Marked elevation of myocardial trace elements in idiopathic dilated cardiomyopathy compared with secondary cardiac dysfunction

OBJECTIVES We sought to investigate the possible pathogenetic role of myocardial trace elements (TE) in patients with various forms of cardiac failure. BACKGROUND Both myocardial TE accumulation and deficiency have been associated with th e development Of heart failure indistinguishable from an idiopathic dilated cardiomyopathy. METHOD Myocardial and muscular content of 32 TE has been assessed in biopsy sample s of 13 patients (pts) with clinical, hemodynamic and histologic diagnosis of idiopathic dilated cardiomyopathy (IDCM), all without past or current ex posure to TE. One muscular and one left ventricular (LV) endomyocardial Spe cimen from each patient, drawn with metal contamination-free technique, wer e analyzed by neutron activation analysis and compared with 1) similar surg ical samples from patients with valvular (12 pts) and ischemic (13 pts) hea rt disease comparable for age and degree of LV dysfunction; 2) papillary an d skeletal muscle surgical biopsies from 10 ts with mitral stenosis and nor mal LV function, and 3) LV endomyocardial biopsies from four normal subject s. RESULTS A large increase (>10,000 times for mercury and antimony) of TE concentrati on has been observed in myocardial but, not in muscular Samples in all pts with IDCM. Patients with Secondary cardiac dysfunction had mild increase (l ess than or equal to 5 times) of myocardial TE and normal muscular TE. In p articular, in pts with IDCM mean mercury concentration was 22,000 times (17 8,400 ng/g vs. 8 ng/g), antimony 12,000 times (19,260 ng/g vs. 1.5 ng/g),go ld 11 times (26 ng/g vs. 2.3 ng/g), chromium 13 times (2,300 ng/g vs. 177 n g/g) and cobalt 1 times (86,5 ng/g vs. 20 ng/g) higher than in control subj ects. CONCLUSION A large, significant increase of myocardial TE is present in IDCM but not i n secondary cardiac dysfunction. The increased concentration of TE in pts w ith IDCM may adversely affect mitochondrial activity and myocardial metabol ism and worsen cellular function. (C) 1998 by the American College of Cardi ology.