Increased left ventricular stiffness impairs filling in dogs with pulmonary emphysema in respiratory failure.

Gómez, Arturo; Mink, Steven N.

doi:10.1172/jci112556

Cited by 12 publications

(15 citation statements)

References 40 publications

(92 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The first studies that reported diastolic dysfunction were based on interventional catheterization (2,3). They were confirmed by experimental research in animals (4,5) and in humans using Doppler ultrasound (6,7). According to these more recent studies, the frequency of abnormalities in LV relaxation has been suggested to be approximately 90% in patients with COPD.…”

mentioning

confidence: 85%

Left Atrial and Ventricular Filling in Chronic Obstructive Pulmonary Disease

Boussuges

Pinet

Molénat

et al. 2000

Am J Respir Crit Care Med

164

100

View full text Add to dashboard Cite

Abnormal left ventricular (LV) diastolic function has frequently been reported in patients with chronic obstructive pulmonary disease (COPD). In the present work, diastolic function was studied by a combined analysis of pulmonary venous and mitral blood flow velocities in 34 patients with COPD clinically stable and without history of heart disease, and 20 control subjects. We confirmed the increased contribution of the atrial contraction to the LV filling in COPD patients in comparison with control subjects; furthermore, a decreased left atrial (LA) filling during the ventricular systole was observed. Changes in LV filling were not the consequence of a systolic dysfunction, because LV systolic function was normal. Doppler indices indicated that LA pressure was below 15 cm H(2)O in all the patients with COPD and control subjects. Several factors can be put forward to explain these changes; the first one is tachycardia. In addition to hypoxemia and medications, echocardiography suggested that a decreased LV preload participated in increased heart rate. Analysis of Doppler transmitral and pulmonary venous flows demonstrated the role of the ventricular interdependence because a correlation existed between LA and LV filling pattern and right ventricle pressure and diameter.

show abstract

mentioning

confidence: 85%

Left Atrial and Ventricular Filling in Chronic Obstructive Pulmonary Disease

Boussuges

Pinet

Molénat

et al. 2000

Am J Respir Crit Care Med

164

100

View full text Add to dashboard Cite

show abstract

“…Emphysema was produced by repeated intrabronchial instillations of the enzyme papain into the lung, in which the procedure was identical to that previously described. 7,8 Briefly, mongrel dogs (n=10) weighing 20-30 kg were anesthetized with sodium pentobarbital (30 mg/kg) and intubated with an endotracheal tube. About 4 cm3 of the enzyme papain (Type IV, Sigma Chemical Co., St. Louis, Mo.)…”

Section: Chronic Emphysema Study (Component 1)mentioning

confidence: 99%

“…7,8 In control dogs (n = 10), the protocol was identical to that performed in the emphysema dogs, except that 40 cm3 of normal saline solution rather than papain was administered into the lower lobes at weekly intervals. The dogs were randomly allocated to either of the two groups.…”

Section: Chronic Emphysema Study (Component 1)mentioning

confidence: 99%

Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema.

1993

Self Cite

View full text Add to dashboard Cite

Background. In chronic obstructive lung disease, a right to left ventricular septal shift that occurs as a consequence of right ventricular pressure overload is the usual mechanism given to explain a decrease in left ventricular (LV) diastolic performance. The purpose of the present study was to examine the extent to which this mechanism could account for a decrease in LV diastolic function in a canine model in which pulmonary artery pressure was elevated to a level found in human disease.Methods and Results. Severe emphysema was produced in dogs by repeated instillations of the enzyme papain into the lung. To assess LV diastolic function, we used sonomicrometry, in which three pairs of subendocardial crystal transducers were implanted along the three orthogonal axes of the LV. LV end-diastolic dimensions and pressure-strain relations along the three axes, as well as the time constant of LV isovolumic relaxation (T), were measured before (baseline) and after 1 year of emphysema (post-l-year study). The results showed that after 1 year of pulmonary hypertension, LV pressure-strain relations were decreased along the septal-lateral and anterior-posterior axes, but a right to left ventricular septal shift was not detected. The relation of average midwall circumferential stress to midwall circumferential strain was used to describe the intrinsic compliance of the LV. The results showed that myocardial stiffness increased in emphysema but that chamber volume was not reduced. At the post-i-year study, T was abnormally increased in the emphysema group in response to augmented preload and afterload compared with preemphysema measurements.Conclusions. We conclude that mechanisms other than ventricular interdependence may be operative in leading to altered LV diastolic filling in chronic emphysema. (Circulation 1993;87:247-260)

show abstract

“…Studies of COPD patients with LV diastolic dysfunction demonstrate that hypoxemia is present when this cardiac complication is diagnosed (5,29). Several mechanisms have been suggested to explain LV diastolic dysfunction in COPD and PH; LV interstitial edema (8), leftward displacement of the septum (29), increased myocardial stiffness (12), and diastolic asynchrony in the apical and lateral walls (4). In our study, light microscopic examination did not reveal any signs of interstitial edema in the hypoxia group, and the collagen depositions in the LV papillary muscles were limited and not likely to be of functional relevance.…”

Section: Discussionmentioning

confidence: 99%

“…The LV diastolic dysfunction has been explained by a leftward displacement of the interventricular septum caused by RV pressure overload (29). However, in a dog model with pulmonary emphysema, LV diastolic dysfunction was present without bowing of the septum to the left (12), suggesting that intrinsic mechanisms in the LV myocardium participate in LV diastolic dysfunction. The molecular mechanisms leading to dysfunction of the LV in chronic alveolar hypoxia are not known.…”

mentioning

confidence: 99%

Alveolar hypoxia induces left ventricular diastolic dysfunction and reduces phosphorylation of phospholamban in mice

Larsen

Sjaastad²,

Svindland³

et al. 2006

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Chronic obstructive pulmonary disease (COPD) may lead to pulmonary hypertension (PH) and reduced function of the right ventricle (RV). However, COPD patients may also develop left ventricular (LV) diastolic dysfunction. We hypothesized that alveolar hypoxia induces LV diastolic dysfunction and changes in proteins governing Ca(2+) removal from cytosol during diastole. Mice exposed to 10% oxygen for 1, 2, or 4 wk were compared with controls. Cardiac hemodynamics were assessed with Doppler echocardiography and a microtransducer catheter under general anesthesia. The pulmonary artery blood flow acceleration time was shorter and RV pressure was higher after 4 wk of hypoxia compared with controls (both P < 0.05). In the RV and LV, 4 wk of hypoxia induced a prolongation of the time constant of isovolumic pressure decay (51% RV, 43% LV) and a reduction in the maximum rate of decline in pressure compared with control (42% RV, 42% LV, all P < 0.05), indicating impaired relaxation and diastolic dysfunction. Alveolar hypoxia induced a 38%, 47%, and 27% reduction in Ser16-phosphorylated phospholamban (PLB) in the RV after 1, 2, and 4 wk of hypoxia, respectively, and at the same time points, Ser16-phosphorylated PLB in the LV was downregulated by 32%, 34%, and 25% (all P < 0.05). The amounts of PLB and sarco(endo)plasmic reticulum Ca(2+) ATPase (SERCA2a) were not changed. In conclusion, chronic alveolar hypoxia induces hypophosphorylation of PLB at Ser16, which might be a mechanism for impaired relaxation and diastolic dysfunction in both the RV and LV.

show abstract

Increased left ventricular stiffness impairs filling in dogs with pulmonary emphysema in respiratory failure.

Cited by 12 publications

References 40 publications

Left Atrial and Ventricular Filling in Chronic Obstructive Pulmonary Disease

Left Atrial and Ventricular Filling in Chronic Obstructive Pulmonary Disease

Altered left ventricular chamber stiffness and isovolumic relaxation in dogs with chronic pulmonary hypertension caused by emphysema.

Alveolar hypoxia induces left ventricular diastolic dysfunction and reduces phosphorylation of phospholamban in mice

Contact Info

Product

Resources

About