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Along with the remarkable progress registered in oncological treatment that led to increased survival of cancer patients, treatment-related comorbidities have also become an issue for these long-term survivors. Of particular interest is the development of cardiotoxic events, which, even when asymptomatic, not only have a negative impact on the patient`s cardiac prognosis, but also considerably restrict therapeutic opportunities. The pathophysiology of cytostatic-induced cardiotoxicity implies a series of complex and intricate mechanisms, whose understanding enables the development of preventive and therapeutic strategies. Securing cardiac function is an ongoing challenge for the pharmaceutical industry and the physicians who have to deal currently with these adverse reactions. This review focuses on the main mechanism of cardiac toxicity induced by anticancer drugs and especially on the current strategies applied for preventing and minimizing the cardiac side effects.

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Femoral head osteonecrosis, also known as avascular necrosis, is a disease with a multifactorial etiology, characterized by a profound change of bone architecture, which leads to the diminishing of bone resistance and femoral head collapse. The main causes that lead to femoral head necrosis are represented by the decrease of local blood perfusion and increase of intraosseous pressure, because of an excessive development of adipose tissue in the areolas of the trabecular bone tissue in the femoral head. The histopathological and immunohistochemical (IHC) study performed by us showed that most of bone trabeculae were damaged by necrotic-involutive processes, their sizes being reduced, both regarding their length and their diameter; generally, the spans were thin, fragmented, distanced among them, which led to the occurrence of some large areolar cavities, full of conjunctive tissue, rich in adipocytes. Some of the residual bone spans even presented microfractures. In the structure of the trabecular bone tissue, numerous cavities showed lack of content, which indicates the death of osteocytes inside, while the endosteum appeared very thin, with few osteoprogenitor, flattened, difficult to highlight cells. The IHC study showed a low reaction of the bone reparatory processes and a reduced multiplication capacity of bone cells involved in the remodeling and remake of the diseased bone tissue. Nevertheless, there were identified numerous young conjunctive cells (fibroblasts, myofibroblasts), positive to proliferating cell nuclear antigen (PCNA), cells that have a high capacity of multiplication, participating in the formation of a fibrous conjunctive tissue (sclerous) instead of the damaged bone trabeculae. The formation of fibrous conjunctive tissue causes the reduction of mechanical resistance of the femoral head and its collapse. The IHC study of the microvascularization in the femoral head damaged by aseptic osteonecrosis showed the presence of a very low vascular system, both in the residual bone trabeculae and in the sclerous conjunctive tissue. Of the inflammatory cells present in the spongy bone tissue of the femoral head affected by osteonecrosis, the most numerous ones were the macrophages. Both macrophages and T-and B-lymphocytes had a heterogenous distribution.