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New-Onset Heart Failure

Educational Objective
Based on this clinical scenario and the accompanying image, understand how to arrive at a correct diagnosis.
1 Credit CME

An adult with a history of alcohol abuse was admitted to the cardiac unit with progressive shortness of breath, lower extremity edema, and tachycardia, which had developed during several days. He had no history of drug use or cardiac events. On physical examination, he had warm extremities. His body temperature was 36.8°C. His blood pressure was 100/60 mm Hg, heart rate was 130 beats/min, respiratory rate was 24 breaths/min, and pulse oximetry was 98% on ambient air. There were bibasilar rales on lung auscultation. The heart sounds were normal, and bilateral ankle edema was present. Laboratory tests revealed hyponatremia (sodium, 124 mEq/L [to convert to millimoles per liter, multiply by 1]), a compensated metabolic acidosis with a bicarbonate concentration of 14 mEq/L (to convert to millimoles per liter, multiply by 1), and a lactate concentration of 82.0 mg/dL (to convert to millimoles per liter, multiply by 0.111). The D-dimer level was 0.0003 μg/mL (to convert to nanomoles per liter, multiply by 5.476), and the pro–brain-type natriuretic peptide level was 6062 pg/mL (to convert to nanograms per liter, multiply by 1). The electrocardiogram on presentation is shown in the Figure. Echocardiography (Video 1 and Video 2) revealed a left ventricular ejection fraction of 50%.

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Shoshin (wet) beriberi

D. Administer intravenous thiamine therapy

At first glance, this case might be interpreted as an ordinary case of severe heart failure due to alcoholic cardiomyopathy. However, echocardiography revealed only a mild reduced left ventricular function, which does not fully explain all the clinical features. In particular, the metabolic acidosis with high lactate levels should trigger an explanation for an alternative diagnosis.

Thiamine deficiency (vitamin B1), also known as beriberi, is a rare condition in developed countries. However, individuals prone to malnourishment, such as individuals with alcoholism, patients receiving total parenteral nutrition without adequate vitamin supplements, or individuals on a diet or after weight loss surgery, are more likely to develop thiamine deficiency.1 Thiamine plays a fundamental role in cellular metabolism, has a half-life of 18 days, and is quickly depleted. Acidosis and the inability to use the Krebs cycle are the major pathophysiologic mechanisms of the clinical manifestations of thiamine deficiency.

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Article Information

Corresponding Author: Kenneth Tandjung, MD, PhD, Department of Cardiology, Dijklander Ziekenhuis, Waterlandlaan 250, 1441 RN Purmerend, the Netherlands (ktandjung@wlz.nl).

Published Online: March 13, 2019. doi:10.1001/jamacardio.2019.0187

Conflict of Interest Disclosures: None reported.

References
1.
Dabar  G, Harmouche  C, Habr  B, Riachi  M, Jaber  B.  Shoshin beriberi in critically-ill patients: case series.  Nutr J. 2015;14:51. doi:10.1186/s12937-015-0039-7PubMedGoogle ScholarCrossref
2.
Attas  M, Hanley  HG, Stultz  D, Jones  MR, McAllister  RG.  Fulminant beriberi heart disease with lactic acidosis: presentation of a case with evaluation of left ventricular function and review of pathophysiologic mechanisms.  Circulation. 1978;58(3, pt 1):566-572. doi:10.1161/01.CIR.58.3.566PubMedGoogle ScholarCrossref
3.
Pereira  VG, Masuda  Z, Katz  A, Tronchini  V  Jr.  Shoshin beriberi: report of two successfully treated patients with hemodynamic documentation.  Am J Cardiol. 1984;53(10):1467. doi:10.1016/S0002-9149(84)91365-1PubMedGoogle ScholarCrossref
4.
Imamura  T, Kinugawa  K.  Shoshin beriberi with low cardiac output and hemodynamic deterioration treated dramatically by thiamine administration.  Int Heart J. 2015;56(5):568-570. doi:10.1536/ihj.15-033PubMedGoogle ScholarCrossref
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