Smoking and growth rate of small abdominal aortic aneurysms

MacSweeney, S. T. R.; Ellis, Mary; Worrell, P.; Greenhalgh, Roger M.; Powell, J.T.

doi:10.1016/s0140-6736(94)92087-7

Cited by 171 publications

(104 citation statements)

References 9 publications

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“…6 Previous studies have identified that AAAs appear to expand faster in current smokers, but most of these studies have been too small to quantify the effect reliably. [15][16][17] We show that smoking increases AAA growth rates by 15% to 20%. Although highly significant, this is a small effect and insufficient to warrant the recommendation of different screening intervals for smokers (Figure 3).…”

Section: Brady Et Al Abdominal Aortic Aneurysm Expansionmentioning

confidence: 76%

Abdominal aortic aneurysm expansion: Risk factors and time intervals for surveillance

Brady¹,

Thompson²,

Fowkes³

et al. 2004

ACC Current Journal Review

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210

360

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on behalf of the UK Small Aneurysm Trial Participants Background-Intervention to reduce abdominal aortic aneurysm (AAA) expansion and optimization of screening intervals would improve current surveillance programs. The aim of this study was to characterize AAA growth in a national cohort of patients with AAA both overall and by cardiovascular risk factors. Methods and Results-In this study, 1743 patients were monitored for changes in AAA diameter by ultrasonography over a mean follow-up of 1.9 years. Mean initial AAA diameter and growth rate were 43 mm (range 28 to 85 mm) and 2.6 mm/year (95% range, Ϫ1.0 to 6.1 mm/year), respectively. Baseline diameter was strongly associated with growth, suggesting that AAA growth accelerates as the aneurysm enlarges. AAA growth rate was lower in those with low ankle/brachial pressure index and diabetes but higher for current smokers (all PϽ0.001). No other factor (including lipids and blood pressure) was associated with AAA growth. Intervals of 36, 24, 12, and 3 months for aneurysms of 35, 40, 45, and 50 mm, respectively, would restrict the probability of breaching the 55-mm limit at rescreening to below 1%. Conclusions

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Section: Brady Et Al Abdominal Aortic Aneurysm Expansionmentioning

confidence: 76%

Abdominal aortic aneurysm expansion: Risk factors and time intervals for surveillance

Brady¹,

Thompson²,

Fowkes³

et al. 2004

ACC Current Journal Review

Self Cite

210

360

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“…35 Studies in humans and mice showed that besides AAA formation, smoking correlates with increased aneurysmal expansion 38,39 and that quitting smoking could reduce the growth rate of small AAAs. 40 In addition, the UK Small Aneurysm Trial showed that smokers with impaired lung function had an increased risk of aneurysm rupture and poorer long-term survival. 41 However, other studies failed to show that smoking influences the outcome of endovascular AAA surgery.…”

Section: Clinical Evidencementioning

confidence: 99%

Smoking and Aortic Diseases

Kakafika

Mikhailidis

2007

Circ J

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Cigarette smoking is a major cause of cardiovascular disease (CVD) and is responsible for approximately 11% of the annual total CVD deaths in the United States. 1 Smoking acts synergistically with other vascular risk factors (eg, hypertension, dyslipidaemia and diabetes) to increase vascular morbidity and mortality. 2 However, smoking has a variable magnitude of increased risk for different vascular diseases: the risk is highest for peripheral arterial disease and aortic aneurysm, and is lowest for coronary artery and cerebrovascular diseases. 2 These effects are thought to reverse after smoking cessation. The constituents of cigarette smoke with the major contribution to pathogenesis of vascular disease are nicotine, carbon monoxide, oxidant gases and polycyclic aromatic hydrocarbons. 2 Nonsmokers who are exposed to "secondhand" smoke experience on average a 30% excess risk of ischemic heart disease and nonfatal myocardial infarction. 3 Secondhand smoke exposure has been shown to activate platelets and to produce endothelial dysfunction, in both experimental animals and humans. 3 The mechanisms by which smoking causes acute cardiovascular events include endothelial dysfunction, thrombosis and inflammation.Endothelial dysfunction is an initiating event in atherogenesis, as well as a major factor in causing acute cardiovascular events. Cigarette smoking impairs flow-mediated endothelium-dependent peripheral arterial vasodilatation, an effect that is, at least partly, reversible after smoking Circulation Journal Vol.71, August 2007 cessation. 4 Smokers without atherosclerosis have coronary vasoconstrictor responses to acetylcholine that, in the presence of normal endothelium, produce vasodilatation. 5 Indeed, the oxidant chemicals of smoke degrade nitric oxide (NO) and reduce NO release, with subsequent impairment of vascular dilation and platelet function. 2 Smokers have lower than normal levels of antioxidant vitamins, reflecting their consumption in response to ongoing oxidant stress. 6 In addition, nicotine itself alters the structural and functional characteristics of vascular smooth muscle cells (VSMC) and endothelial cells. 7,8 Experimental data show that human aortic endothelial cells undergo apoptotic changes when they are exposed to cigarette smoke extracts. 9 This process may be prevented by pre-activation of NO synthase by Larginine. 9,10 Furthermore, smoking causes an increase in vascular superoxide production, which results in decreased NO bioactivity and concomitantly increases production of vasoconstrictor eicosanoids. 11 Cigarette smoke extracts, but not nicotine, also inhibit prostacyclin (PGI2: a vasodilator and inhibitor of platelet aggregation) synthesis in human, rabbit and rat vascular tissue. 12 Smoking-mediated endothelial dysfunction also results in reduced secretion of tissue plasminogen activator (tPA) 13 and increased secretion of plasminogen activator inhibitor (PAI)-1, 1 which results in impaired fibrinolysis. This acts in concert with the increased levels of tissue factor and fibrin...

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“…4,5 The histological features of AAA include atherosclerosis, loss of medial smooth muscle (with evidence of apoptosis), and loss of elastin (with remodeling of the connective tissue). Therefore, we wished to investigate the hypothesis that cadmium, from cigarettes, accumulates in the infrarenal abdominal aorta, thus stimulating aneurysmal dilatation.…”

mentioning

confidence: 99%

Cadmium Accumulation in Aortas of Smokers

Abu‐Hayyeh

Sian

Jones

et al. 2001

ATVB

106

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Abstract-Abdominal aortic aneurysm is a smoking-related disorder. Cadmium, inhaled from cigarettes, may accumulate in the aorta and facilitate weakening of the aorta through adverse effects on smooth muscle cell metabolism. Cadmium was measured by atomic absorption spectrometry in infrarenal aortas from 13 patients with abdominal aortic aneurysm and from 17 age-and sex-matched patients with normal-diameter abdominal aorta. Total cadmium content was associated with smoking, assessed as pack-years (rϭ0.54, Pϭ0.004), but was similar in aneurysmal and undilated aortas. The cadmium content (meanϮSE) was higher in the media (3.25Ϯ0.53 ng/mg dry wt, 7Ϯ1.2 mol/L) than in the intima or adventitia (1.14Ϯ0.24 and 1.87Ϯ0.38 ng/mg dry wt, respectively; ANOVA, PϽ0.005). There was a strong correlation between medial cadmium content and pack-years of smoking (rϭ0.87, PϽ0.001). In aortic smooth muscle cells cultured on fibrillar collagen, cadmium inhibited DNA synthesis and collagen synthesis and diminished cell numbers (IC 50 2 mol/L, 6 mol/L, and 6 mol/L, respectively), but higher concentrations of cadmium were required for upregulation of metallothionein (EC 50 23 mol/L). The cadmium content of the aorta increases in direct proportion to the pack-years of cigarettes smoked, with selective accumulation in the medial layer. However, the cadmium content of aneurysmal aortas was not higher than that of nondilated aortas for patients with matched smoking history. In smokers, the level of cadmium accumulation is probably sufficient to impair the viability of cultured smooth muscle cells. Similar mechanisms could underlie the development of degenerative aortic disease in smokers. Key Words: aortas Ⅲ aneurysm Ⅲ smoking Ⅲ muscle smooth Ⅲ collagen C admium is one of the many toxic components of inhaled tobacco smoke. The amount of cadmium inhaled from each pack of 20 cigarettes is Ϸ16 g. 1 Cadmium has a long elimination time (estimated at 10 to 30 years), providing the possibility for the accumulation of substantial amounts of cadmium during the lifetime of a smoker. There are reports that cadmium alters the metabolism of cultured human aortic smooth muscle cells and the processing of collagen. 2,3 Cadmium also blocks calcium channels and inhibits ATPases and other ion transport systems.Smoking is the most consistent risk factor for the development and expansion of abdominal aortic aneurysms (AAAs). 4,5 The histological features of AAA include atherosclerosis, loss of medial smooth muscle (with evidence of apoptosis), and loss of elastin (with remodeling of the connective tissue). Therefore, we wished to investigate the hypothesis that cadmium, from cigarettes, accumulates in the infrarenal abdominal aorta, thus stimulating aneurysmal dilatation. To test this hypothesis, we compared the concentration of cadmium in infrarenal aortas from patients with and without AAAs.After finding that the highest concentration of cadmium was in the medial layer of the aorta, we investigated whether similar concentrations of cadmium altered the metabol...

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Smoking and growth rate of small abdominal aortic aneurysms

Cited by 171 publications

References 9 publications

Abdominal aortic aneurysm expansion: Risk factors and time intervals for surveillance

Abdominal aortic aneurysm expansion: Risk factors and time intervals for surveillance

Smoking and Aortic Diseases

Cadmium Accumulation in Aortas of Smokers

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