Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease

Détails

ID Serval
serval:BIB_B2AA3EAD469E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease
Périodique
Journal of the American College of Cardiology
Auteur(s)
Nicod  P., Rehr  R., Winniford  M. D., Campbell  W. B., Firth  B. G., Hillis  L. D.
ISSN
0735-1097 (Print)
Statut éditorial
Publié
Date de publication
11/1984
Volume
4
Numéro
5
Pages
964-71
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Nov
Résumé
Previous studies suggested that cigarette smoking 1) inhibits an increase in coronary blood flow that should occur with increased myocardial oxygen demands, and 2) alters thromboxane and prostacyclin production, causing vasoconstriction and platelet aggregation. In 38 smokers (26 men and 12 women, aged 50 +/- 8 years [mean +/- standard deviation] ) with coronary artery disease, systemic and coronary hemodynamic and serologic variables were measured before and after smoking two cigarettes (in 8 to 10 minutes) (21 patients) or 8 to 10 minutes without smoking (17 patients; control group). No variable changed in the control group. Smoking increased (p less than 0.05) heart rate-systolic pressure product, cardiac output and maximal first derivative of left ventricular pressure (dP/dt) without significantly changing the coronary sinus concentrations of thromboxane B2 or 6-keto-prostaglandin F1 alpha (the stable metabolites of thromboxane A2 and prostacyclin, respectively). Smoking did not increase coronary flow in 6 of 11 patients with greater than 70% stenosis of the proximal left anterior descending or circumflex coronary artery, or both, whereas it caused an increase in coronary flow in all 10 patients without proximal stenoses (p = 0.006). To determine if smoking altered the response of coronary flow to increased myocardial oxygen demands, 10 smokers (5 men and 5 women, aged 48 +/- 9 years) underwent atrial pacing for 5 minutes followed 15 minutes later by atrial pacing for 5 minutes during smoking. In the five patients without proximal left coronary artery stenoses, coronary flow increased 26 +/- 29 ml/min with pacing and 45 +/- 21 ml/min with pacing/smoking (p = 0.018).(ABSTRACT TRUNCATED AT 250 WORDS)
Mots-clé
6-Ketoprostaglandin F1 alpha/blood Adult Aged Blood Pressure Cardiac Pacing, Artificial Coronary Circulation Coronary Disease/blood/*physiopathology Female Heart Rate *Hemodynamic Processes Humans Male Middle Aged *Smoking Thromboxane B2/blood
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 14:00
Dernière modification de la notice
20/08/2019 15:21
Données d'usage