{'fraction_non_alphanumeric': 0.017444601603017446, 'fraction_numerical': 0.007072135785007072, 'mean_word_length': 6.120805369127517, '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}}
Evaluation of left ventricular contractile performance from baseline stress‐shortening data in humans: comparison with pharmacological afterload challenge

The purpose of this study was to evaluate whether the baseline stress‐shortening data reflect the contractile state adequately and give results comparable to the evaluation of the end‐systolic stress‐shortening relationships using pharmacological manipulation of afterload. Five groups were studied (total 152 patients): a control group of 30 healthy volunteers, 32 patients after surgical correction of infantile tetralogy of Fallot, 50 patients treated for childhood malignancies with doxorubicin, 17 patients with left ventricular hypertrophy due to systemic hypertension, and 23 patients with congestive cardiomyopathy. In all patients except those with congestive cardiomyopathy, afterload was altered pharmacologically to evaluate the individual stress‐shortening relationship. In all patients the baseline stress‐shortening data were evaluated, as well as their relative positions to two predefined normal ranges for the relationship between end‐systolic stress and shortening. Additionally, a slope value was calculated from the baseline data of the five groups studied and compared with the data obtained by pharmacological afterload increment. Our data show that the comparison of individual baseline data of end‐systolic wall stress and fractional shortening with predefined normal ranges for the relationship between end‐systolic stress and shortening is inadequate. The appropriate normal range to compare with is the 95% confidence interval of baseline stress‐shortening data in normal subjects. Also the calculation of a slope value from the baseline stress‐shortening data of a group of patients seems to be inappropriate. Such a slope value does not necessarily reflect the contractile state, as the specific conditions leading to variations of end‐systolic wall stress are undefined and not standardized, and the correlation between baseline stress‐shortening data depends largely on the influence of the end‐systolic dimension on both parameters.