Hookah Smoking Does Not Constrict Human Coronary Microvessels

Abstract

Hookah (water pipe) smoking has reached epidemic proportions due to unregulated social media marketing to young adults as a safer avant‐garde alternative to cigarettes. In contrast, much is suspected by tobacco researchers—yet little is proven—about hookah's putative health risks. What distinguishes hookah from all other tobacco products is that burning charcoal is used to heat the tobacco. As a result, hookah smoke delivers a large acute exposure not only to carbon monoxide (CO) but also to fine and ultrafine particles, charcoal combustion products that have been suggested—but unproven—by the air pollution and tobacco literature to constitute putative coronary vasoconstrictor stimuli. To test if hookah smoking constricts human coronary microvessels, in 28 young adult hookah smokers (age 27±5 years, mean±SD, 8 women, 20 men) we used myocardial contrast echocardiography (MCE) perfusion imaging with intravenous lipid shelled microbubbles to measure myocardial blood flow and its two components, microvascular flux rate (β) and functional capillary blood volume (A), and measured myocardial oxygen consumption (MVO2 = (7.2 × 10−4) x (heart rate x systolic blood pressure) + 1.42) as well as exhaled CO and plasma nicotine before and immediately after 30 minutes of ad lib hookah smoking in a custom‐built smoking chamber. With hookah smoking, exhaled CO increased from 3.0±0.4 to 25±2.2 ppm (mean ±SE, p<0.001 pre‐vs. post‐hookah), which approximates the CO boost of a typical ad lib hookah smoking session in hookah bars and indicates an exposure to fine and ultrafine particles that is 10 times greater (and to total particles that is 250 times greater) than that with cigarette smoking. On MCE, myocardial blood flow (A x β) did not decrease but rather increased acutely with hookah smoking (88±10 to 120±19 a.u.·s−1, p=0.02). The increased perfusion matched the mild hookah‐induced increase in MVO2 (6.5±0.3 to 7.6±0.4 ml·min−1, p<0.001), indicating physiologic vasodilation, and was manifested primarily by increased microvascular flux rate (0.7±0.1 to 0.9±0.1 s−1, p=0.01) with unchanged capillary blood volume (133±7 to 137±7 a.u., p=ns), a pattern of coronary microvascular response seen previously with a mild b‐adrenergic agonist. Moreover, the increased MVO2 and accompanying decrease in heart rate variability were accompanied by increased plasma nicotine (0.9±0.1 to 7.8±1.3 mg/mL, p<0.001) and almost completely eliminated by intravenous propranolol, documenting b‐adrenergic mediation. Thus, under these experimental conditions, mainstream hookah smoke either is not an acute coronary vasoconstrictor stimulus or one that is too weak to overcome the physiologic dilation of coronary microvessels caused by mild nicotine‐induced cardiac b‐adrenergic stimulation and/or pharmacologic dilation caused by carbon monoxide.