Relationship between Systolic Ejection Time and Inflammation in End-Stage Heart Failure

Systolic ejection time (SET) and systemic inflammation are two essential indicators of heart failure (HF) progression. We aimed to evaluate the associations between SET and inflammatory mediators in end-stage HF.

Participants included 16 patients with end-stage HF recruited from the Heart Failure Clinic at Toronto General Hospital and 16 healthy individuals free of any known cardiovascular disease. SET, end systolic pressure, and levels of inflammatory mediators were documented for each patient, and a Spearman rank correlation coefficient was performed to examine differences between patients with end-stage HF and healthy controls.

The mean SET in patients with HF was shorter than in the healthy controls (283.5 ± 34.3 ms vs 330.1 ± 19.0 ms, P < 0.001). C-reactive protein (P = 0.001), macrophage inflammatory protein-1β (P = 0.041), macrophage-derived chemokine (P = 0.007), and cyclic guanosine monophosphate (P < 0.001) levels were negatively correlated with SET. The levels of other inflammatory mediators-granulocyte-stimulating factor, granulocyte-macrophage colony-stimulating factor, interleukin-8, macrophage inflammatory protein-1, macrophage inflammatory protein-1α, and tumor necrosis factor α-were not significantly correlated with SET.

We found that SET was significantly lower in patients with end-stage HF compared with healthy controls and that reduced SET correlated with increased levels of several inflammatory mediators in patients with HF. By better understanding the relationship between SET and inflammation in HF, a more thorough evaluation could lead to improved risk stratification among patients with HF. Future work should investigate the roles of SET and inflammation in HF.