Heart failure with preserved and slightly impaired ejection fraction and cardiovascular events: Pathogenetic interrelations as a part of the cardiovascular continuum

Abstract

Aim. To evaluate the effect of decompensated HF with preserved or slightly impaired EF on the risk of cardiovascular complications during a 5-year follow-up. Materials and methods. 33 patients with arterial hypertension and HF with preserved or slightly impaired EF (NT-proBNP ≥125 pg/ml, mean, 500.1±590.32 pg/ml and EF ≥40%, mean, 57.0±10.29%) were observed for 5 years. EchoCG, markers of immune inflammation and hormonal changes (endothelin, tumor necrosis factor (TNF), interleukin-6 (IL-6), aldoste-rone, renin) were evaluated at baseline. The endpoint was development of acute fatal and non-fatal cardiovascular events (CVEs). The one-way regression analysis was used to identify predictors of the risk for CVEs. The ROC analysis was used to determine “threshold levels” of significant predictors for this risk. Results. During the 5-year follow-up period, CVEs developed in 13 (39.4%) patients. The CVE predictors included baseline increases in creatinine and IL-6, NT-proBNP and a greater decrease in EF (р<0.05 for each factor). The ROC analysis showed that NT-proBNP ≥235.8 pg/ml was the most effective predictor of CVEs (sensitivity, 92.3%; specificity, 60%; area under the curve, 0.736; р=0.045). Comparison of patient subgroups with baseline values of NT-proBNP higher or lower than the predetermined threshold (n=13 and n=20, respectively) detected an association of more severe HF decompensation with activation of neurohormonal systems and a worse prognosis. Specifically, patients with higher NT-proBNP had also higher levels of IL-6 (р=0.048) and creatinine (р=0.047) and a greater proportion of patients with CVEs (р=0.008). Conclusions. Possible mechanisms of cardiovascular complications in HF with preserved or slightly impaired ejection fraction include activation of immune inflammatory systems. In its turn, the process of heart failure decompensation itself can become a factor intensifying production of proinflammatory cytokines. Heart wall tension may play a special role in the increased activity of inflammatory process and exert an independent effect on development of acute complications in CVDs.