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Cardiotoxicity is the occurrence of heart dysfunction as electric or muscle damage, resulting in heart toxicity. [1] This can cause heart failure, arrhythmia, myocarditis, and cardiomyopathy in patients. [2] Some effects are reversible, while in others, permanent damage requiring further treatment may arise.
Aromatase inhibitors (AIs) are a class of drugs used in the treatment of breast cancer in postmenopausal women and in men, [1] [2] and gynecomastia in men. They may also be used off-label to reduce estrogen conversion when supplementing testosterone exogenously. They may also be used for chemoprevention in women at high risk for breast cancer.
Two distinct drug classes in which cardiotoxicity can occur are in anti-cancer and antiarrhythmic drugs. Anti-cancer drug classes that cause cardiotoxicity include anthracyclines, monoclonal antibodies, and antimetabolites. This form generally manifests as a progressive form of heart failure, but can also manifest as an harmful arrhythmia. [2]
Chemical structure of the endogenous androstenedione. In the human body, the enzyme aromatase converts androstenedione to estrogen. Aromatase is an enzyme that belongs to the cytochrome P450 family located on chromosome 15. In the human body, the aromatase consists of 10 β-strands (1 major sheet and 3 minor sheets) and 12 α-helixes.
The medication has been found to achieve 96.7% to 97.3% inhibition of aromatase at a dosage of 1 mg/day and 98.1% inhibition of aromatase at a dosage of 10 mg/day in humans. [3] [2] As such, 1 mg/day is considered to be the minimal dosage required to achieve maximal suppression of aromatase with anastrozole. [3]
That sound can signal carotid artery stenosis—narrowing of the blood vessels that carry blood from the heart to the brain—or the rare vascular disease fibromuscular dysplasia.
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