Heart failure remains one of the most important problems in cardiology despite the progress in its treatment. A number of recent studies have demonstrated the relationship between the intensification of oxidative stress and chronic inflammation and the severity of left ventricular dysfunction, development of heart failure symptoms, and prediction of future cardiac events. Early detection of changes developing in the heart is key in improving the treatment's effectiveness. It appears that determining specific, sensitive biomarkers reflecting the complex pathophysiology of heart failure and using them to detect asymptomatic cardiac alterations may become a crucial screening tool, assisting in the identification of patients requiring further diagnostic examinations. This article presents an overview of the current knowledge of the role of oxidative stress and inflammation in heart failure; it also discusses the potential role of oxidative stress and inflammatory markers as prognostic factors in heart failure that may be used in screening tests.
The adipose tissue, apart from storing energy, plays a role of an endocrine organ. One of the most important adipokines secreted by adipose tissue is adiponectin, which is also produced by cardiomyocytes and connective tissue cells within the heart. Adiponectin is known for its beneficial effect on the metabolism and cardiovascular system and its low level is a factor of development of many cardiovascular diseases. Paradoxically, in the course of heart failure, adiponectin level gradually increases with the severity of the disease and higher adiponectin level is a factor of poor prognosis. As a result, there is a growing interest in adiponectin as a marker of heart failure progression and a predictor of prognosis in the course of this disease.
Despite advances in prevention and treatment of heart transplant rejection, development of cardiac allograft vasculopathy (CAV) remains the leading factor limiting long-term survival of the graft. Cardiac allograft vasculopathy etiopathogenesis is not fully understood, but a significant role is attributed to endothelial cell damage, caused by immunological and non-immunological mechanisms. Immunological factors include the differences between the recipient's and the donor's HLA systems, the presence of alloreactive antibodies and episodes of acute rejection. Among the non-immunological factors the most important are the age of the donor, ischemia-reperfusion injury and cytomegalovirus infection. The classical cardiovascular risk factors (diabetes, hypertension, obesity and hyperlipidemia) are also important. This study presents an up-to-date overview of current knowledge on the vasculopathy etiopathogenesis and the role played by endothelium and inflammatory processes in CAV, and it also investigates the factors which may serve as risk markers of cardiac allograft vasculopathy.
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