Effects of Acute Cigarette Smoking on Endothelium-Dependent Arterial Dilatation in Normal Subjects

Lekakis, John; Papamichael, Christos; Vemmos, Costas; Stamatelopoulos, Kimon; Voutsas, A.; Stamatelopoulos, Stamatios

doi:10.1016/s0002-9149(98)00098-8

Cited by 111 publications

(68 citation statements)

References 9 publications

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“…24 Lekakis et al showed that endothelial dysfunction persisted for 90 min after smoking. 25 These are possible mechanisms for the acute effects of smoking on the baPWV and CAVI.…”

Section: Acute Effect Of Smoking On Arterial Stiffnessmentioning

confidence: 99%

Acute and Chronic Effects of Smoking on Arterial Stiffness

Kubozono

Miyata

Ueyama

et al. 2011

Circ J

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Background:The brachial-ankle pulse wave velocity (baPWV) and cardio-ankle vascular index (CAVI) are used to evaluate arterial distensibility. The purpose of this study was to elucidate the acute and chronic effects of smoking on arterial stiffness as measured by baPWV and CAVI. Methods and Results:Ten male smokers were studied to evaluate the acute effect of smoking on arterial stiffness. To elucidate the chronic effect of smoking on arterial stiffness, 160 male active smokers were analyzed. CAVI and baPWV were calculated by measuring the pulse volume record, blood pressure (BP), and vascular length from heart to ankle. CAVI and baPWV were measured using a VaSera VS-1000. In the acute study, baPWV and CAVI increased immediately after smoking 1 cigarette. In the chronic study, baPWV and CAVI significantly correlated with mean BP (MBP) and the Brinkman index. In multiple regression analysis, baPWV independently correlated with MBP, and CAVI independently correlated with the Brinkman index, but not with MBP. Receiver-operating characteristics (ROC) curves of baPWV and CAVI to predict Brinkman index ≥500 demonstrated that the area under the ROC curve of CAVI was higher than that of baPWV. Conclusions:Smoking causes a significant increase in arterial stiffness as measured by baPWV and CAVI. CAVI correlated with the Brinkman index, which suggests that CAVI is a useful index of the degree of arterial stiffness caused by smoking. (Circ J 2011; 75: 698 - 702)

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“…24 Lekakis et al showed that endothelial dysfunction persisted for 90 min after smoking. 25 These are possible mechanisms for the acute effects of smoking on the baPWV and CAVI.…”

Section: Acute Effect Of Smoking On Arterial Stiffnessmentioning

confidence: 99%

Acute and Chronic Effects of Smoking on Arterial Stiffness

Kubozono

Miyata

Ueyama

et al. 2011

Circ J

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“…Moreover, smoking elevates the circulating levels of potential blood vessel vasoconstrictor agents such as endothelin-1 and catecholamines that seem to increase immediately after smoking and induce hypertension and endothelial dysfunction [ 26 , 27 ]. Several studies suggest that impaired microvascular function contributes to an increase in blood pressure and heart rate [ 26 ]. We documented that short-term smoking increased blood pressure and heart rate and these changes occurred 5 min after smoking and were not apparent 30 min later.…”

Section: Discussionmentioning

confidence: 70%

Acute cigarette smoking impairs microvascular function in young moderate smokers: A potential model for studying vasoactive properties of food bioactives

et al. 2014

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“…Furthermore, given the demographics of the patients in the adult studies, it is difficult to exclude typical cardiovascular risk factors as contributing to impaired endothelial function. Atherosclerosis 23 , diabetes 24,25 , hypertension 26 , obesity 25 , hypercholesterolemia 25 , and cigarette smoking 27 are all known to impact systemic endothelial function and FMD measurements. Although an adult PAH population may demonstrate these risk factors in proportion to healthy adults 19 , it may be difficult to identify all individuals with subclinical disease.…”

Section: Discussionmentioning

confidence: 99%

153 Systemic Endothelial Dysfunction in Children with Idiopathic Pulmonary Arterial Hypertension Correlates with Disease Severity

Friedman

Szmuszkovicz

Rabai

et al. 2012

The Journal of Heart and Lung Transplantation

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Background-Idiopathic pulmonary arterial hypertension (IPAH) is a life-threatening disease manifested by progressive pulmonary vascular remodeling, compromised pulmonary blood flow and right heart failure. Most studies explore how pulmonary endothelial function modulates disease pathogenesis. We hypothesize that IPAH is a progressive panvasculopathy, affecting both pulmonary and systemic vascular beds, and that systemic endothelial dysfunction correlates with disease severity. Recent studies demonstrate systemic endothelial dysfunction in adults with pulmonary hypertension, however adults often have additional comorbidities affecting endothelial function. Systemic endothelial function has not been explored in children with IPAH.

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Effects of Acute Cigarette Smoking on Endothelium-Dependent Arterial Dilatation in Normal Subjects

Cited by 111 publications

References 9 publications

Acute and Chronic Effects of Smoking on Arterial Stiffness

Acute and Chronic Effects of Smoking on Arterial Stiffness

Acute cigarette smoking impairs microvascular function in young moderate smokers: A potential model for studying vasoactive properties of food bioactives

153 Systemic Endothelial Dysfunction in Children with Idiopathic Pulmonary Arterial Hypertension Correlates with Disease Severity

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