ABSTRACT
The heart propels blood through the lungs and peripheral circulatory system, providing oxygen and nutrients to all tissues. The efficiency and ability of the heart to perform its task depend on the coordinated conduction of the cardiac impulse and the rapid coordinated activation of the contractile apparatus. The morphologic reactions of the heart to toxic injury can be classified into four categories: cardiac hypertrophy; cardiomyopathies; cardiac necrosis, including infarct-like lesions, hypersensitivity (allergic) myocarditis, and toxic myocarditis; and pericarditis. Endocardial mural thickening can occur in association with toxic or ischemic myocardial necrosis. Chemicals can cause myocardial injury also by direct toxic effects which result in cell damage and cell death. Drugs that cause toxic myocarditis, hypersensitivity myocarditis, or large areas of myocardial necrosis often also cause pericarditis by extension of the inflammation to the pericardium, particularly the visceral pericardium.
