Újabb adatok a megtartott ejekciós frakciójú szívelégtelenség (HFPEF), diastolés bal kamrai dysfunctio pathomechanizmusához

Abstract

We investigated whether there is correlation between the presence or absence of diastolic dysfuncton and oxidative stress, inflammation, coagulation parameters and the stiffness of vascular wall. The MacIver theory of the pathogenesis of heart failure with preserved ejection fraction ( HFPEF ) was also studied. We examined 80 patients, who were sixty years old or older ( 70 hypertonic patient, 10 control ). With echocardiography we found mild left ventricular diastolic dysfunction in 46 of 70 patients ( 66% ) ( HTDD+ group ). In 24 of 70 patients ( 34% ) there were not left ventricular diastolic dysfunction ( HTDD- group ). The total scavenger capacity ( TSC ) was in significant negative correlation with the mean of left ventricular maximal strain rate, with the mean strain rate of atrial contraction period, with left atrial volume ( LAV ) and the LAV / body surface area values, and was in positive correlation with the mean values of atrial reservoir strain and strain rate. The levels of interleukin-6 ( IL-6 ), tumor necrosis factor-α ( TNF-α ), and C-reactive protein ( CRP ) were in positive correlation with LAV / body surface area values. The values of left ventricular mass ( LVM ) and LVM / body surface area were significantly increased, the stroke volume ( SV ) was reduced in the HTDD+ group compared to the control group. The values of EF / LVM and EF / ( LVM / body surface area ) were reduced in both HTDD+ and HTDD- groups according to the control. The carotis score was significantly higher in HTDD+ group than in the control. In conclusion, oxidative stress and inflammation might have a primary pathogenetic role in generation of left ventricular diastolic dysfunction and oxidative stress may lead to left ventricular and atrial systolic dysfunction and to reduced atrial reservoir period deformation in hypertonic patients with preserved ejection fraction ( EF ). Our preliminary results confirm the MacIver hypothesis. The preserved ejection fraction is not due to the increased radial systolic function, but the effect of left ventricular hypertrophy and constant absolute radial wall thickening. Instead of EF the EF / LVM and EF / ( LVM / body surface area ) values should be used to characterize the true degree of systolic dysfunction in HFPEF