Pulmonary Vascular Conditions Research Articles

Dual-energy CT in pulmonary vascular disease.

Dual-energy CT (DECT) imaging is a technique that extends the capabilities of CT beyond that of established densitometric evaluations. CT pulmonary angiography (CTPA) performed with dual-energy technique benefits from both the availability of low kVp CT data and also the concurrent ability to quantify iodine enhancement in the lung parenchyma. Parenchymal enhancement, presented as pulmonary perfused blood volume maps, may be considered as a surrogate of pulmonary perfusion. These distinct capabilities have led to new opportunities in the evaluation of pulmonary vascular diseases. Dual-energy CTPA offers the potential for improvements in pulmonary emboli detection, diagnostic confidence, and most notably severity stratification. Furthermore, the appreciated insights of pulmonary vascular physiology conferred by DECT have resulted in increased use for the assessment of pulmonary hypertension, with particular utility in the subset of patients with chronic thromboembolic pulmonary hypertension. With the increasing availability of dual energy-capable CT systems, dual energy CTPA is becoming a standard-of-care protocol for CTPA acquisition in acute PE. Furthermore, qualitative and quantitative pulmonary vascular DECT data heralds promise for the technique as a "one-stop shop" for diagnosis and surveillance assessment in patients with pulmonary hypertension. This review explores the current application, clinical value, and limitations of DECT imaging in acute and chronic pulmonary vascular conditions. It should be noted that certain manufacturers and investigators prefer alternative terms, such as spectral or multi-energy CT imaging. In this review, the term dual energy is utilised, although readers can consider these terms synonymous for purposes of the principles explained.

Characteristics of the pulmonary circulation in infants with complete atrioventricular septal defect.

Infants with complete atrioventricular septal defect occasionally accompany pulmonary hypertension; however, the pulmonary circulation can be altered by pulmonary vascular conditions as well as the left heart lesions. This study aimed to explore whether the left heart lesions were related to the pulmonary circulation among them. We performed echocardiography and cardiac catheterisation in 42 infants with complete atrioventricular septal defect and studied relationships between the pulmonary haemodynamic parameters and the left heart morphology. Age and weight at preoperative evaluation were 65 days (47-114) (the median following interquartile range) and 5.5 kg (4.0-7.1), respectively. There were 27 individuals with Down syndrome. Gestational age was 38 weeks (37-39). Catheterisation showed mean pulmonary arterial pressure: 36 (29-46) mmHg, the ratio of pulmonary to systemic blood flow: 3.45 (2.79-4.98), pulmonary vascular resistance: 2.20 Wood units·m2 (1.53-3.65), and pulmonary arterial compliance: 2.78 (1.86-4.10) ml/Hg/m2. Echocardiography showed the Rastelli classification type A in 28 and type C in 14, moderate or severe left atrioventricular valve regurgitation in 19 patients (45%), atrioventricular valve index of 0.67 (0.56-0.79), left ventricular end-diastolic volume z score of 4.46 (1.96-7.78), and aortic valve diameter z score of -0.70 (-1.91 to 0.20). Multivariable regression analysis revealed that preoperative pulmonary vascular resistance was significantly correlated to gestational age (p = 0.002), and that preoperative pulmonary arterial compliance was significantly correlated to gestational age (p = 0.009) and Down syndrome (p = 0.036). The pulmonary circulation does not depend upon the presence of left heart lesions but gestational age and Down syndrome in infants with complete atrioventricular septal defect.

Pulmonary Hypertension, Cor Pulmonale, and other Pulmonary Vascular Conditions

This review covers the diseases that affect the pulmonary vasculature directly. These conditions include pulmonary hypertension; pulmonary arterial hypertension; chronic thromboembolic pulmonary hypertension; pulmonary hypertension attributed to left heart disease, lung disease and/or hypoxemia, and other disorders; cor pulmonale; pulmonary atriovenous malformations; and pulmonary aneurysms. Figures show changes in the pulmonary vasculature in pulmonary hypertension, pathways involved in the development of pulmonary hypertension, general guidelines for the evaluation of suspected pulmonary hypertension, enlarged proximal pulmonary arteries with pruning of distal pulmonary vasculature (typical of advanced pulmonary arterial hypertension), the remodeling of the heart and continuous-wave Doppler study results observed with chronic pulmonary hypertension, ventilation and perfusion scans of the lungs with results typical of chronic thromboembolic pulmonary hypertension, and a general approach to the treatment of patients with pulmonary arterial hypertension. Tables list the revised nomenclature and classification of pulmonary hypertension, the World Health Organization classification of functional capacity in patients with pulmonary hypertension, advanced vascular medications for pulmonary artery hypertension, and perioperative management of pulmonary arterial hypertension. This review contains 8 highly rendered figures, 4 tables, and 118 references.

Síndrome hepatopulmonar en la era del trasplante hepático

The most common pulmonary complication of liver disease is the disruption of gas exchange, resulting in severe hypoxemia, a factor that alters the clinical course of patients with liver cirrhosis. One of these alterations is the hepatopulmonary syndrome, which is associated with a significant increase in morbidity and mortality, and is defined as a triad that includes liver disease, abnormal arterial oxygenation caused by demonstrable intrapulmonary vascular dilations, with consequent pulmonary shunt, and imbalance in diffusion and perfusion. An abnormal increase in pulmonary vascular resistance may also be found as a consequence of pulmonary arteriolar flow obstruction, resulting in clinical pulmonary hypertension called “portopulmonary hypertension”. This resembles primary pulmonary hypertension, with dyspnoea and fatigue, but without clinical or histopathological responses to therapies such as prostacyclin. These two pulmonary vascular conditions (hepatopulmonary syndrome and portopulmonary hypertension) in cirrhotic patients, or with portal hypertension, may coexist in the same patient, and hepatopulmonary syndrome usually develops before portopulmonary hypertension.Hepatopulmonary syndrome is thought to be mainly caused by two central processes: vasodilation and pulmonary angiogenesis, which are responsible for alterations in gas exchange, imbalance in ventilation-perfusion, and limitation of oxygen diffusion.This syndrome has currently become of special interest in the success of liver transplantation. Although it is rare, it is important to rapidly recognise its clinical expression in order to understand the pathogenesis involved in the patient with clinical, functional, and histological liver cirrhosis, given its progressive course and poor prognosis.

Pulmonary Hypertension, Cor Pulmonale, and other Pulmonary Vascular Conditions

This review covers the diseases that affect the pulmonary vasculature directly. These conditions include pulmonary hypertension; pulmonary arterial hypertension; chronic thromboembolic pulmonary hypertension; pulmonary hypertension attributed to left heart disease, lung disease and/or hypoxemia, and other disorders; cor pulmonale; pulmonary atriovenous malformations; and pulmonary aneurysms. Figures show changes in the pulmonary vasculature in pulmonary hypertension, pathways involved in the development of pulmonary hypertension, general guidelines for the evaluation of suspected pulmonary hypertension, enlarged proximal pulmonary arteries with pruning of distal pulmonary vasculature (typical of advanced pulmonary arterial hypertension), the remodeling of the heart and continuous-wave Doppler study results observed with chronic pulmonary hypertension, ventilation and perfusion scans of the lungs with results typical of chronic thromboembolic pulmonary hypertension, and a general approach to the treatment of patients with pulmonary arterial hypertension. Tables list the revised nomenclature and classification of pulmonary hypertension, the World Health Organization classification of functional capacity in patients with pulmonary hypertension, advanced vascular medications for pulmonary artery hypertension, and perioperative management of pulmonary arterial hypertension. This review contains 8 highly rendered figures, 4 tables, and 118 references.

Measurement of Pulmonary Flow Reserve and Pulmonary Index of Microcirculatory Resistance for Detection of Pulmonary Microvascular Obstruction

BackgroundThe pulmonary microcirculation is the chief regulatory site for resistance in the pulmonary circuit. Despite pulmonary microvascular dysfunction being implicated in the pathogenesis of several pulmonary vascular conditions, there are currently no techniques for the specific assessment of pulmonary microvascular integrity in humans. Peak hyperemic flow assessment using thermodilution-derived mean transit-time (Tmn) facilitate accurate coronary microcirculatory evaluation, but remain unvalidated in the lung circulation. Using a high primate model, we aimed to explore the use of Tmn as a surrogate of pulmonary blood flow for the purpose of measuring the novel indices Pulmonary Flow Reserve [PFR = (maximum hyperemic)/(basal flow)] and Pulmonary Index of Microcirculatory Resistance [PIMR = (maximum hyperemic distal pulmonary artery pressure)×(maximum hyperemic Tmn)]. Ultimately, we aimed to investigate the effect of progressive pulmonary microvascular obstruction on PFR and PIMR.Methods and ResultsTemperature- and pressure-sensor guidewires (TPSG) were placed in segmental pulmonary arteries (SPA) of 13 baboons and intravascular temperature measured. Tmn and hemodynamics were recorded at rest and following intra-SPA administration of the vasodilator agents adenosine (10–400 µg/kg/min) and papaverine (3–24 mg). Temperature did not vary with intra-SPA sensor position (0.010±0.009 v 0.010±0.009°C; distal v proximal; p = 0.1), supporting Tmn use in lung for the purpose of hemodynamic indices derivation. Adenosine (to 200 µg/kg/min) & papaverine (to 24 mg) induced dose-dependent flow augmentations (40±7% & 35±13% Tmn reductions v baseline, respectively; p<0.0001). PFR and PIMR were then calculated before and after progressive administration of ceramic microspheres into the SPA. Cumulative microsphere doses progressively reduced PFR (1.41±0.06, 1.26±0.19, 1.17±0.07 & 1.01±0.03; for 0, 104, 105 & 106 microspheres; p = 0.009) and increased PIMR (5.7±0.6, 6.3±1.0, 6.8±0.6 & 7.6±0.6 mmHg.sec; p = 0.0048).ConclusionsThermodilution-derived mean transit time can be accurately and reproducibly measured in the pulmonary circulation using TPSG. Mean transit time-derived PFR and PIMR can be assessed using a TPSG and adenosine or papaverine as hyperemic agents. These novel indices detect progressive pulmonary microvascular obstruction and thus have with a potential role for pulmonary microcirculatory assessment in humans.

Inhibition of eicosanoids does not prevent neutrophil injury from phorbol in isolated rabbit lung

Studies suggest that pulmonary and neutrophil cyclooxygenase and lipoxygenase products (i.e., eicosanoids) play a role in oxidant lung injury. We tested the hypothesis that such eicosanoids contribute to lung injury from activation of rabbit neutrophils by phorbol myristate acetate (PMA) in the pulmonary circulation of salt-perfused isolated rabbit lung preparations. We measured lung injury from PMA-activated neutrophils under zone 2 pulmonary vascular conditions with transvascular albumin flux by 125I-labeled albumin. We found that this flux was increased; catalase prevented the increase, confirming that the increase was from oxidant injury. However, results were inconsistent: about one-half of the preparations showed a marked increase and about one-half were not elevated. In preparations with a > 40-mmHg increase in pulmonary arterial pressure (Ppa), albumin flux increased, and in those with Ppa < 40 mmHg it did not. In those with Ppa > 40 mmHg, vascular volume, and presumably vascular surface area, was markedly reduced. We next studied PMA-activated neutrophils under zone 3 pulmonary vascular conditions in preparations with Ppa that increased < 40 mmHg. Albumin flux or filtration coefficient (Kf,c) was used to measure injury. Both were elevated. As with albumin flux, catalase prevented increases in Kf,c. BW-755C (a dual lipoxygenase and cyclooxygenase inhibitor) prevented increases in cyclooxygenase products and leukotriene B4 (a lipoxygenase product) but did not prevent increases in Kf,c. We conclude that a marked decrease in vascular volume can occur in zone 2 preparations and may mask the presence of injury as measured by transvascular albumin flux. A zone 3 vascular condition overcomes the vasoconstrictor-induced decrease in surface area and unmasks injury. Finally, oxidant injury from PMA-stimulated rabbit neutrophils in isolated rabbit lungs cannot be readily attributed to formation of eicosanoids.