Genes expressing inflammatory cytokines (TNF- alpha, IL1 etc) and genes involved in apoptosis (Caspase 3, Bax, Bcl-2, Fas) are dysregulated in the skeletal muscles of the patients who have muscle wasting and decreased exercise capacity with CHF. Patients who show benefit from CRT may also show reversal of the inflammatory/apoptotic cascade that accompanies CHF and these patients may be the ones who benefit the most from CRT
1\. The general objective of this study is to: 1. To identify the molecular pathways that may be altered in the blood and skeletal muscles of the patients undergoing CRT by using transcriptional analysis of the blood and skeletal muscle in these patients 2. To identify objective measurable molecular signals, using gene expression profiling, that correlate with clinical improvement in patients undergoing CRT. 3. To identify the molecular profile of patients who are most likely to benefit from CRT with improvement of exercise capacity and reversal of cardiac cachexia. 4. To identify biochemical pathways involved in cardiac cachexia. 5. To identify genes involved in positive remodeling and reversal of apoptotic cascade in the skeletal muscle.
Study Type
OBSERVATIONAL
Enrollment
30
Duke University Medical Center
Durham, North Carolina, United States
Shift of the muscle transcriptome away from Apoptosis/Inflammation. Reversal of active apoptosis in skeletal muscle.Quality of life assessment(Minn.HF Ques) Exercise capacity (6 min walk).
Time frame: 6 months
Improved LV synchrony as determined by TDI, Decrease in blood markers of inflammation and Oxidative stress and catabolism.
Time frame: 6 months
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