C. Federici

Somatic DNA damage in interventional cardiologists: a case-control study

Interventional cardiologists who work in cardiac catheterization laboratories are exposed to low doses of ionizing radiation that could pose a health hazard. DNA damage is considered to be the main initiating event by which radiation damage to cells results in development of cancer and hereditary disease. The aim of the present study was to assess the effects of chronic low‐dose X‐ray radiation exposure on somatic DNA damage of interventional cardiologists working in highvolume cardiac catheterization laboratories. For this analysis, we used peripheral lymphocytes and the assay for micronuclei (MNs), which is considered to be a reliable biological dosimeter for radiation exposure. We obtained peripheral blood from 62 physicians (mean age±se = 40.6±1.5 years): 31 interventional cardiologists (group I, exposed) and 31 age‐ and sex‐matched clinical cardiologists (group II, nonexposed). Interventional cardiologists showed higher MN values (group I=20.5±1.6 vs. group II=12.8±1.3, P=0.001), although some overlap was apparent in the individual subject analysis. A correlation between years of professional activity and MN frequency value was detectable for interventional cardiologists (r=0.428, P=0.02) but not for clinical cardiologists (r=0.253, P=0.17). The results indicated that, overall, interventional cardiologists working in a high‐volume catheterization laboratory have higher levels of somatic DNA damage when compared with clinical cardiologists working outside the catheterization laboratory. The amount of this damage varies and is only weakly related to the duration of professional exposure, which suggests that a dominant modulation of the underlying genetic substrate by environmental factors has a role in determining the harm in individual physicians.

Relation of increased chromosomal damage to future adverse cardiac events in patients with known coronary artery disease.

Somatic deoxyribonucleic acid (DNA) damage has been associated with early-phase and/or acute complications of atherosclerosis. However, it remains unclear whether circulating levels of DNA damage have prognostic value in patients with coronary artery disease (CAD). The aim of this study was to assess the prognostic significance of chromosomal DNA damage in human lymphocytes on the rate of major adverse cardiovascular events in patients with CAD. A follow-up prospective cohort study was carried out of 178 patients (153 men, mean age 61.9 +/- 9.7 years) with angiographically proved CAD who underwent micronucleus assay, a sensitive biomarker of chromosomal damage and genetic instability, from March 1999 and June 2001. During a mean follow-up period of 51.4 +/- 23.8 months, 58 patients had major adverse cardiovascular events (cardiac death, myocardial infarction, stroke, congestive heart failure, unstable angina, or coronary and peripheral revascularization). The overall event-free survival rates were 77.5%, 70.4%, and 49.0% in patients in the lower, middle, and upper tertiles of micronucleus level, respectively (log rank = 11.5, p = 0.003). In a multivariate Cox regression model, only the upper tertiles were significantly associated with a higher risk for major adverse cardiovascular events (hazard ratio 2.2, 95% confidence interval 1.1 to 4.7, p = 0.03). In conclusion, levels of peripheral chromosomal DNA damage may be a new sensitive biomarker of prognostic stratification in patients with known CAD.