The Effects of Diesel Exhaust Inhalation On Exercise Capacity In Patients With Stable Angina Pectoris

Completed

• Conditions: Coronary Heart Disease; Angina Pectoris

• Registration Number: NCT00737958
• Lead Sponsor: University of Edinburgh

Brief Summary

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.

Detailed Description

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.

Study Timeline

• Status Verified: 2008-07
• Study Start: 2008-08
• Study First Submitted: 2008-08-19
• Study First Submitted QC: 2008-08-19
• Study First Posted: 2008-08-20
• Primary Completion: 2008-12
• Study Completion: 2008-12
• Last Update Submitted: 2010-03-30
• Last Update Posted: 2010-03-31

Recruitment & Eligibility

• Status: COMPLETED
• Sex: All
• Target Recruitment: 19

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

Study & Design

• Study Type: OBSERVATIONAL
• Study Design: Not specified

Primary Outcome Measures

Name	Time	Method
Myocardial ischaemia - measured as time to 1mm ST segment depression on the ECG during standard BRUCE exercise stress testing.	Immediately after exposure

Secondary Outcome Measures

Name	Time	Method
Total ischaemic burden - assessed using 24 hour Holter ambulatory ECG monitoring	24hrs after exposure
Total exercise capacity - assessed by maximal work done during exercise stress test	Immediately after exposure
Biochemical evidence of myocardial ischaemia - plasma highly sensitive troponins, ischaemically modified albumin, fatty acid binding protein	Before, after and at 24 hours after exposure

Trial Locations

Locations (1)

University of Edinburgh; 🇬🇧 Edinburgh, Midlothian, United Kingdom