Background & Aims: Liver transplantation is the only curative intervention for terminal liver disease. Accurate long-term quality of life (QOL) data are required in the context of improved surgical outcomes and increasing posttransplant survival. This study reviews the long-term QOL after primary liver transplantation in adult patients surviving 5 or more years after surgery. Methods: A literature search was conducted on PubMed for all studies matching the eligibility criteria between January 2000 and October 2013. Bibliographies of included studies were also reviewed. Two authors independently performed screening of titles and abstracts. Consensus for studies included for review was achieved by discussion between authors based on predetermined eligibility criteria. Quality appraisal and data tabulation were performed using predetermined forms. Results were synthesized by narrative review. Results: Twenty-three studies (5402 patients) were included. QOL following liver transplantation remains superior to preoperative status up to 20 years post-operatively. More post-operative complications predicted worse QOL scores especially in physical domains. Benefits in functional domains persist long-term with independence in self-care and mobility. Employment rates recover in the short-term but decline after 5 years, and differ significantly between various aetiologies of liver disease. Overall QOL improves to a similar level as the general population, but physical function remains worse. Participation in post-operative physical activity is associated with superior QOL outcomes in liver transplant recipients compared to the general population. QOL improvements are similar compared to lung, kidney and heart transplantation. Heterogeneity between studies precluded quantitative analysis. Conclusions: Liver transplantation confers specific long-term QOL and functional benefits when compared to preoperative status. This information can assist in providing a more complete estimate of the overall health of liver transplant recipients and the effectiveness of surgery. Guidelines for future studies are provided.
Therapeutic Level II. See Instructions for Authors for a complete description of levels of evidence.
Objective-The goal of this study was to investigate the role of platelets in systemic and cardiac inflammatory responses and the development of postinfarct ventricular complications, as well as the efficacy of antiplatelet interventions. Methods and Results-Using a mouse myocardial infarction (MI) model, we determined platelet accumulation and severity of inflammation within the infarcted myocardium by immunohistochemistry and biochemical assays, analyzed peripheral blood platelet-leukocyte conjugation using flow cytometry, and tested antiplatelet interventions, including thienopyridines and platelet depletion. Platelets accumulated within the infarcted region early post-MI and colocalized with inflammatory cells. MI evoked early increase in circulating platelet-leukocyte conjugation mediated by P-selectin/P-selectin glycoprotein ligand-1. Antiplatelet interventions inhibited platelet-leukocyte conjugation in peripheral blood, inflammatory infiltration, content of matrix metalloproteinases or plasminogen activation, and expression of inflammatory mediators in the infarcted myocardium (all PϽ0.05) and lowered rupture incidence (PϽ0.01). Clopidogrel therapy alleviated the extent of chronic ventricular dilatation by serial echocardiography. Key Words: ischemic heart disease Ⅲ leukocytes Ⅲ platelets Ⅲ thienopyridines Ⅲ inflammation Ⅲ myocardial infarction Ⅲ ventricular rupture T he role of platelets in atherosclerotic lesions and acute coronary syndrome has been well documented. The proinflammatory actions of platelets have received increasing attention. 1,2 Platelets contribute to inflammatory responses through release of inflammatory mediators and plateletleukocyte interactions by which platelets mediate leukocyte activation and infiltration into inflamed tissues. 1,2 There are several reports of an elevated proportion of platelet-leukocyte aggregates tested ex vivo in blood samples from patients with acute coronary syndromes. [3][4][5] The current rationale for routine use of the platelet P2Y 12 receptor inhibitors thienopyridines (clopidogrel and prasugrel) is to prevent arterial thrombosis following coronary intervention. 6 Thienopyridine treatment is known to inhibit platelet-leukocyte interactions in the peripheral blood of patients with peripheral atherosclerotic vascular disease, coronary artery disease, or renal transplantation. 5,6 Myocardial infarction (MI) evokes intense inflammatory responses both systemically and within the infarcted myocardium, with adverse consequences. 7 The potential contribution of platelets to postinfarct cardiac inflammation remains unexplored. Relevant to this is the question of whether thienopyridines exert cardiac protection through inhibition of platelet's inflammatory action in the infarcted myocardium, independent of vascular thrombosis. Conclusion-PlateletsVentricular wall rupture is a fatal complication of acute MI, with a death rate of 70% to 90%. 8,9 Recent experimental studies, including ours, have provided strong evidence that wall rupture is the consequence o...
THR confers significant mid-term HRQOL benefits across a broad range of health domains. Further studies based on consistent guidelines provided in this review are required.
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