Abstract 3142: Predictors of Heart Failure in Patients with Stable Coronary Artery Disease and Preserved Ejection Fraction
BACKGROUND: Heart failure (HF) is a disease commonly associated with coronary artery disease (CAD). Most risk models for HF development have focused on acute myocardial infarction (MI) patients. Renal disease is an emerging risk factor for cardiovascular morbidity and mortality, and the association between obesity and outcomes has been disparate. The prevention of events with angiotensin-converting enzyme inhibition (PEACE) population enabled the development of a risk model to predict HF in patients with stable CAD and preserved ejection fraction with particular attention to renal disease and obesity.
METHODS: In the 8290 PEACE patients without pre-existing HF, new-onset HF hospitalizations and fatal HF were assessed over a median follow-up of 4.8 years. Covariates with prevalence of >5% were evaluated in a Cox regression multivariable model using backward selection if p<0.05. A risk score was developed and converted to an integer-based scoring system.
RESULTS: Among the PEACE population (age 64±8, female 18%, prior MI 55%), there were 268 cases of fatal and non-fatal HF. 12 characteristics were associated with increased risk of HF (Table⇓) along with several baseline medications. Higher body mass index and lower glomerular filtration rate (GFR) were independently associated with greater risk of HF. Randomization to trandolapril independently reduced risk of HF. There was no interaction between trandolapril treatment and other risk factors for HF. The risk score (range 0 –21) demonstrated excellent discriminatory power (c-statistic 0.80). Risk of HF ranged from 1.75% in patients with a risk score of 0 to 33% in patients with risk score±16.
CONCLUSION: Among patients with stable CAD and preserved EF, lower GFR and higher BMI were independently associated with increased risk of HF. Trandolopril decreased the risk of HF in these patients with preserved EF. These stable CAD patients who remain at increased risk of HF development could be targeted for novel therapies.