Pulmonary circulation
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Pulmonary circulation · Oct 2019
Metabolomics of exercise pulmonary hypertension are intermediate between controls and patients with pulmonary arterial hypertension.
Mechanisms underlying pulmonary arterial hypertension (PAH) remain elusive. Pulmonary arterial hypertension and exercise PH share similar physiologic consequences; it is debated whether they share biologic mechanisms and if exercise PH represents an early phase of pulmonary arterial hypertension. We conducted an observational study to test if there is a graded metabolic disturbance along the severity of PH, which may indicate shared or disparate pathophysiology. ⋯ The metabolic signature of exercise PH was uniquely between that of control and pulmonary arterial hypertension subjects. Accuracy predicting control, exercise PH, and pulmonary arterial hypertension group was 96%, 90%, and 88%, respectively, using paired rest-exercise metabolic changes. Our data suggest the metabolic profile of exercise PH is between that of controls and patients with pulmonary arterial hypertension.
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Pulmonary circulation · Oct 2019
Cytokines trigger disruption of endothelium barrier function and p38 MAP kinase activation in BMPR2-silenced human lung microvascular endothelial cells.
The bone morphogenetic protein receptor II (BMPRII) signaling pathway is impaired in pulmonary arterial hypertension and mutations in the BMPR2 gene have been observed in both heritable and idiopathic pulmonary arterial hypertension. However, all BMPR2 mutation carriers do not develop pulmonary arterial hypertension, and inflammation could trigger the development of the disease in BMPR2 mutation carriers. Circulating levels and/or lung tissue expression of cytokines such as tumor necrosis factor-α or interleukin-18 are elevated in patients with pulmonary arterial hypertension and could be involved in the pathogenesis of pulmonary arterial hypertension. ⋯ Interestingly, tumor necrosis factor-α induced activation of P38MAPK and disrupted endothelial barrier function in BMPR2-silenced HLMVECs. Altogether, our findings showed that stable BMPR2 silencing resulted in impaired endothelial barrier function and activation of P38MAPK in HLMVECs. In BMPR2-silenced HLMVECs, cytokines enhanced adhesiveness capacities, activation of P38MAPK and impaired endothelial barrier function suggesting that cytokines could trigger the development of pulmonary arterial hypertension in a context of impaired BMPRII signaling pathway.
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Pulmonary circulation · Oct 2019
Clinical outcomes of inferior vena cava filter in complicated pulmonary embolism.
Background: Previous observational studies suggest that inferior vena cava filter placement in pulmonary embolism patients complicated with congestive heart failure, mechanical ventilation, and shock may have a mortality benefit. We sought to analyze the survival benefits of inferior vena cava filter in pulmonary embolism patients complicated with acute myocardial infarction, acute respiratory failure, shock, or requiring treatment with thrombolytics. Methods: This retrospective observational study used hospital discharge data from the National Inpatient Sample Data (NIS). ⋯ Clinical outcomes were compared between the inferior vena cava filter group and the non-inferior vena cava filter group. Results: Mortality rate in complicated pulmonary embolism patients with inferior vena cava filter placement was lower (20.9% vs. 33%; NNT = 8.28, 95% confidence interval (CI) 7.91-8.69, E-value = 2.53) and in the subgroups; acute myocardial infarction (17.9% vs. 30.1%; NNT = 8.19, 95% CI 7.52-8.92, E-value = 2.76), acute respiratory failure (19.5% vs. 29.7%; NNT = 9.76, 95% CI 8.67-11.16, E-value = 2.38), shock (30.7% vs. 47.1%; NNT = 6.08, 95% CI 5.73-6.47, E-value = 2.43), and with the use of thrombolytics (7% vs. 12.9 %; NNT 17.1, 95% CI 14.88-20.12, E-value = 3.01) (p < 0.001 for all). Conclusion: Inferior vena cava filter placement in pulmonary embolism complicated with acute myocardial infarction, acute respiratory failure, shock, or requiring thrombolytic therapy was associated with reduced mortality.
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Pulmonary circulation · Oct 2019
Case Reports"Anagrelide-induced pulmonary arterial hypertension": a rare case of drug-induced pulmonary arterial hypertension.
Pulmonary arterial hypertension can be associated with exposure to certain drugs or toxins. However, only a few cases of drug-induced pulmonary arterial hypertension have been previously reported. ⋯ Pulmonary arterial hypertension promptly improved after the discontinuation of anagrelide. Anagrelide-induced pulmonary arterial hypertension is a very rare disease, and our case shows that it might be reversible.