Toxic and radiation injury of the myocardium
- Lesion
Some cancer drugs, cocaine, high adrenaline, thyroid disease and chest radiation can damage the heart muscle directly.
What it is
The myocardium can be injured by toxins and hormones. Anthracyclines (doxorubicin) cause a dose-dependent dilated cardiomyopathy through oxidative and topoisomerase-related damage; trastuzumab causes a mostly reversible dysfunction; immune checkpoint inhibitors cause lymphocytic myocarditis. Catecholamines (pheochromocytoma, cocaine, intense stress, high-dose pressors) cause vasospasm, tachycardia and focal contraction-band necrosis. Thyroid disease changes the heart: hyperthyroidism causes tachycardia, atrial fibrillation and high-output failure; hypothyroidism causes low output and pericardial effusion. Chest radiation causes pericarditis, myocardial fibrosis, valve thickening and accelerated coronary disease.
Structure
- Catecholamine injury: foci of hypercontracted myocytes with dense eosinophilic transverse bands and scattered inflammatory cells.
- Anthracycline injury: on electron microscopy, loss of myofibrils and vacuolisation from dilated sarcoplasmic reticulum.
Toxic and endocrine injury to the myocardium
| Agent | Mechanism | Pathology | Clinical |
|---|---|---|---|
| Anthracyclines | Oxidative stress, topoisomerase II-β damage | Myocyte vacuolisation, myofibril loss, fibrosis | Dose-dependent dilated cardiomyopathy |
| Trastuzumab | Loss of HER2 survival signalling | Little structural damage | Mostly reversible dysfunction |
| Immune checkpoint inhibitors | T-cell attack on myocytes | Lymphocytic myocarditis | Arrhythmia, failure, high mortality |
| Cocaine | Catecholamine excess, spasm, thrombosis | Contraction-band necrosis, infarcts | Chest pain, MI, arrhythmia |
| Pheochromocytoma and stress | Catecholamine excess | Contraction-band necrosis, focal myocarditis | Arrhythmia, stress cardiomyopathy |
| Hyperthyroidism | Increased metabolism and β-adrenergic sensitivity | Hypertrophy, little else | Tachycardia, AF, high-output failure |
| Chest radiation | Endothelial and fibroblast injury | Fibrosis of pericardium, myocardium, valves, coronary arteries | Constriction, restriction, early coronary disease |
Clinical notes
- Patients receiving cardiotoxic cancer therapy are monitored with serial echocardiography (cardio-oncology).
Test yourself
Think of the answer, then tap the question to see it.
What determines anthracycline cardiotoxicity?
Mainly the cumulative dose; the resulting dilated cardiomyopathy is often irreversible.
What is the typical lesion of catecholamine excess in the heart?
Focal contraction-band necrosis of myocytes.
Which cardiac effect is classic for hypothyroidism?
Pericardial effusion with a flabby, low-output heart (also bradycardia).
Elsewhere in DurgiPedia
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Cardiomyopathy | Enlarged Heart | MedlinePlus (MedlinePlus, US National Library of Medicine, 2025); Dilated cardiomyopathy: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.