{'fraction_non_alphanumeric': 0.011235955056179775, 'fraction_numerical': 0.0, 'mean_word_length': 6.060975609756097, '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}}
Angiotensin converting enzyme inhibitors and cardiovascular remodelling.

Regional alterations in left ventricular function are generally present in patients who sustain an acute myocardial infarction. Segmental wall motion abnormalities in left ventricular systolic function can be identified in the hyperacute period and generally persist in patients with myocardial infarction. Through the process of infarct expansion, the infarcted territory may thin and lengthen in the short term following a myocardial infarction. Some infarct survivors are also prone to further progressive alterations in the shape and size of the left ventricle, a process that has been termed "postinfarction ventricular remodelling". Although a component of left ventricular remodelling appears to represent an adaptive process serving to preserve stroke volume and cardiac output following myocardial injury, the enlargement process may have undesirable long term effects on global left ventricular function and on clinical prognosis. Fortunately, recent experimental and clinical evidence shows that ventricular remodelling and its deleterious consequences may be preventable.