{'fraction_non_alphanumeric': 0.022912047302291204, 'fraction_numerical': 0.019216555801921657, 'mean_word_length': 4.991150442477876, '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}}
Attempted diagnosis of ventricular mural thrombi in acute mycardial infarction using 125I-labelled fibrinogen.

In an attempt to diagnose ventricular mural thrombi complicating acute myocardial infarction (AMI), 80 patients have been given 100 muCi 125I-labelled fibrinogen after admission to a CCU. Precordial radioactivity was recorded for the following 6 days over four sites corresponding to chest leads CR1-CR4. A sustained rise in radioactivity of at least 15% of initial recordings was classed as type A pattern, a minor rise or flattened response as type B pattern and a rapid decrease as type C pattern; 28% showed a type A, 19% a type B and 54% a type C pattern. There was no significant difference between the groups in incidence of pericardial friction rub but when patients with suspected pericarditis (as evidenced by characteristic pains) were added, pericarditis was significantly overrepresented in the type A group. Smaller infarctions (SGOT less than 100 U/1) were significantly more common in patients with a type C decay pattern. No differences were noted between the groups as regards type and site of the infarction. A sustained rise in precordial radioactivity after an AMI may be an indication of mural thrombosis but the influence of other factors secondary to an infarction, e.g. pericarditis, cannot be determined at present.