Endovenous varicose vein treatment in patients with right heart failure and tricuspid valve regurgitation – A relative contraindication?

In 2015, four patients in Hamilton New Zealand were identified to have failed endovenous varicose vein treatment. All the patients had one aspect in common, evidence of right heart failure and tricuspid valve regurgitation. This raised the question, should the presence of this cardiac pathology be a relative contraindication for endovenous treatment of varicose veins?

There are reports in the literature of cases of varicose veins associated with right heart failure and tricuspid valve regurgitation. The first case was published in 1962 by Brickner et al. ¹ In all the cases published, surgical techniques were employed to exclude the refluxing vein if conservative measures failed to prevent complications.^2–4 Today, intervention on varicose veins is achieved most frequently through endovenous methods. In Hamilton, we have used endovenous laser ablation therapy, radiofrequency ablation and the latest dual-injury system, ClariVein. Success with Clarivein is reported in initial trials to reach 97%, ⁵ which is fairly consistent with other endovenous methods.

New Zealand has a high rate of right heart failure compared to other parts of the world. The most common cause of right heart failure is left heart failure, and this is no different in New Zealand; however, we also suffer from a high rate of rheumatic heart disease, especially in the Maori population. ⁶ If tricuspid valve regurgitation is present, due to primary valvular disease or high right ventricular pressures, the backflow into the veins from the right heart failure will also be pulsatile. We postulate that it is this pulsatile high-pressure reflux that not only contributes to the formation of varicose veins but also the inability of the current methods of endovenous varicose vein treatments to create the sufficient inflammation and collapse of the treated vein required for success.

Another aspect potentially contributing to the failure of treatment may be the difficulty that a pulsating vein poses for accurate diameter measurement with vascular ultrasonography. Indications for use include that the diameter of the vein treated is under 15 mm, and hence care needs to be taken that the measurement is under this size in all phases of the pulse cycle.

This topic was recently presented for discussion at the Australia and New Zealand Society of Vascular Surgery annual meeting. Comments were limited, which we felt was due to differences in patient population and uptake of endovenous varicose vein treatments. The group did raise the question of the clinical importance of varicose vein pulsatility, because some patients can have it with no apparent negative effects. A prospectively collected database of all patients presenting to have varicose vein scanning in Hamilton who are shown to have pulsatility was initiated this year and will be analysed in a years’ time. The aim would be for all patients with pulsatile varicose veins to have cardiac echocardiography to investigate for cardiac pathology. For a scientific publication, we will aim to clarify the overall incidence of pulsatile varicose veins, the rate of correlating cardiac pathology, and the rate of failure of endovenous varicose vein treatment in this population and the overall population.

We feel that right heart failure and tricuspid valve regurgitation should be a relative contraindication for endovenous varicose vein treatment. Thought needs to be given to open surgery in those patients with right heart failure and tricuspid regurgitation when endovenous treatment seems unlikely to succeed.