Patterns of alveolar fluid clearance in heart failure

Hochberg, Irit; Abassi, Zaid; Azzam, Zaher S.

doi:10.1016/j.ijcard.2008.03.015

Cited by 13 publications

(8 citation statements)

References 52 publications

(56 reference statements)

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“…Interestingly, when looking at the ensemble-averaged ePAD, fluid accumulation evidenced by a drop in impedance occurred at ePAD values higher than those reported in the literature. 16 However, this finding is consistent with the clinical observation that patients with chronic HF may only occasionally develop pulmonary edema despite the presence of chronically elevated filling pressures, 17 suggesting that alternative mechanisms, such as increased lymphatic and alveolar fluid clearance, might partially compensate for the alveolar fluid accumulation. Further studies are needed to explore the interaction between hydrostatic pressure and interstitial accumulation in detail.…”

Section: Hydrostatic Pressure and Interstitial Fluid Accumulationsupporting

confidence: 71%

Continuous Monitoring of Intrathoracic Impedance and Right Ventricular Pressures in Patients With Heart Failure

Vanderheyden¹,

Houben²,

Verstreken³

et al. 2010

Circ: Heart Failure

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Background— Hemodynamic monitoring using implantable devices may provide early warning of volume overload in patients with heart failure (HF). This study was designed to prospectively compare information from intrathoracic impedance monitoring and continuous right ventricular pressure measurements in patients with HF. Methods and Results— Sixteen patients with HF (age, 63.5±13.8 years; left ventricular ejection fraction, 23.2±11.3%; New York Heart Association, II and III) and a previous HF decompensation received both a cardiac resynchronization therapy defibrillator providing a daily average of intrathoracic impedance and an implantable hemodynamic monitor providing an estimate of the pulmonary artery diastolic pressure. At the end of a 6-month investigator-blinded period, baseline reference hemodynamic values were determined over 4 weeks during which the patient was clinically stable. A major HF event was defined as HF decompensation requiring hospitalization, IV diuretic treatment, or leading to death. Sixteen major HF events occurred in 10 patients. Within 30 days and 14 days before a major HF event, impedance decreased by 0.12±0.21 Ω/d and 0.20±0.20 Ω/d, respectively, whereas estimated pulmonary arterial diastolic pressure increased by 0.10±0.20 mm Hg/d and 0.16±0.15 mm Hg/d, respectively. During these periods, impedance decreased by 3.8±5.4 Ω ( P <0.02) and 4.9±6.1 Ω ( P <0.007), respectively, whereas estimated pulmonary arterial diastolic pressure increased by 5.8±5.7 mm Hg ( P <0.002) and 6.8±6.1 mm Hg ( P <0.001), respectively, compared with baseline. In all patients, impedance and estimated pulmonary arterial diastolic pressure were inversely correlated ( r =−0.48±0.25). Within 30 days preceding a major HF event, this correlation improved to r =−0.58±0.24. Conclusions— Decompensated HF develops based on hemodynamic derangements and is preceded by significant changes in intrathoracic impedance and right ventricular pressures during the month prior to a major clinical event. Impedance and pressure changes are moderately correlated. Future research may establish the complementary contribution of both parameters to guide diagnosis and management of patients with HF by implantable devices.

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Section: Hydrostatic Pressure and Interstitial Fluid Accumulationsupporting

confidence: 71%

Continuous Monitoring of Intrathoracic Impedance and Right Ventricular Pressures in Patients With Heart Failure

Vanderheyden¹,

Houben²,

Verstreken³

et al. 2010

Circ: Heart Failure

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“…2-6 Notably, β 2 -AR plays a very important role in regulating lung function in CHF, and in other diseases. 14,15 In our study, there was a decrease in PRA and Ang II levels and an improvement of heart function after administration of olmesartan, which is consistent with some previous studies. 1,13,16,17 One possible mechanism is that olmesartan activation of angiotensin-converting enzyme 2 (ACE2) can hydrolyze Ang II to Ang1-7.…”

Section: Discussionsupporting

confidence: 92%

“…Similar data have been reported, in which β 2 -AR expression had not fundamentally changed in the heart of rats with CHF; β 2 -AR function had been desensitized in CHF to protect the organ. 15,19 After treatment with olmesartan, the expression of β 2 -AR was up-regulated, which could better protect the lung function of rats with CHF. These mechanisms require further research.…”

Section: Discussionmentioning

confidence: 99%

Effects of olmesartan therapy on the expression of lung adrenoceptors in rats with chronic heart failure

Jiang

Cao

et al. 2014

J Renin Angiotensin Aldosterone Syst

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Introduction: Adrenergic receptors (AR) play important roles in regulating lung function. However, there are few reports concerning AR expression and the protective effect of angiotensin II receptor blockers (ARB) on the lung in chronic heart failure (CHF). In this study, we aimed to investigate the protective effects of the ARB olmesartan on the lung in CHF. Materials and methods: Wistar rats were randomly divided into four groups: normal control, sham-operated rats, rats with CHF induced by ligating the left anterior descending coronary arteries, and rats with CHF treated with olmesartan (1 mg/kg) once daily for 8 weeks. Heart function, plasma renin activity (PRA) and angiotensin II (Ang II) levels, lung microscopic structure inspection and mRNA and protein expressions of α1A-, β1- and β2-AR in lung were tested. Results: Compared with the CHF group, PRA and Ang II levels were decreased while heart function and mRNA and protein expression of α1A-AR, β1-AR and β2-AR were up-regulated in the olmesartan group (p<0.05 or p<0.01). The inflammation and cell proliferation in CHF lung tissue were reduced in the olmesartan group. Conclusion: Olmesartan may play a beneficial role in protecting lung in CHF by up-regulating AR and decreasing levels of PRA and Ang II.

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“…31,32 In addition to maintaining the integrity of the epithelial barrier by the tight junctions, epithelial cells need mechanisms to reabsorb the fluids present in the interstitium and alveolar spaces after lung injury mediated by mechanical ventilation. 33 This process is mediated by active transport of Na + through amiloride-sensitive cation channels Epithelial Na + Channels (ENaC) present in the apical cell membranes and the Na + /K + -ATPases localized mainly in the basolateral cell membrane. [34][35][36][37] Electron microscope studies provided clear evidence for the major abnormalities in the blood-gas barrier during lung injury.…”

mentioning

confidence: 99%

Alveolar Type I Epithelial Cells: The Forgotten Cells in Fetal Lung Development and Lung Injury

Najrana¹,

Sanchez‐Esteban²

2016

Pulm Res Respir Med Open J

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Patterns of alveolar fluid clearance in heart failure

Cited by 13 publications

References 52 publications

Continuous Monitoring of Intrathoracic Impedance and Right Ventricular Pressures in Patients With Heart Failure

Continuous Monitoring of Intrathoracic Impedance and Right Ventricular Pressures in Patients With Heart Failure

Effects of olmesartan therapy on the expression of lung adrenoceptors in rats with chronic heart failure

Alveolar Type I Epithelial Cells: The Forgotten Cells in Fetal Lung Development and Lung Injury

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