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
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.
- Patients with poor LV function and an EF of ≤35%
- Patients who are symptomatic with Class II or Class III heart failure on optimal
- Patients with EKG showing QRS duration of greater than 120 ms and meet criteria for
Bi-ventricular ICD implantation.
- Patients with other co-morbid conditions which could contribute to cachexia, such as
end stage renal disease, ongoing malignancy, chronic or acute liver failure, age
greater than 80yrs.
- Patients who are unable to walk and are wheelchair bound or need assistance to walk
for reasons other than CHF.
- Patients with muscular dystrophies and myopathies.
- Patients with untreated hyper or hypothyroidism.
- Patients on Dialysis.
- Patients with recent (<12 weeks) revascularization.
- Patients with recent (<12 weeks) myocardial infarction.