Cardiac beriberi: morphological findings in two fatal cases

Cardiovascular beriberi is categorized into two main groups, according to its cause: alcoholic and non-alcoholic (dietary). Cardiovascular beriberi can also be divided into a fulminant form (Shoshin beriberi) and a chronic form. Shoshin beriberi is characterized by hypotension, tachycardia, and lactic acidosis and is mainly encountered in non-alcoholic patients in Asian countries, although it has also been seen in alcoholics in Western countries. Due to the complex clinical presentation and to the lack of diagnostic tests, thiamine deficiency is still being missed, especially among non-alcoholics patients. We present two fatal cases of non - alcohol associated cardiac beriberi. An acute myocardial infarction was observed in one case; extensive colliquative myocytolisis (grade 2) was described in the second case respectively. Morphologically, myocardial necrosis and colliquative myocytolysis are the histologic hallmarks of this acute, rare clinical entity. An increase in apoptotic myocytes was demonstrated probably sustaining the cardiogenic shock.

[1]  K E Muffly,et al.  Structural Remodeling of Cardiac Myocytes in Patients With Ischemic Cardiomyopathy , 1992, Circulation.

[2]  A. Galinier,et al.  Development of beriberi heart disease 20 years after gastrojejunostomy. , 2003, The American journal of medicine.

[3]  K. Yano,et al.  ST-segment elevation of electrocardiogram in a patient with Shoshin beriberi. , 2005, Internal medicine.

[4]  K. Yano,et al.  Histopathological changes of biopsied myocardium in Shoshin beriberi. , 2005, International heart journal.

[5]  E. Turillazzi,et al.  A systematic study of a myocardial lesion: colliquative myocytolysis. , 2005, International journal of cardiology.

[6]  I. Seong,et al.  Thiamine deficiency as a rare cause of reversible severe pulmonary hypertension. , 2007, International journal of cardiology.

[7]  S. Guatimosim,et al.  Abolition of reperfusion-induced arrhythmias in hearts from thiamine-deficient rats. , 2007, American journal of physiology. Heart and circulatory physiology.

[8]  P. Campos,et al.  Cardiac structural changes and electrical remodeling in a thiamine-deficiency model in rats. , 2009, Life sciences.

[9]  A case of ST-elevation and nystagmus--when coronary thrombosis is not to blame. , 2009, QJM : monthly journal of the Association of Physicians.

[10]  V. Lemos,et al.  Cardiac oxidative stress is involved in heart failure induced by thiamine deprivation in rats. , 2010, American journal of physiology. Heart and circulatory physiology.

[11]  M. Neri,et al.  Insight into stress-induced cardiomyopathy and sudden cardiac death due to stress. A forensic cardio-pathologist point of view. , 2010, Forensic science international.

[12]  S. Bello,et al.  MDMA toxicity and pathological consequences: a review about experimental data and autopsy findings. , 2010, Current pharmaceutical biotechnology.

[13]  S. Bello,et al.  Myocardial expression of TNF-alpha, IL-1beta, IL-6, IL-8, IL-10 and MCP-1 after a single MDMA dose administered in a rat model. , 2010, Current pharmaceutical biotechnology.

[14]  M. Rossi,et al.  Ischemic myocardial injuries after cardiac malformation repair in infants may be associated with oxidative stress mechanisms. , 2011, Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology.

[15]  S. Bello,et al.  Anabolic steroid- and exercise-induced cardio-depressant cytokines and myocardial β1 receptor expression in CD1 mice. , 2011, Current pharmaceutical biotechnology.

[16]  V. Vlachova Editorial [Hot topic: TRP Channels: From Understanding to Action (Guest Editor: Viktorie Vlachova)] , 2011 .