Cardiac response to changes in central venous sonomorphology: Mechanism of impaired heart relaxation in patients with varicose veins of lower extremities.

AIM

This study examines the interactions between central venous and cardiac sonomorphologies to explain the mechanism of impaired heart relaxation in patients with varicose veins of lower extremities.

MATERIAL AND METHODS

Part 1: We performed retrospective analysis of influences of inferior vena cava (IVC) diameters on tricuspid and mitral inflow and annular velocities in 64 patients with primary varicose veins. Part 2: We compared IVC diameters and IVC collapsibility index (IVC CI) in patients with varicose veins with normal values.

RESULTS

We found a significant positive influence of an increase in maximal expiratory and minimal inspiratory IVC diameters on mitral and tricuspid early annular velocities or e-waves (-values < .008), inflow velocities or E-waves (-values < .05) and early to late inflow E/A ratios (-values < .01). Less influenced by the changes in venous biometry (-values > .05) were late mitral and tricuspid inflow, annular and systolic velocities (A-, a-, s-waves).Expiratory and inspiratory diameters in patients with varicose veins were significantly smaller (-values < .05 expiratory; < .0001 inspiratory), and IVC CI was significantly higher (-values < .0001) than the normal values.

CONCLUSION

Chronic venous disease impairs the function and the morphology of the entire inferior caval system and the heart. Impaired relaxation of the heart in patients with varicose veins is the result of two factors: (1) impaired venous return resulting in the low central venous pressure and the low early diastolic cardiac inflow; (2) structural changes in the heart resulting in the compensatory increased late diastolic cardiac inflow. Increase in central venous pressure (IVC diameters) and early diastolic cardiac inflow (E-waves), accompanied by unchanged myocardial response (e-wave) can serve as marker for return to normal physiology.