Vol 77, No 1 (2019)
Original articles
Published online: 2018-11-07

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Inflammatory markers and left ventricular diastolic dysfunction in a family-based population study

Małgorzata Kloch, Katarzyna Stolarz-Skrzypek, Agnieszka Olszanecka, Wiktoria Wojciechowska, Adam Bednarski, Justyna Stefaniak, Danuta Czarnecka
Kardiol Pol 2019;77(1):33-39.

Abstract

Background: Heart failure affects patients with normal left ventricular systolic function (heart failure with preserved ejection fraction [HFPEF]) and those with reduced ejection fraction (HFREF). The treatment of HFPEF remains an unresolved issue.

Aims: We sought to determinate the relationship between inflammatory markers and left ventricular diastolic dysfunction (LVDD) in a family-based population study.

Methods: A total of 303 participants from the general population (55% women, median age 49 years and 45% men, median age 40 years) underwent echocardiography and measurement of serum inflammatory markers: C-reactive protein (CRP), myeloperoxidase (MPO), and interleukin 6 (IL-6).

Results: Serum IL-6 concentration correlated with peak transmitral late diastolic velocity (A) and pulmonary vein systolic-to-di­astolic velocity (S/D) ratio (p < 0.01). Moreover, a significant correlation between IL-6 concentration and E/A ratio and early diastolic peak velocities of the mitral annulus displacement (E’) was observed. The association of IL-6 concentration and peak transmitral early diastolic velocities (E) and the E/E’ ratio (p < 0.05) was noted in men. In addition, the CRP concentration was shown to have an effect on E/A ratio in women (p < 0.05). A significant correlation between the CRP concentration and S/D ratio was observed both in women (p < 0.01) and men (p < 0.05). No significant correlation was found between the level of MPO and LVDD parameters. Additionally, only one predictive model was identified; E’ was found to be dependent on IL-6, age, and heart rate in men (p < 0.001, R2 = 0.611).

Conclusions: The above results suggest that inflammation may lead to the onset of LVDD, probably via vascular endothelial dysfunction.

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