Changes in deceleration capacity of heart rate and heart rate variability induced by ambient air pollution in individuals with coronary artery disease

Background and Objective: Exposure to ambient particles has been
shown to be responsible for cardiovascular effects, especially in
elderly with cardiovascular disease. The study assessed the
association between deceleration capacity (DC) as well as heart
rate variability (HRV) and ambient particulate matter (PM) in
patients with coronary artery disease (CAD). Methods: A prospective
study with up to 12 repeated measurements was conducted in Erfurt,
Germany, between October 2000 and April 2001 in 56 patients with
physician-diagnosed ischemic heart disease, stable angina pectoris
or prior myocardial infarction at an age of at least 50 years.
Twenty-minute ECG recordings were obtained every two weeks and
24-hour ECG recordings every four weeks. Exposure to PM (size range
from 10 nm to 2.5 mu m), and elemental (EC) and organic (OC) carbon
was measured. Additive mixed models were used to analyze the
association between PM and ECG recordings. Results: The short-term
recordings showed decrements in the high-frequency component of HRV
as well as in RMSSD (root-mean-square of successive differences of
NN intervals) in association with increments in EC and OC 0-23
hours prior to the recordings. The long-term recordings revealed
decreased RMSSD and pNN50 (% of adjacent NN intervals that differed
more than 50 ms) in association with EC and OC 24-47 hours prior to
the recordings. In addition, highly significant effects were found
for DC which decreased in association with PM(2.5), EC and OC
concurrent with the ECG recordings as well as with a lag of up to
47 hours. Conclusions: The analysis showed significant effects of
ambient particulate air pollution on DC and HRV parameters
reflecting parasympathetic modulation of the heart in patients with
CAD. An air pollution-related decrease in parasympathetic tone as
well as impaired heart rate deceleration capacity may contribute to
an increased risk for cardiac morbidity and sudden cardiac death in
vulnerable populations.