Right Ventricular Dysfunction in Chronic Lung Disease

Kolb, Todd M.; Hassoun, Paul M.

doi:10.1016/j.ccl.2012.03.005

Cited by 50 publications

(42 citation statements)

References 108 publications

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“…Furthermore, although hypoxia leads to RV hypertrophy, systolic function is generally preserved (Huez et al . , Kolb & Hassoun ). Development of diastolic dysfunction of both right and LV in the experimental mouse model of hypoxia has previously been described by us and these animals also have increased circulating levels of IL‐18 (Larsen et al .…”

Section: Discussionmentioning

confidence: 97%

IL-18 neutralization during alveolar hypoxia improves left ventricular diastolic function in mice

et al. 2014

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Section: Discussionmentioning

confidence: 97%

IL-18 neutralization during alveolar hypoxia improves left ventricular diastolic function in mice

et al. 2014

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“…Subsequently, the RV dilates in response to increased pressure (Voelkel et al, 2006) but becomes unable to compensate over time, and RV failure occurs (Schulman & Matthay, 1992) while LV function is maintained (Zangiabadi, De Pasquale, & Sajkov, 2014). The prevalence of cor pulmonale, in addition to its occurrence either early or later in the progression of IPF, is difficult to determine because of the difficulties in distinguishing chronic lung disease from associated PH and RV failure (Hoeper et al, 2011;Kolb & Hassoun, 2012). Our study using echocardiography to detect longitudinal temporal changes in RV structure and function in mice after BLM exposure revealed changes as early as day 7, concomitant with evidence of vascular remodelling at this point and with the presence of fibrotic markers in the same model (Headley et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

“…The diagnosis of cor pulmonale is challenging because the clinical presentation is often non-specific and is masked by the underlying chronic lung disease (MacNee, 1994;Weitzenblum, 2003). In idiopathic pulmonary fibrosis (IPF), fibrosis and loss of lung parenchyma contribute to PH and RV hypertrophy by obliterating pulmonary vascular beds (Kolb & Hassoun, 2012;Weitzenblum, Ehrhart, Rasaholinjanahary, & Hirth, 1983) and by limiting cardiac filling secondary to relative stiffness of intrathoracic structures (Hsia, 1999;Sietsema, 2001). Pulmonary hypertension is a severe complication of IPF that contributes significantly to morbidity and mortality (Nathan, Noble, & Tuder, 2007), and it has been hypothesized that cor pulmonale drives the mortality in these patients (Handoko et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Alterations in cardiovascular function in an experimental model of lung fibrosis and pulmonary hypertension

Darwiche

Collum

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?We have evaluated changes in cardiovascular physiology using echocardiography in an experimental model of lung fibrosis. What is the main finding and its importance?Remarkably, we report changes in cardiovascular function as early as day 7, concomitant with evidence of vascular remodelling. We also report that isolated pulmonary arteries were hypercontractile in response to a thromboxane A2 agonist. These findings are significant because the development of pulmonary hypertension is one of the most significant predictors of mortality in patients with lung fibrosis, where there are no available therapies and a lack of animal models. Abstract Group III pulmonary hypertension is observed in patients with chronic lung diseases such as chronic obstructive pulmonary disease or idiopathic pulmonary fibrosis. Pulmonary hypertension (PH) develops as a result of extensive pulmonary vascular remodelling and resultant changes in vascular tone that can lead to right ventricle hypertrophy. This eventually leads to right heart failure, which is the leading indicator of mortality in patients with idiopathic pulmonary fibrosis. Treatments for group III PH are not available, in part owing to a lack of viable animal models. Here, we have evaluated the cardiovascular changes in a model of lung fibrosis and PH. Data obtained from this study indicated that structural alterations in the right heart, such as right ventricular wall hypertrophy, occurred as early as day 14, and similar increases in right ventricle chamber size were seen between days 21 and 28. These structural changes were correlated with decreases in the systolic function of the right ventricle and right ventricular cardiac output, which also occurred between the same time points. Characterization of pulmonary artery dynamics also highlighted that PH might be occurring as early as day 21, indicated by reductions in the velocity–time integral; however, evidence for PH is apparent as early as day 7, indicated by the significant reduction in pulmonary acceleration time values. These changes are consistent with evidence of vascular remodelling observed histologically starting on day 7. In addition, we report hyperactivity of bleomycin‐exposed pulmonary arteries to a thromboxane A2 receptor (Tbxa2r) agonist.

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“…The RHC remains the gold standard assessment technique for pulmonary and RV pressures [28]. An increased pressure in the RV is often associated with RV dilatation that causes the septum to shift towards the LV causing LV diastolic dysfunction.…”

Section: Right Heart Catheterisationmentioning

confidence: 99%

“…This in turn causes the RV to become more spherical in structure and impairs LV function. The clinical assessment of RV diastolic dysfunction can be performed (1) non-invasively using imaging techniques such as echocardiography [5,25] and cardiac magnetic resonance (CMR) [26,27] and (2) invasively using right heart catheterisation (RHC) [28], conductance catheterisation [29,30] and radionuclide angiography [31].…”

Section: Non-invasive and Invasive Assessment Of Rv Diastolic Dysfuncmentioning

confidence: 99%

RV diastolic dysfunction: time to re-evaluate its importance in heart failure

et al. 2015

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Right ventricular (RV) diastolic dysfunction was first reported as an indicator for the assessment of ventricular dysfunction in heart failure a little over two decades ago. However, the underlying mechanisms and precise role of RV diastolic dysfunction in heart failure remain poorly described. Complexities in the structure and function of the RV make the detailed assessment of the contractile performance challenging when compared to its left ventricular (LV) counterpart. LV dysfunction is known to directly affect patient outcome in heart failure. As such, the focus has therefore been on LV function. Nevertheless, a strategy for the diagnosis and assessment of RV diastolic dysfunction has not been established. Here, we review the different causal mechanisms underlying RV diastolic dysfunction, summarising the current assessment techniques used in a clinical environment. Finally, we explore the role of load-independent indices of RV contractility, derived from the conductance technique, to fully interrogate the RV and expand our knowledge and understanding of RV diastolic dysfunction. Accurate assessment of RV contractility may yield further important prognostic information that will benefit patients with diastolic heart failure.

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Right Ventricular Dysfunction in Chronic Lung Disease

Cited by 50 publications

References 108 publications

IL-18 neutralization during alveolar hypoxia improves left ventricular diastolic function in mice

IL-18 neutralization during alveolar hypoxia improves left ventricular diastolic function in mice

Alterations in cardiovascular function in an experimental model of lung fibrosis and pulmonary hypertension

RV diastolic dysfunction: time to re-evaluate its importance in heart failure

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