Cardiotoxicity of Cancer Therapy: Mechanisms and Predictors
The overall study objectives are:
1. To determine the longitudinal relationships between circulating NRG-1β levels and
incident risk of adverse cardiovascular outcomes in patients exposed to anthracycline,
trastuzumab, or a combination of the two agents. We hypothesize that a sustained
increase in NRG-1β, indicative of enhanced cardiac stress with exposure to
chemotherapeutic agents, is predictive of an increased risk of cardiac dysfunction and
2. To study the SNP/haplotype variation in the Neuregulin/ErbB signaling pathway on
incident risk of adverse cardiovascular outcomes. We hypothesize that there will be
SNP/haplotypes variations that are associated with incident cardiovascular outcomes.
3. To determine the longitudinal relationships between echocardiographic measures of
strain and strain rate and incident cardiac dysfunction in patients exposed to
anthracycline, trastuzumab, or a combination of the two agents. We hypothesize that
early declines in strain and strain rate are predictive of an increased risk of future
cardiac dysfunction and heart failure.
4. To explore the changes in NRG-1β levels and the relationships with novel
echocardiographic measures of cardiac function.
5. To create a biobank as a future resource for additional questions in novel biomarkers
6. To determine the long-term effects of cancer therapy cardiotoxicity by following
patients yearly for a total of 5 years after their exposure to cancer therapy.
Observational Model: Cohort, Time Perspective: Prospective
Cardiac dysfunction or signs or symptoms of heart failure
Cardiac dysfunction. as defined according to the CREC criteria as a decline in LVEF of 10% to less than 55% without signs or symptoms
United States: Institutional Review Board
|Abramson Cancer Center of the University of Pennsylvania||Philadelphia, Pennsylvania 19104-4283|