Thiamine deficiency is an uncommon nutritional deficiency in the developed world. The population most at risk in North America and Europe has been noted to be alcoholics with poor diets. This nutrient deficiency can manifest as several different syndromes, one of which is “beriberi.” Beriberi was first described by Dr. Wenckebach in the early 1900s who observed the presence of dependent edema, elevated venous pressures, and an enlarged heart in patients who had three or more months of a thiamine deficient diet, with recovery after thiamine administration. What followed years after were several case reports of alcoholics with signs of congestive heart failure who improved drastically with administration of thiamine.
Although today beriberi heart disease is a rare diagnosis, what it does show is that thiamine is an important micronutrient for the heart, and lack of thiamine can cause symptoms of heart failure.
Given that thiamine is excreted through the urine, another population that has been deemed to be at risk for thiamine deficiency is those on high doses of diuretics such as furosemide1. Interestingly, this population includes the difficult-to-control heart failure patients that we see on the wards every day. Biochemically, one study has shown that thiamine uptake in cardiac cells can be inhibited by furosemide2.
Yet, treatment of patients with congestive heart failure on diuretics with thiamine is not currently standard of practice.
Looking at the literature, there have been only two randomized double blind placebo controlled trials on thiamine use in patients with congestive heart failure: Shimon et al 19953 and Schoenenberger et al 20124. Both of these trials showed a statistically significant increase in left ventricular ejection fraction with the use of thiamine in patients presenting with symptomatic congestive heart failure. Granted, the ejection fraction only improved by 3-4% which we could say was due to echocardiography interpretation variability. However, being that thiamine is cheap and there is evidence that points towards its use as a medication in heart failure, should we institute it into our daily practice?
What do you think?
- Katta N, Balla S, Alpert MA. Does Long-Term Furosemide Therapy Cause Thiamine Deficiency in Patients with Heart Failure? A Focused Review. Am J Med. 2016;129(7):753.e7-753.e11.
- Zangen A, Botzer D, Zangen R, Shainberg A. Furosemide and digoxin inhibit thiamine uptake in cardiac cells. Eur J Pharmacol. 1998;361(1):151-5.
- Shimon I, Almog S, Vered Z, et al. Improved left ventricular function after thiamine supplementation in patients with congestive heart failure receiving long-term furosemide therapy. Am J Med. 1995;98(5):485-90.
- Schoenenberger AW, Schoenenberger-berzins R, Der maur CA, Suter PM, Vergopoulos A, Erne P. Thiamine supplementation in symptomatic chronic heart failure: a randomized, double-blind, placebo-controlled, cross-over pilot study. Clin Res Cardiol. 2012;101(3):159-64.
Omid Amidi, MD is a current Internal Medicine Resident Physician at Baylor College of Medicine in Houston, Texas. His research is focused on Chemotherapy-related Cardiotoxicity which is conducted at M.D. Anderson Cancer Center. His blog can be found on www.amidimd.com. @OAmidiMD