Reversible Pulmonary Hypertension Research Articles

357 Comparative Effects of the Drugs Used for Pulmonary Hypertension Reversibility Testing: A Meta-Analysis

pyruvate dehydrogenase kinase (PDK) 2, catalyzing the phosphorylation of pyruvate dehydrogenase (PDH) and thus regulating the flux of pyruvate into the mitochondria, were investigated during SMC proliferation and the development of human IH. Methods and Materials: A novel human intimal hyperplasia (IH) model was established in which balloon-injured human internal mammary arteries (hMA) were transplanted into the abdominal aortic position of nude rats. Results: IH rapidly developed over 21 days and was morphologically and in immunohistochemistry identical to the neointima of human coronary arteries. Over 21 days, we found increased proliferative and decreased apoptotic activity within the IH lesion and luminal obliteration progressed to approx. 60%. Tissue PDK2 expression was significantly elevated and PDH was inhibited.PDGF was markedly elevated in the animal serum during neointima formation. Activation of SMC in vitro with PDGF caused increased PDK2 activity via both PI3K/Akt and Ras/Raf/Erkpathways. We observed an increase of the mitochondrial membrane potential ( m), a decreased release of mitochondrial reactive oxygen species (mROS), as well as enhanced cell proliferation. PDK2 inhibition using dichloroacetate(DCA) or PDK2 shRNA prevented PDGF-induced mitochondrial hyperpolarization and SMC proliferation.In vivo, oral DCAtreatment of rats or pre-implant PDK2 shRNA-transduction of the hMAs prevented the injuryinduced increase of SMC proliferation and significantly decreased IH development. Conclusions: PDK2 is the link between PDGF downstream pathways and mitochondrial metabolic modulation and its activation facilitates SMC proliferation. Pharmacological or genetic inhibition of PDK2 in SMC attenuates PDGF-induced increase in m, cell proliferation and the development of human IH. PDK2 may be a novel target for the prevention of restenosis.

Xenon is not superior to isoflurane on cardiovascular function during experimental acute pulmonary hypertension

Acute right ventricular afterload increase is a known perioperative challenge for the anaesthetic regime especially for patients with a compromised right ventricle. The accused negative inotropic action of volatile anaesthetics, with the exception of xenon, might be crucial for the adaptation of the right ventricle. Reversible pulmonary hypertension (mean pressure 40 mmHg) was induced by an infusion of the stable thromboxane A(2) analog U46619 in a porcine model (n = 35). The effects of 70 vol% xenon and 0.9 vol% isoflurane on biventricular function were studied by conductance catheter technique. Inflammation and myocardial injury was quantified using serum probes [tumour necrosis factor α (TNFα), interleukin 6 (IL-6), troponin] and myocardial tissue [B natriuretic peptide (BNP), TNFα, activated caspase 3] by enzyme-linked immunosorbance assays and reverse-transcription polymerase chain reaction. After wash in of xenon global haemodynamic parameters remained stable whereas isoflurane caused a systemic vasodilation. This led to a significant decrease in mean arterial pressure in the isoflurane group whereas cardiac output remained stable. Both substances did not alter the biventricular contractility nor did they induce changes in preload for both ventricles. Xenon led to an additional increase in right ventricular afterload, whereas isoflurane reduced pulmonary vascular resistance. No effects on systemic inflammatory response and myocardial injury were found, whereas higher apoptosis rate and expression of BNP and IL-6 was determined in the right ventricle. These results do not support the idea that xenon is more beneficial than isoflurane in right ventricular failure during pulmonary hypertension. Isoflurane did not compromise systolic ventricular function during acute PHT it only led to vasodilation in contrast to xenon.

Mechanisms of Pulmonary Hypertension Related to Ventricular Septal Defect in Congenital Heart Disease

The aim of this study was to investigate differences in molecular mechanisms of pulmonary hypertension between patients with complete transposition of the great arteries (TGA) combined with ventricular septal defect (VSD) and those with VSD alone. Twenty-four consecutive patients with pulmonary hypertension (mean pulmonary artery pressure > 30 mm Hg) underwent surgical correction of TGA + VSD (n = 10) or VSD alone (n = 14). Lung specimens were taken from the right middle lobe before cardiopulmonary bypass (CPB). Extent of pulmonary hypertension was graded according to the Heath-Edwards pathologic classification. Enzyme-linked immunosorbent assay (ELISA) was used to determine expression of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), endothelin-1 (ET-1), endothelin A and B receptors (ET-AR, ET-BR), matrix metalloproteinases 2 and 9 (MMP-2, MMP-9), and tissue inhibitor of metalloproteinase (TIMP). There were no statistically significant differences in age, height, weight, VSD diameter, or preoperative pulmonary artery pressure between groups. Hemoglobin level, pulmonary artery oxygen saturation, and reduction in postoperative pulmonary artery pressure were significantly higher in patients undergoing correction of TGA + VSD (p < 0.05). All patients had grade 0 to II Heath-Edwards morphologic changes in lung biopsy samples. Expression of eNOS and MMP-2 was significantly lower in the TGA + VSD group than in the VSD-alone group (eNOS, 280.13 ± 101.92 ng/mg versus 488.41 ± 249.60 ng/mg; p < 0.05; MMP-2, 31.68 ± 15.36 ng/mg versus 69.28 ± 49.12 ng/mg; p < 0.05). There were no statistically significant differences between groups in expression of iNOS, ET-1, ET-AR, ET-BR, MMP-9, or TIMP. In patients with TGA + VSD, high oxygenation in the pulmonary circulation decreases expression of MMP-2 and eNOS, which may affect the progress and reversibility of pulmonary hypertension.

Which Drug Is the Best for Pulmonary Hypertension Reversibility Testing?

Multiple drugs are used to test the reversibility of pulmonary hypertension (PH) in advanced heart failure (HF), especially in the process of heart transplant evaluation. Effects of these drugs were never systematically compared.

Fully reversible pulmonary arterial hypertension associated with dasatinib treatment for chronic myeloid leukaemia

To the Editors: Pulmonary arterial hypertension (PAH) is a devastating disease that is characterised by a progressive increase in pulmonary vascular resistance (PVR), chronic right heart failure and premature death. Pulmonary hypertension (PH) is defined by a mean pulmonary artery pressure ( P pa) ≥25 mmHg at rest, and the haemodynamic definition discerns pre- and post-capillary PH [1]. Furthermore, PAH is distinguished from other forms of PH that may occur secondary to various underlying causes, including left heart disease, chronic lung disorders and thromboembolic disease [1]. Although the development of targeted PAH therapies, such as endothelin receptor antagonists, phosphodiesterase type-5 inhibitors (PDE5i) and prostanoids, has markedly improved the clinical situation and outcome of affected patients, the current medical treatment of PAH is not satisfactory. Recently, tyrosine kinase inhibitors (TKIs), particularly imatinib, have been proposed as a potential novel treatment option in PAH [2–7]. Imatinib was the first TKI that achieved regulatory approval for the treatment of chronic myeloid leukaemia (CML) and has become the standard of care for patients with this disease, as it inhibits the hybrid BCR–ABL oncogene that is pathogenic in the development of CML. Imatinib inhibits several tyrosine kinases, including BCR–ABL, the platelet-derived growth factor receptor (PDGFR) and c-Kit. More recently, additional TKIs, including dasatinib and nilotinib, have been introduced for the treatment of CML in patients who are intolerant or unresponsive to imatinib. The potential efficacy of imatinib in PAH is attributable to its inhibitory effect on the PDGFR. Platelet-derived growth factor (PDGF) is thought to play a pivotal role in the pathobiology of PAH by initiating and maintaining the underlying pulmonary vascular remodelling [7, 8]. Consistent with this, inhibition of PDGFR signalling by imatinib was recently shown to reverse PAH in animal models, and to …

Congenital diaphragmatic hernia: optimising outcomes through a consistent care bundle approach

St Michael's NICU (StMH) provides pre and postoperative care for all newborns with an ante/postnatal diagnosis of congenital diaphragmatic hernia (CDH) in South-West England. A consistent care bundle is followed...

Reversible pulmonary hypertension in a cat

A 13-year-old, neutered female domestic shorthair cat was presented for sudden respiratory distress following palliative radiotherapy and the combined administration of a single dose of carboplatin for the treatment of recurrent fibrosarcoma. Clinical and radiographic findings were suggestive of pleural effusion. Echocardiography revealed marked right-sided cardiac enlargement associated with tricuspid regurgitation and Doppler evidence of pulmonary hypertension. After 25 days of treatment for congestive heart failure and suspected pulmonary thromboembolism, clinical signs and echocardiographic and Doppler evidence of right-sided cardiac enlargement and pulmonary hypertension had completely resolved. To the best of the authors' knowledge, this is the first report of reversible pulmonary hypertension, likely secondary to pulmonary thromboembolism, in a cat.

Cell-based therapies in pulmonary hypertension: who, what, and when?

pulmonary hypertension (PH), diagnosed when mean pulmonary arterial pressure exceeds the upper limits of normal (i.e., >25 mmHg) at rest (2), occurs in a variety of clinical situations and is associated with a broad spectrum of histological patterns and abnormalities. PH is currently classified into five distinct World Health Organization (WHO) groups, based on common clinical parameters, potential etiological mechanisms, and responses to treatment (22). Although any form of PH can contribute to increased patient morbidity and mortality, pulmonary arterial hypertension (PAH) (WHO group 1) is a particularly severe and progressive form associated with right heart failure and premature death (1). At present, therapeutic approaches to stabilize or reverse this debilitating condition involve treatment with one or a combination of up to three specific classes of agents, including prostacyclin analogs, endothelin-1 receptor antagonists, and/or phosphodiesterase-5 inhibitors. Retrospective (meta)analyses of these therapeutic strategies have demonstrated a reduction in mortality with their use (7, 12); however, many experts believe that current PAH treatment is inadequate given the persistently high mortality rate and functional hemodynamic impairment in many patients. These observations have led to continued intensive investigation into pathogenetic mechanisms and many proposals for additional alternative new therapies (20, 24). Among the potential new therapies, increasing interest in the role of endothelial progenitor cells (EPCs) as a cell-based therapy has emerged. However, issues remain regarding what group of PH patients are most likely to benefit from treatment, at what point in the disease is treatment most likely to be successful, and what types of cells should be utilized for therapy.

Reversibility of fixed pulmonary hypertension in left ventricular assist device support recipients

Conflicting data still exist concerning the reversibility of secondary severe 'fixed' pulmonary hypertension (PH) by the use of left ventricular assist device (LVAD) support in terms of time necessary to provide a bridge to 'transplantability'. We retrospectively reviewed 145 patients with heart failure and severe PH treated by LVAD support between 2000 and 2009. There were 133 men (91.7%) and 12 women (8.3%) with a mean age of 52.95±12.01 years. Patients were divided into two groups depending on preoperative PH reversibility. Fixed PH was defined by a mean pulmonary arterial pressure (mPAP) >25 mmHg, a pulmonary vascular resistance (PVR) >2.5 Wood Unit (WU) and a transpulmonary gradient (TPG) >12 mmHg, despite pharmacological treatment. Fifty-six patients had fixed PH (group A) and 89 reversible PH (group B). Only 27 patients of group A underwent right heart catheterization evaluation during LVAD support; the remaining 29 patients had other contraindications to heart transplantation (HTx). The 27 patients were divided into three subgroups on the basis of examination time during LVAD support: <6 months (11 patients), between 6 and 12 months (six patients) and >12 months (10 patients). The mPAP, PVR, and TPG decreased significantly during LVAD support (mPAP, 37.26±6.35 mmHg vs 21.00±7.51 mmHg, p=0.007; PVR, 3.49±1.47 WU vs 1.53±0.66 WU, p=0.000; and TPG, 15.04±5.22 mmHg vs 7.78±3.21 mmHg, p=0.019). A significant reduction of all parameters was observed during the first 6 months and later on there was no further decrease. There were no significant differences between the three subgroups (mPAP, p=0.680; PVR, p=0.723; and TPG, p=0.679) in terms of time of reversibility. LVAD support allowed 19 patients to be transplanted. Patients with fixed PH can be treated with LVAD support. Our data suggest that 6 months after LVAD implantation it is possible to observe an important reduction of PH and evaluate the potential transplantability of patients. Longer support does not add any effect of LVAD on PH.

Mechanistic Insights into Reversal of Pulmonary Hypertension by Estrogen Therapy

Severe pulmonary hypertension(PH) leads to right-ventricular failure(RVF) and death. Estrogen(E2) pretreatment has been shown to attenuate development of PH. Here, we tested the hypothesis that E2 may also reverse advanced PH and investigated its underlying mechanisms. Male rats were treated with monocrotaline(MCT,60 mg/kg) to induce PH(n=36). At day-21 when PH had established, one group was euthanized(PH, n=8), and 5 other groups for 10 days received either i) E2 (0.017 mg/day, n=12) ii) E2 plus angiogenesis inhibitor TNP-470 (1.2 mg/day, n=3) iii) ERb-agonist DPN(0.34 mg/day, n=3) iv) ERa-agonist PPT(0.34 mg/day, n=3) or v) left untreated(RVF, n=7). Saline-treated rats served as controls(CTRL, n=6). Echocardiography, cardiac catheterization, RT-PCR, Western-blot and immunocytochemistry were performed. MCT-group developed severe PH at day21 as RV-pressure (RVP) increased from 31±2 in CTRL to 69±2 mmHg. E2 reversed PH(RVP=38±2mmHg, P<0.05) completely resulting in full recovery. Interestingly, E2 failed to rescue PH when applied together with TNP. VGEF protein in RV and lungs was reduced significantly ∼5fold in PH and E2 increased VEGF significantly ∼10 fold. Reduced RV capillary-density in PH was restored fully by E2. E2 reduced cardiopulmonary inflammation as IL-6 transcript upregulation in PH(∼22 fold in lung, ∼7 folds in RV) was partially reversed by E2. Lungs showed 4-fold increase in ED1-inflammatory cells in PH and E2 reversed this increase. Lung ERb-transcripts, but not ERa, were significantly reduced 6-fold in PH and were restored by E2. ERb protein in lung and RV was also significantly reduced ∼2 fold in PH and E2 restored ERb. ERb agonist DPN was as effective as E2 to rescue PH (RVP=34±1 mmHg), whereas PPT was not as effective. In conclusion, E2 rescues PH by stimulating cardiopulmonary neoangiogenesis and suppressing inflammation mainly via ERb.

Reversible Pulmonary Hypertension in Adolescent with Left Atrial Myxoma

We report a patient of left atrial huge myxoma presenting with severe pulmonary hypertension in adolescents. A patient was a 14-year-old boy presented with sudden onset dyspnea. Transthoracic echocardiographic study revealed the presence of a nodular, 4.34 × 8.11 cm sized, mobile, hyperechoic mass in the left atrium and severe pulmonary hypertension with tricuspid insufficiency. After surgical therapy, tricuspid regurgitation and pulmonary hypertension was decreased and the patient was stabilized and had an uneventful clinical course.

A Case of Ascites and Extensive Abdominal Distension Caused by Reversible Pulmonary Arterial Hypertension Associated with Graves' Disease

Patients with hyperthyroidism can develop left ventricular dysfunction and heart failure, but severe pulmonary hypertension association with hyperthyroidism is rarely seen. Herein, we describe the case of a 27-year-old female who presented with abdominal distension accompanied by pulmonary arterial hypertension and Graves’ disease. Her pulmonary arterial hypertension was improved by treating the hyperthyroidism and pulmonary artery hypertension. Additionally, the patient’s symptoms of right-side heart failure improved after pulmonary arterial pressure was reduced. Hyperthyroidism should be regarded as a reversible cause of associated pulmonary arterial hypertension. (Endocrinol Metab 26:248-252, 2011)

Pharmacological test with sildenafil at pulmonary hypertension assessing in children with congenital heart diseases

The paper considers the devised author’s method of pulmonary hypertension assessment in children with congenital heart diseases. 51 patients were made the test. According to the ECG data two types of reaction were noted after sildenafil intake: positive and negative. Positive reaction indicates pulmonary hypertension reversibility. This fact is the main condition for successful surgical heart disease correction.

Pulmonary hypertension (PH) in patients (pts) with CML treated with tyrosine kinase inhibitors (TKIs).

6597 Background: TKIs are the current standard therapy for patients with CML. Fluid retention and pleural effusions have been reported in pts treated with TKIs, particularly with dasatinib. Although TKIs have been shown to reverse PH in animal models, there have been some reports of development of reversible PH with dasatinib. Methods: We conducted a retrospective analysis on 401 CML pts in CP who were treated with TKIs (imatinib, dasatinib or nilotinib) as initial therapy for CML and had a transthoracic echocardiogram done (TTE) at some point during the course of therapy. PH was diagnosed if the patient had an estimated right ventricular systolic pressure (RVSP) of 35 mm Hg or greater. Secondary causes of PH (systolic or diastolic dysfunction on TTE, chronic obstructive pulmonary diseases [COPD], obstructive sleep apnea [OSA] and pulmonary embolism) were investigated during chart review. Results: Twenty pts had at least one TTE; median age 57 years, 46% males. Six pts (30%) received nilotinib 400 mg BID, 4 (20%) pts imatinib (400 mg; n = 1, 600 mg; n = 1 and 800 mg daily; n = 2), and 10 (50%) pts received dasatinib (dose between 40 mg to 140 mg daily). Five (25%) pts had coronary artery disease, 9 (45%) pts had systemic hypertension, 2 (10%) pts had COPD and 3 (15%) pts had OSA. Thirteen pts had serial TTE to compare the progression of PH including 6 (7%) who had a TTE prior to starting TKI. Among these 13 pts with serial TTE, 7 had rising RVSP with one patient having mild global hypokinesia, another with diastolic dysfunction and another with OSA. Four of those 7 patients had normal RVSP on their TTE prior to starting therapy. Five other pts had improvement in the RVSP on serial TTE, 4 of them with systemic hypertension. Two of those 5 pts had elevated RVSP on their TTE prior to starting therapy. One pt had no change. Eleven pts had pleural effusions (7 dasatinib, 3 imatinib, 1 nilotinib) associated with PH. Conclusions: TKI therapy is occasionally associated with development of PH, but RVSP may improve spontaneously in some pts. A prospective study is needed to further investigate the relationship between TKIs and the development of PH. Author Disclosure Employment or Leadership Position Consultant or Advisory Role Stock Ownership Honoraria Research Funding Expert Testimony Other Remuneration Bristol-Myers Squibb, Novartis

Portopulmonary hypertension and right heart failure in patients with cirrhosis

In 5-6% of patients with portal hypertension a pathological state exists in which changes in the pulmonary vasculature cause an increase in pulmonary vascular resistance. The resultant increased work of the right ventricle may cause right heart failure and liver congestion. Patients with cirrhosis are at increased risk of mortality and transplant graft failure. The present review examines the latest advances in diagnosis, treatment and management of portopulmonary hypertension. Portopulmonary hypertension may be screened with transthoracic echocardiography and following up with a right heart catheterization in patients in whom the right ventricular systolic pressure is calculated to be 50 mmHg or greater. Therapy with prostanoids, endothelin-1 inhibitors and phosphodiesterase-5 inhibitors, or a combination of therapies, may be very effective in moderating pulmonary artery hypertension and, in selected patients, allowing liver transplantation to proceed safely. The model for end-stage liver disease (MELD) score is being weighted to accelerate responders on the waiting list for a transplant. Advances in diagnosis and therapy of portopulmonary hypertension allow patients with cirrhosis who respond to vasodilators to undergo liver transplantation safely. Unfortunately liver transplantation does not always result in reversal of pulmonary hypertension. There are now reports of de-novo pulmonary hypertension after liver transplantation.

Comparison of Endothelial Biomarkers According to Reversibility of Pulmonary Hypertension Secondary to Congenital Heart Disease

The reversibility of pulmonary arterial hypertension (PAH) in children with congenital heart disease (CHD) is strongly associated with the degree of intimal proliferation, vessel narrowing, and number of circulating endothelial cells (CECs). Circulating endothelial cells may arise from either endothelial damage or accelerated turnover during vessel remodeling, but nothing is known about endothelial microparticles (EMPs) and other biomarkers reflecting endothelial alterations. This study aimed to document endothelial markers further according to the irreversibility of PAH secondary to CHD. The study investigated soluble markers of endothelial damage or activation (thrombomodulin, soluble endothelial protein C receptor, and soluble E-selectin), inflammation (interleukin-6), and angiogenic cytokine levels [vascular endothelial growth factor (VEGF) and placental growth factor (PlGF)] in 26 patients with CHD, 16 with reversible PAH (median age, 2 years) and 10 with irreversible PAH (median age, 9 years). Endothelial activation/apoptosis was evaluated by measuring EMP levels. Plasma procoagulant activity also was measured. The results show that the levels of soluble markers indicating endothelial activation were not predictors of PAH irreversibility. Lower levels of PlGF were observed in reversible compared with irreversible PAH but were not associated with the CEC level, the mean pulmonary artery pressure (mPAP), or age. No significant difference in procoagulant activity or EMP level was found between irreversible and reversible PAH. Among a large panel of biomarkers reflecting endothelial activation, regeneration, and injury, the high CEC levels previously described proved to be the only marker allowing discrimination between reversible and irreversible PAH secondary to CHD.

Reversible Pulmonary Hypertension, Lactic Acidosis, and Rapidly Evolving Multiple Organ Failure as Manifestations of Shoshin Beriberi

Reversible Pulmonary Hypertension, Lactic Acidosis, and Rapidly Evolving Multiple Organ Failure as Manifestations of Shoshin Beriberi

Pulmonary hypertension in heart transplantation: Discrepant prognostic impact of pre-operative compared with 1-year post-operative right heart hemodynamics

The prognostic impact of pulmonary hypertension (PH) before and after heart transplantation (HTx) is debated. We investigated: (i) the significance of pre-operative reversible PH on post-operative survival; (ii) the value of recatheterization while on the waiting list; (iii) the evolution of right heart hemodynamics (RHH) after HTx; and (iv) the prognostic impact of PH at 1 year after HTx. We reviewed the records of 500 HTx recipients transplanted between 1983 and 2007. Pre-operatively, a non-PH group (Group 1, n = 365) fulfilled directly our RHH criteria for HTx, while a PH group (Group 2, n = 135) was accepted after reversibility of PH by acute vasodilatory testing. Recatheterization was performed every third month while on the waiting list and repeatedly after transplantation. With a follow-up of 6.8 +/- 5.1 years and a 50% survival rate of 12.1 +/- 5.4 years, our main findings were as follows: (i) Patients with reversible PH on vasodilatory testing had a survival rate similar to that of patients without PH (11.7 +/- 0.8 vs 12.1 +/- 0.5 years, p = 0.80). (ii) Pre-operative recatheterization was of limited value as RHH remained stable. Five percent of patients died while on the waiting list and 2 improved clinically and were removed. (iii) Mean pulmonary artery pressure (MAP) was reduced from 28 +/- 9 and 40 +/- 8 mm Hg pre-operatively to 21 +/- 7 and 24 +/- 6 mm Hg after 2 weeks and 16 +/- 7 and 18 +/- 8 mm Hg at 3 years in Groups 1 and 2, respectively. (iv) Recipients with MAP >20 mm Hg at 1 year post-HTx had significantly lower survival than those with MAP <or=20 mm Hg (11.5 +/- 0.7 vs 15.6 +/- 0.6 years, p < 0.001). Elevated pulmonary pressure 1 year after HTx provides significant prognostic information regarding long-term outcome, whereas pre-operative reversible PH in this group does not influence survival.

Selective Serotonin Reuptake Inhibitors and the Incidence and Outcome of Pulmonary Hypertension

Selective serotonin reuptake inhibitors (SSRIs) prevent the development of and reverse pulmonary hypertension (PH) in animal models. We sought to determine whether SSRIs are associated with a decreased incidence of PH in at-risk patients and whether SSRIs are associated with decreased mortality in patients with established PH. In a case-control study of patients enrolled in the Surveillance of Pulmonary Hypertension in America (SOPHIA) registry, we tested whether patients without PH (no-PH group; n = 155) were more likely to be receiving SSRIs when compared to those with confirmed PH (n = 1,180). In a separate cohort study of adults with documented PH in the referral-based Pulmonary Hypertension Connection (PHC) registry (n = 542), we classified patients into categories by SSRI use, and we examined whether SSRI use was associated with decreased mortality. In SOPHIA, the confirmed PH group was less likely to be receiving SSRIs compared with the no-PH group (univariate odds ratio [OR], 0.56 [95% confidence interval (CI), 0.39 to 0.82]; p = 0.003; multivariate OR, 0.71l [95% CI, 0.48 to 1.06]; p = 0.09). In the PHC, 69 of 542 patients (13%) were receiving SSRIs at the time of referral. During a mean (+/- SD) follow-up period of 4.0 +/- 3.1 years, 12% of patients receiving SSRIs vs 23% of patients not receiving SSRIs died (hazard ratio [HR], 0.35; 95% CI, 0.14 to 0.87; p = 0.023). The association between SSRI use and decreased mortality persisted after adjusting for age, gender, etiology of PH, and obesity (HR, 0.35; 95% CI, 0.14 to 0.88; p = 0.026). SSRIs appear to be associated with a decreased development of PH and a decreased mortality in PH. These findings provide a rationale for clinical trials of SSRIs in PH.

Treprostinil to Reverse Pulmonary Hypertension Associated With Idiopathic Pulmonary Fibrosis as a Bridge to Single-Lung Transplantation

The available therapies and prognosis of idiopathic pulmonary fibrosis remain relatively poor, and concurrent pulmonary hypertension further increases the risk of death and complications after lung transplantation. Limited data exist for the treatment of pulmonary hypertension associated with idiopathic pulmonary fibrosis. We describe a case where intravenous treprostinil was used to bridge an elderly patient with idiopathic pulmonary fibrosis with severe pulmonary hypertension to successful single-lung transplantation.