Experimental ‏review ‏of ‏cobalt ‏induced cardiomyopathy

Abstract

The heart is a target of injury for many chemical compounds, both medically prescribed and not. Pathophysiological mechanisms underlying development of chemical-induced cardiomyopathies vary depending on the inciting agent, and can include: direct toxic effects, neurohormonal activation, altered calcium homeostasis, and oxidative stress. The fact that drug-induced heart disease, and in particular cobalt-induced cardiomyopathy, does not occur more often, as would be expected from the diversity of various mechanisms, is perhaps surprising. In spite of this, cardiotoxicity remains a major problem of hundreds of pharmaceutical agents, industrial chemicals and naturally occurring products and is often a limiting factor in treatment of certain diseases. Hence, it must be taken in account in the process of clinical decision making and treatment as well as in the process of drug research and development. The primary morphological alteration is mitochondrial damage that possibly reflects an enzymatic block of oxidative decarboxylation at pyruvate and ketogluterate levels. Due to that myofibrils of the myocardial cells were affected highlighting that the main cause of myofibril reduction could be a lower oxygen intake in the perinuclear area. The reduction of the contractile support of myocardial cells can explain the possible myocardial dysfunction. Nuclear changes were consistent with sarcoplasmic alterations, our study showing deformed, twisted, hyperchromatic nuclei with heterogeneous chromatin and even disintegrating nuclei. Changes of the interstitial connective tissue were sometimes extensive and sometimes barely noticeable. The most common alteration of this structure was the onset and development of a mainly perivascular collagen fibrillogenetic process.

Keywords

• cobalt
• heart
• rats
• cardiomyocytes
• mitochondria