RNA from three control and three banded rats each were processed according to the One-Cycle Target Labeling protocol (GeneChip Expression Analysis, Affymetrix, Santa Clara, USA). Before and after amplifications, the total RNA/complementary RNA concentrations were checked with NanoDrop ND-1000 (Thermo Scientific, Wilmington, USA) and quality was controlled (Experion electrophoresis station, BioRad; Hercules, USA). Samples were hybridized to GeneChipÂ® Rat Genome 230 2.0 arrays (Affymetrix; Santa Clara, USA) containing 31,000 probe sets covering 28,000 rat genes.

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The diastolic pulmonary gradient does not predict survival in patients with pulmonary hypertension due to left heart disease.

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The diastolic pulmonary gradient does not predict survival in patients with pulmonary hypertension due to left heart disease.

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