Phlebology | 2021
Varicose vein and diastolic dysfunction: Is there an interaction?
Abstract
Dear Editor, We have read with great interest the article published by Rusninovich Y and Rusinovich V and congratulate the authors for assessing and reporting the cardiac Doppler findings in patients with varicose vein (VV) for the first time. They have examined the characteristics of cardiac Doppler in patients with primary VVs of lower extremities and compared them with normal subjects without VV. Patients with primary VVs in comparison with normal controls have impaired relaxation of right and left ventricles documented by lower early diastolic mitral and tricuspid inflow velocities. Moreover, they have reported higher systolic mitral and tricuspid annular velocities. Eventually they have commented that increased atrial ejection fraction due to altered preload in patients with primary VVs are the possible mechanisms of these cardiac Doppler findings in patients with primary varicose veins. We would like to make further evaluation on their comments. Echocardiographic assessment of patients with varicose vein or chronic venous insufficiency would certainly improve our understanding on the pathophysiology and hemodynamic consequences of VVs. Beyond the limitations such as retrospective, single center design and low number of patients which have been already mentioned by the authors, cardiac Doppler findings give rise several issues which need to be discussed carefully. The association between the echocardiographic findings revealing impaired diastolic relaxation and VV might have been arisen from the influence of hemodynamic consequences of VV on the cardiac filling pressure and subsequent diastolic and systolic functions of the heart. Unfortunately we don’t have too much knowledge in literature regarding the effects of peripheral VV on cardiac filling pressures and volumes. Impaired relaxation might be attributed to increase in atrial volumes which results in forceful atrial contraction. However impaired diastolic relaxation, namely grade I diastolic dysfunction does not necessitate increased volume inflow into heart chambers. Impaired relaxation of right and left ventricles themselves is the other major mechanism of diastolic dysfunction. Recently, VV has been classified under the term of dilating venous diseases with the presumption that it is the local manifestation of systemic vascular wall abnormality. In this context, not only the hemodynamic changes but also the ultra-structural changes in vascular wall and extracellular matrix in heart chambers may be responsible for the impaired relaxation of the heart in patients with VV. Likewise coronary artery ectasia which has been defined as a member of dilating vascular disease, has shown to be associated with left ventricular diastolic dysfunction. However this issue needs to be clarified in future studies focusing on the cardiac filling volumes and pressures directly. Hemodynamic and morphologic changes of heart chambers in association with contribution of hemodynamic and morphologic changes of vena cava should be assesses in patients with VVs or dilating venous disease.