Left Ventricular Structure and Function in Relation to Environmental Exposure to Lead and Cadmium

Abstract

Background Experimental studies have demonstrated that lead and cadmium have direct toxic effects on the myocardium, but the few human studies are limited by design, assessment of exposure, and use of heart failure as a late‐stage endpoint. Methods and Results In a prospective population study, we studied the association of left ventricular ( LV ) function with blood lead (BPb) and 24‐hour urinary cadmium (UCd). In 179 participants randomly recruited from a Flemish population (50.3% women; mean age 39.1 years), geometric mean BP b and UC d at enrollment (1985‐2000) were 0.20 μmol/L and 6.1 nmol, respectively. We assessed systolic and diastolic LV function 11.9 years (median) later (2005‐2010) by using Doppler imaging of the transmitral blood flow and the mitral annular movement and speckle tracking. In multivariable‐adjusted linear regression, LV systolic function decreased with BP b. For a doubling of exposure, estimates were −0.392% for global longitudinal strain ( P =0.034), −0.618% and −0.113 s −1 for regional longitudinal strain ( P =0.028) and strain rate ( P =0.008), and −0.056 s −1 for regional radial strain rate ( P =0.050). Regional longitudinal strain rate (−0.066 s −1 , P =0.009) and regional radial strain (−2.848%, P =0.015) also decreased with UC d. Models including both exposure indexes did not allow differentiating whether LV dysfunction was predominately related to BP b or UC d. Diastolic LV function was not associated with BP b or UC d ( P ≥0.159). Conclusions Although effect sizes were small, our results suggest that environmental exposure to lead, cadmium, or both might be a risk factor for systolic LV dysfunction, a condition often proceeding to heart failure.