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Norbert F Voelkel - One of the best experts on this subject based on the ideXlab platform.
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the need to recognize the pulmonary Circulation and the right ventricle as an integrated functional unit facts and hypotheses 2013 grover conference series
Pulmonary circulation, 2015Co-Authors: Norbert F Voelkel, Harm Jan Bogaard, Jose GomezarroyoAbstract:AbstractFor many patients with severe pulmonary arterial hypertension, heart failure—and, in particular, right heart failure—is the final chapter of their chronic illness. Targeted therapy for pulmonary hypertension is effective only if the right ventricular ejection fraction is maintained or improved. Because improvement of right heart function and reversal of right heart failure are treatment goals, it is important to investigate the cellular and molecular mechanisms that cause right heart failure. Here, we propose that right ventricular capillary rarefaction is an important hallmark of right heart failure and consider that the “sick Lung Circulation” and the pressure-overloaded right ventricle constitute a functional unit.
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The Sick Lung Circulation and the Failing Right Ventricle
The Right Ventricle in Health and Disease, 2014Co-Authors: Norbert F VoelkelAbstract:The global hypothesis proposed is that the health of the Lung Circulation affects the health and function of the right ventricle (RV). The activated, injured, and phenotypically altered cells of the vast Lung microCirculation emit signals and inform the downstream coronary microvasculature and the systemic vessels. Injured Lung endothelial cells can release microparticles-containing microRNA which can be taken up by coronary and systemic vessel endothelial cells. This mechanism can account in part for reprogramming—via altered gene expression—of recipient endothelium. In addition, there are inflammatory mediators, which after being released by sick Lung endothelial cells, activate distal systemic and coronary vessels, and cell-free double-stranded DNA, as found circulating in the plasma of patients with thromboembolic disease, can be toxic to distal vascular beds. Finally, inflammatory mediators and growth factors released from the sick Lung Circulation are likely participating in the release of precursor cells from the bone marrow which in turn can affect the behavior of the Lung- and coronary microvessels.
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The Right Ventricle in Chronic Lung Diseases
The Right Ventricle in Health and Disease, 2014Co-Authors: Norbert F Voelkel, Otto C. BurghuberAbstract:In this chapter the concept of the “sick Lung Circulation informing the heart” is applied to chronic Lung diseases. The concept of signals emanating from the injured Lung vessels—both precapillary and postcapillary—and influencing the performance of the right and left ventricle by inducing a myocardial microangiopathy, is discussed in the setting of COPD/emphysema, pulmonary fibrosis, and cystic fibrosis and the pertinent literature is reviewed. The concept is supported in COPD patients where right heart dysfunction can occur while significant pulmonary hypertension is absent. In patients with interstitial pulmonary fibrosis, the outcome is more closely related to the right ventricular function than to the pulmonary artery pressure, and there are reports that provide evidence in support of early right heart dysfunction in cystic fibrosis patients.
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Treatment for pulmonary arterial hypertension-associated right ventricular dysfunction.
Annals of the American Thoracic Society, 2014Co-Authors: Jose Gomez-arroyo, Norbert F Voelkel, Julio Sandoval, Marc A. Simon, Erick Dominguez-cano, Harm Jan BogaardAbstract:Pulmonary arterial hypertension (PAH) includes a heterogeneous group of diseases characterized by pulmonary vasoconstriction and remodeling of the Lung Circulation. Although PAH is a disease of the Lungs, patients with PAH frequently die of right heart failure. Indeed, survival of patients with PAH depends on the adaptive response of the right ventricle (RV) to the changes in the Lung Circulation. PAH-specific drugs affect the function of the RV through afterload reduction and perhaps also through direct effects on the myocardium. Prostacyclins, type 5 phosphodiesterase inhibitors, and guanylyl cyclase stimulators may directly enhance myocardial contractility through increased cyclic adenosine and guanosine monophosphate availability. Although this may initially improve cardiac performance, the long-term effects on myocardial oxygen consumption and function are unclear. Cardiac effects of endothelin receptor antagonists may be opposite, as endothelin-1 is known to suppress cardiac contractility. Because P...
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Pulmonary Hypertension and Right Ventricular Dysfunction in Chronic Lung Diseases: New Pathobiologic Concepts
Current Respiratory Medicine Reviews, 2012Co-Authors: Jose Gomez-arroyo, Herman J. Bogaard, Laszlo Farkas, Antonio Abbate, Norbert F VoelkelAbstract:Here we provide background information for the pathobiological concept of a "sick Lung Circulation", and how it may affect cardiac function. We propose that in most chronic and progressive Lung diseases, but in particular COPD/emphysema and interstitial Lung diseases (ILD), there are significant pathological changes of the small pulmonary vessels. Complementing the WHO classification of pulmonary vascular diseases we provide a classification which is based on pathogenetic mechanisms such as inflammation, hypoxia and angioproliferation. We also propose that chronic Lung disease - related 'cor pulmonale' is insufficiently explained by an elevation of the pulmonary arterial pressure. © 2012 Bentham Science Publishers.
Steven H. Abman - One of the best experts on this subject based on the ideXlab platform.
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Pulmonary Vascular Disease in Bronchopulmonary Dysplasia
Advances in Pulmonary Hypertension, 2016Co-Authors: Steven H. Abman, Alicia Grenolds, Peter M. MouraniAbstract:Pulmonary vascular disease and pulmonary hypertension (PH) contributes significantly to the pathogenesis, pathophysiology, and clinical course of infants with bronchopulmonary dysplasia (BPD). This article briefly reviews the impact of premature birth on the developing Lung Circulation, mechanisms that contribute to the development of PH in premature newborns, and the diagnostic evaluation and management of severe PH in infants with BPD.
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Unique aspects of the developing Lung Circulation: structural development and regulation of vasomotor tone
Pulmonary circulation, 2016Co-Authors: Yuangsheng Gao, Steven H. Abman, Kurt R. Stenmark, David N. Cornfield, Bernard Thébaud, J. Usha RajAbstract:This review summarizes our current knowledge on Lung vasculogenesis and angiogenesis during normal Lung development and the regulation of fetal and postnatal pulmonary vascular tone. In comparison to that of the adult, the pulmonary Circulation of the fetus and newborn displays many unique characteristics. Moreover, altered development of pulmonary vasculature plays a more prominent role in compromised pulmonary vasoreactivity than in the adult. Clinically, a better understanding of the developmental changes in pulmonary vasculature and vasomotor tone and the mechanisms that are disrupted in disease states can lead to the development of new therapies for Lung diseases characterized by impaired alveolar structure and pulmonary hypertension.
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Impaired Vascular Endothelial Growth Factor Signaling in the Pathogenesis of Neonatal Pulmonary Vascular Disease
Advances in experimental medicine and biology, 2009Co-Authors: Steven H. AbmanAbstract:Abstract Of diverse growth factors that contribute to normal Lung development, vascular endothelial growth factor (VEGF) plays an especially prominent role in the normal growth and development of the pulmonary Circulation in the fetus and newborn. Strong experimental and clinical data support the role of impaired VEGF signaling in the pathogenesis of two major clinical disorders of the developing Lung Circulation: persistent pulmonary hypertension of the newborn (PPHN) and bronchopulmonary dysplasia (BPD). These disorders are each characterized by impaired vascular growth, structure and reactivity, which are at least partly due to endothelial cell dysfunction. This chapter will briefly discuss VEGF signaling during normal Lung development and how disruption of VEGF signaling contribute to the pathogenesis of neonatal pulmonary vascular disease in these settings.
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recent advances in the pathogenesis and treatment of persistent pulmonary hypertension of the newborn
Neonatology, 2007Co-Authors: Steven H. AbmanAbstract:Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome characterized by failure of the Lung Circulation to achieve or sustain the normal drop in pulmonary vascular resistance (PVR) at birth. Past laboratory studies identified the important role of nitric oxide (NO)-cGMP signaling in the regulation of the perinatal Lung Circulation, leading to the development and application of inhaled NO therapy for PPHN. Although inhaled NO therapy has improved the clinical course and outcomes of many infants, pulmonary hypertension can be refractory to inhaled NO, suggesting the need for additional approaches to severe PPHN. To develop novel therapeutic strategies for PPHN, ongoing studies continue to explore basic mechanisms underlying the pathobiology of PPHN in experimental models, including strategies to enhance NO-cGMP signaling. Recent studies have demonstrated that impaired vascular endothelial growth factor (VEGF) signaling may contribute to the pathogenesis of PPHN. Lung VEGF expression is markedly decreased in an experimental model of PPHN in sheep; inhibition of VEGF mimics the structural and functional abnormalities of PPHN, and VEGF treatment improves pulmonary hypertension through upregulation of NO production. Other studies have shown that enhanced NO-cGMP activity through the use of cGMP-specific phosphodiesterase inhibitors (sildenafil), soluble guanylate cyclase activators (BAY 41-2272), superoxide scavengers (superoxide dismutase), and rho-kinase inhibitors (fasudil) can lead to potent and sustained pulmonary vasodilation in experimental PPHN. Overall, these laboratory studies suggest novel pharmacologic strategies for the treatment of refractory PPHN.
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Chapter 7 – Developmental Physiology of the Pulmonary Circulation
The Lung, 2004Co-Authors: Steven H. AbmanAbstract:Publisher Summary This chapter reviews the physiologic regulation of the developing pulmonary Circulation, including mechanisms that regulate vascular tone and reactivity in the fetal Lung; mechanisms that contribute to adaptive changes at birth and the early postnatal period; and mechanisms that may contribute to the failure of pulmonary vascular resistance (PVR) to fall in neonates with severe pulmonary hypertension. Postnatal survival depends upon the ability of the pulmonary Circulation to undergo rapid and dramatic vasodilation during the first minutes after birth. Normal development of the Lung Circulation is determined by the precise coordination of numerous signals from multiple cell types, which include diverse transcription factors, growth factors, chemokines, cytokines, vasoactive products, matrix proteins and others. Physiologically, the fetal pulmonary Circulation is characterized by the presence of high vascular resistance, and the ability to oppose vasodilation and maintain low blood flow in utero. The ability to respond to vasoactive stimuli increases with maturation. The NO-cGMP cascade plays an important role in the regulation of vascular tone and reactivity of the fetal and transitional pulmonary Circulation, and abnormalities in this system contribute to abnormal pulmonary vascular tone and reactivity in an experimental model of persistent pulmonary hypertension of the newborn (PPHN).
Harm Jan Bogaard - One of the best experts on this subject based on the ideXlab platform.
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the need to recognize the pulmonary Circulation and the right ventricle as an integrated functional unit facts and hypotheses 2013 grover conference series
Pulmonary circulation, 2015Co-Authors: Norbert F Voelkel, Harm Jan Bogaard, Jose GomezarroyoAbstract:AbstractFor many patients with severe pulmonary arterial hypertension, heart failure—and, in particular, right heart failure—is the final chapter of their chronic illness. Targeted therapy for pulmonary hypertension is effective only if the right ventricular ejection fraction is maintained or improved. Because improvement of right heart function and reversal of right heart failure are treatment goals, it is important to investigate the cellular and molecular mechanisms that cause right heart failure. Here, we propose that right ventricular capillary rarefaction is an important hallmark of right heart failure and consider that the “sick Lung Circulation” and the pressure-overloaded right ventricle constitute a functional unit.
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Treatment for pulmonary arterial hypertension-associated right ventricular dysfunction.
Annals of the American Thoracic Society, 2014Co-Authors: Jose Gomez-arroyo, Norbert F Voelkel, Julio Sandoval, Marc A. Simon, Erick Dominguez-cano, Harm Jan BogaardAbstract:Pulmonary arterial hypertension (PAH) includes a heterogeneous group of diseases characterized by pulmonary vasoconstriction and remodeling of the Lung Circulation. Although PAH is a disease of the Lungs, patients with PAH frequently die of right heart failure. Indeed, survival of patients with PAH depends on the adaptive response of the right ventricle (RV) to the changes in the Lung Circulation. PAH-specific drugs affect the function of the RV through afterload reduction and perhaps also through direct effects on the myocardium. Prostacyclins, type 5 phosphodiesterase inhibitors, and guanylyl cyclase stimulators may directly enhance myocardial contractility through increased cyclic adenosine and guanosine monophosphate availability. Although this may initially improve cardiac performance, the long-term effects on myocardial oxygen consumption and function are unclear. Cardiac effects of endothelin receptor antagonists may be opposite, as endothelin-1 is known to suppress cardiac contractility. Because P...
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chronic pulmonary artery pressure elevation is insufficient to explain right heart failure
Circulation, 2009Co-Authors: Harm Jan Bogaard, Ramesh Natarajan, Scott C Henderson, Carlin S Long, Donatas Kraskauskas, Lisa Smithson, Ramzi A Ockaili, Joe M Mccord, Norbert F VoelkelAbstract:Background—The most important determinant of longevity in pulmonary arterial hypertension is right ventricular (RV) function, but in contrast to experimental work elucidating the pathobiology of left ventricular failure, there is a paucity of data on the cellular and molecular mechanisms of RV failure. Methods and Results—A mechanical animal model of chronic progressive RV pressure overload (pulmonary artery banding, not associated with structural alterations of the Lung Circulation) was compared with an established model of angioproliferative pulmonary hypertension associated with fatal RV failure. Isolated RV pressure overload induced RV hypertrophy without failure, whereas in the context of angioproliferative pulmonary hypertension, RV failure developed that was associated with myocardial apoptosis, fibrosis, a decreased RV capillary density, and a decreased vascular endothelial growth factor mRNA and protein expression despite increased nuclear stabilization of hypoxia-induced factor-1. Induction of myocardial nuclear factor E2-related factor 2 and heme-oxygenase 1 with a dietary supplement (Protandim) prevented fibrosis and capillary loss and preserved RV function despite continuing pressure overload. Conclusion—These data brought into question the commonly held concept that RV failure associated with pulmonary hypertension is due strictly to the increased RV afterload. (Circulation. 2009;120:1951-1960.)
Bengt Rundqvist - One of the best experts on this subject based on the ideXlab platform.
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growth factors and interleukin 6 across the Lung Circulation in pulmonary hypertension
European Respiratory Journal, 2009Co-Authors: Nedim Selimovic, Bert Andersson, Claes-håkan Bergh, Egidija Sakiniene, Hans Carlsten, Bengt RundqvistAbstract:The aim of our study was to assess the levels of growth factors and interleukin (IL)-6 across the pulmonary Circulation in patients with pulmonary arterial hypertension (PAH) and correlate them with clinical and haemodynamic data and outcome. Simultaneous arterial and pulmonary arterial blood samples in patients with PAH (n = 44) and controls (n = 20) were obtained during right heart catheterisation. Vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF)-BB, transforming growth factor (TGF)-β1 and IL-6 were measured using ELISA. Arterial median (interquartile range) values for VEGF, PDGF-BB, TGF-β1 and IL-6 were significantly higher in patients (377 (218–588) versus 9.0 pg·mL −1 ; 1,955 (1,371–2,519) versus 306 (131–502) pg·mL −1 ; 26.42 (11.3–41.1) versus 7.0 (1.8–18.4) ng·mL −1 ; and 3.98 (0.7–8.1) versus 0.7 pg·mL −1 , respectively; p Our findings indicate increased release and/or decreased clearance of growth factors at the Lung vascular level, which may contribute to vascular remodelling in PAH.
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growth factors and interleukin 6 across the Lung Circulation in pulmonary hypertension
European Respiratory Journal, 2009Co-Authors: Nedim Selimovic, Bert Andersson, Claes-håkan Bergh, Egidija Sakiniene, Hans Carlsten, Bengt RundqvistAbstract:The aim of our study was to assess the levels of growth factors and interleukin (IL)-6 across the pulmonary Circulation in patients with pulmonary arterial hypertension (PAH) and correlate them with clinical and haemodynamic data and outcome. Simultaneous arterial and pulmonary arterial blood samples in patients with PAH (n = 44) and controls (n = 20) were obtained during right heart catheterisation. Vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF)-BB, transforming growth factor (TGF)-beta1 and IL-6 were measured using ELISA. Arterial median (interquartile range) values for VEGF, PDGF-BB, TGF-beta1 and IL-6 were significantly higher in patients (377 (218-588) versus 9.0 pg.mL(-1); 1,955 (1,371-2,519) versus 306 (131-502) pg.mL(-1); 26.42 (11.3-41.1) versus 7.0 (1.8-18.4) ng.mL(-1); and 3.98 (0.7-8.1) versus 0.7 pg.mL(-1), respectively; p<0.001 for all variables). There was a consistent step-up of VEGF, PDGF-BB and TGF-beta1 across the Lungs in PAH patients (p<0.001, p = 0.002 and p<0.001, respectively), whereas in controls, arterial and pulmonary arterial serum levels of IL-6 and growth factors were similar (statistically nonsignificant). In multivariate analysis, increased IL-6 levels predicted mortality (hazard ratio 1.08 (95% confidence interval 1.02-1.15); p = 0.012). Our findings indicate increased release and/or decreased clearance of growth factors at the Lung vascular level, which may contribute to vascular remodelling in PAH.
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Growth factors and interleukin-6 across the Lung Circulation in pulmonary hypertension
The European respiratory journal, 2009Co-Authors: Nedim Selimovic, Bert Andersson, Claes-håkan Bergh, Egidija Sakiniene, Hans Carlsten, Bengt RundqvistAbstract:The aim of our study was to assess the levels of growth factors and interleukin (IL)-6 across the pulmonary Circulation in patients with pulmonary arterial hypertension (PAH) and correlate them with clinical and haemodynamic data and outcome. Simultaneous arterial and pulmonary arterial blood samples in patients with PAH (n = 44) and controls (n = 20) were obtained during right heart catheterisation. Vascular endothelial growth factor (VEGF), platelet-derived growth factor (PDGF)-BB, transforming growth factor (TGF)-beta1 and IL-6 were measured using ELISA. Arterial median (interquartile range) values for VEGF, PDGF-BB, TGF-beta1 and IL-6 were significantly higher in patients (377 (218-588) versus 9.0 pg.mL(-1); 1,955 (1,371-2,519) versus 306 (131-502) pg.mL(-1); 26.42 (11.3-41.1) versus 7.0 (1.8-18.4) ng.mL(-1); and 3.98 (0.7-8.1) versus 0.7 pg.mL(-1), respectively; p
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Endothelin-1 Across the Lung Circulation in Patients With Pulmonary Arterial Hypertension and Influence of Epoprostenol Infusion
The Journal of heart and lung transplantation : the official publication of the International Society for Heart Transplantation, 2009Co-Authors: Nedim Selimovic, Bert Andersson, Claes-håkan Bergh, Egidija Sakiniene, Hans Carlsten, Bengt RundqvistAbstract:Background The endothelin-1 (ET-1) system plays a pathophysiologic role in patients with pulmonary arterial hypertension (PAH). Results from previous studies assessing the transpulmonary gradient of ET-1 have been inconsistent. The influence of an intravenous epoprostenol infusion on the transpulmonary ET-1 gradient is unknown. Methods In a prospective investigation, serum concentrations of ET-1 were measured in 39 consecutive patients (31 women; mean age, 20–77 years) with pulmonary hypertension (33 with PAH) and compared with 20 controls. The effect of intravenous epoprostenol administration on the transpulmonary gradient of ET-1 was analyzed in 13 patients with pulmonary hypertension. Blood samples were taken simultaneously from the pulmonary artery and radial artery. Results The serum levels of ET-1 were significantly higher in the arterial (3.9 ± 1.28 vs 2.53 ± 0.24 pg/ml, p p p = 0.79). During intravenous epoprostenol infusion, there were no changes in the mean transpulmonary ET-1 gradient (0.98 ± 0.07 vs 0.96 ± 0.09, p = 0.52), despite significant hemodynamic changes. Conclusion The ET-1 radial artery/pulmonary artery ratio of unity indicates a balanced release and clearance of ET-1 across the Lung Circulation in controls and in patients with different forms of pulmonary hypertension. ET-1 levels across the pulmonary Circulation did not change during epoprostenol infusion.
Bruce D. Johnson - One of the best experts on this subject based on the ideXlab platform.
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Lung-to-Lung Circulation times during exercise in heart failure
European journal of applied physiology, 2009Co-Authors: Norman R. Morris, Eric M. Snyder, Kenneth C. Beck, Bruce D. JohnsonAbstract:Circulation time (the transit time for a bolus of blood through the circulatory system) is a potential index of cardiac dysfunction in chronic heart failure (HF). In healthy subjects, Circulation time falls as cardiac output (Q) rises during exercise, however little is known about this index in HF. In this study we examined the relationship between Lung-to-Lung Circulation time (LLCT) during exercise in ten HF (53 ± 14 year, resting ejection fraction = 23 ± 8%) and control subjects (51 ± 18 year). We hypothesized that HF patients would have slower LLCT times during exercise when compared to control subjects. Each subject completed two identical incremental exercise tests during which LLCT was measured in one test and Q measured in the other. Q was measured using the open circuit C2H2 washin technique and Circulation time measured using an inert gas technique. In HF patients and control subjects, LLCT decreased and Q increased from rest (HF:LLCT = 53.6 ± 8.2 s, Q = 4.3 ± 1.1 l min−1; control: LLCT = 55.3 ± 10.9 s, Q = 4.5 ± 0.5 l min−1) to peak exercise (HF:LLCT = 20.6 ± 3.9* s, Q = 8.8 ± 2.5* l min−1; control:LLCT = 14.9 ± 2.4 s, Q = 16.5 ± 1.2 l min−1; *P < 0.05 vs control). LLCT was significantly (P < 0.05) slower for the HF group when compared to the control group during submaximal exercise and at peak exercise. However, at a fixed Q the HF subjects had a faster LLCT. We hypothesize that the faster LLCT at a fixed Q for HF patients, may be the result of a more intensive peripheral vasoconstriction of non-active beds and a better redistribution of blood flow.
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The relationship between resting Lung-to-Lung Circulation time and peak exercise capacity in chronic heart failure patients.
Journal of cardiac failure, 2007Co-Authors: Norman R. Morris, Eric M. Snyder, Kenneth C. Beck, Luke J. Haseler, Lyle J. Olson, Bruce D. JohnsonAbstract:Abstract Background Peak exercise capacity (VO 2peak ) is a measure of the severity of chronic heart failure (CHF); however, few indices of resting cardiopulmonary function have been shown to predict VO 2peak . A prolonged Circulation time has been suggested as an index of increased severity of CHF. The aim of this study was to investigate the relationship between resting Lung-to-Lung Circulation time (LLCT) and VO 2peak in CHF. Methods and Results Thirty CHF patients (59 ± 13 years, New York Heart Association: 1.9 ± 1.0) undertook the study. Each subject completed resting pulmonary and echocardiography measures and an incremental exercise test. LLCT was measured using the reappearance of end-tidal acetylene (P ET ,C 2 H 2 ) after a single inhalation. Univariate and multivariate stepwise linear regression was used to determine the predictors of VO 2peak . Univariate correlates of VO 2peak (group mean 1.53 ± 0.44 L/min −1 ) included LLCT ( r = −0.75), inspiratory capacity ( r = 0.41), ejection fraction ( r = 0.33), peak early flow velocity ( r = −0.39), and the ratio of early to late flow velocity ( r = −0.31). LLCT was the only independent predictor where VO 2peak = 3.923–0.045 (LLCT); r 2 = 54%. Conclusions These results suggest that resting LLCT determined using the soluble inert gas technique represents a simple, noninvasive method that provides additional information regarding exercise capacity in CHF.
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Resting cirulation time as a predictor of exercise capacity in heart failure patients
2005Co-Authors: Norman R. Morris, Eric M. Snyder, Kenneth C. Beck, Lyle J. Olson, T.p. Oslon, Bruce D. JohnsonAbstract:Body: The factors that predict exercise capacity in CHF are not well understood. It is clear the systolic factors such as ejection fraction (EF) are poor predictors of exercise capacity (VO2peak) in CHF. Recently some studies have suggested that other cardiovascular factors such as diastolic function and left ventricular stiffness may be better predictors of VO2peak. We have recently developed a method of measuring Lung-to-Lung Circulation time (circ time) using the reappearance of end tidal acetylene (PetC2H2) in the expired air following a single inhalation. This measure of circ time is not only dependent on cardiac function but also on blood flow distribution and thus may provide additional information on the cardiovascular impairment to exercise in CHF. We hypothesized that resting circ time may be a predictor of VO2peak in CHF, with longer resting circ times indicating poorer exercise capacity. Twenty-one CHF patients (age 58Რyr, NYHA = 1.92; EF = 27.5Ხ0 %, meanᓅM) participated in the study. Exercise capacity was determined using an incremental treadmill test, while resting circ time was measured using acetylene inhalation. The mean peak exercise capacity (VO2peak) for the CHF patients was 18.7ᱮ1 ml.kg-1.min-1 and the resting circ time was 53.7ᱮ8 s. Peak exercise capacity was strongly correlated with resting circ time (r=-0.74, P
