{'fraction_non_alphanumeric': 0.02717391304347826, 'fraction_numerical': 0.012907608695652174, 'mean_word_length': 5.517699115044247, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Cocaine and apoptosis in myocardial cells

Toxic effects of cocaine on the heart muscle have been known for many years. Cardiovascular complications related to cocaine abuse include myocardial ischemia and infarction, inflammation, and disease of the heart muscle, rhythm disturbances, and sudden cardiac death. Cocaine toxicity‐related cardiac morbidity and mortality are often due to several interacting mechanisms. Cocaine also has a potent pharmacological effect, indirectly stimulating the sympathetic nervous system, and it has a direct toxic effect on the heart. Although apoptosis (also called programmed cell death) has been shown to play an important role in the pathogenesis of several diseases in the heart, including heart failure and ischemic myocardial infarction, the role of apoptosis in the toxic effect of cocaine on the heart has not been explored. Recent studies indicated that cocaine causes apoptotic cell death in both adult and fetal heart muscles. Increased oxidative stress and reactive oxygen species, and the subsequent activation of a “stress responsive” enzyme (p38‐mitogen‐activated protein kinase) in the heart may play an important role in cocaine‐induced apoptosis in the heart muscle. These findings suggest a new way to understand the cardiotoxic effects of cocaine, and may have potential clinical implications in the better management of cocaine‐induced heart diseases. Anat Rec (New Anat): 257:208–216, 1999. © 1999 Wiley‐Liss, Inc.