Myocardial Glycogen Deposition in a Patient With Streptococcal Toxic Shock Syndrome

A 39-year-old Japanese woman was admitted because of dyspnea. Blood pressure was 70/44 mmHg, pulse rate 93/min irregular, and body temperature 36.8℃. Laboratory data were as follows: white blood cells, 31,000/µL; C-reactive protein, 2.8 mg/dL; blood urea nitrogen, 35 mg/dL; creatinine, 3.43 mg/dL; total bilirubin, 2.7 mg/dL; aspartate aminotransferase, 12,400 IU/L; alanine aminotransferase, 4,670 IU/L; lactate dehydrogenase, 17,920 IU/L; creatinine kinase (CK), 24,006 IU/L; CKMB, 21 IU/L; N-terminal pro-B-type natriuretic peptide, 5,620 pg/mL. ECG showed atrial fibrillation. Echocardiography and left ventriculography revealed diffuse severe hypokinesis of the left ventricle (LV) (ejection fraction (EF), 20%) (Figure A,B). Coronary angiography was normal, and cardiac catheterization showed mean postcapillary wedge pressure, 25 mmHg, mean pulmonary artery pressure, 36 mmHg, and cardiac index, 2.88 L/min/m². Therefore, a right ventricular endomyocardial biopsy was obtained. Histological finding was cytoplasmic vacuolation in the myocytes without inflammatory cellular infiltration or necrosis (Figure C). Periodic acid-Schiff staining showed a positive reaction in the cytoplasm (Figure D). Electron microscopy disclosed glycogen deposition in the myocytes without necrosis/apoptosis (Figure E-1,E-2).

Figure.

Left ventriculography on admission (A, end-diastolic phase; B, end-systolic phase). Microphotographs of biopsied myocardium (C, hematoxylin and eosin staining, ×200; D, periodic acid Schiff staining, ×200). Electron microscopy photographs (E-1; E-2 (inset of E-1)). Transthoracic echocardiography after recovery (F).

She was treated with sulbactam/ampicillin, 3 g/day in addition to diuretics and catecholamine. Two weeks after admission, echocardiography showed normal LVEF (66%) (Figure G), and the antistreptokinase antibody titer was increased from 512 to 5,120. She was diagnosed with streptococcal toxic shock syndrome (STSS), and these histological features may suggest myocardial hibernation in STSS.¹

Disclosures

K.M. is a member of Circulation Journal’s Editorial Team. The authors declare no conflicts of interest.

Reference

• 1.   Levy RJ, Piel DA, Acton PD, Zhou R, Ferrari VA, Karp JS, et al. Evidence of myocardial hibernation in the septic heart. Crit Care Med 2005; 33: 2752–2756.