Abstract
We examined cardiovascular function in 637 volunteers (19–72 years) without antihypertensive medication in never smokers (n = 365), present smokers (n = 81) and previous smokers (n = 191, median abstinence 10 years). Haemodynamics during passive head-up tilt were recorded using whole-body impedance cardiography and radial pulse wave analysis. Results were adjusted for age, sex, body mass index, LDL cholesterol and alcohol use. Systolic and diastolic blood pressure, heart rate, and pulse wave velocity were not different between the groups. Supine aortic reflection times did not differ, while upright values were shorter in present versus previous smokers (p = 0.04). Heart rate adjusted augmentation index was increased in the supine position in present smokers versus controls (p = 0.045), and in present (p < 0.001) and previous (p = 0.031) smokers versus controls in the upright position. Supine and upright cardiac output was higher (p ≤ 0.016) and systemic vascular resistance lower (p ≤ 0.001) in present versus previous smokers. In spite of the long abstinence, in the upright position previous smokers had lower cardiac output (p = 0.032) and higher systemic vascular resistance (p = 0.014) than never smokers. In the absence of differences in blood pressure and arterial stiffness, present smokers presented with hyperdynamic circulation and enhanced wave reflection compared with previous smokers.
Highlights
Cigarette smoking is one of the most important preventable risk factors for mortality in the Western world[1,2], accounting for more than 5 million premature deaths globally per year[3]
body mass index (BMI) was higher in previous smokers compared to never- and present smokers
In the office systolic blood pressure (BP) was ~6 mmHg higher in previous smokers versus present smokers, while diastolic BP was higher in previous smokers compared to never and present smokers
Summary
Cigarette smoking is one of the most important preventable risk factors for mortality in the Western world[1,2], accounting for more than 5 million premature deaths globally per year[3]. In a study with 10,914 patients the progression of atherosclerosis in current smokers was increased by 50% versus non-smokers, documented using measurements of IMT in the carotid artery[7]. Gropelli et al reported that smoking causes an acute 15–20 mmHg rise in systolic BP, but the effect starts declining after 10 minutes and can be missed if BP is measured more than 30 minutes after smoking[15]. Some studies reported that smokers have lower BP than non-smokers[17,18]. Many studies have reported that chronic smoking is a risk factor for increased arterial stiffness, a number of investigations have not found differences in arterial stiffness between smokers and never smokers[22,23]. Polonia et al found that AIx was reduced by about 9 percentage points in subjects who stopped smoking for 6 months, whereas there was an increase of 1.7 percentage points in those who continued smoking[28]
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