Effect of Paroxetine on Smokers' Cardiovascular Response to Stress - 1

This study has been completed.
Sponsor:
Collaborator:
Information provided by (Responsible Party):
University of Minnesota - Clinical and Translational Science Institute
ClinicalTrials.gov Identifier:
NCT00218439
First received: September 16, 2005
Last updated: April 28, 2014
Last verified: April 2014

September 16, 2005
April 28, 2014
October 2005
August 2010   (final data collection date for primary outcome measure)
Systolic Blood Pressure Response to Stress [ Time Frame: After 4 weeks of paroxetine / placebo ] [ Designated as safety issue: No ]
Change in systolic blood pressure from Resting period to that observed during a speech delivered immediately after smoking a cigarette
  • Physiological response to stress; measured at Weeks 4 and 8, immediately folllowing mental stress test
  • Psychological response to stress; measured at Weeks 4 and 8, immediately following mental stress test
Complete list of historical versions of study NCT00218439 on ClinicalTrials.gov Archive Site
Not Provided
Not Provided
  • Diastolic Blood Pressure Response to Stress [ Time Frame: After 4 weeks of paroxetine / placebo ] [ Designated as safety issue: No ]
    Change in diastolic blood pressure from Resting period to that observed during a speech delivered immediately after smoking a cigarette
  • Heart Rate Response to Stress [ Time Frame: After 4 weeks of paroxetine / placebo ] [ Designated as safety issue: No ]
    Change in heart rate from Resting period to that observed during a speech delivered immediately after smoking a cigarette
  • Plasma Epinephrine Concentration Response to Stress [ Time Frame: After 4 weeks of paroxetine / placebo ] [ Designated as safety issue: No ]
    Change in plasma epinephrine concentrations from Resting period to those observed during a speech delivered immediately after smoking a cigarette
  • Plasma Norepinephrine Concentration Response to Stress [ Time Frame: After 4 weeks of paroxetine / placebo ] [ Designated as safety issue: No ]
    Change in plasma norepinephrine concentrations from Resting period to those observed during a speech delivered immediately after smoking a cigarette
Not Provided
 
Effect of Paroxetine on Smokers' Cardiovascular Response to Stress - 1
Smoking, Antidepressants, and Response to Mental Stress

Smokers report that they often smoke cigarettes during stressful times. The combined effect of smoking and exposure to stress leads to exaggerated increases in blood pressure, heart rate and other measures of stress response. This combination may result in greater cardiovascular harm than either smoking or stress alone. The purpose of this study is to determine the effects of paroxetine on the response to stress after smoking.

Smokers report that they often smoke cigarettes during stressful times. Smoking and stress produce similar physiological responses such as increases in heart rate, blood pressure, and adrenaline levels. The combination of smoking and stress results in greater increases in these physiological responses compared to smoking or stress alone. Such increases are thought to be harmful to cardiovascular health. Additionally, smokers with exaggerated responses to stress may be more likely to relapse following a smoking cessation attempt. The purpose of this study is to assess the effects of paroxetine, a selective serotonin reuptake inhibitor (SSRI), on the cardiovascular response to stress after smoking.

Participants in this double-blind, placebo-controlled study will receive 1 month of paroxetine and 1 month of placebo with the order of which is taken during the first month randomly assigned. Paroxetine will be administered at a daily dose of 10 mg for the first week and increased to a daily dose of 20 mg for the remainder of the study. After one month of medication, participants will abstain from smoking for one night and then undergo mental stress testing the following day. Immediately prior to the mental stress testing, participants will smoke a cigarette. Mental stressors will include speaking and math tasks. Physiological measures of stress (e.g., blood pressure, heart rate, and plasma catecholamine concentrations) and subjective measures of stress will be evaluated. Following the second month of medication, participants will again undergo the procedure for mental stress testing and evaluation.

Interventional
Not Provided
Allocation: Randomized
Endpoint Classification: Pharmacodynamics Study
Intervention Model: Crossover Assignment
Masking: Double Blind (Subject, Investigator)
Primary Purpose: Treatment
Tobacco Use Disorder
  • Drug: Paroxetine
    10 mg for 1 week followed by 20 mg for 3 weeks
  • Drug: Placebo
  • Experimental: 1
    Active medication for 4 weeks followed by placebo for 4 weeks
    Interventions:
    • Drug: Paroxetine
    • Drug: Placebo
  • Experimental: 2
    Placebo for 4 weeks followed by active for 4 weeks
    Interventions:
    • Drug: Paroxetine
    • Drug: Placebo
Kotlyar M, al'Absi M, Thuras P, Vuchetich JP, Adson DE, Nowack AL, Hatsukami DK. Effect of paroxetine on physiological response to stress and smoking. Psychosom Med. 2013 Apr;75(3):236-43. doi: 10.1097/PSY.0b013e3182898f6d. Epub 2013 Mar 15.

*   Includes publications given by the data provider as well as publications identified by ClinicalTrials.gov Identifier (NCT Number) in Medline.
 
Completed
105
August 2010
August 2010   (final data collection date for primary outcome measure)

Inclusion Criteria:

  • Smokes an average of at least 10 cigarettes per day during the year prior to enrollment

Exclusion Criteria:

  • Interested in quitting smoking within the 3 months following enrollment
  • Current unstable medical condition
  • Substance abuse within the year prior to enrollment
  • Current use of any medications (e.g., psychoactive medications, antihypertensives) that, in the opinion of the investigators, might interfere with study measures or that would be expected to interact with paroxetine (e.g., CYP2D6 substrates)
  • Smoking cessation therapy within the 3 months prior to enrollment
  • Regular use of any form of tobacco other than cigarettes
  • Significant psychiatric disorders as assessed by the PRIME-MD and verified by a clinician
  • History of hypersensitivity to any selective serotonin reuptake inhibitor
  • Pregnancy or breastfeeding
Both
18 Years to 65 Years
Yes
Contact information is only displayed when the study is recruiting subjects
United States
 
NCT00218439
NIDA-17307-1, K23DA017307-01, DPMC
Not Provided
University of Minnesota - Clinical and Translational Science Institute
University of Minnesota - Clinical and Translational Science Institute
National Institute on Drug Abuse (NIDA)
Principal Investigator: Michael Kotlyar University of Minnesota - Clinical and Translational Science Institute
University of Minnesota - Clinical and Translational Science Institute
April 2014

ICMJE     Data element required by the International Committee of Medical Journal Editors and the World Health Organization ICTRP