Chronic heart failure (CHF) remains an important and increasing public health care problem. It is a complex syndrome affecting many body systems. Body wasting (i.e., cardiac cachexia) has long been recognised as a serious complication of CHF. Cardiac cachexia is associated with poor prognosis, independently of functional disease severity, age, and measures of exercise capacity and cardiac function. Patients with cardiac cachexia suffer from a general loss of fat tissue, lean tissue, and bone tissue. Cachectic CHF patients are weaker and fatigue earlier, which is due to both reduced skeletal muscle mass and impaired muscle quality. The pathophysiologic alterations leading to cardiac cachexia remain unclear, but there is increasing evidence that metabolic, neurohormonal and immune abnormalities may play an important role. Cachectic CHF patients show raised plasma levels of epinephrine, norepinephrine, and cortisol, and they show high plasma renin activity and increased plasma aldosterone level. Several studies have also shown that cardiac cachexia is linked to raised plasma levels of tumour necrosis factor alpha and other inflammatory cytokines. The degree of body wasting is strongly correlated with neurohormonal and immune abnormalities. The available evidence suggests that cardiac cachexia is a multifactorial neuroendocrine and metabolic disorder with a poor prognosis. A complex imbalance of different body systems may cause the development of body wasting.

Chronic heart failure (CHF) is a leading cause of morbidity and mortality worldwide. Whilst anaemia is known to cause heart failure, CHF may also frequently cause anaemia. There is a positive correlation between the severity of heart failure and the prevalence and severity of anaemia in CHE The presence of anaemia in CHF independently predicts increased mortality in HF. There are many potential reasons for the development of anaemia in CHF but most of the anaemia seen in CHF is the "anaemia of chronic illness". This review will discuss the prevalence of anaemia in CHF, its causes, and its prognostic importance.

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Background: Bortezomib has shown significant anti-tumor activity in multiple myeloma. There are varied protocols including bortezomib, doxorubicin and dexamethason with different application rates. We observed in a retrospective analysis a wide range of toxicity, so that we have to modified our standard approach. The purpose of our analysis was to assess the frequency of toxicity and their alteration after changing the protocol. Patients and methods: Eleven patients were treated for two 28-day cycles using our standard protocol. Bortezomib was given at 1.3 mg/m2 (days 1,4,8,11) and dexamethason at 40 mg (days 1–4, 9–12, 17–20) as well as doxorubicin at 9 mg/m2 (days 1–4). Seven patients received a third modified cycle composed of Bortezomib at 1.3 mg/m2 (days 1,4,8,11), dexamethason at 40 mg days 1–4 and doxorubicin at 20 mg/m2 days 1 and 4. Results: One patient had unergone prior autologous transplantation, the other ten patients (90%) were newly diagnosed. All patients reported moderate peripheral neuropathic pain during the first two cycles. Eight patients (72%) developed severe adverse effects, twenty-five percent during the first cycle and seventy-five percent after the second one. The age of the affected patients range from 65 to 77 years (average age 70.5 years), the mean age of the unaffected is 64.7 years (54 to 72 years). Grade 3–4 toxic effects included infections (100%), neutropenia (25%), acute renal insufficiency (25%) and pulmonary edema (1 patient). Within the group of infections a pneumonia were diagnosed in six patients (75%), herpes zoster in two patients (25%) and an erysipelas in one patient. Two patients (25%) with pneumonia are died from a septic-toxic shock. The seven patients receiving the modiefied third cycle were without any grade 3–4 toxicity. Conclusions: The age seems to have an influence on adverse effects (p=0.19) but there is a high significant benefit concerning the toxicity of bortezomib depending on application rates of doxorubicin and dexamethason.