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Biomedical subjects

J T Powell

Publications and source records attributed to J T Powell.

At least 55 records · Page 3Linked to original sources
PubMed1998

The effects of potassium channel openers on saphenous vein exposed to arterial flow.

OBJECTIVES: To assess the sensitivity of saphenous vein to potassium channel opening drugs (KCOs). METHODS: Saphenous vein, harvested at bypass surgery or high ligation for correction of varicose veins, was exposed to an in vitro flow circuit and vasomotor responses assessed by organ bath pharmacology. OUTCOME MEASURES: Effective drug concentrations for 50% reduction in vein ring tension (IC50). RESULTS: Vein rings pre-contracted with phenylephrine showed a concentration-dependent relaxation to all the KCOs tested with a potency ranking of HOE 234 > cromakalim > pinacidil > diazoxide. The relaxation to cromakalim was endothelium-independent and was inhibited by glibenclamide (an ATP-sensitive K+ channel blocker). The sensitivity of vein rings to cromakalim increased after exposure to arterial flow conditions for 90 minutes (IC50 before 1.7 +/- 0.25 microM and after 0.25 +/- 0.08 microM, p > 0.001). This effect was not evident after 90 min of venous flow conditions, 2.19 +/- 0.49 microM. When the workload on vein, exposed to arterial flow conditions, was reduced mechanically by external stenting with PTFE the increased sensitivity to cromakalim was abolished. CONCLUSIONS: Saphenous vein has ATP-sensitive K+ channels responsive to KCOs. The increased sensitivity to cromakalim, induced by arterial flow conditions, may represent an endogenous protective mechanism limiting ischaemic damage resulting from the higher workload imposed on grafted vein.

Arteries↗
PubMed1998

Molecular and cellular changes in vein grafts: influence of pulsatile stretch.

Adaptation of saphenous vein, with its intrinsic myogenic tone, from the low-pressure, minimally pulsatile flow of the venous system to the pulsatile flow of the arterial circulation is a minor miracle. Changes in gene expression caused by the pulsatile circumferential deformation (cyclic strain) initiate changes in gene expression, which lead to both vein graft adaptation and pathology. Removal of circumferential deformation by external stenting attenuates the early changes in gene expression and the later development of intimal hyperplasia. Pathways for the transduction of cyclic strain into cellular events have been elucidated in cultured vascular cells. The important second messengers include calcium and reactive oxygen species.

Animals↗
PubMed1998

Vascular damage from smoking: disease mechanisms at the arterial wall.

The products of tobacco combustion are absorbed into the systemic circulation. Absorbed nicotine stimulates the release of catecholamines, whilst other products (perhaps including nicotine) injure the arterial endothelium and promote atherogenesis. Free radicals and aromatic compounds diminish the endothelial synthesis of nitric oxide, causing impaired endothelium-dependent relaxation of arteries, the earliest clinical sign of endothelial dysfunction. Smoking alters the shear forces and rheology at the endothelial surface and these changes enhance the effects of products of tobacco combustion to upregulate leucocyte adhesion molecules on the endothelial surface. The increased oxidation of low density lipoprotein (LDL) in smokers has synergistic effects to promote monocyte adhesion and monocyte migration into the subintimal space. Continued stimulation of intimal cells by oxidized LDL leads to the development of atherosclerosis. Many of these effects are ameliorated by high concentrations of vitamin C. Smoking also potentiates thrombosis at the dysfunctional endothelium by increasing the concentration of plasma fibrinogen and altering the activity of platelets. All these proatherogenic effects of smoking to injure the endothelium also are observed, albeit to lesser extent, in passive smokers.

Arteries↗
PubMed1997

Circumferential deformation and shear stress induce differential responses in saphenous vein endothelium exposed to arterial flow.

Adaptation of saphenous vein to the hemodynamic stresses of the arterial circulation is critical to the maturation of vein bypass grafts. We have investigated early adaptive responses of venous endothelium by placing excised human saphenous vein in a bypass circuit with either venous or arterial flow conditions, using external stenting to resolve the effects of longitudinal (shear) from circumferential stress. Endothelial protein concentrations were assessed by immunostaining area (ratio of protein/CD31) and Western blotting of endothelial cell lysates (staining ratio protein/vWf). In both unstented and stented veins nitric oxide synthase increased after 90 min of arterial flow: twofold increase of immunostaining area (P = 0.001), four- to fivefold increase by Western blotting (P = 0.02), and increased A23187mediated maximum endothelium-dependent relaxation of vein rings (P = 0.01). In unstented veins, ICAM-1 concentration was increased after 45 min of arterial flow: twofold increase by immunostaining (P = 0.001) and Western blotting (P = 0.038), with maximum fibrinogen-mediated endothelium-dependent relaxation increasing from 55.9+/-4.9 to 97+/-2.1% (P = 0.01). In contrast, in unstented veins there was a threefold decrease of VCAM-1 and no change in P-selectin after arterial flow for 45 and 90 min, respectively. However, no changes in ICAM-1 and VCAM-1 were observed in stented veins. The flow-induced alterations in nitric oxide synthase, ICAM-1, and VCAM-1 were abolished when 3 mM tetraethylammonium ion (K+ channel blocker) was included in the vein perfusate. The very rapid changes in ICAM-1 and VCAM-1 expression are a response to circumferential stress, whereas the slower upregulation of nitric oxide synthase is a response to longitudinal (shear) stress. Similar changes could influence the adhesiveness of endothelium in newly implanted saphenous vein bypass grafts.

Arteries↗
PubMed1997

Risk factors associated with the development of peripheral arterial disease in smokers: a case-control study.

PURPOSE AND METHOD: A hospital based case-control study was designed to investigate what aspects of smoking and what co-factors of smoking are associated with the development of peripheral arterial disease (PAD). Cases were 291 smokers, newly referred with PAD, and controls were 828 age and sex matched smokers without PAD. RESULTS: Reported recent tobacco usage was similar in cases and controls but total tobacco exposure was associated with the risk of PAD-adjusted odds ratios (ORs) increasing with tertile of pack-years smoked to reach 1.63 (95% CI, 1.11-2.39; P = 0.011), for the highest tertile ( > 48 pack-years) compared with smokers in the lowest tertile (< 31 pack-years). Cases reported smoking significantly lower tar and nicotine yield cigarettes than controls, but tended to inhale more deeply, and had significantly higher plasma concentrations of cotinine. ORs for PAD were significantly and independently increased by systolic blood pressure > 160 mmHg (8.1 (5.2 13.0); P < 0.0001), history of hypertension (2.4 (1.5-3.2); P = 0.0003) and apolipoprotein B > 0.9 g/l(3.8 (2.3-7.6); P = 0.008). CONCLUSIONS: Increased total exposure to tobacco and the ability to smoke tobacco in a way which maximises nicotine yield are associated with increased risk of smokers developing PAD. There is no evidence that smoking low tar cigarettes reduces this risk, whereas both hypertension (particularly systolic) and high levels of apolipoprotein B, increase this risk.

Aged↗
PubMed1997

Unrestricted usage of immunoglobulin heavy chain genes in B cells infiltrating the wall of atherosclerotic abdominal aortic aneurysms.

The aim of this study was to provide evidence for the hypothesis that the B cell rich infiltrate concentrated in the adventitia of atherosclerotic abdominal aortic aneurysms is an autoimmune response to specific tissue antigens. Detailed histological examination of biopsies from 26 atherosclerotic abdominal aortic aneurysms showed in the adventitia, the presence of lymphoid follicles in 7/26 (27%) and of plasma cells in all cases. DNA prepared from the outer aneurysm wall (n = 25) was amplified using the polymerase chain reaction to investigate the repertoire of the immunoglobulin heavy chain (VH) genes used. Amplification of the VDJ region of VH, using both framework 2 and 3 primers, revealed unrestricted usage of the VH gene in 24/25 cases. The only case where restricted usage of the VH genes was observed, might have been attributable to severe virally-induced tissue inflammation. These results indicate that, in the vast majority of atherosclerotic abdominal aortic aneurysms, the B cell rich adventitial infiltrates are not an autoimmune response to a limited repertoire of tissue antigens.

Aged↗
PubMed1997

Development of an in vitro model to study the response of saphenous vein endothelium to pulsatile arterial flow and circumferential deformation.

OBJECTIVES: To develop an in vitro model of human saphenous vein bypass to facilitate study of the early adaptive responses of venous endothelium to arterial flow conditions. DESIGN MATERIAL AND METHODS: Segments of human saphenous vein (with or without external polytetrafluoroethylene (PTFE) stents to limit circumferential and radial deformation) were mounted in a bypass circuit and subjected to pulsatile flow with oxygenated Krebs solution to simulate arterial or venous flow conditions for a period of 90 min. The viability of the vein was assessed by the tissue ATP concentration and vasomotor responses to phenylephrine, sodium nitroprusside and bradykinin (endothelium-dependent). Immunohistochemistry was used to assess both endothelial preservation (CD31) and the expression of proteins involved in leukocyte adhesion: E-selectin, P-selectin and ICAM-1. Freshly excised veins were used as controls. RESULTS: The concentration of ATP was 320 +/- 11 nmol/g in freshly excised vein (n = 8) and following exposure to the arterial flow circuit increased to 566 +/- 60 nmol/g (n = 8, paired t-test, p = 0.003) in unstented veins and to 421 +/- 49 nmol/g (n = 8, paired t-test, p = 0.002) in externally stented veins (with PTFE). Both endothelium-dependent and sodium nitroprusside-induced vasodilatation responses were preserved after veins were exposed to the arterial flow circuit, but the sensitivity to phenylephrine was increased: EC50 decreasing from 9 microM, p = 0.008. There was a 5-10% decrease in staining area for CD31 after veins, stented or unstented, were exposed to the arterial flow circuit. However, after exposure to the arterial flow circuit, the staining area ratio for ICAM-1/CD31, which remained unchanged in externally stented veins, increased two-fold in unstented veins, p > 0.01: there were no changes in the staining area ratio P-selectin/CD31 and no staining for E-selectin was observed. CONCLUSION: Vasomotor responses and tissue ATP concentration indicate that the viability of saphenous vein can be maintained for up to 90 min in an ex vivo flow circuit and the CD31 staining indicated endothelial preservation. This opens up the possibility of investigating the early changes in saphenous vein endothelium following exposure to arterial pressure, as at bypass surgery. First results suggest that there is rapid upregulation of the leukocyte adhesion molecule ICAM-1, which can be prevented by limiting the circumferential deformation of the vein with an external PTFE stent.

Adaptation, Physiological↗
PubMed1997

Dilatation of saphenous vein grafts by nitric oxide.

OBJECTIVES: To investigate firstly whether flow-dependent vasodilation is maintained in vein grafts, and secondly whether nitric oxide donors dilate vein grafts to improve the flow through graft stenoses. DESIGN, MATERIALS AND METHODS: The vasodilatation of mature patent vein grafts, in response to reactive hyperaemia and glyceryl trinitrate (GTN), was assessed by the change in external diameter using duplex ultrasonography. The severity (ratio of proximal systolic velocity, V1, to peak systolic velocity at the stenosis, V2, of vein graft stenoses was determined by duplex ultrasonography before and after 24 h of local application of GTN patches. RESULTS: In post-occlusion hyperaemia the diameter of patent distal vein grafts (n = 7) increased to a maximum of 112 +/- 1.9% of resting diameter after 2 min, p = 0.026. The diameter increased further to 117 +/- 2.5% of the resting value 5 min after oral GTN (n = 5), p = 0.007. The velocity ratio, V2/V1, through graft stenoses (n = 6) decreased by 20 +/- 5% after application of GTN patches, principally as a result of reduction in V2, mean difference 0.8, p = 0.15. The changes in response to GTN were more evident for proximal than distal vein graft stenoses. CONCLUSION: Flow-induced vasodilatation responses, which have been attributed to the endothelial release of nitric oxide, are maintained in patent vein grafts: the grafts dilate even further in response to GTN. The application of GTN patches close to a vein graft stenoses appears to reduce the velocity ratio through vein graft stenoses. GTN patches might be used to reduce the risk of graft occlusion when there is a delay between the detection and the treatment of haemodynamically significant graft stenoses.

Administration, Cutaneous↗
PubMed1997

An association between arterial pulse pressure and variation in the fibrillin-1 gene.

OBJECTIVE: To investigate whether variation in the fibrillin-1 gene was associated with blood pressure in healthy middle aged men, as had been observed in patients with abdominal aortic aneurysm. DESIGN, SETTING, AND PATIENTS: Middle aged men (n = 245), aged 50 to 61 years, were recruited from one of the nine general practices participating in the second Northwick Park heart study. Blood samples were obtained for the preparation of genomic DNA and analysis of plasma variables. MAIN OUTCOME MEASURES: Systolic, diastolic, and pulse pressures; fibrillin-1 genotype characterised with a four allele variable tandem nucleotide repeat polymorphism in intron 28. RESULTS: In healthy middle aged men only three common genotypes were observed: 2-2 (frequency 54.1%), 2-3 (16%) and 2-4 (15%). The mean arterial systolic (and pulse) pressure varied according to fibrillin-1 genotype: 2-4 genotype, 126-3 (47.6) mm Hg; 2-2 genotype, 131.0 (51.3) mm Hg; and 2-3 genotype, 135.5 (54.2) mm Hg. The median pulse pressure was 50 mm Hg. Distribution of men around the median pulse pressure, according to genotype, showed a significant trend for patients of 2-4 genotype to have the lowest pulse pressures, those of 2-2 genotype to have intermediate pressures, and those of 2-3 genotype to have the highest pulse pressures (p = 0.003 for healthy men). CONCLUSIONS: There appears to be a significant association between fibrillin-1 genotype and arterial pulse pressure in men aged 50 to 61 years.

Alleles↗
PubMed1997

Influence of hypercholesterolemia and adventitial inflammation on the development of aortic aneurysm in rabbits.

Abdominal aortic aneurysms are characterized by intimal atherosclerosis, disruption and attenuation of the elastic media, and a variable adventitial inflammatory infiltrate. We have developed an animal model of this disorder to evaluate the contribution of hypercholesterolemia, medial injury, and adventitial inflammation to aneurysmal dilatation. To accomplish this, we used periaortic application of calcium chloride, which induced both medial injury with calcification and endothelial injury. Ultrasonography was used to demonstrate the dilatation and thickening of the aortic wall. Over the first 3 weeks after periaortic application of 0.25 mol/L CaCl2, the external aortic diameter increased from 3.5 +/- 0.5 to 4.2 +/- 0.8 mm, but the ID remained unchanged. This apparent wall thickening was accompanied by vascular remodeling, and biochemical changes included approximately 50% reduction in tissue hydroxyproline concentration and increased activity of gelatinases (matrix metalloproteinase [MMP]-2 and MMP-9). Independently, cholesterol feeding to induce hypercholesterolemia or the concomitant periaortic application of thioglycollate had little effect on the histological, biochemical, or diameter changes. Together, hypercholesterolemia and thioglycollate were associated with rapid aortic dilatation in CaCl2, treated animals but not controls: after 3 weeks, the ID and OD had doubled, the OD increasing from 3.5 +/- 0.4 to 7.1 +/- 0.4 mm, P = .005. The remarkable feature that accompanied this dilatation was the infiltration of cells, mostly foamy macrophages, into the adventitia, with a further reduction in hydroxyproline concentration. Adventitial inflammation may provide the critical stimulus to dilatation of an aorta with preexisting intimal and medial injury.

Animals↗
PubMed1997

The influence of diabetes on the vasomotor responses of saphenous vein and the development of infra-inguinal vein graft stenosis.

There has been a prejudice that diabetes modulates the function of saphenous vein in a manner that predisposes to bypass graft failure, although most of the evidence accrues from animal studies. We have investigated the effect of diabetes on the vasodilator responses and ultrastructure of saphenous vein harvested from patients undergoing infrainguinal bypass surgery for limb salvage and the development of stenoses within the vein grafts. Of 55 consecutive patients undergoing vein bypass surgery for critical ischemia, 16 (29%) were diabetic: diabetes was not a risk factor for graft stenosis, which occurred in 17 of 56 (30%) grafts. Endothelium-dependent relaxation by nitric oxide pathways stimulated after receptor activation (bradykinin and thrombin) was not different in vein rings from diabetic (n = 12) and nondiabetic patients (n = 12). Prostarioid-mediated vasorelaxation was absent in vein rings from diabetic patients, and the production of 6-keto prostaglandin F(1alpha) (PGF(1alpha)) from diabetic vein was only 66 +/- 27 pg x cm-2 x min-1 compared with 112 +/- 20 pg x cm-2 x min-1 from control vein (P = 0.011). Fibrinogen-mediated vasorelaxation, normally inhibited by K+ channel blockers, was negligible in vein from diabetic patients. No ultrastructural differences were observed between the endothelium of saphenous vein harvested from diabetic and nondiabetic patients. However, diabetes was associated significantly with the presence of spiraled collagen in media. The maintenance of receptor-activated stimulation of nitric oxide pathways and the damping of the response to fibrinogen in saphenous vein endothelium may provide, in part, for the good prognosis of vein graft surgery in diabetic patients: diabetes is not a risk factor for early (12 months) infrainguinal vein graft stenosis.

Aged↗
PubMed1996

Interaction between fibrillin genotype and blood pressure and the development of aneurysmal disease.

Debate as to whether abdominal aortic aneurysms (AAA) are caused by atherosclerosis or whether they have a strong genetic etiology continues. We have investigated the hypothesis that risk factors are likely to be strongest in patients with generalized aneurysmal disease. We screened 232 consecutive AAA patients for popliteal aneurysm and investigated cardiovascular and genetic risk factors in these patients. Ultrasonography demonstrated the presence of a popliteal aneurysm in 24 of 232 (10%) patients. Multivariate analysis identified four independent factors associated with popliteal aneurysm: age (p = 0.013), height (p = 0.017), triglyceride concentration (p = 0.009), and systolic blood pressure (p = 0.037). In the AAA patients a significant association of fibrillin-1 genotype was present, determined by a tandem repeat polymorphism, with both systolic and pulse pressure. The genotypes associated with the highest pressures were significantly more common among the patients with popliteal aneurysm, p = 0.03. Following these findings we investigated whether there was an association between fibrillin-1 genotype and blood pressure in a healthy population, 245 men aged 50-61 years. Again we found a significant association between fibrillin genotype and pulse pressure, p = 0.003. We suggest that a strong interaction occurs between fibrillin genotype and blood pressure which contributes to the development of aneurysmal disease.

Aging↗
PubMed1996

Vasoactive effects of fibrinogen on saphenous vein.

Normal plasma fibrinogen concentrations are critical to haemostasis. Higher fibrinogen concentrations are associated with increasing risk of atherosclerotic disease and with graft stenosis and occlusion after saphenous vein bypass surgery. Vein graft stenosis is characterized by the localized proliferation of intimal smooth muscle cells, causing narrowing of the graft with increased risk of thrombotic occlusion. In rabbit arteries, fibrinopeptide B is reported to have both vasoconstrictor and mitogenic properties. We report here that fibrinopeptides had no vasoactive effects on saphenous vein rings; however, fibrinogen (0-2 microM) affected an endothelium-dependent relaxation, followed by recontraction at higher concentrations. The fibrinogen-mediated relaxation was inhibited by K+-channel blockers and antibodies to ICAM-1. Coupled signalling pathways for the synthesis of vasoactive mediators and mitogens could underlie the association between fibrinogen and the development of vein graft pathology.

Animals↗
PubMed1996

Unravelling the familial tendency to aneurysmal disease: popliteal aneurysm, hypertension and fibrillin genotype.

PURPOSE: To screen patients with abdominal aortic aneurysm for popliteal aneurysm and investigate cardiovascular and genetic risk factors associated with aneurysmal disease at more than one site (generalised aneurysmal disease). SUBJECTS, DESIGN AND SETTING: All patients referred to the Regional Vascular Surgical Service at Charing Cross Hospital with unruptured abdominal aortic aneurysm between 1989 and 1993 were screened for popliteal aneurysms, using ultrasonography. MAIN OUTCOME MEASURES: Palpation of a popliteal aneurysm or ultrasonographic detection of popliteal dilatation, where the ratio maximum popliteal fossa diameter/suprageniculate popliteal diameter was > or = 1.5, in relation to cardiovascular and genetic risk factors. RESULTS: Clinical examination detected popliteal aneurysms in only 11/232 patients (5%), but ultrasonography demonstrated the presence of popliteal aneurysm in a further 13 patients, 24/232 in total (10%). Multivariate regression identified four independent factors associated with popliteal dilatation disease: age (p = 0.046), height (p = 0.006), systolic hypertension (p = 0.037) and triglyceride concentration (p = 0.009). Generalised aneurysmal disease and systolic blood pressure were associated with polymorphic variation in the fibrillin-1 gene, but not with variations in the apolipoprotein B and type III collagen genes. CONCLUSIONS: Few patients with abdominal aortic aneurysm (10%) also have popliteal aneurysms: the risk of popliteal dilatation increases with age, height, systolic blood pressure, triglyceride concentration and fibrillin genotype. The strong interaction between fibrillin genotype and blood pressure may contribute to the familial tendency to aortic aneurysm.

Age Factors↗
PubMed1996

The influence of smoking cessation and hypertriglyceridaemia on the progression of peripheral arterial disease and the onset of critical ischaemia.

OBJECTIVE: To investigate whether smoking and other cardiovascular risk factors were associated with deterioration of ankle/brachial pressure index or onset of critical ischaemia in patients with mild to moderate intermittent claudication. DESIGN AND SETTING: Longitudinal study in a London teaching hospital. SUBJECTS: 415 consecutive smokers, with symptoms of intermittent claudication and an ankle/brachial pressure index of <0.9, referred for a surgical opinion between April 1985 and December 1990, who were not considered for an immediate surgical procedure. MAIN OUTCOME RESULTS: Reduction in ankle/brachial pressure index of >0.14, onset of critical limb ischaemia. RESULTS: After one year of follow up 183 patients (44%) had stopped smoking (as evaluated by biochemical markers). With longer follow up only 110 patients (27%) had maintained smoking cessation. There were no differences in age, sex, and previous tobacco exposure between stoppers and smokers, but the proportion of diabetics among stoppers (20%) was greater than among those who continued smoking (10%) [p=0.01]. The annual rate of deterioration of ABPI was 21, 16 and 17% respectively in the first, second and third year of follow-up and the onset of critical ischaemia was observed in 52 patients (12.5%) during the period of follow-up. In univariate analyses, continued smoking, diabetes and presence of ischaemic heart disease were not associated with an increased risk of deterioration of ABPI, but hypertriglyceridaemia (> or = 2.2 mmol/l) was, [relative risk 1.7(95% CI 1.21-2.37), p=0.003], and patients having systolic blood pressure in the middle tertile (153-170 mmHg had a reduced risk of deterioration of ABPI, p=0.026. Hypertriglyceridaemia (> or = 2.2mmol/l) was the only independent factor associated with deterioration of ABPI in multivariate analysis [relative risk 1.8(95% CI:1.23-2.59), p=0.003] and also was associated with a relative risk of onset of critical ischaemia of 1.9 [(95% CI: 1.08-2.87), p=0.035], compared with triglyceride levels of <2.2mmol/l. CONCLUSION: For those with mild to moderate claudication, the lack of immediate benefit from cessation of smoking appears to be associated with a gradual return to smoking. Hypertriglyceridaemia was identified as the most important independent factor associated with the progression of peripheral arterial disease and onset of critical ischaemia.

Aged↗
PubMed1996

Risk factors for abdominal aortic aneurysms in smokers.

OBJECTIVE: To investigate features of the smoking habit and other cardiovascular risk factors associated with the development of abdominal aortic aneurysm in smokers. DESIGN AND SETTING: Case control study of smokers recruited, between 1989 and 1992, in a London teaching hospital. SUBJECTS: Consecutive smokers referred with abdominal aortic aneurysm (cases n=44) and 244 age and sex-matched smokers attending Dermatology, Orthopaedic and Urology clinics (controls). MAIN RESULTS: Hypertension was more common amongst the patients with aneurysm (30%) than the controls (19%). Measured systolic and diastolic blood pressures were significantly higher in the aneurysm patients. The relative risk of having an abdominal aortic aneurysm increased 3.4-fold (95% CI 1.06-10.89) for those with a diastolic blood pressure of >90mmHg, p=0.035 and 4.1-fold (95% CI 1.27-13.16) for those with a mean arterial pressure > or = 100mmHg, p=0.009. Plasma lipids, fibrinogen and cotinine were similar amongst patients with aneurysm and controls. The cumulative smoking exposure was similar in the patients with aneurysm and controls, median 49 and 44 pack-years respectively. The relative risk of developing an aneurysm increased with the number of cigarettes currently smoked, p=0.008, and with increasing depth of inhalation, p=0.025, but was not associated with the tar or nicotine yield of current cigarettes. CONCLUSIONS: In smokers, the risk of developing an abdominal aortic aneurysm increases with increasing mean arterial and diastolic blood pressure and two aspects of current smoking habit: the number of cigarettes currently smoked and the depth of inhalation.

Aged↗