Background P wave indices and PR interval from 12-lead electrocardiograms (ECGs) are predictors of cardiovascular morbidity and mortality, but their repeatability has not been examined. Objectives Determine the short-term repeatability of P wave indices (P axis, maximum P area and duration, P dispersion and P terminal force in V1) and PR interval. Methods Participants (n=63) underwent two standard ECGs at each of two visits, two weeks apart. We calculated the intra-class correlation coefficient (ICC), weighted Kappa, and minimal detectable change and difference. Results ICCs were 0.93 for PR interval, 0.78 for P axis, 0.77 for maximum P area, and 0.58 for maximum P duration. Within- and between-visit Kappa were 0.30 and 0.11 for P dispersion, and 0.68 and 0.46 for P terminal force. Conclusion Repeatability of PR duration was excellent, that of P wave axis and maximum area was fair, and maximum P wave duration and terminal force was poor. Repeatability of P wave dispersion was fair within visit, yet poor between visits. These results illustrate potential biases when measurement error of some P wave indices is ignored in clinical and epidemiologic studies.
Background The electrocardiographic (ECG) Tpeak-Tend interval (TpTe) is associated with arrhythmias and sudden cardiac death. TpTe offers a supplementary measure for the QT interval (QT), yet its repeatability has not been established. Purpose Evaluate short-term repeatability of TpTe and QT. Methods Four ECGs were obtained on sixty participants. The sources of variation, intra-class correlation coefficient (ICC) - an index of reproducibility, and minimal detectable change (MDC) were estimated for TpTe and QT. The impact of repeated measurements on repeatability was estimated for a hypothetical clinical trial designed to detect drug-induced prolongation of TpTe and QT. Results We used heart rate-adjusted QT [(QT)a] but TpTe in the study group was rate-invariant. The ICC [95% confidence interval (CI)] was 0.77 (0.69, 0.85) for TpTe, 0.75 (0.65, 0.85) for QT and 0.68 (0.57, 0.79) for (QT)a. The MDC (ms) was 21, 32 and 26 for TpTe, QT and (QT)a respectively. Conclusion TpTe has excellent repeatability supporting its use as a supplement to QT in observational and clinical studies.
Pulmonary macrophages are an important component of immune defense against inhaled foreign particles and microorganisms. In humans and other mammals, exposure to moderate amounts of ozone (O3) can inhibit functional capacities of alveolar macrophages. In many wilderness areas downwind of urban centers, ozone levels frequently exceed national standards. We report results of 4-h inhalation exposures to 0.8 parts per million O3 on pulmonary macrophage viability and phagocytosis capacity in marine toads, Bufo marinus. At 1 and 24 h after ozone exposure, macrophages had reduced in vitro capacity to phagocytize fluorescent polystyrene microspheres. By 48 h postexposure, there were no differences in these macrophage functions between ozone- and air-exposed toads. Macrophage yield did not differ among exposure groups nor did exposure to elevated temperatures (30 degrees C) for up to 48 h affect recovery of macrophages. However, compared with the millions of macrophages per milliliter recovered in mammals by similar procedures, pulmonary macrophage yield was typically in the range of 50 to 200 x 10(3) per milliliter extracted fluid. These results are the first to report effects of an air pollutant on amphibian immune system function and suggest a possible role of oxidant air pollutants in regional declines of amphibian populations.
Background Excess adiposity, which affects 69% of US adults, increases coronary heart disease ( CHD ) risk in an association that manifests below conventional obesity cut points. The population‐level impact on CHD risk that is attainable through modest adiposity reductions in populations is not well characterized. We estimated the effect of hypothetical reductions in both body mass index ( BMI ) and waist circumference ( WC ) on CHD incidence. Methods and Results The study population included 13 610 ARIC (Atherosclerosis Risk in Communities) participants. Our hypothetical reduction in BMI or WC was applied relative to the temporal trend, with no hypothetical reduction among those with BMI >24 or WC >88 cm, respectively. This threshold for hypothetical reduction is near the clinical guidelines for excess adiposity. CHD risk differences compared the hypothetical reduction with no reduction. Sensitivity analysis was conducted to estimate the effect of applying the hypothetical BMI reduction at the established overweight cut point of 25. Cumulative 12‐year CHD incidence with no intervention was 6.3% (95% CI, 5.9–6.8%). Risk differences following the hypothetical BMI and WC reductions were −0.6% (95% CI, −1.0% to −0.1%) and −1.0% (95% CI, −1.4% to −0.5%), respectively. These results were robust for the sensitivity analyses. Consequently, we estimated that this hypothetical reduction of 5% in BMI and WC, respectively, could have prevented 9% and 16%, respectively, of the CHD events occurring in this study population over 12 years, after adjustment for established CHD risk factors. Conclusions Meaningful CHD risk reductions could derive from modest reductions in adiposity attainable through lifestyle modification.
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