Harnessing vascular biology to rescue CVI sufferers

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Despite affecting 25 million Americans, including two to six million with ulcer conditions, chronic venous insufficiency is relatively understudied compared to other vascular diseases. Yet for patients with venous leg ulcers, their condition is debilitating, painful and embarrassing.

Dr. Ulka Sachdev is studying the condition, hoping her “bench-side research” will develop “bedside” solutions. She received a five-year, National Institutes of Health K08 and SVS Foundation grants in 2012 and an SVS Foundation Clinical Research Seed Grant in 2017. “Their ulcers are very difficult to manage,” she said. “They are large, open, painful and wet. Patients’ daily routines are negatively affected by their wounds. It’s really sad.”

Since she regularly treats CVI patients, Dr. Sachdev wondered why some patients have benign venous insufficiency that ulcerates and why some ulcers recur. “If we could determine at an earlier stage how to mitigate the risk of new ulceration or recurrence, I think it would be worth it,” she said.

In her previous, K08-supported research she hypothesized that wound healing during ischemia is promoted by inflammatory proteins released by damaged tissue. She found that certain proteins known as danger signals can be released by damaged tissue and promote regenerative effects.

“My hypothesis is that specific danger signals can be manipulated, ideally with an oral drug,” Dr. Sachdev said. “If it works, this could be a mechanism that allows a dying muscle cell to say, ‘Hey, I need help.’ This might mean that someone who cannot get a bypass or a stent might not have to face amputation.’”

Her recent grant is for studying study patterns of inflammation in chronic venous insufficiency.

The goal of her studies is to determine whether patients with benign varicose veins and those with ulcerations express inflammatory mediators that predict their response to treatment. Later, perhaps, effective treatments will be found that change these patients’ lives.

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