Acute Effect of Hookah Smoking on the Human Coronary Microcirculation

Abstract

Hookah (water pipe) smoking is a major new understudied epidemic affecting youth. Because burning charcoal is used to heat the tobacco product, hookah smoke delivers not only nicotine but also large amounts of charcoal combustion products, including carbon-rich nanoparticles that constitute putative coronary vasoconstrictor stimuli and carbon monoxide, a known coronary vasodilator. We used myocardial contrast echocardiography perfusion imaging with intravenous lipid shelled microbubbles in young adult hookah smokers to determine the net effect of smoking hookah on myocardial blood flow. In 9 hookah smokers (age 27 ± 5 years, mean ± SD), we measured myocardial blood flow velocity (β), myocardial blood volume (A), myocardial blood flow (A × β) as well as myocardial oxygen consumption (MVO2) before and immediately after 30 minutes of ad lib hookah smoking. Myocardial blood flow did not decrease with hookah smoking but rather increased acutely (88 ± 10 to 120 ± 19 a.u./s, mean ± SE, p = 0.02), matching a mild increase in MVO2 (6.5 ± 0.3 to 7.6 ± 0.4 ml·minute(-1), p <0.001). This was manifested primarily by increased myocardial blood flow velocity (0.7 ± 0.1 to 0.9 ± 0.1 second(-1), p = 0.01) with unchanged myocardial blood volume (133 ± 7 to 137 ± 7 a.u., p = ns), the same pattern of coronary microvascular response seen with a low-dose β-adrenergic agonist. Indeed, with hookah, the increased MVO2 was accompanied by decreased heart rate variability, an indirect index of adrenergic overactivity, and eliminated by β-adrenergic blockade (i.v. propranolol). In conclusion, nanoparticle-enriched hookah smoke either is not an acute coronary vasoconstrictor stimulus or its vasoconstrictor effect is too weak to overcome the physiologic dilation of coronary microvessels matching mild cardiac β-adrenergic stimulation.

Figure 1

Hookah Smoking Chamber and Water pipe Schematic. The Plexiglass and aluminum smoking chamber with a procedure chair enclosed. Multiple airtight rubber ports on the front and side panels allow wires and tubing to be connected to recording equipment outside the closed chamber (Left panel). Closeup of a mock subject holding the water pipe. A fan within the exhaust system continuously pulls air out through the vent (arrow) in the ceiling (Middle panel). The water pipe schematic showing the burning charcoal used to heat the tobacco (Right panel).

Figure 2

Effect of hookah smoking on myocardial blood flow by MCE. Illustrative MCE images of the left ventricle at various time intervals after the destructive pulse sequence (denoted as T0) in one subject. The rate of bubble replenishment in the myocardium was faster after hookah smoking (Top panel). Time-video intensity plot before and after hookah smoking in the same subject. The reappearance rate (myocardial blood flow velocity, β) was faster after hookah smoking, whereas the peak video intensity (myocardial blood volume, A) was unchanged (Bottom left panel). Summary data for myocardial blood flow (A × β) and myocardial blood flow normalized to myocardial oxygen consumption (MVO₂) before and after hookah smoking (Bottom right bar graphs). Data are mean ± SE for 9 subjects, *p <0.05.

Figure 3

Effect of hookah smoking on heart rate variability before and after β-adrenergic blockade (i.v. propranolol). Panels illustrate heart rate, normalized high frequency power (HFnu), normalized low frequency power (LFnu), and the LF/HF ratio before (white bars) and immediately after (black bars) 30 minutes of hookah smoking with and without β blockade. Summary data for 4 subjects reported as mean ± SE, *p <0.05. HFnu = high frequency normalized units; LFnu = low frequency normalized units.