The Effects of Diesel Exhaust Inhalation On Exercise Capacity In Patients With Stable Angina Pectoris
The purpose of this study is to determine whether exposure to diesel exhaust (air pollution) has a functional impact on patients with stable angina pectoris.
Coronary Heart Disease
|Study Design:||Observational Model: Case-Crossover
Time Perspective: Prospective
|Official Title:||The Effects of Diesel Exhaust Inhalation On Exercise Capacity In Patients With Stable Angina Pectoris|
- Myocardial ischaemia - measured as time to 1mm ST segment depression on the ECG during standard BRUCE exercise stress testing. [ Time Frame: Immediately after exposure ] [ Designated as safety issue: No ]
- Total ischaemic burden - assessed using 24 hour Holter ambulatory ECG monitoring [ Time Frame: 24hrs after exposure ] [ Designated as safety issue: No ]
- Total exercise capacity - assessed by maximal work done during exercise stress test [ Time Frame: Immediately after exposure ] [ Designated as safety issue: No ]
- Biochemical evidence of myocardial ischaemia - plasma highly sensitive troponins, ischaemically modified albumin, fatty acid binding protein [ Time Frame: Before, after and at 24 hours after exposure ] [ Designated as safety issue: No ]
Biospecimen Retention: Samples Without DNA
Plasma samples Serum samples
|Study Start Date:||August 2008|
|Study Completion Date:||December 2008|
|Primary Completion Date:||December 2008 (Final data collection date for primary outcome measure)|
Patients with documented stable coronary artery disease, symptoms of stable angina pectoris, and a positive standard BRUCE exercise stress test at 3 - 13 minutes.
Air pollution is a major cause of cardiovascular morbidity and mortality. The mechanism and components of air pollution responsible for these cardiovascular effects are unknown but small combustion-derived particles are suspected to be the major cause. Using a unique exposure system in Umeå Sweden, we have demonstrated that healthy volunteers who inhale dilute diesel exhaust develop an impairment of two important, highly relevant and complementary aspects of vascular function: the regulation of vascular tone and endogenous fibrinolysis. We have recently extended these findings and have shown that brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in patients with stable asymptomatic coronary heart disease. We now wish to extend these findings to patients with chronic stable angina pectoris. In particular, we wish to determine the functional impact of diesel exhaust inhalation as well as describe the time course and minimum exposure that can induce these detrimental effects.
|University of Edinburgh|
|Edinburgh, Midlothian, United Kingdom, EH16 4SB|
|Study Director:||David E Newby, MD FRCP||University of Edinburgh|