Acute effects of smoking on left ventricular function and neuro‐humoral responses in patients with known or suspected ischaemic heart disease

Abstract

Systolic left ventricular function was examined by radionuclide ventriculography in 12 habitual smokers with known or suspected ischaemic heart disease, aged 33-69 years, before, during, and after smoking of two cigarettes in a row and was repeated on a non-smoking control day. Plasma concentrations of adrenaline, noradrenaline, renin, and angiotensin II were determined on the smoking day, before and immediately after smoking. During smoking, there were significant increases in heart rate (+27%), rate-pressure product (+23%), and cardiac output (+14%) in the face of a significant increase in left ventricular end-systolic volume (+5%) and significant decreases in ejection fraction (-6%) and stroke volume (-8%). Blood pressure was virtually unchanged, and total peripheral resistance remained constant. Plasma adrenaline increased by 100%, renin decreased by 21%, and noradrenaline and angiotensin II did not change. The humoral changes were not correlated to changes in any of the haemodynamic variables. Areas of myocardial hypokinesis emerged or widened during smoking in 11 of 12 patients. Thus, in patients with known or suspected ischaemic heart disease, smoking was associated with an acute decrease in systolic ventricular function and development of widespread hypokinesis despite adrenaline stimulation.

Ethnic differences in arterial stiffness and wave reflections after cigarette smoking

“…Nicotine acutely increases the sympathetic tone [4,18,19] by releasing both epinephrine and norepinephrine, which are a-adrenergic, b 1 -adrenergic and b 2 -adrenergic receptor agonists [20,21]. Vasodilatation of peripheral muscular [45,46] and large central arteries [47] in responses to isoproterenol, a b 1 -adrenergic and b 2 -adrenergic agonist, are attenuated in healthy Black normotensive patients as compared with Whites.…”

“…Nicotine releases catecholamines, which are a-adrenergic, b 1 -adrenergic and b 2 -adrenergic receptor agonists [20,21]. The nicotine intake per cigarette has been reported to be 30% greater in Blacks as compared with Whites [22].…”

Effect of Exposure to Second-Hand Smoke on the Quality of Life: A Nationwide Population-Based Study from South Korea

“…Although the pathophysiological mechanisms of SHS exposure responsible for such detrimental effects on HRQOL remain unclear, there is indirect biological evidence to support our findings. In this respect, it is known that active smoking is associated with higher serum concentrations of epinephrine and norepinephrine and a lower concentration of renin, suggesting a potential interaction of exposure to smoke and the sympathetic regulatory system [ 29 , 30 ]. Moreover, the increased exposure to chemical substances present in smoke, including nicotine and carbon monoxide, can cause peripheral vasoconstriction and impaired tissue oxygenation, leading to possible psychological derangement [ 14 , 31 ].…”

Secondhand Smoke Exposure and Quality of Life in Patients With Heart Failure

“…26 In habitual smokers, smoking 2 cigarettes was associated with a 100% increase in plasma adrenaline (epinephrine) and a 21% decrease in plasma renin; angiotensin II levels did not change significantly. 27 These data suggest a potential interaction of smoke exposure on this important regulatory system, although data from animal models of myocardial infarction have been unable to confirm this. 28 An increase in platelet aggregability has also been implicated in the increased risk of cardiovascular events associated with SHS.…”