Altered Pulmonary Hemodynamics Research Articles

Right Ventricular Subclinical Dysfunction as a Predictor of Postoperative Adverse Clinical Outcomes in Patients with Femoral Fracture.

Femoral fractures often lead to complications such as altered pulmonary hemodynamics. Right ventricular global longitudinal strain (RV GLS), which correlates with pulmonary hemodynamics, indicates the subclinical function of the right ventricle (RV). This study aimed to investigate the predictive value of RV GLS for the risk of adverse clinical composite outcomes in patients with femoral fractures. Data were obtained from a prospective single-center cohort of patients hospitalized for femoral fractures and followed up for at least 1 year between March 2021 and October 2022. The primary outcome was the development of an adverse composite clinical event, which included pneumonia, pulmonary oedema or effusion, pulmonary thromboembolism, and all-cause mortality within the 1-year period following surgery. Among the 163 patients, 36 (22.09%) experienced adverse composite clinical events during 1-year follow-up. The adverse outcome group demonstrated poorer RV GLS and RV free wall strain values than the non-adverse outcome group. The optimal cut-off value of RV GLS for predicting composite adverse clinical events was -12.55%. The cumulative composite event-free survival rate was significantly lower in the RV GLS ≥ -12.55% group (log-rank p-value = 0.003). After adjusting for confounding factors, multivariate Cox proportional hazards regression analyses showed that RV GLS ≥ -12.55% independently increased the risk of composite adverse clinical events by 2.65-fold. Poor RV GLS is a significant predictor of adverse clinical outcomes in patients with femoral fractures. Specifically, an RV GLS value of ≥ -12.55% indicated a substantially increased risk of adverse events.

The importance of pulmonary pulse transit time in indicating right ventricular dysfunction and pulmonary arterial stiffness in rheumatoid arthritis.

Rheumatoid arthritis patients are at risk of developing cardiovascular disease such as right heart failure and pulmonary hypertension (PH). Arterial stiffness can be used to assess pulmonary hemodynamics. Noninvasive approaches can also be used to assess pulmonary hemodynamics. Recently, there have been reports that pulmonary pulse transit time (PPTT) may also be a useful measure. This study aims to examine the effects of pulmonary hemodynamic alterations on PPTT in RA patients. Forty RA patients and 40 healthy controls were included in the study. Sociodemographic characteristics, laboratory data, and echocardiographic examinations were performed in both groups. Conventional echocardiographic examination included left and right ventricular systolic and diastolic diameters, right ventricular myocardial performance index (RVMPI), right ventricular diastolic function, estimated pulmonary artery systolic pressure (sPAP), tricuspid annular plane systolic excursion (TAPSE), pulmonary artery stiffness (PAS), and PPTT. Right ventricular diastolic and systolic volumes, right ventricular ejection fraction (RVEF), and right ventricular fractional area change (RVFAC) were determined by four-dimensional echocardiography (4DE). There was no difference between the sPAP values of the patients. RVMPI and PAS were increased in RA patients compared with controls. The PPTT was shortened in RA patients and correlated with RVEF, RVFAC, RVMPI, TAPSE/sPAP, disease duration, and C-reactive protein (CRP). In univariate linear regression analysis, PPTT (p < .001) was thought to be an independent predictor of PAS. RVFAC, disease duration, and PAS were also independent predictors of PPTT. In RA patients, PPTT may be the first evidence of early abnormalities in pulmonary vascular hemodynamics. PPTT and PAS are the values that may predict each other in RA patients. Due to its more practical application, PPTT can be used instead of PAS to assess pulmonary hemodynamics.

Eliminating Senescent Cells Can Promote Pulmonary Hypertension Development and Progression.

Senescent cells (SCs) are involved in proliferative disorders, but their role in pulmonary hypertension remains undefined. We investigated SCs in patients with pulmonary arterial hypertension and the role of SCs in animal pulmonary hypertension models. We investigated senescence (p16, p21) and DNA damage (γ-H2AX, 53BP1) markers in patients with pulmonary arterial hypertension and murine models. We monitored p16 activation by luminescence imaging in p16-luciferase (p16LUC/+) knock-in mice. SC clearance was obtained by a suicide gene (p16 promoter-driven killer gene construct in p16-ATTAC mice), senolytic drugs (ABT263 and cell-permeable FOXO4-p53 interfering peptide [FOXO4-DRI]), and p16 inactivation in p16LUC/LUC mice. We investigated pulmonary hypertension in mice exposed to normoxia, chronic hypoxia, or hypoxia+Sugen, mice overexpressing the serotonin transporter (SM22-5-HTT+), and rats given monocrotaline. Patients with pulmonary arterial hypertension compared with controls exhibited high lung p16, p21, and γ-H2AX protein levels, with abundant vascular cells costained for p16, γ-H2AX, and 53BP1. Hypoxia increased thoracic bioluminescence in p16LUC/+ mice. In wild-type mice, hypoxia increased lung levels of senescence and DNA-damage markers, senescence-associated secretory phenotype components, and p16 staining of pulmonary endothelial cells (P-ECs, 30% of lung SCs in normoxia), and pulmonary artery smooth muscle cells. SC elimination by suicide gene or ABT263 increased the right ventricular systolic pressure and hypertrophy index, increased vessel remodeling (higher dividing proliferating cell nuclear antigen-stained vascular cell counts during both normoxia and hypoxia), and markedly decreased lung P-ECs. Pulmonary hemodynamic alterations and lung P-EC loss occurred in older p16LUC/LUC mice, wild-type mice exposed to Sugen or hypoxia+Sugen, and SM22-5-HTT+ mice given either ABT263 or FOXO4-DRI, compared with relevant controls. The severity of monocrotaline-induced pulmonary hypertension in rats was decreased slightly by ABT263 for 1 week but was aggravated at 3 weeks, with loss of P-ECs. Elimination of senescent P-ECs by senolytic interventions may worsen pulmonary hemodynamics. These results invite consideration of the potential impact on pulmonary vessels of strategies aimed at controlling cell senescence in various contexts.

Mild pulmonary hemodynamic alterations in patients with systemic sclerosis: relevance of the new 2022 ESC/ERS definition of pulmonary hypertension and impact on mortality

Background and objectiveThe definition of pre-capillary pulmonary hypertension (PH) has been modified, with lowering of the mean pulmonary arterial pressure (mPAP) threshold from 25 to 20 mmHg and addition of a mandatory criterion of pulmonary vascular resistance (PVR) ≥ 2 Wood units (WU). Our objectives were: 1/ to estimate the proportion of patients reclassified as having pre-capillary PH when using the new 2022 ESC/ERS hemodynamic criteria (i.e. mPAP 21-24 mmHg and PVR ≥ 2 WU), and to describe their clinical characteristics and outcome; and 2/ to study the relationship between PVR and survival in patients with mPAP > 20 mmHg.MethodsWe retrospectively analyzed consecutive SSc patients included in our National Reference Center for a first right-heart catheterization between 2003 and 2018. The association between survival and PVR was studied using smoothing splines.ResultsWe included 126 SSc patients with mPAP > 20 mmHg. Among them, 16 (13%) had a baseline mPAP value between 21 and 24 mmHg and PVR ≥ 2 mmHg and were reclassified as pre-capillary PH; 10 of which (62%) raised their mPAP ≥ 25 mmHg during follow-up. In patients with mPAP > 20 mmHg, we observed a linear relation between PVR and mortality for values < 6 WU.ConclusionA significant proportion of SSc patients is reclassified as having pre-capillary PH with the new 2022 ESC/ERS hemodynamic definition. Lowering the PVR threshold from 3 to 2 WU captures patients at risk of raising their mPAP > 25 mmHg, with a possibly less severe disease.

Right ventricular dysfunction and right ventricular-arterial uncoupling at admission increase the in-hospital mortality in patients with COVID-19 disease.

BackgroundCoronavirus disease 2019 (COVID‐19) frequently involves cardiovascular manifestations such as right ventricular (RV) dysfunction and alterations in pulmonary hemodynamics. We evaluated the application of the critical care ultrasonography ORACLE protocol to identify the most frequent alterations and their influence on adverse outcomes, especially those involving the RV (dilatation and dysfunction).MethodsThis cross‐sectional study included 204 adult patients with confirmed COVID‐19 admitted at three centers. Echocardiography and lung ultrasound images were acquired on admission using the ORACLE ultrasonography algorithm.ResultsTwo‐hundred and four consecutive patients were evaluated: 22 (11.9%) demonstrated a fractional shortening of < 35%; 33 (17.1%) a tricuspid annular plane systolic excursion (TAPSE) of < 17 mm; 26 (13.5%) a tricuspid peak systolic S wave tissue Doppler velocity of < 9.5 cm/sec; 69 (37.5%) a RV basal diameter of > 41 mm; 119 (58.3%) a pulmonary artery systolic pressure (PASP) of > 35 mm Hg; and 14 (11%) a TAPSE/PASP ratio of < .31. The in‐hospital mortality rate was 37.6% (n = 71). Multiple logistic regression modeling showed that PASP > 35 mm Hg, RV FS of < 35%, TAPSE < 17 mm, RV S wave < 9.5, and TAPSE/PASP ratio < .31 mm/mm Hg were associated with this outcome. PASP and the TAPSE/PASP ratio had the lowest feasibility of being obtained among the investigators (62.2%).ConclusionThe presence of RV dysfunction, pulmonary hypertension, and alteration of the RV–arterial coupling conveys an increased risk of in‐hospital mortality in patients presenting with COVID‐19 upon admission; therefore, searching for these alterations should be routine. These parameters can be obtained quickly and safely with the ORACLE protocol.

Pulmonary Hypertension in COVID-19 Pneumoniae: It Is Not Always as It Seems

COVID-19 patients, even if previously well, can have pulmonary hypertension due to other causes.The cause of pulmonary hypertension should always be sought and not assumed, even in COVID-19 patients.

Degree of Portal and Systemic Hemodynamic Alterations Predict Recurrent AKI and Chronic Kidney Disease in Patients With Cirrhosis.

The relevance of hemodynamic derangements on the incidence of recurrent acute kidney injury (AKI) and chronic kidney disease (CKD) in patients with cirrhosis is largely unknown. Consecutive patients with cirrhosis with a complete record of baseline hemodynamics were followed for identifying risk factors for the development of recurrent AKI and CKD by using negative binomial regression and competing risk analysis, respectively. Consecutive patients with cirrhosis (n = 2013, age 50.1 ± 11.8 years, 80% male, Child A:B:C percentage 13.7:52.9:33.4, and mean Child‐Turcotte‐Pugh score 8.6 ± 1.8) were enrolled, 893 (44.3%) of whom received beta‐blockers, with 44.2% responders. Prior AKI was noted in 12.4% at enrollment. At a median follow‐up of 379 (interquartile range: 68‐869) days, AKI developed at a rate of 0.37 episodes per person‐year, and 26% patients developed CKD. A lower mean number of AKI episodes (0.05 ± 0.25 vs. 0.42 ± 0.868; P < 0.001), CKD (subdistribution hazard ratio 0.74 [0.54‐1.02]), and mortality (hazard ratio 0.21 [0.06‐0.73]) were observed in beta‐blocker responders. Albuminuria was an independent risk factor for recurrent AKI, CKD, and mortality (P < 0.05). Lower systemic vascular resistance index predicted hemodynamic response (odds ratio 2.04 [1.29‐3.22]), cumulative AKI episodes (ratio of means 0.10 [0.08‐0.14]), and development of CKD (subdistribution hazard ratio 0.70 [0.58‐0.83]). Higher hepatic venous pressure gradient (≥17 mm Hg) predicted AKI episodes (ratio of means 1.76 [1.32‐2.35]) but not CKD. Conclusion: High portal pressure and severe vasodilatation predispose patients with cirrhosis to repeated AKI episodes and development of CKD. Response to beta‐blockers and therapies targeting the vasodilatory state could prevent frequent AKI and the risk of CKD development. Albuminuria could serve as an early marker of renal dysfunction in patients with cirrhosis.

Relationship Between Lung Diffusion And Exercise Capacity In Heart Failure With Preserved Ejection Fraction

PURPOSE: Patients with heart failure with preserved ejection fraction (HFpEF) have impaired lung diffusion (DL) at rest and during exercise which may contribute to a reduced exercise capacity. However, it is unclear whether these impairments are solely due to alterations in pulmonary hemodynamics or related to other cardiopulmonary factors which may impair oxygen uptake such as the inability to recruit lung surface area. Therefore this study examined simultaneous measurements of DL for carbon monoxide (DLCO) and nitric oxide (DLNO), which allows for partitioning of DL into its alveolar-capillary membrane (Dm) and pulmonary capillary blood volume (Vc) components, to better understand the relationship between exertional changes in lung diffusion and exercise capacity. METHODS: HFpEF patients (N=17, age=62±9y, BMI=36±8kg/m2) undergoing exercise right heart catheterization performed simultaneous rebreathe DLCO/NO tests at rest and during each stage of incremental supine cycling exercise, and membrane conductance (Dm) and pulmonary capillary blood volume (Vc) were calculated. Breath-by-breath pulmonary gas exchange was recorded throughout rest and exercise. RESULTS: All patients were hemodynamically diagnosed with HFpEF (pulmonary capillary wedge pressure >15 at rest and/or >25 mmHg during exercise). Overall lung and alveolar-capillary membrane diffusion increased from rest to peak exercise (DLCO: 11.8±4.0 to 16.2±7.4 ml/min/mmHg, DLNO: 33.1±11.5 to 48.4±21.9 ml/min/mmHg, Dm: 18.9±7.2 to 28.3±13.1 ml/min/mmHg; p’s<0.01). The change in DL was related to exercise capacity (change in DLCO vs. peak VO2: R=0.69, p<0.01, change in DLNO vs. peak VO2: R=0.65, p<0.01) and this was primarily driven by changes in Dm (change in Dm vs. peak VO2: R=0.63, p<0.01) but not Vc (change in Vc vs. peak VO2: R=0.15, p=0.582). CONCLUSIONS: These data highlight that a limited increase in lung diffusion and alveolar-capillary membrane conductance during exercise are associated with a lower VO2 peak in HFpEF patients. In addition to hemodynamic constraints previously reported in HFpEF, an inability to recruit lung surface area during exercise may also contribute to the reduced exercise capacity in these patients.

Serial pulmonary vascular resistance assessment in patients late after ventricular septal defect repair

BackgroundThe long-term evolution of pulmonary vascular resistance (PVR) after ventricular septal defect (VSD) repair is unknown. This study serially evaluated resting and exercise PVR after VSD repair in childhood. MethodsPatients were enrolled from the outpatient Adult Congenital Heart Disease clinic of the University Hospitals Leuven and compared to age- and gender-matched controls. Participants underwent resting and exercise echocardiography and cardiopulmonary exercise testing at baseline and follow-up. Total PVR was calculated as the ratio of mean pulmonary artery pressure (mPAP) to cardiac output (CO). The slope of the mPAP-CO curve (exercise PVR) was obtained using linear regression analysis. ResultsTwenty-seven patients (mean age 31 ± 7 years, 70% male) and 18 controls were included. At baseline, patients had larger right ventricular (RV) end-diastolic areas (10 ± 2 vs 9 ± 1 cm2/m2, p = 0.001) and lower tricuspid annular plane systolic excursion (TAPSE) (17 (17–19) vs 26 (22–28) mm, p < 0.001). After 1.1 (1.0–1.5) years follow-up, similar differences in RV areas and TAPSE were found. Patients reached lower peak workload and cardiac index compared to controls at each time point. Peak total PVR was higher (Baseline: 2.7 ± 0.8 vs 2.2 ± 0.3 mm Hg/L/min, p = 0.005; Follow-up: 2.9 ± 0.9 vs 2.1 ± 0.3 mm Hg/L/min, p < 0.001) and the mPAP-CO slope was steeper (Baseline: 2.2 ± 0.8 vs 1.7 ± 0.3 mm Hg/L/min, p = 0.008; Follow-up: 2.5 ± 0.9 vs 1.6 ± 0.3 mm Hg/L/min, p < 0.001) in patients. The mPAP-CO slope in patients correlated inversely with peak oxygen uptake (R = −0.41 and − 0.45, p = 0.036 and 0.022, baseline and follow-up, respectively). ConclusionDespite repair, VSD patients seem to show altered pulmonary hemodynamics and RV impairment at rest and exercise, supporting life-long follow-up.

Role of pulmonary hemodynamics in determining 6-minute walk test result in atrial septal defect: an observational study

BackgroundThe presence of altered pulmonary hemodynamics in adult patients with atrial septal defect (ASD) is common. However, there are no observational studies which evaluate the impact of altered pulmonary hemodynamics on the 6-min walk test (6MWT) result. This study aimed to investigate the role of pulmonary hemodynamics in determining 6MWT result of patients with ASD.MethodForty-six consecutive adult patients with ASD were included in this study. Right heart catheterization was performed to obtain the pulmonary hemodynamics profile. Meanwhile, 6MWT was presented as high or low with cut-off point 350 m. Receiver operating characteristic (ROC) was used for analytical methods.ResultAbnormal functional capacity was indicated by ROC result of mPAP cut-off value of > 24 mmHg (p = 0.0243; AUC = 0.681). The value of PVR > 3.42 woods unit (WU) showed high specificity in determining abnormal functional capacity (p = 0.0069; AUC = 0.713). Flow ratio with cut-off point ≤4.89 had the highest sensitivity (100%) (p = 0.8300; AUC = 0.520).ConclusionPulmonary hemodynamics can serve as an indicator of 6MWT result in adult ASD patients with values of mPAP> 24 mmHg and PVR > 3.42 WU.

Right ventricular strain as predictor of pulmonary complications in patients with femur fracture.

SummaryBackground:Following femur fracture, medullary fat enters the systemic circulation and altered pulmonary haemodynamics may contribute to pulmonary complications. This study evaluated the association between right ventricular (RV) function and pulmonary complications in patients with femur fracture.Methods:Patients with a femur fracture who had undergone pre-operative echocardiography that included RV peak global longitudinal strain (RV GLS) were evaluated retrospectively between March 2015 and February 2016. Pulmonary complications were defined as the development of pneumonia or pulmonary thromboembolism during the first postoperative month.Results:Among 78 patients, pulmonary complications developed in eight (10.3%). The RV GLS value of all patients was lower than the normal range. In addition, the RV GLS value of patients with pulmonary complications was significantly lower than that of patients without pulmonary complications. Multivariate regression analyses found that worse RV GLS values independently predicted pulmonary complications [odds ratio (OR) 2.09, 95% confidence interval (CI) 1.047–4.151, p = 0.037]. Receiver operating characteristic curve analysis found that a RV GLS value of –14.85% was the best cut-off value to predict pulmonary complications; sensitivity: 75.0%; specificity: 62.9%. Moreover, patients with RV GLS values > –14.85% had significantly lower pulmonary complication-free survival.Conclusions:In patients with femur fracture, RV GLS values could help predict pulmonary complications. Therefore, patients with RV GLS values > –14.85 should be monitored closely before and after surgery for femur fracture.

Reliability of echocardiographic speckle-tracking derived bi-atrial strain assessment under different hemodynamic conditions

The aim of this study was to assess intra- and inter-observer variability of left (LA) and right atrial (RA) strain indices obtained by two-dimensional speckle-tracking echocardiography (2D-STE) in a healthy group of individuals at low-altitude and after rapid ascent to high-altitude in order to provoke altered systemic and pulmonary hemodynamics otherwise seen in various cardiac diseases. Twenty healthy subjects underwent transthoracic echocardiography during a baseline examination at low-altitude (424 m) as well as 7, 20 and 44 h after arrival at high-altitude (4559 m). Atrial strain indices (i.e. reservoir, conduit and contractile strain) were determined off-line by two independent observers. Intra- and inter-observer reproducibility of variables was assessed by intra-class correlation coefficients (ICCs), coefficients of variation and Bland Altman plots. Heart rate, systemic blood pressure and pulmonary artery pressure increased significantly from low-altitude to the first examination at high-altitude. Intra-observer ICCs were ≥0.90 except for RA conduit strain with an ICC of 0.86. The mean intra-observer differences were small and limits of agreement of relative differences were narrow for all atrial strain parameters (<3 and <16%, respectively). Inter-observer ICCs (0.80–0.90), mean biases and limits of agreement (<4 and <20%, respectively) were greater than intra-observer results for all parameters. Intra- and inter-obserer ICCs for all atrial strain variables did not differ between low- and high-altitude. 2D-STE-derived bi-atrial strain indices have excellent intra- and moderate inter-observer reproducibility with no effect of high-altitude-induced hemodynamic changes on reliability results.

Delayed Microvascular Shear Adaptation in Pulmonary Arterial Hypertension. Role of Platelet Endothelial Cell Adhesion Molecule-1 Cleavage.

Altered pulmonary hemodynamics and fluid flow-induced high shear stress (HSS) are characteristic hallmarks in the pathogenesis of pulmonary arterial hypertension (PAH). However, the contribution of HSS to cellular and vascular alterations in PAH is unclear. We hypothesize that failing shear adaptation is an essential part of the endothelial dysfunction in all forms of PAH and tested whether microvascular endothelial cells (MVECs) or pulmonary arterial endothelial cells (PAECs) from lungs of patients with PAH adapt to HSS and if the shear defect partakes in vascular remodeling in vivo. PAH MVEC (n = 7) and PAH PAEC (n = 3) morphology, function, protein, and gene expressions were compared with control MVEC (n = 8) under static culture conditions and after 24, 72, and 120 hours of HSS. PAH MVEC showed a significantly delayed morphological shear adaptation (P = 0.03) and evidence of cell injury at sites of nonuniform shear profiles that are critical loci for vascular remodeling in PAH. In clear contrast, PAEC isolated from the same PAH lungs showed no impairments. PAH MVEC gene expression and transcriptional shear activation were not altered but showed significant decreased protein levels (P = 0.02) and disturbed interendothelial localization of the shear sensor platelet endothelial cell adhesion molecule-1 (PECAM-1). The decreased PECAM-1 levels were caused by caspase-mediated cytoplasmic cleavage but not increased cell apoptosis. Caspase blockade stabilized PECAM-1 levels, restored endothelial shear responsiveness in vitro, and attenuated occlusive vascular remodeling in chronically hypoxic Sugen5416-treated rats modeling severe PAH. Delayed shear adaptation, which promotes shear-induced endothelial injury, is a newly identified dysfunction specific to the microvascular endothelium in PAH. The shear response is normalized on stabilization of PECAM-1, which reverses intimal remodeling in vivo.

SHAPE OF THE RIGHT VENTRICULAR OUTFLOW TRACT DOPPLER ENVELOPE IS A SENSITIVE PREDICTOR OF ALTERED PULMONARY HEMODYNAMICS IN PEDIATRIC PATIENTS

The shape of the RV outflow tract (RVOT) Doppler velocity envelope (DVE) has been shown to be a sensitive marker of altered pulmonary hemodynamics in adults, but this has not been validated in children. Systolic deceleration or ‘‘notching’’ of the RVOT DVE relates to the pathologic wave

Cerebral fat embolism after bone fractures

After a forklift accident, a 44-year-old man was admitted to our hospital in July, 2014, with fractures of the right fi bula and tibia, the left femur, and the pelvis. A proximal femoral nail antirotation was done to stabilise the left femur. 1 h after the operation, he developed acute respiratory failure, requiring reintubation and admission to the intensive care unit. CT angiography of the thorax showed bilateral ground-glass opacities and distinct nodular opacities (fi gure), without pulmonary embolism or aspiration. Despite intensive mechanical ventilation, severe hypoxaemia persisted (partial pressure of blood oxygen 6·7 kPa; normal range 11–13 kPa). We started antibiotic therapy because he had fever and tachycardia. 4 days later, we stopped sedative medication to allow neurological assessment, which showed he had a Glasgow Coma Scale score of 3. He developed axillar and inguinal petechiae, so 10 days after surgery we did MRI of the brain, which showed bilateral confl uent white matter abnormalities with diff usion restriction (fi gure). This pattern of cytotoxic cerebral oedema, with lesions in the white matter rather than the grey matter, is indicative of the subacute stage of fat embolism (5–14 days after an embolic event). Electro encepha lography showed diff use encephalopathy. On the basis of acute respiratory failure, petechiae in non-dependent areas, and typical fi ndings on MRI, we diagnosed cerebral fat embolism syndrome. Cardiographic imaging showed no evidence of a patent foramen ovale or rightto-left shunt. We continued supportive care, and 16 days after surgery the patient was extubated following respiratory and neurological recovery. At the end of August, 2014, our patient was transferred to a neurorehabilitation centre. The clinical triad of respiratory failure, unconsciousness, and petechiae observed in cerebral fat embolism syndrome is a direct consequence of mobilisation of bone marrow. The syndrome typically results from fractures of the pelvis and long bones, or fracture stabilisation with intramedullary devices. After trauma, medullary fat enters the circulation and can embolise to the lung. Altered pulmonary haemodynamics and the systemic infl ammatory reaction to trauma are thought to contribute to acute respiratory failure. The pliable nature of the fat emboli allows subsequent passage through the pulmonary capillaries with systemic embolisation to the skin and brain, causing petechiae and cerebral ischaemia with neurological symptoms. Although cerebral fat embolism is a clinical diagnosis, MRI showing a starfi eld pattern of scattered spot lesions with diff usion restriction in the acute phase (1–4 days) or confl uent cytotoxic cerebral oedema in periventricular and subcortical white matter in the subacute phase (5–14 days), supports the diagnosis.

Dual-energy CT pulmonary angiography in patients with suspected pulmonary embolism: value for the detection and quantification of pulmonary venous congestion.

To evaluate if vascular and pulmonary parenchymal enhancement values in dual-energy (DE) CT pulmonary angiography (CTPA) can suggest the diagnosis of pulmonary congestion. DE-CTPA images of 90 out of 1321 patients negative for pulmonary embolism showed signs of congestive heart failure. We measured DE-derived pulmonary parenchymal [perfused blood volume (PBV)], pulmonary artery (PA) and left atrium (LA) enhancement values in these patients and in 142 control patients. Enhancement values were compared between the populations and correlated with serum values of B-type natriuretic peptide (BNP) and proBNP, where available. No significant difference of PBV but significant differences of mean PA and LA enhancement and individual enhancement differences (PA - LA) were found between the populations. PA - LA was higher in patients with elevated BNP and proBNP and was positively correlated with these values. Receiver operating characteristic analysis revealed a moderate discriminatory power of the PA - LA difference for the presence of cardiac biomarker elevations. PBV in DE-CTPA is not altered in patients with signs of congestive heart failure. However, differences in enhancement values in the pre- and post-pulmonary vessels were found in comparison with the control population. Altered pulmonary vascular haemodynamics in pulmonary venous congestion are not reflected in dual-energy-derived PBV maps. In the diagnosis of left heart failure in patients with chest pain and dyspnoea, density measurements in the pulmonary artery and in the left atrium in CTPA images may be a helpful diagnostic tool.

TCT-731 TRANSCATHETER AORTIC VALVE IMPLANTATION (TAVI) REDUCES SYMPATHETIC ACTIVITY AND NORMALIZES ARTERIAL SPONTANEOUS BAROREFLEX IN PATIENTS WITH AORTIC STENOSIS

BACKGROUND: In patients with aortic stenosis, reduced cardiac output or altered pulmonary hemodynamics may increase sympathetic nerve activity. However, the magnitude of the increase in sympathetic...

Heat Shock Protein -70 (HSP- 70) A Novel Surrogate Marker for Hypoxia Induced Liver Injury (HILI): A Prospective Open Label Control Clinical Pilot Study

Purpose: Hypoxic hepatopathy (HH) is a common entity in hospital with impaired hepatic perfusion secondary to transient altered cardio pulmonary hemodynamics, manifesting with sharp rise of transaminases with perfusion injury rarely requiring transplantation. Transaminases are non-specific index of reperfusion injury (IR). HSP are reperfusion signal proteins represent sheer-stress. HSP -70 is one of specific signals of IR impacts on specific target. This study evaluates the utility of a novel marker of HILI. Methods: Sixty (n=60) patients were recruited from Hospital. Group A control (n=20) Group B (n=20) HILI, Group C (n=20) Acute Hepatitis [(Tylenol 8/20 (40%), Acute hepatitis B8/20 (40%) herpes simplex 1/20 (5%) EBV 1/20 (5%) acute hepatitis A 1/20 (5%) unknown 1/20 (5%). All groups underwent serial blood levels of HSP70, Liver and renal functions, MELD score, SOFA score, from day 0, 4,7 and 10. Exclusion; Cardio respiratory failure, renal failure, acute alcoholic hepatitis, sepsis, organ transplant hemolytic syndromes, CVA, MELD > 20, MAP< 90. Results: Group A; HSP 70 was normal. Group B was intermediate on day 0 and very high on day 4, 7 and reverting back to lower levels on day 10. Group C had a low level (mildly elevated) of HSP-70 on all days with the exception of the Tylenol group where it was intermediate levels. View Table - Results.Table: [332] ResultsConclusion: HSP -70 is a relevant surrogate marker for hypoxia induced hepatopathy. HSP-70 levels strongly correlated with HILI and poorly with Tylenol induced liver injury. But negatively with other non-vascular liver injuries. Larger study needed to validate this finding.

Impact of pulmonary hemodynamics on 6-min walk test in idiopathic pulmonary fibrosis

Pulmonary hypertension (PH) has been associated with decreased functional capacity in patients with advanced idiopathic pulmonary fibrosis (IPF). We aimed to evaluate the true impact of altered pulmonary hemodynamics on functional capacity in a cohort of patients with IPF. Between January 1990 and December 2007, 124 patients [73M/51F; 111 Caucasians] with IPF underwent right heart catheterization and 6-min walk test (6MWT). Pulmonary arterial hypertension (PAH) was defined as mPAP≥25 and pulmonary artery occlusion pressure (PAOP)≤15mmHg, and Pre-PH as mPAP>20 and <25mmHg with PAOP<15mmHg. Demographic, hemodynamic, spirometric, and 6MWT data were collected. Fifty four (44%) patients had PH. There were no significant differences between the PH and the non-PH groups in measures of pulmonary function other than PaO(2). Patients with PH and PAH had significantly lower 6-min walk distance (6MWD) (p=0.008 and p=0.03 respectively) and distance saturation product (DSP) (p=0.002 and p=0.006 respectively) compared to non-PH patients. Mean pulmonary arterial pressure (mPAP) was the best predictor of 6MWD by multivariate analysis (p=0.0006). Increasing mPAP was associated with a statistically significant decline in 6MWD (p=0.02) and DSP (p=0.01). Patients with 'Pre-PH' had lower 6MWD compared to patients with mPAP≤20mmHg (p=0.07). Relative to measures of pulmonary function and hypoxia, altered pulmonary hemodynamics had a greater impact on 6MWD in patients with IPF. Higher mPAP was associated with more significant exercise impairment. Mild abnormalities in pulmonary hemodynamics (so called 'Pre-PH') were associated with reduced 6MWD.

PWE-269 Heat shock protein-70 (hsp-70) a novel surrogate marker for hypoxia induced liver injury (HILI)—a prospective open level control clinical pilot study

IntroductionHypoxic hepatopathy (HH) is a common entity in hospital with impaired hepatic perfusion secondary to transient altered cardio pulmonary haemodynamics, manifesting with sharp rise of transaminases with perfusion injury rarely...