Reverse cardiac remodelling in patients with primary pulmonary hypertension after isolated lung transplantation*1

Kasimir, Marie-Theres; Seebacher, Gernot; Jaksch, Péter; Winkler, G.; Schmid, Katharina; Marta, Gabriel; Simon, Paul; Klepetko, Walter

doi:10.1016/j.ejcts.2004.05.057

Cited by 81 publications

(62 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Reversal of RV function and remodeling in patients with PH after LTx has been reported. [12][13][14][15] Because ill patients are currently treated with combination therapy of PAH-targeted drugs, LTx should be reserved for patients whose RV function deteriorates despite such therapy. However, reverse RV remodeling after LTx in patients with end-stage PAH despite combination therapy of PAH-targeted drugs has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Reverse Right Ventricular Remodeling After Lung Transplantation in Patients With Pulmonary Arterial Hypertension Under Combination Therapy of Targeted Medical Drugs

Sarashina

Nakamura

Akagi

et al. 2017

Circ J

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Reverse Right Ventricular Remodeling After Lung Transplantation in Patients With Pulmonary Arterial Hypertension Under Combination Therapy of Targeted Medical Drugs

Sarashina

Nakamura

Akagi

et al. 2017

Circ J

View full text Add to dashboard Cite

“…9 Compared with volume-overload states, histological changes are more pronounced in RV pressure-overload states as demonstrated by the increased density of myocardial connective tissue seen in both animal and human studies. 10,11 In acute pressure-overload states such as pulmonary embolism (PE), an adult with a previously normal RV is incapable of acutely generating a mean pulmonary artery pressure Ͼ40 mm Hg, and RV failure occurs early in the presence of a significant embolic burden. 12 In most patients with idiopathic PAH, progressive RV dilatation and RV dysfunction occur.…”

Section: Pathophysiologymentioning

confidence: 99%

Right Ventricular Function in Cardiovascular Disease, Part II

et al. 2008

View full text Add to dashboard Cite

R ight ventricular (RV) function may be impaired in pulmonary hypertension (PH), congenital heart disease (CHD), and coronary artery disease and in patients with left-sided heart failure (HF) or valvular heart disease. In recent years, many studies have demonstrated the prognostic value of RV function in cardiovascular disease. In the past, however, the importance of RV function has been underestimated. This perception originated from studies on openpericardium dog models and from the observation that patients may survive without a functional subpulmonary RV (Fontan procedure). In the 1940s, studies using openpericardium dog models showed that cauterization of the RV lateral wall did not result in a decrease in cardiac output or an increase in systemic venous pressure. 1-3 As was later demonstrated, the open-pericardium model did not take into account the complex nature of ventricular interaction. In 1982, Goldstein and colleagues 2 showed that RV myocardial infarction (RVMI) in a closed-chest dog model led to significant hemodynamic compromise. These findings were further supported by clinical studies demonstrating an increased risk of death, arrhythmia, and shock in patients with RVMI. 4 The study of the RV is a relatively young field. In 2006, the National Heart, Lung, and Blood Institute identified RV physiology as a priority in cardiovascular research. 5 The goal of this review is to present a clinical perspective on RV physiology and pathobiology. In the first article of the series, the anatomy, physiology, embryology, and assessment of the RV were discussed. In this second part, we discuss the pathophysiology, clinical importance, and management of RV failure.

show abstract

“…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%

“…Improvements included a return of the leftward-bowing interventricular septum (IVS) to its physiological position and a disappearance of high-grade tricuspid insufficiency. 55,56 Whether there is a point of no return is to be seen, but so far numerous data on therapies for PAH, including cell therapies, indicate re-versibility of PAH-induced RVF, albeit slow and maybe incomplete.…”

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

View full text Add to dashboard Cite

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

show abstract

Reverse cardiac remodelling in patients with primary pulmonary hypertension after isolated lung transplantation*1

Cited by 81 publications

References 23 publications

Reverse Right Ventricular Remodeling After Lung Transplantation in Patients With Pulmonary Arterial Hypertension Under Combination Therapy of Targeted Medical Drugs

Reverse Right Ventricular Remodeling After Lung Transplantation in Patients With Pulmonary Arterial Hypertension Under Combination Therapy of Targeted Medical Drugs

Right Ventricular Function in Cardiovascular Disease, Part II

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

Contact Info

Product

Resources

About