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Respiratory tract infection has been implicated as a factor leading
to the onset of acute myocardial infarction. In contrast to previous
data, Clayton et al. did not observe a significant association between
recent respiratory infection and myocardial infarction, but they did find
a strong association of infarction with chest pain on breathing within the
preceding week or with fever.
In industrialised countries, particularly in urban areas,
considerable levels of anthropogenic air pollutants can be expected.
Exposure to elevated air pollution is linked to increased respiratory
Illnesses and mortality. Air pollution induces an increased oxidative
stress and cytokine release and produces local pulmonary inflammation. At
the same time, epidemiological and clinical evidence for the association
between air pollution, including both gaseous pollutants and particulate
matter, and occurrence of acute myocardial infarction has continued to
grow.[5,6] It is believed that local pulmonary inflammation causes a
systemic response which may elevate the risk of acute myocardial
infarction by inducing plaque destabilisation, hypercoagulability and
disturbance of the autonomic nervous system. As an indicator of tightly
integrated cardiopulmonary affectability, Zanobetti and Schwartz have
recently reported on a slightly higher increase in risk of myocardial
infarction due to air pollution in association with chronic obstructive
lung disease and intercurrent pneumonia.
Since air pollution may influence both respiratory pathology and
occurrence of myocardial infarction, the study of Clayton et al would be
more conclusive if controls for two important factors, i.e. the level of air
pollutants and chronic lung diseases had been established. One might
expect that increased body temperature and pain on breathing, at least in
some patients in this study, could be related to the enhanced inflammation
and exacerbation of preexisting lung disease associated with elevated air
pollution. In turn, this may be one of the reasons why Clayton et al found
an association of myocardial infarction only with chest symptoms or fever,
but not with clearly diagnosed acute respiratory infection.
The proposed mechanisms of increased risk for myocardial infarction
associated with acute respiratory infection are similar to those
associated with elevated air pollution and include increased
thrombogeneicity and risk of plaque rupture.[1,2] There is a possibility
that air pollution may independently increase the incidence of myocardial
infarction by increasing the intensity of nonspecific pulmonary
inflammatory processes as well as by increasing the incidence of acute
respiratory infections. Further investigations need to focus on acute and
chronic inflammatory response as an important pathophysiological pathway,
and on its modulation as a possible mean of prevention. Better insight
into the specific adverse effects of air pollutants and respiratory
infections may allow additional improvement of preventive strategies
especially in some populations with a higher than normal risk of a
coronary event, for example in patients with ischemic heart disease and an
accompanying lung disease.
1. Meier CR, Jick SS, Derby LE, et al. Acute respiratory-tract infections
and risk of first-time acute myocardial infarction. Lancet 1998;351:1467-
2. Clayton TC, Capps NE, Stephens NG, et al. Recent respiratory infection
and the risk of myocardial infarction. Heart 2005;91:1601-2.
3. Schwartz J. Air pollution and hospital admissions for respiratory
disease. Epidemiology 1996;7:20-8.
4. Stieb DM, Judek S, Burnett RT. Meta-analysis of time-series studies of
air pollution and mortality: effects of gases and particles and the
influence of cause of death, age, and season. J Air Waste Manag Assoc
5. Routledge HC, Ayres JG, Townend JN. Why cardiologists should be
interested in air pollution. Heart 2003;89:1383-8.
6. Zanobetti A, Schwartz J. The effect of particulate air pollution on
emergency admissions for myocardial infarction: a multicity case-crossover
analysis. Environ Health Perspect 2005;113:978-82.