Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease
Details
Serval ID
serval:BIB_B2AA3EAD469E
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Acute systemic and coronary hemodynamic and serologic responses to cigarette smoking in long-term smokers with atherosclerotic coronary artery disease
Journal
Journal of the American College of Cardiology
ISSN
0735-1097 (Print)
Publication state
Published
Issued date
11/1984
Volume
4
Number
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
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Nov
Abstract
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)
Keywords
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
Yes
Create date
25/01/2008 15:00
Last modification date
20/08/2019 16:21