Relation Between Heavy Metals and Left Ventricular Diastolic Function in Patients with Coronary Artery Disease

Abstract

One of the earliest detectable abnormalities in patients with coronary artery disease is left ventricular diastolic dysfunction. Its main cause is myocardial ischaemia, but still many of other mechanisms are possible. The aim of this study was to investigate the relation of cadmium, lead, copper, zinc, and selenium with left ventricular diastolic function indices in patients with coronary artery disease. The study included 33 patients (14 with single-vessel disease and 19 with multivessel disease on angiography) who were not exposed occupationally to heavy metals. Control group consisted of 18 patients with normal coronary arteries. The blood cadmium and lead concentrations and serum zinc, selenium and copper concentrations were determined using atomic absorption spectrophotometry. Left ventricular diastolic function parameters were estimated by echo-Doppler and colour M-mode. All heavy metal concentrations were within the standard ranges in all studied groups. Patients with single-vessel disease, multivessel disease and control group did not differ in concentrations of studied metals. On univariate and multivariate analysis only cadmium significantly correlated with echocardiographic parameters of left ventricular diastolic function: peak early to peak late mitral inflow velocity ratio (r = -0.36, p < 0.05) and deceleration time of early mitral inflow (r = 0.43, p < 0.01) in patients with CAD. No significant correlations between concentrations of heavy metals and indices of left ventricular diastolic function were found in control group. The present data suggest that cadmium in concentrations even below the threshold limit value for unexposed population may contribute to development of left ventricular diastolic dysfunction in patients with CAD, potentializing the effect of myocardial ischaemia.

Lead Exposure and Cardiovascular Disease—A Systematic Review

“…Blood lead levels were substantially lower in more recent compared with older studies. Case–control studies assessed lead exposure on the basis of lead levels in blood (Kosmala et al 2004), plasma (Mansoor et al 2000), and urine (Pan et al 1993; Tsai et al 2004), on a job exposure matrix (Gustavsson et al 2001), and on lead levels in the air of the residential neighborhood of study participants (Dulskiene 2003). None of these studies determined lead in bone.…”

“…General populations Occupational populations Cohort studies CC and CS studies Prosp. Retrospective cohort studies PMS Pocock et al 1988Kromhout 1988Møller and Kristensen 1992Lustberg and Silbergeld 2002Menke et al 2006Pan et al 1993Mansoor et al 2000Gustavsson et al 2001Dulskiene 2003Tsai et al 2004Kosmala et al 2004Muntner et al 2005Robinson 1974Tollestrup et al 1995Dingwall-Fordyce and Lane 1963Malcolm 1971, Malcolm and Barnett 1982Sheffet et al 1982Davies 1984Cooper et al 1985Belli et al 1989Michaels 1991Steenland et al 1992Cocco et al 1994…”

Declining exposures to lead and cadmium contribute to explaining the reduction of cardiovascular mortality in the US population, 1988–2004

“…9,10,28 Potential mechanisms include disruption of redox balance, 7-9,29-32 epigenetic 33 and endocrine 34 pathways. Epidemiologic studies from different geographical locations and time periods have reported positive associations of lead and cadmium with atherosclerotic disease, 5,6 including cardiovascular mortality and the prevalence and incidence of endpoints such as myocardial infarction and coronary heart disease, [35][36][37][38][39][40] stroke, 36,39,41,42 heart failure, [41][42][43] peripheral arterial disease, 4,15,[44][45][46][47] and carotid atherosclerosis. 28,48,49 Metaanalysis and systematic reviews of observational studies add to the body of evidence supporting the role of lead and cadmium as cardiovascular risk factors.…”

“…In NHANES 1988-94, urine cadmium was measured in duplicate by GFAA spectrometry (model 3030; PerkinElmer, Norwalk, CT, USA) with Zeeman background correction, and the average of the two measurements was reported. 14 In NHANES 1999-2004 cadmium was measured only in a random one-third subsample of the study population by ICP-MS spectrometry (ELAN, PerkinElmer) in 1999-2002 and by ICP-dynamic reaction cell (DRC)-MS (ELAN DRC, PerkinElmer) in 2003-04. The remaining two-thirds of 1999-2004 NHANES participants who were not selected for urine cadmium measurements (N ¼ 4852) had cadmium concentrations missing completely at random and we imputed their cadmium concentrations as the median of each participant's posterior cadmium distribution generated from a Markov Chain Monte Carlo with Gibbs sampling under a prediction model based on urine cadmium determinants.…”

Atomic spectrometry update. Clinical and biological materials, foods and beverages

“…Kosmala et al 74 believed that they might have discovered evidence that low level Cd exposure might contribute to the development of left ventricular diastolic dysfunction in patients with coronary artery disease. Using AAS techniques, they measured blood Cd and Pb, serum Cu, Se and Zn in samples from patients with indices of left ventricular diastolic dysfunction and in samples from subjects with normal coronary arteries.…”