Risk Factors For Pulmonary Hypertension Research Articles

Nephrectomy and high-salt diet inducing pulmonary hypertension and kidney damage by increasing Ang II concentration in rats

BackgroundChronic kidney disease (CKD) is a significant risk factor for pulmonary hypertension (PH), a complication that adversely affects patient prognosis. However, the mechanisms underlying this association remain poorly understood. A major obstacle to progress in this field is the lack of a reliable animal model replicating CKD-PH.MethodsThis study aimed to establish a stable rat model of CKD-PH. We employed a combined approach, inducing CKD through a 5/6 nephrectomy and concurrently exposing the rats to a high-salt diet. The model's hemodynamics were evaluated dynamically, alongside a comprehensive assessment of pathological changes in multiple organs. Lung tissues and serum samples were collected from the CKD-PH rats to analyze the expression of angiotensin-converting enzyme 2 (ACE2), evaluate the activity of key vascular components within the renin–angiotensin–aldosterone system (RAAS), and characterize alterations in the serum metabolic profile.ResultsAt 14 weeks post-surgery, the CKD-PH rats displayed significant changes in hemodynamic parameters indicative of pulmonary arterial hypertension. Additionally, right ventricular hypertrophy was observed. Notably, no evidence of pulmonary vascular remodeling was found. Further analysis revealed RAAS dysregulation and downregulated ACE2 expression within the pulmonary vascular endothelium of CKD-PH rats. Moreover, the serum metabolic profile of these animals differed markedly from the sham surgery group.ConclusionsOur findings suggest that the development of pulmonary arterial hypertension in CKD-PH rats is likely a consequence of a combined effect: RAAS dysregulation, decreased ACE2 expression in pulmonary vascular endothelial cells, and metabolic disturbances.Graphical

Periodontitis exacerbates pulmonary hypertension by promoting IFNγ+ T cell infiltration in mice

Uncovering the risk factors of pulmonary hypertension and its mechanisms is crucial for the prevention and treatment of the disease. In the current study, we showed that experimental periodontitis, which was established by ligation of molars followed by orally smearing subgingival plaques from patients with periodontitis, exacerbated hypoxia-induced pulmonary hypertension in mice. Mechanistically, periodontitis dysregulated the pulmonary microbiota by promoting ectopic colonization and enrichment of oral bacteria in the lungs, contributing to pulmonary infiltration of interferon gamma positive (IFNγ+) T cells and aggravating the progression of pulmonary hypertension. In addition, we identified Prevotella zoogleoformans as the critical periodontitis-associated bacterium driving the exacerbation of pulmonary hypertension by periodontitis, and the exacerbation was potently ameliorated by both cervical lymph node excision and IFNγ neutralizing antibodies. Our study suggests a proof of concept that the combined prevention and treatment of periodontitis and pulmonary hypertension are necessary.

Cardiac Implications of Adenotonsillar Hypertrophy and Obstructive Sleep Apnea in Pediatric Patients: A Comprehensive Systematic Review.

This review investigates the relationship between pediatric obstructive sleep apnea, often associated with adenotonsillar hypertrophy, and cardiovascular health, particularly pulmonary hypertension. We conducted a comprehensive literature search using electronic databases, including Medline Pub-Med, Scopus, and the Web of Science. The study analyzed a total of 230 articles and screened 48 articles, with 20 included in the final analysis, involving 2429 children. The PRISMA flowchart visually illustrates the selection process, and the ROBINS-E and -I tools help ensure the reliability and validity of the evidence produced by these studies. These studies explored various aspects, including the severity of obstructive sleep apnea, cardiac anomalies, cardiac stress markers, risk factors for pulmonary hypertension, and the impact of adenoidectomy and tonsillectomy on cardiac function. The research found that adenotonsillar hypertrophy and obstructive sleep apnea are significant risk factors for cardiovascular complications, especially pulmonary hypertension, in children. Adenoidectomy and tonsillectomy may provide effective treatments. Following adenoidectomy in relation to obstructive sleep apnea, there appears to be a reduction in mean pulmonary artery pressure during echocardiographic examination. However, the efficacy of these procedures can vary based on the severity of obstructive sleep apnea and individual cardiac conditions. The study also identified concerns regarding data bias. The authors emphasize the need for well-designed clinical studies, including both healthy patients with adenotonsillar hypertrophy and vulnerable children with genetic disorders, to ensure that clinical decisions are based on solid scientific evidence.

Pathophysiology and Risk Factors of Pulmonary Hypertension in Patients with Thalassemia

Pathophysiology and Risk Factors of Pulmonary Hypertension in Patients with Thalassemia

Impact of inhalation exposure to cigarette smoke on the pathogenesis of pulmonary hypertension primed by monocrotaline in rats.

Extensive, long-term exposure to cigarette smoke (CS) was recently suggested to be a risk factor for pulmonary hypertension, although further validation is required. The vascular effects of CS share similarities with the etiology of pulmonary hypertension, including vascular inflammation and remodeling. Thus, we examined the influence of CS exposure on the pathogenesis of monocrotaline (MCT)-induced pulmonary hypertension, hypothesizing that smoking might accelerate the development of primed pulmonary hypertension. CS was generated from 3R4F reference cigarettes, and rats were exposed to CS by inhalation at total particulate matter concentrations of 100-300 μg/L for 4h/day, 7days/week for 4weeks. Following 1 week of initial exposure, rats received 60 mg/kg MCT and were sacrificed and analyzed after an additional 3weeks of exposure. MCT induced hypertrophy in pulmonary arterioles and increased the Fulton index, a measure of right ventricular hypertrophy. Additional CS exposure exacerbated arteriolar hypertrophy but did not further elevate the Fulton index. No significant alterations were observed in levels of endothelin-1 and vascular endothelial growth factor, or in hematological and serum biochemical parameters. Short-term inhalation exposure to CS exacerbated arteriolar hypertrophy in the lung, although this effect did not directly aggravate the overworked heart under the current experimental conditions.

Phenotypes of Sarcoidosis-Associated Pulmonary Hypertension-A Challenging Mystery.

Sarcoidosis has been a well-recognised risk factor for pulmonary hypertension (PH) for a long time, but still, the knowledge about this concatenation is incomplete. Sarcoidosis-associated PH (SAPH) is an uncommon but serious complication associated with increased morbidity and mortality among sarcoidosis patients. The real epidemiology of SAPH remains unknown, and its pathomechanisms are not fully explained. Sarcoidosis is a heterogeneous and dynamic condition, and SAPH pathogenesis is believed to be multifactorial. The main roles in SAPH development play: parenchymal lung disease with the destruction of pulmonary vessels, the extrinsic compression of pulmonary vessels by conglomerate masses, lymphadenopathy or fibrosing mediastinitis, pulmonary vasculopathy, LV dysfunction, and portal hypertension. Recently, it has been recommended to individually tailor SAPH management according to the predominant pathomechanism, i.e., SAPH phenotype. Unfortunately, SAPH phenotyping is not a straightforward process. First, there are gaps in our understanding of undergoing processes. Second, the assessment of such a pivotal element as pulmonary vasculature on a microscopic level is non-feasible in SAPH patients antemortem. Finally, SAPH is a dynamic condition, multiple phenotypes usually coexist, and patients can switch between phenotypes during the course of sarcoidosis. In this article, we summarise the basic knowledge of SAPH, describe SAPH phenotypes, and highlight some practical problems related to SAPH phenotyping.

Assessment of risk factors for bronchopulmonary dysplasia with pulmonary hypertension and construction of a prediction nomogram model

Objective: To explore the risk factors of pulmonary hypertension (PH) in premature infants with bronchopulmonary dysplasia (BPD), and to establish a prediction model for early PH. Methods: This was a retrospective cohort study. Data of 777 BPD preterm infants with the gestational age of <32 weeks were collected from 7 collaborative units of the Su Xinyun Neonatal Perinatal Collaboration Network platform in Jiangsu Province from January 2019 to December 2022. The subjects were randomly divided into a training cohort and a validation cohort at a ratio of 8∶2 by computer, and non-parametric test or χ2 test was used to examine the differences between the two retrospective cohorts. Univariate Logistic regression and multivariate logistic regression analyses were used in the training cohort to screen the risk factors affecting the PH associated with BPD. A nomogram model was constructed based on the severity of BPD and its risk factors,which was internally validated by the Bootstrap method. Finally, the differential, calibration and clinical applicability of the prediction model were evaluated using the training and verification queues. Results: A total of 130 among the 777 preterm infants with BPD had PH, with an incidence of 16.7%, and the gestational age was 28.7 (27.7, 30.0) weeks, including 454 males (58.4%) and 323 females (41.6%). There were 622 preterm infants in the training cohort, including 105 preterm infants in the PH group. A total of 155 patients were enrolled in the verification cohort, including 25 patients in the PH group. Multivariate Logistic regression analysis revealed that low 5 min Apgar score (OR=0.87, 95%CI 0.76-0.99), cesarean section (OR=1.97, 95%CI 1.13-3.43), small for gestational age (OR=9.30, 95%CI 4.30-20.13), hemodynamically significant patent ductus arteriosus (hsPDA) (OR=4.49, 95%CI 2.58-7.80), late-onset sepsis (LOS) (OR=3.52, 95%CI 1.94-6.38), and ventilator-associated pneumonia (VAP) (OR=8.67, 95%CI 3.98-18.91) were all independent risk factors for PH (all P<0.05). The independent risk factors and the severity of BPD were combined to construct a nomogram map model. The area under the receiver operating characteristic (ROC) curve of the nomogram model in the training cohort and the validation cohort were 0.83 (95%CI 0.79-0.88) and 0.87 (95%CI 0.79-0.95), respectively, and the calibration curve was close to the ideal diagonal. Conclusions: Risk of PH with BPD increases in preterm infants with low 5 minute Apgar score, cesarean section, small for gestational age, hamodynamically significant patent ductus arteriosus, late-onset sepsis, and ventilator-associated pneumonia. This nomogram model serves as a useful tool for predicting the risk of PH with BPD in premature infants, which may facilitate individualized early intervention.

Preterm birth: An important risk factor for pulmonary hypertension.

Preterm birth: An important risk factor for pulmonary hypertension.

Left Ventricular Filling Pressure in Chronic Thromboembolic Pulmonary Hypertension

BackgroundChronic thromboembolic pulmonary hypertension (CTEPH) is characterized by obstruction of major pulmonary arteries with organized thrombi. Clinical risk factors for pulmonary hypertension due to left heart disease including metabolic syndrome, left-sided valvular heart disease, and ischemic heart disease are common in CTEPH patients. ObjectivesThe authors sought to investigate prevalence and prognostic implications of elevated left ventricular filling pressures (LVFP) in CTEPH. MethodsA total of 593 consecutive CTEPH patients undergoing a first diagnostic right and left heart catheterization were included in this study. Mean pulmonary arterial wedge pressure (mPAWP) and left ventricular end-diastolic pressure (LVEDP) were utilized for assessment of LVFP. Two cutoffs were applied to identify patients with elevated LVFP: 1) for the primary analysis mPAWP and/or LVEDP >15 mm Hg, as recommended by the current pulmonary hypertension guidelines; and 2) for the secondary analysis mPAWP and/or LVEDP >11 mm Hg, representing the upper limit of normal. Clinical and echocardiographic features, and long-term mortality were assessed. ResultsLVFP was >15 mm Hg in 63 (10.6%) and >11 mm Hg in 222 patients (37.4%). Univariable logistic regression analysis identified age, systemic hypertension, diabetes, atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial volume as significant predictors of elevated LVFP. Atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial volume remained independent determinants of LVFP in adjusted analysis. At follow-up, higher LVFPs were measured in patients who had meanwhile undergone pulmonary endarterectomy (P = 0.002). LVFP >15 mm Hg (P = 0.021) and >11 mm Hg (P = 0.006) were both associated with worse long-term survival. ConclusionsElevated LVFP is common, appears to be due to comorbid left heart disease, and predicts prognosis in CTEPH.

Diazoxide for Neonatal Hyperinsulinemic Hypoglycemia and Pulmonary Hypertension.

Hypoglycemia in neonates is associated with long-term neurodevelopmental effects. Hyperinsulinemic hypoglycemia (HH) is the most common cause of persistent hypoglycemia in neonatal intensive care units. Diazoxide is the only medication that is currently recommended for treatment of HH in neonates. However, the use of diazoxide in neonates is associated with pulmonary hypertension as an adverse effect. In this article, we review the literature on the mechanism of action and adverse effects with the use of diazoxide in neonatal hyperinsulinism. We then present a case series of neonates treated with diazoxide in our neonatal intensive care unit over a 5-year period. Among 23 neonates who received diazoxide, 4 developed pulmonary hypertension and 1 died. All infants who developed pulmonary hypertension were born preterm at less than 36 weeks gestation and had pre-existing risk factors for pulmonary hypertension. HH in preterm neonates, with pre-existing pulmonary hypertension or with risk factors for pulmonary hypertension requires thoughtful management.

Pulmonary artery pressures and right ventricular dimensions of post-COVID-19 patients without previous significant cardiovascular pathology

BackgroundPulmonary hypertension is a significant complication of COVID-19, but follow-up data on pulmonary artery pressure after recovery from COVID-19 are limited. ObjectivesTo investigate pulmonary artery pressure and heart dimensions in post-COVID-19 patients without a history of significant cardiac pathology. MethodsData for 91 eligible adult patients were subjected to 2 analyses. First, patients were grouped according to where they received COVID-19 treatment: the ICU, COVID-19 ward, or outpatient clinic. Second, the severity of COVID-19 was grouped as no pulmonary involvement, non-severe pulmonary involvement, or severe pulmonary involvement based on thoracic computed tomography scores. Heart dimensions were measured and pulmonary artery pressure was estimated using transthoracic echocardiography. The correlation between transthoracic echocardiography findings and COVID-19 severity was assessed. ResultsPulmonary artery pressure and right-heart dimensions were significantly elevated in the post-COVID-19 patients without a history of risk factors for pulmonary hypertension that presented to the cardiology outpatient clinic with cardiac complaints. Both of these findings were correlated with the severity of COVID-19 and the extent of lung involvement based on thoracic computed tomography. ConclusionThe present findings confirm that increases in systolic pulmonary artery pressure and right ventricular dimensions persist 2-3 months after recovery from COVID-19 in patients without a history of risk factor for pulmonary hypertension. Furthermore, the increase in pulmonary artery pressure and right ventricular dimensions correlate with the severity of COVID-19 and the extent of lung involvement based on thoracic computed tomography.

Incidence and Risk Factors of Pulmonary Hypertension After Venous Thromboembolism: An Analysis of a Large Health Care Database.

Background Pulmonary hypertension (PH) is a devastating potential complication of pulmonary embolism, a manifestation of venous thromboembolism (VTE). The incidence of and risk factors for PH in those with prior VTE are poorly characterized. Methods and Results International Classification of Diseases (ICD) codes from inpatient and outpatient medical claims from MarketScan administrative databases for years 2011 to 2018 were used to identify cases of VTE, comorbidities before the VTE event, and PH occurring subsequent to the VTE event. Cumulative incidence and hazard ratios (HR), and their 95% CI, were calculated. The 170021 VTE cases included in the analysis were on average (±SD) 57.5±15.8years old and 50.5% were female. A total of 5943 PH cases accrued over an average follow-up of 1.94years. Two years after incident VTE, the cumulative incidence (95% CI) of PH was 3.5% (3.4%-3.7%) overall. It was higher among older individuals, among women (3.9% [3.8%-4.1%]) than men (3.2% [3.0%-3.3%]), and among patients presenting with pulmonary embolism (6.2% [6.0%-6.5%]) than those presenting with deep vein thrombosis only (1.1% [1.0%-1.2%]). Adjusting for age and sex, risk of PH was higher among patients with VTE with underlying comorbidities. Using the Charlson comorbidity index, there was a dose-response relationship, whereby greater scores were associated with increased PH risk (score ≥5 versus 0: HR, (2.50 [2.30-2.71])). When evaluating individual comorbidities, the strongest associations were observed with concomitant heart failure (HR, 2.17 [2.04-2.31]), chronic pulmonary disease (2.01 [1.90-2.14]), and alcohol abuse (1.66 [1.29-2.13]). Conclusions In this large, real-world population of insured people with VTE, 3.5% developed PH in the 2years following their initial VTE event. Risk was higher among women, with increasing age, and in those with additional comorbidities at the time of the VTE event. These data provide insights into the burden of PH and risk factors for PH among patients with VTE.

Screening Echocardiography Identifies Risk Factors for Pulmonary Hypertension at Discharge in Premature Infants with Bronchopulmonary Dysplasia.

Premature infants with bronchopulmonary dysplasia (BPD) are at increased risk of secondary pulmonary hypertension (BPD-PH). Prior studies yielded mixed results on the utility of echocardiographic screening at 36weeks post-menstrual age (PMA). We present our experience using echocardiographic screening at the time of BPD diagnosis to identify infants at highest risk of BPD-PH at discharge. Retrospective cohort analysis of clinical/ demographic data and screening echocardiograms in patients with BPD.Discharge echocardiograms identified infants with or without BPD-PH at discharge. 36weeks PMA screening echocardiograms and clinical data were then reviewed to identify which factors were associated with increased odds of BPD-PH at discharge. Associations between echocardiographic findings were evaluated with 2- and 3-variable models to predict increased risk of BPD-PH at discharge. In our cohort of 64 infants with severe BPD, BPD-PH was present in 22/64 (34%) infants at discharge. There were no clinical differences at time of 36weeks PMA screening evaluation (mean PMA 36.6 ± 2.9weeks). PH at screening was poorly predictive of PH at discharge as PH at screening resolved in 49% of patients. However, having an ASD, RV dilation, hypertrophy, or reduced function on screening, especially in combination, were associated with BPD-PH at discharge. In our cohort of premature infants with BPD, 36weeks PMA screening echocardiogram identified patients at increased risk for BPD-PH at discharge when ASD, RVH, or impaired RV function were present. Larger prospective studies are indicated to validate these findings.

Phosphatidylserine and the thrombin–antithrombin complex as markers for hypercoagulability in Egyptian beta-thalassemia patients

Background Hypercoagulability is a known complication of thalassemia, in particular, thalassemia intermedia. Several factors contribute to this hypercoagulability, including chronic platelet activation and the presence of other comorbid conditions. In addition, the oxidation of globin subunits in thalassemic red blood cells (RBCs) triggers the formation of reactive oxygen species. These factors lead to the exposure of negatively charged phospholipids like phosphatidylserine (PS), which ultimately causes increased thrombin generation, particularly in splenectomized patients. Aim This study aimed to assess the risk for hypercoagulability in thalassemic patients using PS expression on RBCs and the thrombin–antithrombin (TAT) complex in plasma. Patients and methods This study included 50 thalassemic patients (19 patients with splenectomy and 31 patients without splenectomy) and 30 apparently healthy individuals as a control group. Patients were subjected to assessment of history for deep venous thrombosis or pulmonary hypertension by echocardiography. Annexin V was used to detect PS expression on RBCs by flow cytometry, while the enzyme-linked immunosorbent assay was used to detect the TAT complex in plasma. Results Erythrocyte PS expression was significantly higher (P<0.001) in thalassemic patients than in the control group. The TAT complex level revealed no significant difference between thalassemia patients and the control group (P=0.468). Patients with pulmonary hypertension showed a statistically significant higher PS expression and TAT complex level. However, there was no significant increase in PS expression or TAT level in patients with a history of deep venous thrombosis only. Conclusion Increased PS expression and TAT complex level may be a risk factor for pulmonary hypertension in thalassemia patients with splenectomy.

Ischaemic versus non-ischaemic: how does heart failure aetiology affect pulmonary arterial capacitance and pulmonary artery pulsatility index in end-stage heart failure?

Background The aetiology of heart failure may have different effects on right ventricular (RV) function, pulmonary pressures and RV afterload. Pulmonary arterial capacitance (PAC) and pulmonary artery pulsatility index (PAPi) are novel haemodynamic indices used in determining RV afterload and RV function, respectively. We aimed to investigate whether there was a difference in PAC and PAPi between ischaemic cardiomyopathy (ICMP) and non-ischaemic cardiomyopathy (NICMP) in patients with end-stage heart failure. Methods and results A total of 215 subjects undergoing evaluation for heart transplantation or left ventricular (LV) assist device were classified into two groups: ICMP (n = 101) and NICMP (n = 114). The patients with LV ejection fraction ≤ 25% were included in the study. ICMP group had lower PAC and higher PAPi values compared to NICMP group [1.25 (0.82–1.86) vs. 1.58 (1.02–2.21), p = 0.002 and 3.4 (2.2–5.0) vs. 2.5 (1.7–4.0); p = 0.007]. Pulmonary vascular resistance, pulmonary artery systolic and mean pressure were higher in ICMP group compared to NICMP group [3.5 ± 1.8 vs. 2.9 ± 2.3, p = 0.004; 59.0 (42.0–73.0) vs. 46.0 (37.0–59.0), p < 0.001, 35.0 (27.0–46.0) vs. 31.0 (23.0–39.0), p = 0.002]. The patients with ICMP had higher tricuspid annular plane systolic excursion and less RV dilatation. ICMP was an independent risk factor for pulmonary hypertension (OR: 4.02, 95% CI: 1.13-14.24, p = 0.031). Conclusion ICMP was associated with lower PAC and higher PAPi. These results indicated that an ischaemic aetiology is associated with higher RV afterload and better RV function in the end-stage heart failure.

Risk Factors of Pulmonary Hypertension in Patients on Hemodialysis: A Single Center Study.

IntroductionPulmonary hypertension (PH) is an underestimated cardiovascular consequence and a mortality predictor in patients on hemodialysis (HD). Thus, we studied its prevalence, risk factors, association with inflammation/oxidative stress, and cardiac changes in HD patients.MethodsThis was a single-center cross-sectional observational study conducted at a tertiary care hospital. Patients aged >18 years on hemodialysis for at least three months were included and divided into those with and without PH; patients with secondary causes for PH were excluded. Clinical characteristics, HD-related factors, lab parameters (C-reactive protein and malondialdehyde with thiol assay were used as markers of inflammation and oxidative stress, respectively), and echocardiography details were compared. PH was defined as a mean pulmonary artery pressure of >25 mmHg at rest, and it was further divided as mild (25–40 mmHg), moderate (40–60 mmHg), and severe (>60 mmHg).ResultsOf 52 patients, 28 patients had PH (mild 24, moderate 4, and none had severe PH) with prevalence of 54%. No difference was found in clinical characteristics, dialysis-related factors, biochemical parameters including inflammation (C-reactive protein; p=0.76), or oxidative stress (thiol; p=0.36 and MDA; p=0.46) between the groups. When compared to individuals without PH, HD patients with PH exhibited significantly more mitral regurgitation (p=0.002).ConclusionHemodialysis patients have a high prevalence of PH. PH was significantly associated with the presence of mitral regurgitation on echocardiography. Our study did not find differences in traditional risk factors, HD-related factors, and inflammation/oxidative markers between the groups with and without PH.

Characteristics and Risk Factors of Pulmonary Hypertension in Patients With Hyperthyroidism

ObjectiveThis study aimed to comprehensively assess the characteristics and risk factors of hyperthyroidism with pulmonary hypertension (PH). MethodsThis was a retrospective cross-sectional analysis of 315 consecutive patients with hyperthyroidism admitted to the endocrinology department of Tongji Hospital from February 2016 to December 2017. PH was defined as a pulmonary arterial systolic pressure above 35 mm Hg measured by echocardiography. ResultsAmong the 315 patients, 208 were females, the median age was 42 (30-51) years, and the median disease duration was 12 (3-48) months. Thirty-five percent (111/315) of patients were identified with PH. Patients with hyperthyroidism and PH showed significantly higher serum concentrations of free thyroxine (FT4), free triiodothyronine, thyroid receptor antibodies, total bilirubin (TB), direct and indirect bilirubin, lower serum levels of hemoglobin and creatinine, and more severe cardiac load (P < .05 for each) compared with patients without PH. Levels of serum FT4, free triiodothyronine, thyroid receptor antibodies, and thyroid peroxidase antibody were different among groups of patients with different levels of pulmonary arterial systolic pressure (P < .05 for each). Multivariate logistic regression analysis indicated that serum FT4 (odds ratio, 1.02; 95% CI, 1.01-1.04; P = .004) and TB (OR, 1.03; 95% CI, 1.00-1.06; P = .030) were independent risk factors for PH in patients with hyperthyroidism. ConclusionElevated serum FT4 and TB levels may be independent risk factors for PH in patients with hyperthyroidism and valuable indicators for the identification and treatment of patients with PH and hyperthyroidism.

Prevalence and risk factors for Pulmonary Hypertension associated with chronic Myeloproliferative Neoplasms.

Pulmonary hypertension (PH) is commonly reported in Philadelphia-chromosome negative myeloproliferative neoplasms (MPNs) including polycythemia vera (PV), essential thrombocythemia (ET), and myelofibrosis (MF). PH may be diagnosed directly by right heart catheterization (RHC) or estimated by transthoracic echocardiography (TTE). Survival is shortened by PH but despite the potential significance of PH to management and prognosis of MPN, estimates of its prevalence in MPNs vary and risk factors for the condition are poorly established. We performed a systematic review and meta-analysis of available studies to fill this void. We searched EMBASE, MEDLINE, and Clinicaltrials.gov for the terms "pulmonary hypertension," "myeloproliferative disorders," "polycythemia vera," "essential thrombocythemia," and "myelofibrosis." We restricted analysis to the 1999-2019 window to improve uniformity of MPN diagnostic criteria. We retrieved 221 records and, after abstract and full-text screening, identified 17 papers meeting criteria for inclusion in our meta-analysis. A modified Newcastle-Ottawa scale was used to assess quality. Results for 935 patients were available, 309 of these having PH (33%). Using logistic mixed-effect regression, we found that diagnosis mode (RHC vs TTE) and MPN duration influenced PH prevalence. Studies employing predominantly TTE yielded prevalence estimates ~5-fold higher than those using RHC (35% vs 7.2%). We identified MF and duration of MPN as significant risk factors for development of PH. Prevalence of PH in MPNs is poorly understood with estimates ranging from 3.8% to 58%. Patients with MF and longer duration of disease seem at particularly high risk and should be carefully monitored for PH.

Prevalence and risk factors of pulmonary hypertension among adult patients with HIV infection in Ethiopia.

Globally, non-communicable diseases are increasing in people living with HIV. Pulmonary hypertension is a rare non-communicable disease in people living with HIV with a reported prevalence of <1%. However, data on pulmonary hypertension in people living with HIV from Africa are scarce and are non-existent from Ethiopia. This study aimed to examine the prevalence and severity of echocardiographic pulmonary hypertension and risk factors associated with pulmonary hypertension in people living with HIV in Ethiopia. A total of 315 consecutive adult people living with HIV followed at the Tikur Anbessa Specialized Hospital HIV Referral Clinic were enrolled from June 2018 to February 2019. Those with established pulmonary hypertension of known causes were excluded. A structured questionnaire was used to collect data on demographics, respiratory symptoms, physical findings, physician-diagnosed lung disease, and possible risk factors. Pulmonary hypertension was defined by a tricuspid regurgitant velocity of ≥2.9 m/sec on transthoracic echocardiography. A tricuspid regurgitant velocity ≥3.5, which translates into a pulmonary arterial pressure/right ventricular systolic pressure of ≥50 mmHg, was considered moderate-to-severe pulmonary hypertension. The mean age of the participants was 44.5 ± 9.8 years and 229 (72.7%) were females. Pulmonary hypertension was diagnosed in 44 (14.0%) of participants, of whom 9 (20.5%) had moderate-to-severe disease. In those with pulmonary hypertension, 17 (38.6%) were symptomatic: exertional dyspnea, cough, and leg swelling were seen in 12 (27.3%), 9 (20.5%), and 4 (9.1%), respectively. There was no significant difference in those with pulmonary hypertension compared to those without the disease by gender, cigarette smoking, previous history of pulmonary tuberculosis treatment, physician-diagnosed chronic obstructive pulmonary disease or bronchial asthma, duration of anti-retroviral therapy therapy or anti-retroviral regimen type. Pulmonary hypertension looks to be a frequent complication in people living with HIV in Ethiopia and is often associated with significant cardiopulmonary symptoms. Further studies using right heart catheterization are needed to better determine the etiology and prevalence of pulmonary hypertension in people living with HIV in Ethiopia compared to other countries.

PULMONARY HYPERTENSION IN POST TUBERCULOSIS PULMONARY SEQUELAE: ATTENTION NEEDED

TYPE: Abstract Publication TOPIC: Pulmonary Vascular Disease PURPOSE: To assess the prevalence and risk factors of pulmonary hypertension in post tuberculosis pulmonary sequelae. METHODS: It is a cross sectional study conducted in Tirunelveli Medical College from January 2018-June 2019. Patients with history of pulmonary tuberculosis and features of sequelae in chest X-ray were included. Data collected for risk factors, like age, sex, BMI, smoking history, drug sensitivity, treatment outcome and number of tuberculosis history, extension and type of sequelae in chest X-Ray and spirometry pattern. Transthoracic echocardiography was done. RESULTS: 46 patients with sequelae were assessed. 21(45.65%) had pulmonary hypertension, out of which 15(71.43%) had cor pulmonale. Underweight (p=0.03;OR:4) and ATT defaulted patients(p=0.03;OR:3.94) had significant risk. Number of zones (p<0.001) and extension of disease (p=0.002) showed significant relationship, with odds ratio for ≥3zones 14.6 and bilateral disease 8.13. Most common lesion was fibrosis (82.2%). Patients with combined sequelae lesion had more risk than with single lesion (p=0.026;OR:4). 61.9% had mixed pattern in spirometry with significant risk (p=0.01) than patients with either one. CONCLUSIONS: Pulmonary hypertension in post pulmonary tuberculosis sequelae is a significant complication. Undernourishment, defaulting treatment and extensive lesion had higher risk. CLINICAL IMPLICATIONS: The high prevalence of pulmonary hypertension in post tuberculosis pulmonary sequelae emphasizes the need for early detection, treatment with adequate regimen and ensuring compliance with treatment of pulmonary tuberculosis. Recommendations regarding long term follow up of these patients to prevent morbidity and mortality associated with pulmonary hypertension should be included in national and international tuberculosis programs. DISCLOSURE: No significant relationships. KEYWORDS: tuberculosis, pulmonary hypertension, Post tuberculosis sequelae