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Morris‐Thurgood, Jayne; Frenneaux, Michael

doi:10.1023/a:1026555012135

Cited by 36 publications

(6 citation statements)

References 86 publications

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“…Those modifications are concomitant with a decrease in phosphorylated metabolites concentrations in CH hearts, mainly phosphocreatine (PCr) [8], [9]. Altogether, these results evidence the development of a global heart failure in CH hearts [1], [10], [11].…”

Section: Introductionmentioning

confidence: 76%

Improved Energy Supply Regulation in Chronic Hypoxic Mouse Counteracts Hypoxia-Induced Altered Cardiac Energetics

et al. 2010

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BackgroundHypoxic states of the cardiovacular system are undoubtedly associated with the most frequent diseases of modern time. Therefore, understanding hypoxic resistance encountered after physiological adaptation such as chronic hypoxia, is crucial to better deal with hypoxic insult. In this study, we examine the role of energetic modifications induced by chronic hypoxia (CH) in the higher tolerance to oxygen deprivation.Methodology/Principal FindingsSwiss mice were exposed to a simulated altitude of 5500 m in a barochamber for 21 days. Isolated perfused hearts were used to study the effects of a decreased oxygen concentration in the perfusate on contractile performance (RPP) and phosphocreatine (PCr) concentration (assessed by 31P-NMR), and to describe the integrated changes in cardiac energetics regulation by using Modular Control Analysis (MoCA). Oxygen reduction induced a concomitant decrease in RPP (−46%) and in [PCr] (−23%) in Control hearts while CH hearts energetics was unchanged. MoCA demonstrated that this adaptation to hypoxia is the direct consequence of the higher responsiveness (elasticity) of ATP production of CH hearts compared with Controls (−1.88±0.38 vs −0.89±0.41, p<0.01) measured under low oxygen perfusion. This higher elasticity induces an improved response of energy supply to cellular energy demand. The result is the conservation of a healthy control pattern of contraction in CH hearts, whereas Control hearts are severely controlled by energy supply.Conclusions/SignificanceAs suggested by the present study, the mechanisms responsible for this increase in elasticity and the consequent improved ability of CH heart metabolism to respond to oxygen deprivation could participate to limit the damages induced by hypoxia.

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Section: Introductionmentioning

confidence: 76%

Improved Energy Supply Regulation in Chronic Hypoxic Mouse Counteracts Hypoxia-Induced Altered Cardiac Energetics

et al. 2010

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“…Ventricular interdependence corresponds to the forces transmitted from the left ventricle to the other and vice versa through the myocardium and pericardium and occurs because the two ventricles have common myocardial fibers, share the interventricular septum, and are wrapped within the pericardium [32]. Accordingly, RV diastolic function can influence that of the left ventricle by several mechanisms including RV pressure overload [33][34][35]. However, in the present study, LV diastolic alterations of both IPF and no-IPF patients were evident in the presence and in the absence of PAH and cannot be therefore ascribed to an impairment of LV myocardial diastolic properties occurring as the consequence of septal wall distortion towards the left ventricle due to RV pressure overload [33,36,37].…”

Section: Diastolic and Systolic Functionmentioning

confidence: 99%

“…Accordingly, RV diastolic function can influence that of the left ventricle by several mechanisms including RV pressure overload [33][34][35]. However, in the present study, LV diastolic alterations of both IPF and no-IPF patients were evident in the presence and in the absence of PAH and cannot be therefore ascribed to an impairment of LV myocardial diastolic properties occurring as the consequence of septal wall distortion towards the left ventricle due to RV pressure overload [33,36,37]. It is also worthy of note that only in IPF patients, LV GLS, but not LV EF, was significantly lower in comparison with both healthy controls and no-IPF.…”

Section: Diastolic and Systolic Functionmentioning

confidence: 99%

Impaired Right and Left Ventricular Longitudinal Function in Patients with Fibrotic Interstitial Lung Diseases

Buonauro

Santoro

Galderisi

et al. 2020

JCM

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Background: Left ventricular (LV) and right ventricular (RV) dysfunction is recognized in idiopathic pulmonary fibrosis (IPF). Little is known about cardiac involvement in non-idiopathic pulmonary fibrosis (no-IPF). This issue can be explored by advanced echocardiography. Methods: Thirty-three clinically stable and therapy-naive fibrotic IPF and 28 no-IPF patients, and 30 healthy controls were enrolled. Exclusion criteria were autoimmune systemic diseases, coronary disease, heart failure, primary cardiomyopathies, chronic obstructive lung diseases, pulmonary embolism, primary pulmonary hypertension. Lung damage was evaluated by diffusion capacity for carbon monoxide (DLCOsb). All participants underwent an echo-Doppler exam including 2D global longitudinal strain (GLS) of both ventricles and 3D echocardiographic RV ejection fraction (RVEF). Results: We observed LV diastolic dysfunction in IPF and no-IPF, and LV GLS but not LV EF reduction only in IPF. RV diastolic and RV GLS abnormalities were observed in IPF versus both controls and no-IPF. RV EF did not differ significantly between IPF and no-IPF. DLCOsb and RV GLS were associated in the pooled pulmonary fibrosis population and in the IPF subgroup (β = 0.708, p < 0.001), independently of confounders including pulmonary arterial systolic pressure. Conclusion: Our data highlight the unique diagnostic capabilities of GLS in distinguishing early cardiac damage of IPF from no-IPF patients.

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“…More importantly, the LV was impeded by the leftward movement of the septum and had a reduction in left ventricular diastolic area. As described by Morris-Thurgood and Frenneaux [12], further volume loading in this case can have detrimental effects enhancing diastolic ventricular interaction. Belenkie and colleagues [13] studied volume loading in a canine model, before and after pulmonary embolization.…”

Section: Pathophysiology Of Right Ventricular Failurementioning

confidence: 85%

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2006

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Right ventricular failure (RVF) is an underestimated problem in intensive care. This review explores the physiology and pathophysiology of right ventricular function and the pulmonary circulation. When RVF is secondary to an acute increase in afterload, the picture is one of acute cor pulmonale, as occurs in the context of acute respiratory distress syndrome, pulmonary embolism and sepsis. RVF can also be caused by right myocardial dysfunction. Pulmonary arterial catheterization and echocardiography are discussed in terms of their roles in diagnosis and treatment. Treatments include options to reduce right ventricular afterload, specific pulmonary vasodilators and inotropes.

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Cited by 36 publications

References 86 publications

Improved Energy Supply Regulation in Chronic Hypoxic Mouse Counteracts Hypoxia-Induced Altered Cardiac Energetics

Improved Energy Supply Regulation in Chronic Hypoxic Mouse Counteracts Hypoxia-Induced Altered Cardiac Energetics

Impaired Right and Left Ventricular Longitudinal Function in Patients with Fibrotic Interstitial Lung Diseases

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