Direct Contribution of Anemia to Cardiac Overload Determined by Natriuretic Peptide and Covariance Structure Analyses

Background: While anemia can occur concomitantly with chronic kidney disease (CKD), the adverse cardiovascular effects of anemia, including heart failure (HF), remain unclear. Thus, the direct effects of anemia on the left ventricular ejection fraction (LVEF), as a marker of systolic function, and the plasma B-type natriuretic peptide (BNP) level, as a marker of cardiac overload, were investigated. Methods: Covariance structure analyses were proposed for 1536 inpatients to examine the interactions among the estimated glomerular filtration rate, hemoglobin (Hb), LVEF, and LogBNP. Results: The theoretical path models revealed that CKD was a significant causal factor of not only decreases in both LVEF and Hb (standardized regression coefficients (β): 0.150 and 0.157, respectively) but also an increase in LogBNP (β: −0.200), suggesting that CKD decreases cardiac function and increases cardiac overload. The apparent response of systolic function to anemia (β from Hb to LVEF: −0.070) tempered cardiac overload (β from LVEF to LogBNP: −0.455), but anemia was a cause of significant increase in LogBNP (β from Hb to LogBNP: −0.352), confirming that anemia is an enhancing factor of cardiac overload. Conclusion: Anemia was found to be a substantial risk factor for worsening cardiac overload; however, this disadvantage could be unclear and underestimated because of the concomitant effects of CKD as well as the apparent augmentation of systolic function due to anemia.