Document Detail


Ischemic and thrombotic effects of dilute diesel-exhaust inhalation in men with coronary heart disease.
MedLine Citation:
PMID:  17855668     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Exposure to air pollution from traffic is associated with adverse cardiovascular events. The mechanisms for this association are unknown. We conducted a controlled exposure to dilute diesel exhaust in patients with stable coronary heart disease to determine the direct effect of air pollution on myocardial, vascular, and fibrinolytic function. METHODS: In a double-blind, randomized, crossover study, 20 men with prior myocardial infarction were exposed, in two separate sessions, to dilute diesel exhaust (300 mug per cubic meter) or filtered air for 1 hour during periods of rest and moderate exercise in a controlled-exposure facility. During the exposure, myocardial ischemia was quantified by ST-segment analysis using continuous 12-lead electrocardiography. Six hours after exposure, vasomotor and fibrinolytic function were assessed by means of intraarterial agonist infusions. RESULTS: During both exposure sessions, the heart rate increased with exercise (P<0.001); the increase was similar during exposure to diesel exhaust and exposure to filtered air (P=0.67). Exercise-induced ST-segment depression was present in all patients, but there was a greater increase in the ischemic burden during exposure to diesel exhaust (-22+/-4 vs. -8+/-6 millivolt seconds, P<0.001). Exposure to diesel exhaust did not aggravate preexisting vasomotor dysfunction, but it did reduce the acute release of endothelial tissue plasminogen activator (P=0.009; 35% decrease in the area under the curve). CONCLUSIONS: Brief exposure to dilute diesel exhaust promotes myocardial ischemia and inhibits endogenous fibrinolytic capacity in men with stable coronary heart disease. Our findings point to ischemic and thrombotic mechanisms that may explain in part the observation that exposure to combustion-derived air pollution is associated with adverse cardiovascular events. (ClinicalTrials.gov number, NCT00437138 [ClinicalTrials.gov].).
Authors:
Nicholas L Mills; Håkan Törnqvist; Manuel C Gonzalez; Elen Vink; Simon D Robinson; Stefan Söderberg; Nicholas A Boon; Ken Donaldson; Thomas Sandström; Anders Blomberg; David E Newby
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Publication Detail:
Type:  Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The New England journal of medicine     Volume:  357     ISSN:  1533-4406     ISO Abbreviation:  N. Engl. J. Med.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-09-14     Completed Date:  2007-09-21     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0255562     Medline TA:  N Engl J Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1075-82     Citation Subset:  AIM; IM    
Copyright Information:
Copyright 2007 Massachusetts Medical Society.
Affiliation:
Centre for Cardiovascular Science, Edinburgh University, Edinburgh, Sweden. nick.mills@ed.ac.uk
Data Bank Information
Bank Name/Acc. No.:
ClinicalTrials.gov/NCT00437138
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MeSH Terms
Descriptor/Qualifier:
Air Pollution / adverse effects*
Cardiovascular System / drug effects*,  physiopathology
Coronary Disease / physiopathology*
Cross-Over Studies
Double-Blind Method
Environmental Exposure / adverse effects
Exercise / physiology
Fibrinolysis / drug effects
Humans
Inhalation
Male
Middle Aged
Myocardial Infarction
Myocardial Ischemia / etiology*
Particulate Matter / adverse effects*
Thrombosis / etiology
Vasodilator Agents / pharmacology
Vehicle Emissions / toxicity*
Chemical
Reg. No./Substance:
0/Particulate Matter; 0/Vasodilator Agents; 0/Vehicle Emissions
Comments/Corrections
Comment In:
N Engl J Med. 2007 Sep 13;357(11):1147-9   [PMID:  17855676 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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