Abstract
Chagas disease (CD) remains a major cause of cardiomyopathy and stroke in developing countries. Brain damage in CD has been attributed exclusively to the effects of structural heart disease on the brain, including cardioembolism and low cardiac output symptoms. However, CD patients also develop stroke and brain atrophy independently of cardiac disease severity. Chronic inflammation directed against T. cruzi may act as a trigger for endothelial damage, platelet activation, acceleration of atherosclerosis and apoptosis, all of which lead to stroke and brain atrophy. In the present article, evidence supporting this new theory is presented, along with considerations towards mechanistically-based targeted treatment.
Highlights
Chagas disease (CD) remains a major cause of cardiomyopathy and stroke in developing countries
The numbers are awe-striking: in endemic areas, up to 25% of the population bear positive serologic tests for Chagas disease,[4] usually infected as children; 30% will go on to develop a chronic form of cardiopathy and 10% will suffer a stroke often as young adults.[5]
Most interest in Chagas disease has been directed at two more recent phenomena: the possibility of blood-borne transmission from immigrants of endemic areas;[6,7,8] and the resurgence of acute forms of Chagas disease, including encephalitic forms, in patients with HIV co-infection.[9,10]. These forms will not be discussed here. While both are potentially important, the present article will focus on three more general questions relevant to all individuals infected with T. cruzi: is there evidence for brain involvement in Chagas disease? If so, what are the mechanisms for this involvement? what potential treatments exist?
Summary
Abstract – Chagas disease (CD) remains a major cause of cardiomyopathy and stroke in developing countries. In the chronic cardiomyopathy phase, no parasites were found in the brain in the series described, except for rare patients co-infected by HIV.[9,10] Most changes are attributable to passive congestion by left ventricular heart failure, low cardiac output, neuronal ischemia, and brain infarcts frequently stemming from a left ventricular apical thrombus.
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