Effect of lung transplantation on right and left ventricular volumes and function measured by magnetic resonance imaging.

Globits, Sebastian; Burghuber, Otto Chris; Koller, Jeanette; Schenk, Peter; Frank, Herbert; Grimm, M; End, Adelheid; Glogar, Dietmar; Imhof, Herwig; Klepetko, Walter

doi:10.1164/ajrccm.149.4.8143034

Cited by 37 publications

(11 citation statements)

References 22 publications

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“…Strategies to normalize the rarefied myocardial capillary bed may be employed (34) and perhaps strategies to reverse myocardial autophagy-or repair dysfunctional and ineffective processing of misfolded proteins and facilitate the secretion of proteins from ER stressed cells (94,120). Ideally, treatment of severe PAH reduces the PVR (67), is antiangiogenic, and improves RV function. The model of severe PAH and RV failure discussed above is being used to assess the effects of interventions on the lung circulation and on the heart (Table 5) (150).…”

Section: Discussionmentioning

confidence: 99%

Right Ventricle in Pulmonary Hypertension

Voelkel

Natarajan

Drake

et al. 2011

Comprehensive Physiology

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During heart development chamber specification is controlled and directed by a number of genes and a fetal heart gene expression pattern is revisited during heart failure. In the setting of chronic pulmonary hypertension the right ventricle undergoes hypertrophy, which is likely initially adaptive, but often followed by decompensation, dilatation and failure. Here we discuss differences between the right ventricle and the left ventricle of the heart and begin to describe the cellular and molecular changes which characterize right heart failure. A prevention and treatment of right ventricle failure becomes a treatment goal for patients with severe pulmonary hypertension it follows that we need to understand the pathobiology of right heart hypertrophy and the transition to right heart failure.

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Section: Discussionmentioning

confidence: 99%

Right Ventricle in Pulmonary Hypertension

Voelkel

Natarajan

Drake

et al. 2011

Comprehensive Physiology

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“…As soon as RV afterload is relieved, the right ventricle enters a dramatic remodelling process, leading to near-normalization of volume indices and function. 44 …”

Section: Correction Of Rv Pressure Overload 2 Decreasing Afterloadmentioning

confidence: 99%

Management of acute and chronic RV dysfunction

Lang

2007

European Heart Journal Supplements

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The aim of this article was to outline contemporary treatments of right ventricular (RV) dysfunction and failure. Despite the heterogeneity of disorders underlying RV failure, RV function is a main determinant of long-term prognosis. Therefore, the unique therapeutic goal is to preserve or ameliorate RV function. Although, in advanced stages of RV failure, there is a considerable overlap of pathophysiological mechanisms, the principle targets of treatment are RV contractility, RV pressure overload, and RV volume overload. Apart from surgical strategies such as pulmonary endarterectomy, lung transplantation, closure of shunt lesions, and interventional structural cardiology procedures such as closure of abnormal communications and defects, or graded blade balloon atrial septostomy, targeted pharmacological treatments have become available over the past years. In addition, global strategies such as exercise training, arrhythmia correction, and synchronization treatments may become a new standard of care in the near future. KEYWORDS Right ventricular dysfunction; Right ventricular failure DefinitionRight ventricular (RV) dysfunction has been defined as a state where stroke volume still increases in the presence of increased RV end-diastolic volume. In contrast, RV failure is present when stroke volume cannot increase any further in parallel to increased RV end-diastolic volume. The compromise of the systemic circulation by the septal shift and interventricular dependence causing a severe left ventricular (LV) filling disorder, offsets a vicious cycle. On a molecular basis, it appears that there is a recapitulation of the fetal gene pattern with a decrease in the a-myosin heavy chain gene and an increase in the expression of the fetal b-myosin heavy chain in dysfunctional or failing RV myocardium. Although excessive and longstanding elevation of RV afterload is a major and prevalent cause of RV dysfunction/ failure, evidence accumulates that RV ischemia, 2 excessive sympathetic and renin-angiotensin system stimulation, 3 and volume overload that is accelerated by tricuspid regurgitation 4 contribute. This transition from dysfunction to failure may be ongoing fast or slowly over years, with an unknown genetic component underlying the ability of the RV to resist pressure and volume overload and to maintain stroke volume. RV hypertrophy is a mechanism accounting for preserved RV function. Recent work has demonstrated that in COPD, concentric RV hypertrophy is the earliest sign of RV pressure overload. However, this early structural adaptation of the heart does not yet compromise RV and LV systolic function. 5In practice, the distinction between RV dysfunction and failure can be revealed by a short-time inhalation of NO which, because of its high pulmonary vascular selectivity, 6 will increase RV stroke volume only in the case of a predominantly pulmonary vascular alteration, i.e. in the presence of RV dysfunction.Taken together, pressure, volume, and contractility are main determinants of RV function, and as such, are ...

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“…An improvement in right ventricular dysfunction occurs after transplantation as evidenced by echocardiography and magnetic resonance imaging, even in patients with relatively preserved baseline right ventricular function (106,107). Patients with pulmonary hypertension undergoing single lung transplantation have post-transplant pulmonary artery pressures that are within the normal range (40, 108).…”

Section: Pulmonary Hemodynamicsmentioning

confidence: 99%

Transplantation in Chronic Obstructive Pulmonary Disease

Patel

Criner

2006

COPD: Journal of Chronic Obstructive Pulmonary Disease

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Lung transplantation is a surgical option for patients who fail optimization of medical treatment for the severe symptoms that result from COPD. This review will discuss patient selection, transplant listing, and the surgical technique for transplantation in COPD. Furthermore, it will describe transplant outcomes and its effects on recipient survival, pulmonary function, exercise capacity, respiratory muscle function, and quality of life. The respective roles of transplantation and lung volume reduction surgery as therapies for advanced disease will be outlined.

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Effect of lung transplantation on right and left ventricular volumes and function measured by magnetic resonance imaging.

Cited by 37 publications

References 22 publications

Right Ventricle in Pulmonary Hypertension

Right Ventricle in Pulmonary Hypertension

Management of acute and chronic RV dysfunction

Transplantation in Chronic Obstructive Pulmonary Disease

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