Echocardiographic findings of the heart resembling dilated cardiomyopathy during hypokalemic myopathy due to licorice-induced pseudoaldosteronism.

Abstract

Dear Sir, Although licorice-induced pseudoaldosteronism is known to be a cause of hypokalemic myopathy, it is not recognized as a cause of secondary cardiomyopathy. In order to manage potentially reversible secondarily caused cardiomyopathy, it is necessary to distinguish this disease from idiopathic dilated cardiomyopathy. Although M-mode, two-dimensional, and Doppler echocardiography are useful in detecting and assessing the degree of impairment of left ventricular function, it is dif~cult to identify secondary causes of dilated cardiomyopathy, such as alcoholic cardiomyopathy, uremic cardiomyopathy, hypophosphatemia, hypocalcemia, iron overload, pheochromocytoma, sarcoid heart disease, and acute in_ammatory myopericarditis. We describe a unique case of hypokalemic myopathy due to licorice-induced pseudoaldosteronism that presented ~ndings similar to dilated cardiomyopathy as an another cause of secondary cardiomyopathy. A 65-year-old man was admitted to our hospital complaining of dif~culty walking and maintaining the seated position. He had a 13-year history of diabetes mellitus and a several year history of alcoholic liver cirrhosis and chronic gastritis. For a few years he had been taking a very small dose of licorice containing stomachics (0.06 g licorice extract in total granules of 3.0 g/day). For 2 months, due to worsened liver dysfunction, he had been receiving 40 mg/day of glycyrrhizin (total 800 mg) intravenously. Physical examinations showed an irregular pulse rate of 64/min with a blood pressure of 104/60 mmHg. A pansystolic murmur (2/6) was audible but no rales were detected. Mild hepatomegaly was detected with no ascites or pretibial edema. Generalized muscle weakness was noted. The chest roentogenogram showed mild cardiomegaly (CTR 5 52.9%). An electrocardiogram showed atrial ~brillation, depression in the ST segment, a _at T wave, and a markedly augmented U wave in multiple leads. Complete blood cell counts showed mild anemia (red blood cell count 299 3 104). Blood chemistry showed severe hypokalemia of 1.7 mEq/L and a marked increase in muscle enzymes; for example, myogrobin, 5310 (normally ,50) ng/mL; creatinine phosphokinase (CK), 8160 IU/L; aldolase, 41.2 U/L. Analysis of the CK isozymes showed a marked increase in not only the MM fraction but also the MB fraction, which originated from cardiac muscles. Hormonal studies showed no abnormalities except for a reduction in plasma renin activity (,0.15 ng/mL/h of the detecting limit) and aldosterone (,25.0 pg/mL of the limit). Arterial blood gas showed metabolic alkalosis of pH 7.596 with a bicarbonate of 46.3 mmol/L and a base excess of 22.9 mmol/L. Two-dimensional echocardiography showed enlargement of the left ventricle (Dd 5 56.3 mm) and a reduction in contractility (ejection fraction 39%, fractional shortening 19%, and mean VCF 0.59 circ/s) without left ventricular hypertrophy. Color Doppler _ow mapping revealed the presence of mitral regurgitation (third degree; Figure 1, upper panel) and mild regurgitation in the pulmonary and tricuspid valves. These ~ndings were consistent with a diagnosis of pseudoaldosteronism with hypokalemic myopathy and a condition resembling dilated cardiomyopathy. Although a myocardial biopsy was not performed, it has been reported that hypokalemia alone does not cause cardiomyopathy [1] and that hypokalemia increases the myocardial contractile force [2]. Volume infusion–induced left ventricular dilatation causes mitral regurgitation by increasing the effective regurgitant ori~ce [3]. Ballester et al. [4] reported that the degree of left ventricular dilatation plays an important role in the mechanism of mitral regurgitation in dilated