Pulmonary Hypertension Patients Research Articles

The diverging roles of insulin-like growth factor binding proteins in pulmonary arterial hypertension.

Pulmonary hypertension (PH) is a progressive, severe and to date not curable disease of the pulmonary vasculature. Alterations of the insulin-like growth factor 1 (IGF-1) system are known to play a role in vascular pathologies and IGF-binding proteins (IGFBPs) are important regulators of the bioavailability and function of IGFs. In this study, we show that circulating plasma levels of IGFBP-1, IGFBP-2 and IGFBP-3 are increased in idiopathic pulmonary arterial hypertension (IPAH) patients compared to healthy individuals. These binding proteins inhibit the IGF-1 induced IGF-1 receptor (IGF1R) phosphorylation and exhibit diverging effects on the IGF-1 induced signaling pathways in human pulmonary arterial cells (i.e. healthy as well as IPAH-hPASMCs, and healthy hPAECs). Furthermore, IGFBPs are differentially expressed in an experimental mouse model of PH. In hypoxic mouse lungs, IGFBP-1 mRNA expression is decreased whereas the mRNA for IGFBP-2 is increased. In contrast to IGFBP-1, IGFBP-2 shows vaso-constrictive properties in the murine pulmonary vasculature. Our analyses show that IGFBP-1 and IGFBP-2 exhibit diverging effects on IGF-1 signaling and display a unique IGF1R-independent kinase activation pattern in human pulmonary arterial smooth muscle cells (hPASMCs), which represent a major contributor of PAH pathobiology. Furthermore, we could show that IGFBP-2, in contrast to IGFBP-1, induces epidermal growth factor receptor (EGFR) signaling, Stat-3 activation and expression of Stat-3 target genes. Based on our results, we conclude that the IGFBP family, especially IGFBP-1, IGFBP-2 and IGFBP-3, are deregulated in PAH, that they affect IGF signaling and thereby regulate the cellular phenotype in PH.

Invasive Implanted Hemodynamic Monitoring in Patients with Complex Congenital Heart Disease: State-of-the-Art Review.

As the number of patients with congenital heart disease (CHD) continues to increase, the burden of heart failure (HF) in this population requires innovative strategies to individualize management. Given the success of implanted invasive hemodynamic monitoring (IHM) with the CardioMEMSTM HF system in adults with acquired HF, this is often suggested for use in patients with CHD, though published data are limited to case reports and case series. Therefore, this review summarizes the available published reports on the use of IHM in patients with complex CHD, describes novel applications, and highlights future directions for study. In patients with CHD, IHM has been used across the lifespan, from age 3 years to adulthood, with minimal device-related complications reported. IHM uses include (1) prevention of HF hospitalizations; (2) reassessment of hemodynamics after titration of medical therapy without repeated cardiac catheterization; (3) serial monitoring of at-risk patients for pulmonary hypertension to optimize timing of heart transplant referral; (4) and hemodynamic assessment with exercise (5) or after ventricular assist device placement. IHM has the potential to reduce the number of cardiac catheterizations in anatomically complex patients and, in patients with Fontan circulation, IHM pressures may have prognostic implications. In conclusion, though further studies are needed, as patients with CHD age and HF is more prevalent, this tool may assist CHD physicians in caring for this complex patient population.

The acute effect of inhaled nitric oxide on the exercise capacity of patients with advanced interstitial lung disease: a randomized controlled trial

BackgroundInhaled nitric oxide (iNO) selectively acts on the pulmonary vasculature of ventilated lung tissue by reducing pulmonary vascular resistance and intrapulmonary shunt. This effect may reduce ventilation/perfusion mismatch and decrease pulmonary hypertension in patients with interstitial lung disease.MethodsIn a prospective, single-blinded, randomized, placebo-controlled trial, participants with advanced interstitial lung disease, underwent two separate six-minute walk tests (6MWT): one with iNO and the other with a placebo. The primary outcome measured the difference in meters between the distances covered in the two tests. Secondary outcomes included oxygen saturation levels, distance-saturation product, and Borg dyspnea score. A predefined subgroup analysis was conducted for patients with pulmonary hypertension.ResultsOverall, 44 patients were included in the final analysis. The 6MWT distance was similar for iNO treatment and placebo, median 362 m (IQR 265-409) vs 371 m (IQR 250-407), respectively (p = 0.29). Subgroup analysis for patients with pulmonary hypertension showed no difference in 6MWT distance with iNO and placebo, median 339 (256-402) vs 332 (238-403) for the iNO and placebo tests respectively (P=0.50). No correlation was observed between mean pulmonary artery pressure values and the change in 6MWT distance with iNO versus placebo (spearman correlation Coefficient 0.24, P=0.33).ConclusionIn patients with advanced interstitial lung disease, both with and without concurrent pulmonary hypertension, the administration of inhaled nitric oxide failed to elicit beneficial effects on the six-minute walk distance and oxygen saturation. The use of inhaled NO was found to be safe and did not lead to any serious side effects.Trial registration(NCT03873298, MOH_2018-04-24_002331).

Risk factors associated with pulmonary hypertension in patients with active tuberculosis and tuberculous destroyed lung: a retrospective study

Pulmonary tuberculosis (TB) can result in irreversible damage and lead to tuberculous destructive lung (TDL), a severe chronic lung disease that is associated with a high mortality rate. Additionally, pulmonary hypertension (PH) is a hemodynamic disorder that can be caused by lung diseases. The objective of this study is to investigate the risk factors associated with PH in active TB patients diagnosed with TDL. We conducted a retrospective review of the medical records of 237 patients who were diagnosed with TDL, active pulmonary tuberculosis, and underwent echocardiography at the Third People’ Hospital of Shenzhen from January 1, 2016, to June 30, 2023. Univariate and multivariate logistic regression analyses were performed to identify factors that correlated with the development of pulmonary hypertension. Univariate and multivariate logistic regression analyses revealed that several factors were associated with an increased risk of pulmonary hypertension (PH) in individuals with tuberculosis destroyed lung (TDL). These factors included age (OR = 1.055), dyspnea (OR = 10.728), D-dimer (OR = 1.27), PaCO2 (OR = 1.040), number of destroyed lung lobes (OR = 5.584), bronchiectasis (OR = 3.205), and chronic pleuritis (OR = 2.841). When age, D-dimer, PaCO2, and number of destroyed lung lobes were combined, the predictive value for PH in patients with TDL was found to be 80.6% (95% CI 0.739–0.873),with a sensitivity of 76.6% and specificity of 73.2%. Advanced age, elevated D-dimer levels, hypercapnia, and severe lung damage were strongly correlated with the onset of PH in individuals with active pulmonary tuberculosis (PTB) and TDL. Furthermore, a model incorporating age, D-dimer, PaCO2, and the number of destroyed lung lobes might be valuable in predicting the occurrence of PH in patients with active PTB and TDL.

D-42 | Determinants and Factors for Readmission and In-Hospital Mortality in Pulmonary Arterial Hypertension Patients Undergoing CTO-PCI

D-42 | Determinants and Factors for Readmission and In-Hospital Mortality in Pulmonary Arterial Hypertension Patients Undergoing CTO-PCI

Clinical Features and Multimodality Diagnostic Tools of Pulmonary Hypertension

Pulmonary hypertension (PH) is defined as an increase in mean pulmonary arterial pressure (mPAP) above normal (> 20 mmHg) and an increase in pulmonary vascular resistance (pulmonary vascular resistance / PVR) above normal in resting settings. The pathophysiology of PH involves remodeling of the pulmonary vessels, from the main pulmonary arteries, lobar arteries, segmental arteries, distal arteries, pulmonary arterioles, capillaries to the postcapillary pulmonary veins. In general, the epidemiological figures for PH are not known with certainty. The United Kingdom reported a PH prevalence of 97 cases per one million people, with a female-to-male ratio of 1.8. The diagnostic strategy for PH focuses primarily on two issues. The primary objective is to improve the early detection of PH and expedite the transfer of patients at high risk for PAH, CTEPH, or other forms of severe PH to a PH center. The second objective is to identify the underlying disease, including left heart disease (Group 2 PH) and lung disease (Group 3 PH), as well as comorbidities, in order to assure proper classification, risk assessment, and therapy. The gold standard for detecting and categorizing pulmonary hypertension is right heart catheterization (RHC). Clinical scoring in the form of shortness of breath without any obvious cause accompanied by physical examination, ECG and Thorax X-ray images which depict an enlarged right heart have good specificity and sensitivity for the diagnosis of pulmonary hypertension in patients with congenital heart disease. A high right ventricular pressure, mean PAP, and BNP values during observation, as well as heart size on chest X-ray can be predictors of a poorer prognosis in this population. Keyword: Clinical Risk Scoring, Pulmonary Hypertension, Right Heart Catheterization.

ATP13A3 variants promote pulmonary arterial hypertension by disrupting polyamine transport

Abstract Aims Potential loss-of-function variants of ATP13A3, the gene encoding a P5B-type transport ATPase of undefined function, were recently identified in pulmonary arterial hypertension (PAH) patients. ATP13A3 is implicated in polyamine transport but its function has not been fully elucidated. Here, we sought to determine the biological function of ATP13A3 in vascular endothelial cells and how PAH-associated variants may contribute to disease pathogenesis. Methods and Results We studied the impact of ATP13A3 deficiency and overexpression in endothelial cell (EC) models (human pulmonary ECs, blood outgrowth ECs (BOECs) and HMEC-1 cells), including a PAH patient-derived BOEC line harbouring an ATP13A3 variant (LK726X). We also generated mice harbouring an Atp13a3 variant analogous to a human disease-associated variant to establish whether these mice develop PAH. ATP13A3 localised to the recycling endosomes of human ECs. Knockdown of ATP13A3 in ECs generally reduced the basal polyamine content and altered the expression of enzymes involved in polyamine metabolism. Conversely, overexpression of wild-type ATP13A3 increased polyamine uptake. Functionally, loss of ATP13A3 was associated with reduced EC proliferation, increased apoptosis in serum starvation and increased monolayer permeability to thrombin. Assessment of five PAH-associated missense ATP13A3 variants (L675V, M850I, V855M, R858H, L956P) confirmed loss-of-function phenotypes represented by impaired polyamine transport and dysregulated EC function. Furthermore, mice carrying a heterozygous germ-line Atp13a3 frameshift variant representing a human variant spontaneously developed a PAH phenotype, with increased pulmonary pressures, right ventricular remodelling and muscularisation of pulmonary vessels. Conclusion We identify ATP13A3 as a polyamine transporter controlling polyamine homeostasis in ECs, deficiency of which leads to EC dysfunction and predisposes to PAH. This suggests a need for targeted therapies to alleviate the imbalances in polyamine homeostasis and EC dysfunction in PAH.

Serum PM20D1 levels in patients with idiopathic pulmonary arterial hypertension and its clinical significance

ObjectiveThis study aimed to investigate the serum levels of Peptidase M20 domain containing 1 (PM20D1) in idiopathic pulmonary arterial hypertension (IPAH) patients and examine its association with lipid metabolism, echocardiography, and hemodynamic parameters.MethodsThis prospective observational research enrolled 103 IPAH patients from January 2018 to January 2022. Enzyme-linked immunosorbent assay (ELISA) was used to measure the serum PM20D1 levels in all patients before treatment within 24 h of admission. Demographic data, echocardiography, hemodynamic parameters and serum biomarkers were also collected.ResultsThe IPAH patients in the deceased group had significantly elevated age, right atrial (RA), mean pulmonary arterial pressure (mPAP), mean right atrial pressure (mRAP), pulmonary capillary wedge pressure (PCWP), pulmonary vascular resistance (PVR) and significantly decreased 6 min walking distance (6MWD) and tricuspid annulus peak systolic velocity (TASPV). IPAH patients showed significant decreases in serum PM20D1, low-density lipoprotein cholesterol (LDL-C), and albumin (ALB). Additionally, PM20D1 was negatively correlated with RA, NT-proBNP and positively correlated with PVR, ALB, 6MWD, and TAPSV. Moreover, PM20D1 has the potential as a biomarker for predicting IPAH patients’ prognosis. Finally, logistic regression analysis indicated that PM20D1, ALB, NT-proBNP, PVR, TASPV, RA and 6MWD were identified as risk factors for mortality in IPAH patients.ConclusionOur findings indicated that the serum levels of PM20D1 were significantly decreased in IPAH patients with poor prognosis. Moreover, PM20D1 was identified as a risk factor associated with mortality in IPAH patients.

Predominance of M2 macrophages in organized thrombi in chronic thromboembolic pulmonary hypertension patients.

Chronic thromboembolic pulmonary hypertension (CTEPH) is a debilitating disease characterized by thrombotic occlusion of pulmonary arteries and vasculopathy, leading to increased pulmonary vascular resistance and progressive right-sided heart failure. Thrombotic lesions in CTEPH contain CD68+ macrophages, and increasing evidence supports their role in disease pathogenesis. Macrophages are classically divided into pro-inflammatory M1 macrophages and anti-inflammatory M2 macrophages, which are involved in wound healing and tissue repair. Currently, the phenotype of macrophages and their localization within thrombotic lesions of CTEPH are largely unknown. In our study, we subclassified thrombotic lesions of CTEPH patients into developing fresh thrombi (FT) and organized thrombi (OT), based on the degree of fibrosis and remodeling. We used multiplex immunofluorescence histology to identify immune cell infiltrates in thrombotic lesions of CPTEH patients. Utilizing software-assisted cell detection and quantification, increased proportions of macrophages were observed in immune cell infiltrates of OT lesions, compared with FT. Strikingly, the proportions with a CD206+INOS- M2 phenotype were significantly higher in OT than in FT, which mainly contained unpolarized macrophages. Taken together, we observed a shift from unpolarized macrophages in FT toward an expanded population of M2 macrophages in OT, indicating a dynamic role of macrophages during CTEPH pathogenesis.

(651) - The Effect of Antifibrotics on the Progression of Pulmonary Hypertension in Patients with Interstitial Lung Disease Listed for Lung Transplantation

(651) - The Effect of Antifibrotics on the Progression of Pulmonary Hypertension in Patients with Interstitial Lung Disease Listed for Lung Transplantation

Collagen triple helix repeat-containing protein 1 is a novel biomarker of right ventricular involvement in pulmonary hypertension

BackgroundPulmonary hypertension leads to right ventricular failure, which is a major determinant of prognosis. Circulating biomarkers for right ventricular function are poorly explored in pulmonary hypertension. This study aimed to clarify the significance of collagen triple helix repeat-containing protein 1 (CTHRC1) as a biomarker of right ventricular failure in pulmonary hypertension. MethodsA monocrotaline-induced pulmonary hypertension rat model was used to evaluate right ventricular CTHRC1 expression and its relationship with fibrosis. Next, human plasma CTHRC1 levels were measured in controls (n = 20), pulmonary arterial hypertension (n = 46), and chronic thromboembolic pulmonary hypertension (CTEPH) patients (n = 64) before the first and after the final balloon pulmonary angioplasty. ResultsCTHRC1 expression was higher in the right ventricles of rats with monocrotaline-induced pulmonary hypertension than in those of controls. CTHRC1 was co-localized with vimentin and associated with fibrosis in the right ventricles. Plasma CTHRC1 levels were higher in human pulmonary arterial hypertension (P = 0.006) and CTEPH patients (P = 0.011) than in controls. Plasma CTHRC levels were correlated with B-type natriuretic peptide (R = 0.355, P < 0.001), tricuspid lateral annular peak systolic velocity (R = -0.213, P = 0.029), and right ventricular fractional area change (R = -0.225, P = 0.017). Finally, plasma CTHRC1 levels were decreased after the final balloon pulmonary angioplasty (P < 0.001) in CTEPH. ConclusionsCTHRC1 can be a circulating biomarker associated with right ventricular function and fibrosis in pulmonary hypertension and might reflect the therapeutic efficacy of balloon pulmonary angioplasty in CTEPH.

(444) - Similar Waitlist and Post-Lung Transplant Outcomes in Pulmonary Arterial Hypertension Patients When Compared with Other Etiologies of End-Stage Lung Disease, a Propensity-Match Analysis

(444) - Similar Waitlist and Post-Lung Transplant Outcomes in Pulmonary Arterial Hypertension Patients When Compared with Other Etiologies of End-Stage Lung Disease, a Propensity-Match Analysis

A Case Report: A Successful Management of Extrinsic Compression of the Left Main Coronary Artery by a Dilated Pulmonary Artery in Patients with Pulmonary Arterial Hypertension

Extrinsic compression of the left main coronary artery (LMCA) by a dilated pulmonary artery can be life threatening in pulmonary arterial hypertension patients; however, it can be treated with percutaneous coronary intervention. In this case report, we presented a successful treatment with the stenting of the LMCA stenosis associated with extrinsic compression of LMCA by a dilated pulmonary artery.

A single institution anesthetic experience with catheterization of pediatric pulmonary hypertension patients.

Cardiac catheterization remains the gold standard for the diagnosis and management of pediatric pulmonary hypertension (PH). There is lack of consensus regarding optimal anesthetic and airway regimen. This retrospective study describes the anesthetic/airway experience of our single center cohort of pediatric PH patients undergoing catheterization, in which obtaining hemodynamic data during spontaneous breathing is preferential. A total of 448 catheterizations were performed in 232 patients. Of the 379 cases that began with a natural airway, 274 (72%) completed the procedure without an invasive airway, 90 (24%) received a planned invasive airway, and 15 (4%) required an unplanned invasive airway. Median age was 3.4 years (interquartile range [IQR] 0.7-9.7); the majority were either Nice Classification Group 1 (48%) or Group 3 (42%). Vasoactive medications and cardiopulmonary resuscitation were required in 14 (3.7%) and eight (2.1%) cases, respectively; there was one death. Characteristics associated with use of an invasive airway included age <1 year, Group 3, congenital heart disease, trisomy 21, prematurity, bronchopulmonary dysplasia, WHO functional class III/IV, no PH therapy at time of case, preoperative respiratory support, and having had an intervention (p < 0.05). A composite predictor of age <1 year, Group 3, prematurity, and any preoperative respiratory support was significantly associated with unplanned airway escalation (26.7% vs. 6.9%, odds ratio: 4.9, confidence interval: 1.4-17.0). This approach appears safe, with serious adverse event rates similar to previous reports despite the predominant use of natural airways. However, research is needed to further investigate the optimal anesthetic regimen and respiratory support for pediatric PH patients undergoing cardiac catheterization.

Prevalence of Pulmonary Hypertension in Liver Cirrhosis Patients: A Cross-Sectional Analytical Study.

Liver cirrhosis (LC) is a common complication of chronic liver disease. Its prevalence has increased markedly over the last few years. With liver cirrhosis comes cardiovascular morbidity and mortality. It is important that the detection of the abnormalities by echocardiography be given priority, as this can change the clinical outcome of these patients with cardiovascular abnormalities in liver cirrhosis. This study aims to determine the prevalence of pulmonary hypertension in LC patients. A cross-sectional analytical study was carried out at JUTH (Jos University Teaching Hospital) over a period of one year. We recruited 210 adult patients with liver cirrhosis from the gastroenterology clinic and wards for this study. Data from these patients were collected with questionnaires administered by the interviewer and analysed using SPSS 23 statistical software (IBM Corp., Armonk, NY). The data obtained are presented in tables and charts. Categorical variables were expressed as proportions and frequencies, while continuous data were expressed as the median, mean, and standard deviation. Pulmonary hypertension was found in 30.5% of the participants, with mild pulmonary hypertension being the most common. No one had severe pulmonary hypertension. There was an increased risk of developing pulmonary hypertension in patients with coughs, easy fatigability, bilateral leg swelling, abdominal swelling, and ascites (P<0.05). The result showed that there is a high prevalence of pulmonary hypertension in patients with liver cirrhosis.

Pulmonary Hypertension and the Risk of 30-Day Postoperative Pulmonary Complications after Gastrointestinal Surgical or Endoscopic Procedures: A Retrospective Propensity Score-Weighted Cohort Analysis.

Background: Pulmonary hypertension (PH) patients are at higher risk of postoperative complications. We analyzed the association of PH with 30-day postoperative pulmonary complications (PPCs). Methods: A single-center propensity score overlap weighting (OW) retrospective cohort study was conducted on 164 patients with a mean pulmonary artery pressure (mPAP) of >20 mmHg within 24 months of undergoing elective inpatient abdominal surgery or endoscopic procedures under general anesthesia and a control cohort (N = 1981). The primary outcome was PPCs, and the secondary outcomes were PPC sub-composites, namely respiratory failure (RF), pneumonia (PNA), aspiration pneumonia/pneumonitis (ASP), pulmonary embolism (PE), length of stay (LOS), and 30-day mortality. Results: PPCs were higher in the PH cohort (29.9% vs. 11.2%, p < 0.001). When sub-composites were analyzed, higher rates of RF (19.3% vs. 6.6%, p < 0.001) and PNA (11.2% vs. 5.7%, p = 0.01) were observed. After OW, PH was still associated with greater PPCs (RR 1.66, 95% CI (1.05-2.71), p = 0.036) and increased LOS (median 8.0 days vs. 4.9 days) but not 30-day mortality. Sub-cohort analysis showed no difference in PPCs between pre- and post-capillary PH patients. Conclusions: After covariate balancing, PH was associated with a higher risk for PPCs and prolonged LOS. This elevated PPC risk should be considered during preoperative risk assessment.

The clinical and hemodynamic characteristics of pulmonary hypertension in patients with OSA-COPD overlap syndrome

BackgroundOur study aimed to assess the clinical and hemodynamic characteristics of pulmonary hypertension (PH) in patients with overlapping obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD), referred to OSA-COPD overlap syndrome (OS). MethodsWe enrolled a total of 116 patients with OS, COPD, or OSA who underwent right heart catheterization (RHC) due to suspected PH. We conducted a retrospective analysis of the clinical and hemodynamic characteristics of these patients. ResultsAmong the three groups (OS group, n = 26; COPD group, n = 36; OSA group, n = 54), the prevalence of PH was higher in the OS group (n = 17, 65.4%)compared to OSA group (n = 26,48.1%) and COPD group (n = 20,55.6 %). Among three groups with PH, the superior vena cava pressure (CVP) and right ventricular pressure (RAP) were higher in the OS group than in the OSA group (P < 0.05). Patients in the OS and COPD groups had higher pulmonary artery wedge pressure (PAWP) than in the OSA group (14.88 ± 4.79 mmHg, 13.45 ± 3.68 mmHg vs. 11.00 ± 3.51 mmHg, respectively, P < 0.05). OS patients with PH exhibited higher respiratory event index (REI), time spent with SpO2 <90%, oxygen desaturation index (ODI), minimal SpO2 (MinSpO2) and mean SpO2 (MSpO2) compared to OS patients without PH. After adjusting for potential covariates, we found that MinSpO2 (OR 0.937, 95 % CI 0.882–0.994, P = 0.032), MSpO2 (OR 0.805, 95% CI 0.682–0.949, P = 0.010), time spent with SpO2 <90% (OR 1.422, 95% CI 1.137–1.780, P = 0.002), and FEV1 % pred (OR 0.977, 95 % CI 0.962–0.993, P = 0.005) were related to the development of PH. ConclusionsPatients with OS showed higher prevalence of PH, along with higher PAWP, CVP and RAP. Worse nocturnal hypoxemia was found in OS patients with PH.

Evaluation of handgrip strength in children with pulmonary hypertension.

Handgrip strength is a crucial indicator of upper extremity muscular strength and is vital for monitoring disorders like cardiac diseases that restrict a patient's physical activity and result in muscle atrophy. The aim of our study was to evaluate whether muscle strength loss is present in patients with pulmonary hypertension and whether this test can be an alternative to 6-minute walk test. The study included 39 healthy children who were admitted to the outpatient clinic and 16 children with a diagnosis of pulmonary hypertension who were being followed in our centre. We assessed the differences in upper extremity handgrip strength using the Jamar Hydraulic Hand Dynamometer device among both healthy children and those diagnosed with pulmonary hypertension. Moreover, we compared the handgrip strength of pulmonary hypertension patients with significant prognostic indicators such as NYHA class, 6-minute walk test, and pro-brain natriuretic peptide. The mean dominant handgrip strength was 20.8 ± 12 kg in the patient group and 21.6 ± 12.4 kg in the control group (p = 0.970). Handgrip strength was shown to be negatively connected with pro-brain natriuretic peptide (r = -0.565, p = 0.023) and positively correlated with 6-minute walk test (r = 0.586, p = 0.022) during the patient group evaluation. Six-minute walk test needs a customised physical area (30 m of a straight hallway) and trained personnel for applying the test. The handgrip strength test, a different muscle strength indicator, can be used to more clearly and simply indicate the decline in patients' ability for effort. Additionally, it was found in our study that handgrip strength decreased as pro-brain natriuretic peptide levels rose, a crucial measure in the monitoring of pulmonary hypertension.

IDF23-0066 Prevalence of pulmonary hypertension in patients with diabetic kidney disease

IDF23-0066 Prevalence of pulmonary hypertension in patients with diabetic kidney disease

The Effect of Phosphodiesterase-5 Inhibitor on Pulmonary Hypertension in Patients with Idiopathic Pulmonary Fibrosis, A Single Centre Study

The Effect of Phosphodiesterase-5 Inhibitor on Pulmonary Hypertension in Patients with Idiopathic Pulmonary Fibrosis, A Single Centre Study