Varicose Veins: Systemic Hemodynamic Disorder or Systemic Vascular Wall Pathology?

Abstract

Dear Editor,We have read the article published by Kalinin et al 1 with great interest and enthusiasm. Briefly, they have included 583 patients and studied duplex sonography. They have also assessed diastolic function in 46 out of 583 patients by echocardiography. Statistically significant differences in the diameter of the great saphenous vein, diameter of the perforator veins (PVs), and the velocity reflux flow through the PVs have been reported between class C2 and C4 varicose veins. Engrossingly, they have also assessed diastolic dysfunction in patients with chronic venous insufficiency (CVI). They have reported that higher clinical classes of varicose disease are associated with an increased incidence of nonrestrictive blood flow through the tricuspid valve, which might be associated with a decreased inflow into the right heart in subjects with advanced CVI. No restrictive filling patterns have been identified in patients with varicose disease. Importantly, they have noted an increase in right heart chambers and right ventricular thickness. We would like to add further comments on the echocardiographic findings of patients. Echocardiographic examination of 46 out of 583 patients might have been a selection bias. Chest discomfort as an indication for echocardiography might have resulted in selecting patients who have diastolic dysfunction. Although the authors excluded the patients with pulmonary hypertension, in the presence of increased right heart chambers in association with increased right ventricular wall thickness and normal systolic functions of right and left ventricle, someone might expect to see either pulmonary hypertension or a volume load in right ventricle which contradicts the decreased inflow theory into the right heart. Comparison of diastolic filling pattern in patients with and without CVI would certainly improve our understanding of the association between CVI and the heart. We agree with the authors that the pathophysiology of varicose vein may affect the hemodynamics of the heart or diastolic filling patterns. However, this effect may come not only from hemodynamic changes but also from the ultrastructural changes in extracellular matrix tissue in vessel wall and myocardial tissue as well. In this context, we have already defined peripheral varicose vein as a local manifestation of systemic vessel wall abnormality. 2 Accordingly, we have classified peripheral varicose vein, varicocele, pelvic congestion syndrome, and hemorrhoids under the term of "dilating venous disease" 3,4 . Further studies evaluating the diastolic filling patterns of heart in patients with and without CVI would help us to include heart as an integral part of "varicose disease" or "dilating vascular diseases."