An observational study in Coronary Heart Disease and Angina Pectoris, sponsored by University of Edinburgh. Completed at 1 site in United Kingdom. Per ClinicalTrials.gov, last updated 2010-03-31.
Sponsored by University of Edinburgh · Observational
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.
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.
3,639 studies on the registry are indexed under Heart Diseases; 461 are open to participants now.
This study's enrollment of 19 is below the median of 294 across 1,241 observational studies indexed under Heart Diseases.
Browse Heart Diseases studies →University of Edinburgh is the lead sponsor of 393 studies on the registry; 64 are open to participants now.
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Patients will be recruited from the cardiology outpatient clinics
Exclusion Criteria:
Patients with documented stable coronary artery disease, symptoms of stable angina pectoris, and a positive standard BRUCE exercise stress test at 3 - 13 minutes.
Myocardial ischaemia - measured as time to 1mm ST segment depression on the ECG during standard BRUCE exercise stress testing.
Time frame: Immediately after exposure
Total ischaemic burden - assessed using 24 hour Holter ambulatory ECG monitoring
Time frame: 24hrs after exposure
Total exercise capacity - assessed by maximal work done during exercise stress test
Time frame: Immediately after exposure
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
This study is completed, as verified in Jul 2008. You cannot join it, but the record below documents what was studied.
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University of Edinburgh