E-cigarettes deliver nicotine by creating an aerosol of ultrafine particles. Many questions remain about the size and composition and especially about the potential toxicity of these particles. Thus, a key unanswered question-and the research question proposed-is whether e-cigarette aerosol triggers the same acute impairment in coronary microvessel function as does conventional cigarette smoke, which delivers a very well-defined exposure to fine particles and many fold greater exposure to toxic (combustion) products including volatile organic compounds (such as acrolein) that have been implicated in the pathogenesis of tobacco-related coronary disease. Because the effects of nicotine on the human coronary microcirculation remain incompletely defined-with multiple potential vasodilator and vasoconstrictor actions each of which may vary by dose-we will determine the comparative effects of conventional cigarette smoke against e-cigarette aerosol with no nicotine, with low-dose nicotine, and with high-dose nicotine.
Study Type
INTERVENTIONAL
Allocation
NON_RANDOMIZED
Purpose
OTHER
Masking
NONE
Enrollment
20
Subjects will smoke a standard cigarette (yield: tar 12 mg, nicotine 1 mg)
Subjects will smoke nicotine free e-liquid with an e-cigarette.
Subjects will smoke low nicotine (4-6 mg/mL) e-liquid with an e-cigarette.
Subjects will smoke low nicotine (18-24 mg/mL) e-liquid with an e-cigarette.
Cedars-Sinai Medical Center
Los Angeles, California, United States
Myocardial Perfusion (change in microvascular flux rate from baseline at 30 minutes)
Myocardial contrast echocardiography will be used to measure regional myocardial perfusion - microvascular flux rate
Time frame: Baseline and 30 minutes after smoking
Myocardial Perfusion (change in capillary blood volume from baseline at 30 minutes)
Myocardial contrast echocardiography will be used to measure regional myocardial perfusion - capillary blood volume
Time frame: Baseline and 30 minutes after smoking
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