Role of cadmium and magnesium in pathogenesis of idiopathic dilated cardiomyopathy

doi:10.1016/0002-9149(86)90082-2

The American Journal of Cardiology

Volume 58, Issue 3, 1 August 1986, Pages 364-366

https://doi.org/10.1016/0002-9149(86)90082-2 Get rights and content

Abstract

Many investigators have focused attention on the deviation of essential metal profile and the occurrence of pathologic cardiovascular effects. Magnesium deficiency ¹ and cadmium excess² are suspected to be involved in the pathogenesis of coronary heart disease and sudden death. In idiopathic dilated cardiomyopathy (IDC), the role of cobalt³ and selenium⁴ as etiologic factors is well documented. No report exists concerning an association between cadmium concentration and clinical data in IDC, whereas magnesium loss appears to be a factor in pathogenesis of arrhythmias.⁵

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Citation Excerpt :
Several studies have suggested that cadmium plays a role in the pathogenesis of DCM, and cadmium blood and urine levels have been shown to be significantly elevated in patients with DCM compared to controls. Importantly, control patients with DCM have been shown to exhibit a two-fold increase in blood cadmium levels compared with smokers, ex-smokers, and non-smokers.39 An epidemiological study of 12 049 US participants demonstrated that urinary cadmium levels were significantly correlated with the self-reported prevalence of HF.40
Cadmium is a widely distributed toxic heavy metal that has been associated with many diseases including chronic renal dysfunction, osteomalacia, acute heart failure, secondary hypertension, and atherosclerosis. Although several studies have suggested that cadmium may affect multiple systems by inducing lipid per oxidation in cells and disturbing the antioxidant system, the mechanism by which cadmium affects the cardiovascular system remains unclear. Recent studies on heart failure and acute myocardial infarction have shown that cadmium has good predictive ability for mortality in patients with cardiovascular disease. In this study, we briefly review the role of cadmium in cardiovascular disease, which may prompt further studies to investigate the potential association between cadmium and mortality in patients with cardiovascular disease.
O cádmio é um metal tóxico pesado amplamente distribuído que está associado a muitas doenças, inclusive a disfunção renal crónica, a osteomalacia, a insuficiência cardíaca aguda, a hipertensão secundária e a aterosclerose. Embora vários estudos tenham sugerido que o cádmio pode afetar sistemas múltiplos através da indução da perioxidação dos lípidos nas células e da distribuição do sistema antioxidante, o mecanismo através do qual o cádmio afeta o sistema cardiovascular permanece pouco claro. Estudos recentes sobre insuficiência cardíaca e sobre enfarte agudo do miocárdio demonstraram a capacidade preditiva deste metal na mortalidade em doentes com doença cardiovascular. Neste estudo, apresentamos uma breve revisão do papel do cádmio na doença cardiovascular que poderá num futuro próximo motivar novos estudos para investigação da associação potencial entre o cádmio e a mortalidade em doentes com patologia cardiovascular.
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Cadmium (Cd) is reported to produce cardiotoxicity at doses and exposure conditions that cause no effect in kidney or liver. The purpose of the present investigation was to examine the cytotoxicity of Cd to neonatal rat cardiomyocytes in primary culture and to elucidate the transport characteristics of Cd in these cells at a nontoxic concentration. Cd concentrations of 0.1 μM and higher that are well tolerated by hepatocytes and renal cortical epithelial cells were toxic to the cardiomyocyte. The plot of initial uptake rate of Cd at various concentrations was nonlinear suggesting that, in addition to simple diffusion, other processes may also be involved. These processes required metabolic energy as pretreatment with dinitrophenol or sodium fluoride inhibited 58 and 59% of the Cd uptake, respectively. The uptake of Cd was also affected by the incubation temperature and lowering the temperature from 37 to 4°C reduced Cd uptake over 30 min by 61%. Cd uptake required interaction with membrane sulfhydryl groups; pretreatment withp-chloromercuribenzenesulfonic acid or mercuric chloride reduced Cd uptake by 46 and 58%, respectively. Cd utilized the transport pathways for calcium (Ca), zinc (Zn), and copper (Cu). Coincubation with 1.26 mM Ca competitively inhibited Cd uptake by 77%. In the presence of Ca, 30 μM Zn or Cu further inhibited Cd accumulation competitively by as much as 63 and 32%, respectively. Cd could enter the cardiomyocytes through Ca channels and Ca channel blocker, verapamil, inhibited up to 76% of Cd uptake. From the above results it can be concluded that Cd is highly toxic to the cardiomyocytes. A majority of Cd enters these cells through transport processes that exist for Ca, Zn, and Cu. The transport processes utilized by Cd are temperature sensitive and dependent on metabolic energy. Furthermore, these involve membrane sulfhydryl groups and include Ca channels.
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Brief reportRole of cadmium and magnesium in pathogenesis of idiopathic dilated cardiomyopathy

Abstract

Lancet

Am Heart J

Cardiovascular disease and environmental exposure

Br J Ind Med

Brief report
Role of cadmium and magnesium in pathogenesis of idiopathic dilated cardiomyopathy