Résumé :
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Communication n° 201 Familial myopathies are due to primary molecular alterations of striated skeletal and cardiac cells. During cardiomyopathies evolution, patients develop secondary alterations characterized by an abnormal cardiac electric activity and structural modifications of the myocardium leading to heart failure. Heart rate variability (HRV) reflects the functional status of the autonomic nervous system and its effects on sinus node. HRV analysis in patients with heart failure may help to identify those who are at risk of cardiac death. Finally, the autonomic innervation of the heart determines the efficiency of beta-blockers, which are commonly used in heart failure treatment. The aim of the study was to quantify early modifications of HRV in young cardiomyopathic hamsters (CHF147) at the stage of compensated heart failure. CHF147 hamster strain which is totally deficient in delta-sarcoglycan is a suitable model for dilated cardiomyopathies leading to heart failure. ECG monitoring using telemetry allowed performing long-term recordings on unrestrained animals (CHF147 vs. control). Quantitative analysis of time series were carried out on several segments of 1 minute each and allowed us to determine mean NN intervals (NNm), standard deviation of all normal NN intervals (SDNN) and Poincaré plots. In the second set of experiments we performed pharmacological assays to study both sympathetic and vagal tone. ECGs analysis showed a decrease in the NNm revealing a depressed HRV in cardiomyopathic hamsters even at an early stage of the myopathy. These results were confirmed by SDNN analysis of diseased animals compared to healthy wild types. Results were further confirmed by Poincaré plot analysis. Moreover, pharmacological assays allowed identifying an increase in the sympathetic tone that translates a high sympathetic activity. Thus, in addition to the genetic modifications responsible for the myopathy, there is a secondary impairment in the neurovegetative system even at early
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