cardiovascular diseases

Nickel Concentrations in Serum of Patients with Acute Myocardial Infarction or Unstable Angina Pectoris.

Leach CN Jr, Linden JV, Hopfer SM, Crisostomo MC, Sunderman FW Jr.

Abstract

Nickel was measured, by electrothermal atomic absorption spectrophotometry, in sera from (a) 30 healthy adults, (b) 54 patients with acute myocardial infarction, (c) 33 patients with unstable angina pectoris without infarction, and (d) five patients with coronary atherosclerosis who developed cardiac ischemia during treadmill exercise. Mean (and SD) concentrations in Group a were 0.3 (0.3) microgram/L (range less than 0.05-1.1 microgram/L). Within 72 h after hospital admission, hypernickelemia (Ni greater than or equal to 1.2 microgrheart-1414885-639x650am/L) was found in 41 patients of group b (76%) and in 16 patients of group c (48%). Hypernickelemia was found before and after exercise in one patient of Group d (20%). Peak values averaged 3.0 micrograms/L (range 0.4-21 micrograms/L) in Group b, 1.5 microgram/L (range less than 0.05-3.3 micrograms/L) in Group c. In Group b, the mean time interval between the peak values for creatine kinase activity and for nickel was 18 h. Serum nickel concentrations were unrelated to age, sex, time of day, cigarette smoking, medications, clinical complications, or outcome. Mechanisms and sources of release of nickel into the serum of patients with acute myocardial infarction or unstable angina pectoris are conjectural, but hypernickelemia may be related to the pathogenesis of ischemic myocardial injury.

www.clinchem.org/content/31/4/556.full.pdf

Blood lead below 0.48 micromol/L (10 microg/dL) and mortality among US adults.

Menke A1, Muntner P, Batuman V, Silbergeld EK, Guallar E.

Abstract

Background— Blood lead levels above 0.48 μmol/L (10 μg/dL) in adults have been associated with increased risk of cardiovascular, cancer, and all-cause mortality. The objective of the present study was to determine the association between blood lead levels below 0.48 μmol/L and mortality in the general US population.

Methods and Results— Blood leadlead-1565598-640x480 levels were measured in a nationally representative sample of 13 946 adult participants of the Third National Health and Nutrition Examination Survey recruited in 1988 to 1994 and followed up for up to 12 years for all-cause and cause-specific mortality. The geometric mean blood lead level in study participants was 0.12 μmol/L (2.58 μg/dL). After multivariate adjustment, the hazard ratios (95% CI) for comparisons of participants in the highest tertile of blood lead (≥0.17 μmol/L [≥3.62 μg/dL]) with those in the lowest tertile (<0.09 μmol/L [<1.94 μg/dL]) were 1.25 (1.04 to 1.51; Ptrend across tertiles=0.002) for all-cause mortality and 1.55 (1.08 to 2.24; Ptrend across tertiles=0.003) for cardiovascular mortality. Blood lead level was significantly associated with both myocardial infarction and stroke mortality, and the association was evident at levels >0.10 μmol/L (≥2 μg/dL). There was no association between blood lead and cancer mortality in this range of exposure.

Conclusions— The association between blood lead levels and increased all-cause and cardiovascular mortality was observed at substantially lower blood lead levels than previously reported. Despite the marked decrease in blood lead levels over the past 3 decades, environmental lead exposures remain a significant determinant of cardiovascular mortality in the general population, constituting a major public health problem.

http://circ.ahajournals.org/content/114/13/1388.long