Abstract 1995: Chronic Kidney Disease, Ejection Fraction and Heart Failure in Patients with Occluded Infarct-Related Arteries Post-Myocardial Infarction: Data from the Occluded Artery Trial
Background Chronic kidney disease (CKD) is associated with adverse outcomes following MI, including heart failure (HF). The prevalence of CKD and whether CKD is associated with HF in a non-reperfused MI population is unknown.
Method OAT is a randomized trial of PCI vs medical therapy in asymptomatic high risk pts with occluded infarct-related artery (IRA) 3–28 days after MI and creatinine ≤ 2.5 mg/dl. 2,114 of 2,176 patients were grouped into CKD Stages by GFR (ml/min, MDRD formula) at enrollment (Stg 1 ≥ 90, Stg 2 60 – 89, Stg 3 30 –59, Stg 4 15–29). HF was defined as Killip Class > 1 during index MI. Preserved and depressed EF were defined by EF cut-point of 45% (median EF in OAT).
Results (Table⇓) The prevalence of CKD (Stage > 1) was 71% (56.6% Stg 2, 14.5% Stg 3, 0.4% Stg 4). CKD was associated with older age, female gender, diabetes, hypertension, mitral regurgitation and higher Troponin I. Inducible ischemia, number of diseased vessels, IRA location, collaterals and EF were similar across CKD stgs. Prevalence of HF was higher with increasing CKD Stage overall (Stg 1: 15.5%, Stg 2: 18.0%, Stg 3: 29.3% – p < 0.0001); in pts with EF ≥ 45% (Stg 1: 9.5%, Stg 2: 14.5%, Stg 3: 23.2% – p < 0.0001) and in pts with EF < 45% (Stg 1: 26.6%, Stg 2: 23.9%, Stg 3: 37.5% – p = 0.004). In a logistic regression model for correlates of HF, there was a significant interaction between GFR and EF (Wald score 38.620, p < 0.0001). GFR was an independent correlate of HF overall and in pts with preserved EF but not in pts with depressed EF (Table⇓).
Conclusion In pts with occluded IRA post MI, there was a high prevalence of CKD, despite excluding pts with creatinine > 2.5. The effect of CKD on HF was independent of and not additive to the effect of depressed EF. This suggests that HF may result from either CKD or systolic dysfunction post-MI, both of which are independent pathophysiologic states that impair sodium and fluid homeostasis.