{'fraction_non_alphanumeric': 0.018613607188703467, 'fraction_numerical': 0.004492939666238768, 'mean_word_length': 5.837719298245614, '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}}
Cardiac effects of ACE inhibition.

Hypertension frequently is associated with a number of changes in heart structure and function, such as left ventricular hypertrophy, disturbed diastolic function, and subnormal stroke volume during exercise. Most of these changes probably are related to myocardial fibrosis. Antihypertensive agents reverse the structural and functional changes to different degrees. The hemodynamic changes in central hemodynamics at rest and during exercise were studied before and after angiotensin-converting enzyme (ACE) inhibition in 68 patients with essential hypertension (ranging from severe to moderately severe). In patients with moderately severe hypertension who were administered perindoprilat intravenously, mean arterial pressure was reduced by approximately 17% due to reduction in total peripheral resistance and no changes in heart pump function. Chronic treatment with captopril, enalapril, or lisinopril for 6-12 months induced reduction in blood pressure associated with decreased peripheral resistance. In general, there were only minor changes in cardiac output, stroke volume, and heart rate. Studies from other laboratories have shown that ACE inhibitors reverse left ventricular hypertrophy and improve left ventricular diastolic function. Captopril also appears to improve coronary circulation. The effect of ACE inhibitors on heart structure and function appears promising with regard to cardioprotection during chronic use, but long-term studies are needed to prove that this will occur in clinical practice.