The smoker's--a hemodynamic reality?
BACKGROUND
Smoking is a well-known cardiovascular risk factor. Despite this, smokers seem to have a better prognosis after an acute coronary syndrome (ACS). It has been suggested that the thrombogenicity of smoke could explain this phenomenon; by causing occlusions or sub-occlusions in minor coronary lesions and leading to earlier ACS in terms of coronary disease.


OBJECTIVE
To compare the clinical and hemodynamic characteristics of patients hospitalized for ACS, according to their smoking status.


METHODS
The population of patients hospitalized for ACS between January 1, 2001 and September 30 2002 was divided into two groups, according to the existence (F) or not (NF) of a history of smoking. We compared clinical and epidemiologic characteristics, ECG presentation, coronary anatomy, peak troponin, mortality rate, duration of hospital stay and ejection fraction at date of discharge.


RESULTS
Of the 903 patients hospitalized for ACS, 369--mean age 54 years (24-88), 95% men--had a history of smoking. In the NF group mean age was 69 years (29-93), 51% being women. Hypertension and diabetes were more prevalent in NF (71 vs. 47% and 33 vs. 17%). Dyslipidemia was more frequent in F. Presentation with ST elevation was more common in F (38 vs. 24%) (p < 0.01) and peak troponin was also higher in this group (22.4 vs. 16.2 ng/ml) (p < 0.01). Coronary catheterization showed a larger number of vessels with critical disease and with diffuse disease in NF, although without statistical significance. Hospital stay was longer and the mortality rate was higher in NF (7.3 days vs. 6.9 days (NS) and 6.6% vs. 2.6% (p < 0.01), respectively). There was no difference between the two groups in ejection fraction at discharge. After adjustment for age and sex there were no statistically significant differences between the two groups for any of the variables studied.


CONCLUSIONS
The population of patients with a history of smoking who suffer an ACS is significantly younger than those with ACS who never smoked. This may explain the differences found in coronary anatomy between the two groups. The differences found at presentation and the more favorable in-hospital evolution that we found in the F group can also be explained by the epidemiologic differences of both populations and do not stand up to multivariate analysis. Therefore, in the population studied, it is not possible to confirm the hypothesis of a hemodynamic cause for the "smoker's paradox".
Bettencourt
Nuno
N
Centro Hospitalar de Vila Nova de Gaia-Serviço de Cardiologia, Vila Nova de Gaia, Portugal. nunobett@netcabo.pt
Mateus
Pedro
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Dias
Carla
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Santos
Lino
L
Adão
Luís
L
Gonçalves
Carlos
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Simões
Lino
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Gama
Vasc
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D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000789:Angina, Unstable / Q000503:physiopathology; D005260:Female; D006439:Hemodynamics; D006801:Humans; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000503:physiopathology; D012189:Retrospective Studies; D012907:Smoking / Q000503:physiopathology*; D013577:Syndrome