Abstract

Hypertension is the leading cause of cardiovascular diseases Nevertheless diagnosed hypertension can be controlled and monitored with adequate drug regimens. Yet once cardiac hypertrophy is established, a number of patients develop diastolic cardiac dysfunction resulting from cardiac remodeling with fibrosis and cell death. The present study aims to test the hypothesis that animals with aortic stenosis for five weeks can restore cardiac function after the removal of the aortic constriction. Male mice with 10 weeks of age were randomized in three groups Sham , Rem , and Tac . After five weeks of the establishment of cardiac hypertrophy the aortic constriction was removed and the animals were followed for additional five weeks Rem . The positive control group Tac remained with the clip until ten weeks. Echocardiography was performed after 72 hours of the removal of the five weeks stenosis Rem and at the end of ten weeks. We also used cutoff points based on sham group for the ejection fraction EF≥45% and the ratio of E wave per e’ E/e’≤35 . The Rem group was separated into two outcomes according to the presence of dysfunction. Results were expressed as mean ± standard error of the mean SEM. Statistical analyses were performed and p≤0.05 were considered statistically significant. Septum thickness increased after five weeks of stenosis in both Rem 0.812±0.01mm and Tac 0.764±0.02mm groups as compared to sham group 0.675±0.01mm p≤0.05. Left ventricle mass was significantly different in Sham vs Tac 73.98±2.40mg vs 111.79±11.81mg p<0.0001 After 10 weeks the REM group did not present any hypertrophy markers. Among 18 animals of Rem group, 9 had reduced EF compared to sham after 5 weeks 36.97±1.87%vs52,74±4.17% p<0.0001 and after 10 weeks 49±1.13%vs40±1.06% p<0.0001 constituting an occurrence of systolic problems of 50%. When we analyzed E/e’ 13 animals presented diastolic dysfunction and an increased ratio compared to sham animals 41.07±1.12vs30.79±1.95 p<0.05 at 5 weeks. Therefore, the occurrence of diastolic dysfunction reached 72%. The proposed model induced hypertrophy. Despite that, only half the Rem animals had a reduction in ejection fraction, whereas most developed diastolic dysfunction. These findings open a new path for the investigation of these distinct outcomes

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