Variability of Right Ventricular Functional Recovery After Lung Transplantation

Schulman, Larry L.; Leibowitz, David; Anandarangam, Thiruvengadam; DiTullio, Marco R.; McGregor, Carlton C.; Smith, Craig R.; Homma, Shunichi

doi:10.1097/00007890-199609150-00014

Cited by 30 publications

(19 citation statements)

References 13 publications

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“…The mechanism by which a severely dilated "end-stage" right ventricle repairs itself after lung transplantation is also uncertain. 13,14 Figure 1. In idiopathic pulmonary arterial hypertension (IPAH), the right ventricle (RV) is characterized by increased end-diastolic volume, change of the normal ventricular conformation tetrahedron to a crescentic trapezoid, and varying degrees of right ventricular hypertrophy (B).…”

Section: The Right Ventricle In Pulmonary Hypertensionmentioning

confidence: 99%

Right Ventricular Function and Failure

et al. 2006

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Section: The Right Ventricle In Pulmonary Hypertensionmentioning

confidence: 99%

Right Ventricular Function and Failure

et al. 2006

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“…Opponents of this procedure argue that isolated lung transplantation alone will result in immediate and long-term normalization of pulmonary vascular resistance and RV ejection fraction. 27,28,49,50 The donor heart can be used for isolated cardiac transplantation. Patients subjected to HLT are also at risk for accelerated graft coronary disease, although the incidence in the series from Stanford University was only 8% at 5 years following the transplant.…”

Section: Choice Of Transplant Operationmentioning

confidence: 99%

Atrial Septostomy and Transplantation for Patients with Pulmonary Arterial Hypertension

Corris

2009

Semin Respir Crit Care Med

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The development of specific disease-targeted therapy for pulmonary arterial hypertension has offered a major advancement in the management of patients, and these medical treatments have been shown to improve both quality and quantity of life. Nevertheless, many patients deteriorate with time and will require consideration of other approaches. This article focuses on the roles of atrial septostomy and lung transplantation.

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“…Other convincing evidence of the reversible nature of PAH-induced RVF comes from studies that have addressed RV function after lung transplantation for end-stage PAH [53][54][55] and after successful pulmonary endarterectomy in patients with chronic thromboembolic PH. 56 Following these surgical interventions, RV function slowly recovered to normal, and this recovery was sustained in long-term follow-up.…”

Section: Pah-induced Rvf: Reversible or Not?mentioning

confidence: 99%

Stem and Progenitor Cell Therapy for Pulmonary Arterial Hypertension: Effects on the Right Ventricle (2013 Grover Conference Series)

2015

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In experimental animals and in patients with pulmonary arterial hypertension (PAH), a wide spectrum of structural and functional conditions is known that may be responsible for the switch of a state of "compensated" right ventricular (RV) hypertrophy to a state of RV failure. In recent years, therapy with differentiated cells, endothelial progenitor cells, and mesenchymal stem cells has been shown to cause partial or complete reversal of pathological characteristics of PAH. The therapeutic effects of stem or progenitor cell therapy are considered to be (1) paracrine effects from stem or progenitor cells that had engrafted in the myocardium (or elsewhere), by compounds that have anti-inflammatory, antiapoptotic, and proangiogenic actions and (2) unloading effects on the right ventricle due to stem or progenitor cellinduced decrease in pulmonary vascular resistance and decrease in pulmonary artery pressure. Pulmonary arterial hypertension (PAH) is associated with right ventricular (RV) hypertrophy (RVH) or RV failure (RVF), considered to be the result of RV pressure overload. Pharmacotherapy, gene therapy, stem and progenitor cell therapy, and combinations of these treatment modalities have been shown to treat PAH, by lowering pulmonary artery pressure, lowering RV weight, and relieving RVF, thereby improving exercise capacity and life span. 1 Here we review the evidence that, in animals with PAH, stem and progenitor cell therapy leads to lower RV weight and relief of RVF by mechanisms that can be ascribed to (1) lowering of RV afterload and (2) direct effects of the stem and progenitor cells on RV myocardial structure and function. RVH DUE TO PAH-INDUCED RV OVERLOAD: PATHOLOGICAL OR PHYSIOLOGICAL HYPERTROPHY?Originally, left ventricular (LV) hypertrophy (LVH) secondary to pressure overload was considered to be "compensatory," 2 but several studies have clearly demonstrated that LVH is a risk factor and has unfavorable prognostic implications. [3][4][5] On the other hand, the athlete's heart often implies the presence of LVH, but this LVH is considered an adaptation to volume overload that occurs during longlasting rowing, running, and cycling. 6 To date, the healthy aspects of exercise training have been documented firmly and are not restricted to healthy individuals, such as athletes, but even to patients with heart failure. 7,8 The two main forms of myocardial hypertrophy are often termed "pathological" hypertrophy, as occurs secondary to pressure overload, and "physiological" hypertrophy, as occurs in the athlete's heart. Pathological and physiological hypertrophy have been characterized in detail, 9-13 and the most significant differences are found in the membrane receptor and signaling pathways that convey the message to the nucleus, where hypertrophy is effectuated with or without changes in gene expression. In pathological hypertrophy, Ca 2+ -dependent calcineurin activation and calcineurin-induced dephosphorylation of

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Variability of Right Ventricular Functional Recovery After Lung Transplantation

Cited by 30 publications

References 13 publications

Right Ventricular Function and Failure

Right Ventricular Function and Failure

Atrial Septostomy and Transplantation for Patients with Pulmonary Arterial Hypertension

Stem and Progenitor Cell Therapy for Pulmonary Arterial Hypertension: Effects on the Right Ventricle (2013 Grover Conference Series)

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