{'fraction_non_alphanumeric': 0.020855057351407715, 'fraction_numerical': 0.0, 'mean_word_length': 6.007299270072993, '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}}
Update of antibiotic trials for secondary prevention of coronary heart disease.

The possibility that infection is a stimulus for the vascular inflammation that promotes atherogenesis has spawned clinical trials of antibiotics. These have focused primarily on Chlamydia pneumoniae as a potential atherogenic agent. In contrast to pilot studies, recent large trials, capped by the Azithromycin and Coronary Events Study and PRavastatin Or AtorVastatin Evaluation and Infection Therapy mega trials, indicate that standard antibiotics (e.g., azithromycin and gatifloxacin) are ineffective for secondary cardiovascular prevention. Despite this, observations continue to mount that infection can be a stimulus for atherothrombosis. Thus, one should rethink, revise and reformulate hypotheses, and research strategies, including novel antibiotics and treatment at earlier stages of disease, rather than discard infection prematurely as a potential etiologic factor.