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.

Inclusion Criteria:

• Documented coronary heart disease
• Symptoms of stable angina pectoris

Exclusion Criteria:

• History of arrhythmia
• Severe 3 vessel coronary artery disease or left main stem stenosis that has not been revascularised
• Resting conduction abnormality
• Digoxin therapy
• Uncontrolled hypertension
• Renal or hepatic failure
• Patients with unstable disease (ACS or unstable symptoms within 3 months)
• Asthma
• Intercurrent illness

Patients will be recruited from the cardiology outpatient clinics