Hypertension Smoking Research Articles

Thrombophilia and Cardiovascular Risk Factors On the Absolute Risk of First and Recurrent Venous Thrombosis. Results From a Retrospective Family Cohort Study Involving 2097 Relatives.

Abstract 2974Poster Board II-951 Introduction:Arterial and venous thromboembolism (VTE) share or seem to share cardiovascular risk factors such as older age, overweight and obesity, and possibly also hypertension, diabetes mellitus, dyslipidemia, and smoking. Little is known if subjects with common thrombophilia, (i.e. factor V Leiden, prothrombin G20210A or high factor VIII levels) are at higher risk of first or recurrent VTE due to cardiovascular risk factors. For subjects with rare thrombophilia (i.e. antithrombin, protein C or protein S deficiency), or non-carriers of thrombophilia no information is currently available whether contribution of cardiovascular risk factors increases the risk of first or recurrent VTE. Methods:In a multi-center retrospective cohort study of families with thrombophilia, we performed a post-hoc analysis to identify if relatives with rare thrombophilia, common thrombophilia, and relatives without one of these thrombophilic defects were at increased risk of first or recurrent VTE due to cardiovascular risk factors. Known cardiovascular risk factors were recorded: hypertension, hyperlipidemia, the presence of diabetes mellitus, smoking habits and overweight/obesity defined by body mass index (BMI) ≥25-30 kg/m2 or ≥30 kg/m2, respectively. Observation time for first VTE started at the age of 15, and for recurrent VTE on the date when initial anticoagulant treatment was withdrawn. Observation time ended on the date of first VTE or recurrence, respectively, or at date of enrollment. First, the absolute risk of first VTE for cardiovascular risk factors was calculated for the whole cohort. Sensitivity analyses were performed to assess the effect of idiopathic or provoked classification of initial thrombotic event and type of event (deep vein thrombosis or pulmonary embolism). When a positive association was found, a further stratification was subsequently made to analyze whether relatives with rare, common, or no thrombophilia influenced these risks. A Cox-proportional hazards model was used to evaluate risks between groups for adjustments of age and sex. Results:Of a total of 2097 relatives, 55% were female, 180 (12%) had first VTE at a median age of 35 years and 52 (2%) had a recurrence at a median age of 40 years. Of relatives, 20% had hypertension, 13% dyslipidemia, 5% diabetes mellitus, 22% were previous smokers, 35% were overweight and 15% were obese. Point estimates of adjusted hazard ratios in relatives with hypertension, hyperlipidemia, diabetes mellitus or previous smokers, compared to their reference groups ranged between 0.9 and 1.1 and were not statistically significant. Relatives with VTE were heavier than relatives without VTE (mean BMI 27.0 vs 25.5 kg/m2, P< 0.001); adjusted hazard ratio for each 1-point increase in BMI was 1.035 (95% CI, 1.010-1.066). Absolute risk of first VTE in normal weight, overweight or obese subjects was 0.16% (95% CI, 0.12-0.20), 0.20% (95% CI, 0.16-0.25), and 0.26% (95% CI, 0.19-0.36), respectively. Sensitivity analyses did not change these outcomes. Annual incidences of first VTE in non-carriers of thrombophilia, common thrombophilia carriers and rare thrombophilia carriers were 0.04%, 0.20% and 0.97%. In the non-carrier group, adjusted hazard ratios for first VTE in overweight or obese relatives were 6.1 (95% CI, 1.3-28.1) and 6.7 (95% CI, 1.2-37.6), compared to non-carriers of normal weight. In common thrombophilia carriers these risks were 1.7 (95% CI, 1.0-2.9) and 2.1 (95% CI, 1.2-3.8) fold increased. In rare thrombophilia carriers, overweight or obesity was not associated with an increased risk of first VTE (adjusted hazard ratios 0.8; 95% CI, 0.5-1.4 and 0.8; 95% CI, 0.4-1.7, respectively). For recurrence, overweight and obese relatives with common or rare thrombophilia seemed to have a slightly higher risk of recurrence than normal weight relatives, but the overall 10 year recurrence rate in both groups was similar. Conclusion:Venous thrombotic risk increases with increasing BMI in non-carriers and common thrombophilia carriers. This effect is overruled in carriers of rare thrombophilia, where a deficiency itself irrespective of BMI apparently is sufficient to generate very high risk of thrombosis. Overweight and obesity seemed to increase the risk of recurrence in carriers of both common and rare thrombophilia. Other cardiovascular risk factors did not increase the risk of VTE in this thrombophilic family cohort. Disclosures:No relevant conflicts of interest to declare.

Evaluation of the Genetic Variants of Kinesin Motor Protein in Ischemic Stroke

The kinesin light-chain 1 genetic variants G56836C, A185C, and C406T were earlier found to amplify the development of leukoaraiosis in hypertensive smokers. These 3 variants were presumed to affect the function of the mitochondria, thereby giving rise to sensitivity to a chronic ischemic state. We have now extended our investigations to examine how the above genetic variants affect the occurrence of ischemic stroke. Genetic and clinical data on 650 ischemic stroke and 340 neuroimaging alteration-free subjects were analyzed. Univariate and logistic regression approaches were used. None of the above genetic variants proved to be risk factors of ischemic stroke, either alone or in combination with other clinical factors. The examined 3 genetic variants seem to influence the responses of the glial cells to a slight chronic hypoxia state, rather than the mechanisms resulting in cerebral infarcts themselves.

Gene–environmental effects behind leukoaraiosis: a silent genetic variant of the kinesin protein can be activated in a subject with poorly controlled long-lasting hypertension

Objectives The rs8702 variant of the kinesin light chain 1 was earlier found to be a risk factor for vascular white matter demyelinization, referred to as leukoaraiosis (LA), in hypertensive smokers. The aim of this study was to determine the extent to which this genetic variant gives rise to the occurrence of LA and its severity, if the subject is exposed to long-lasting, severe and poorly controlled hypertension. Design and methods The clinical and genetic data on 204 LA patients without infarction and 240 neuroimaging alteration-free subjects were analyzed. Results The rs8702 CC genotype proved to exert strong amplifying effects on the occurrence and severity of LA in patients with long-lasting poorly controlled severe hypertension (a 25.9-fold risk of LA in carriers relative to non-carriers; p < 0.001). Conclusion The previous data on hypertensive smokers and the present findings suggest that the rs8702 CC variant is increasingly unfavorable as regards LA if the hypertension is more severe and poorly controlled. This draws attention to a need for stricter preventive measures in CC carriers.

The Multiple Risk Factor Intervention Trial (MRFIT)—Importance Then and Now

The 356 222 men aged 35 to 57 years, who were free of a history of hospitalization for myocardial infarction, screened by the Multiple Risk Factor Intervention Trial (MRFIT) in its recruitment effort, constitute the largest cohort with standardized serum cholesterol measurements and long-term mortality follow-up. For each five-year age group, the relationship between serum cholesterol and coronary heart disease (CHD) death rate was continuous, graded, and strong. For the entire group aged 35 to 57 years at entry, the age-adjusted risks of CHD death in cholesterol quintiles 2 through 5 (182 to 202, 203 to 220, 221 to 244, and ≥245 mg/dL [4.71 to 5.22, 5.25 to 5.69, 5.72 to 6.31, and ≥6.34 mmol/L]) relative to the lowest quintile were 1.29, 1.73, 2.21, and 3.42. Of all CHD deaths, 46% were estimated to be excess deaths attributable to serum cholesterol levels 180 mg/dL or greater (≥4.65 mmol/L), with almost half the excess deaths in serum cholesterol quintiles 2 through 4. The pattern of a continuous, graded, strong relationship between serum cholesterol and six-year age-adjusted CHD death rate prevailed for nonhypertensive nonsmokers, nonhypertensive smokers, hypertensive nonsmokers, and hypertensive smokers. These data of high precision show that the relationship between serum cholesterol and CHD is not a threshold one, with increased risk confined to the two highest quintiles, but rather is a continuously graded one that powerfully affects risk for the great majority of middle-aged American men.See PDF for full text of the original JAMA article.

Making hypertensive smokers motivated in quitting: developing ‘blood pressure equivalence of smoking’

To express the increased risk from smoking in terms of 'blood pressure' so that hypertensive smokers are motivated into quitting. Mortality risks of smokers were compared with nonsmokers in a large worker cohort in Taiwan (n = 23755 with a 17-year follow-up) for all-cause and for cardiovascular diseases. The blood pressure equivalence of smoking was then identified by the difference in mortality risks between smokers and nonsmokers. Some interaction between hypertension and smoking was found to be synergistic. When hypertension and smoking co-existed, the all-cause mortality outcome [relative risk (RR) = 4.25] was larger than the sum or product of each individual risk for hypertension (RR = 2.16) or for smoking (RR = 1.97). The excess mortality risks of smoking for smokers were converted into a 'blood pressure equivalence'. The results demonstrate that the addition of smoking was similar to an increase of mortality risk approximately equivalent to an increase in blood pressure of 40 mmHg. Smoking cessation in hypertensive patients could provide a reduction of mortality risks similar to a permanent reduction of 40 mmHg in blood pressure, over and above any antihypertensive medications. Appreciating this relationship enables physicians to bridge the clinical disconnection and motivates hypertensive smokers to seek smoking cessation. The use of a 'blood pressure equivalence of smoking' can link the two separate risk factors and may lead to a paradigm shift in overcoming an existing clinical challenge.

Homocysteinemia, hypertension, and family history of diabetes in a smoking male population in Saudi Arabia

AbstractArabs have a lower incidence of atherosclerosis than other ethnicities, but few studies have examined homocysteine (HCYS) as a risk factor for cardiovascular disease in this population. Here, we investigated the association between serum HYCS levels and risk factors for cardiovascular disease (smoking, hypertension, and family history of diabetes) in Saudi males. A total of 50 smokers and 72 nonsmokers completed a general health questionnaire. In addition, their lipid profiles were measured using routine methods and HCYS levels by high-performance liquid chromatograph with electrochemical detection. Regression analysis showed negative associations between HCYS and glucose (r = −0.22; P &lt; 0.05) as well as family history of diabetes (r = −0.21; P &lt; 0.05). HCYS levels were similar between hypertensive and nonhypertensive smokers, but they were significantly elevated in hypertensive nonsmokers (P = 0.027) and lower in smokers with family history of diabetes (P = 0.01). Levels of HCYS among nonsmokers inversely correlated with history of diabetes and elevated glucose. Nonsmokers’ HCYS levels were significantly elevated in the presence of hypertension and correlated with diastolic blood pressure. Thus, HCYS may be a predictor of hypertension among nonsmokers. Until further trials are conducted, we recommend vitamin B6/folic acid supplementation for the Saudi hypertensive population as an adjuvant therapy.

Beneficial Effect of Angiotensin II Type 1 Receptor Blocker Antihypertensive Treatment on Arterial Stiffness: The Role of Smoking

The purpose of the present study was to assess angiotensin receptor blocker (ARB) treatment on arterial stiffness in select hypertensive patients and define possible differences between smokers and nonsmokers. The authors evaluated 81 consecutive, nondiabetic patients (mean age, 52 years; 47 men) with uncomplicated essential hypertension with high plasma renin activity who were administered monotherapy with irbesartan, an ARB, at maximal dose. Patients were divided into smokers (n=24) and nonsmokers (n=57). Carotid-radial pulse wave velocity (PWVc-r), carotid-femoral pulse wave velocity (PWVc-f), and augmentation index (AIx) were measured before and 6 months after ARB antihypertensive treatment. All mean values of elastic effect indices were decreased after irbesartan monotherapy (AIx, from 26.3%to 21.2% [P<.01;] PWVc-f, from 7.7 m/s to 7.3 m/s [P<.05], and PWVc-r, from 8.9 m/s to 8.3 m/s [P<.001]). When comparing smokers vs nonsmokers, no difference was noted in AIx and PWVc-f change (P=not significant), while PWVc-r change was greater in smokers compared with nonsmokers (P<.05). Chronic ARB treatment may favorably affect arterial stiffness and wave reflections in hypertensive chronic smokers with elevated plasma renin levels.

Clinical Significance of High-Molecular Weight Form of Adiponectin in Male Patients With Coronary Artery Disease

The author (N. Komura) apologizes for errors which appeared in the Table 1, page 25, Vol. 72. The numbers and proportion of hypertension or current smokers were 72 (55%), 61 (47%) in non-diabetic patients, and 39 (70%), 26 (46%) in diabetic patients, respectively. The corrected Table 1 is given below. (Circ J 2008; 72: 23 - 28)

Evaluation of the roles of the A185C and C406T kinesin light-chain 1 variants in the development of leukoaraiosis

Vascular white matter demyelinization of the brain is referred to as leukoaraiosis (LA). This frequent age-associated entity leads to a cognitive decline or dementia. The background of LA has been hypothesized to be a chronic hypoxia-induced functional cytoskeleton malfunction. Setting out from this assumption, we earlier found that the kinesin light-chain 1 (KNS2) cytoskeleton motor protein 56836CC single nucleotide polymorphism conferred a risk of LA in hypertensive smokers. The aim of the present study was to extend our observations as to how the KNS2 A185C and C406T single nucleotide polymorphisms in the 5'-untranslated sequence region affect the susceptibility to LA. These two latter variants were presumed to influence the transcription of the KNS2 mRNA by locating in a function-enhancer region. An association analysis of these genetic variants was conducted on 242 patients with LA and 251 neuroimaging alteration-free controls. The KNS2 AA185-406TT haplotype increased the risk of LA 3.56-fold in hypertensive smokers as compared with those not carrying the KNS2 AA185-406TT genotype, which was similar to our previous findings for the KNS2 56836CC intron variant. Moreover, the three homozygous KNS2 variants (56936CC-AA185-406TT) coincided to an extent of 82.2%. Overall, although the 56836CC intron variant appears to be the most important of the three kinesin variants as regards the development of LA, the contribution of the AA185-406TT haplotype to the unfavorable phenotype of LA cannot be ruled out. The present finding supports the involvement of the cytoskeleton in the development of vascular white matter damage, thereby opening up novel fields in the research into LA.

A Genetic Variant in Cytoskeleton Motors Amplifies Susceptibility to Leukoaraiosis in Hypertensive Smokers: Gene–Environmental Interactions Behind Vascular White Matter Demyelinization

One of the most frequent causes of an age-associated cognitive decline is the vascular white matter demyelinization of the brain referred to as leukoaraiosis (LA). The wide range of severity of the cognitive decline caused by LA can have numerous deleterious effects on the quality of life, leading overall to far-reaching public health problems. Besides clinical risk factors such as hypertension and advanced age, genetic susceptibility factors are presumed to be of great importance in the development of LA. The protein kinesin, which is the main motor protein in the trafficking system of the mitochondria, can undergo functional damage under the circumstances of chronic hypoxia. This may give rise to a slowly developing metabolic crisis in the glia cells, a phenomenon hypothesized to account for the evolution of LA. Setting out from this assumption, we examined how the kinesin light-chain 1 (KNS2) G56836C single nucleotide polymorphism in intron 13 affects the susceptibility to LA. This genetic variant was found to be associated with cognitive disturbances and neurodegeneration, and it was presumed to affect the function of kinesin. The association analysis of the above genetic variant was performed in 229 patients with LA and 264 neuroimaging alteration-free controls. The KNS2 56836CC variant increased the risk of LA 7.76-fold in hypertensive smokers as compared with those not carrying this variant. This finding may be useful in everyday clinical practice by indicating the need for stricter preventive measures in CC carriers.

Trial design: Blood pressure control and weight gain prevention in prehypertensive and hypertensive smokers: The treatment and prevention study

Background Cigarette smokers with elevated blood pressure (BP) are at substantially higher risk for cardiovascular events compared to normotensive smokers. Although smoking cessation should be a primary treatment goal for these patients, increases in body weight accompanying smoking abstinence may further increase BP. Intervention strategies that facilitate smoking cessation and modify adverse changes in body weight and BP are needed. Methods We describe an ongoing multi-site, two-phase, five-year randomized clinical trial. Participants are cigarette smokers with Prehypertension or Stage I Hypertension. In the first phase, participants receive a smoking cessation intervention combining behavioral counseling and nicotine replacement in an open-label fashion. In the second phase, participants who successfully quit smoking are randomly assigned to one of three lifestyle interventions: 1) weight gain prevention, 2) blood pressure control, or 3) usual lifestyle. Participants are followed for one year to assess changes in blood pressure, body weight, dietary intake, and physical activity. Conclusions Results from the proposed study will provide important insights into the efficacy of various approaches to lifestyle modification in smokers at increased risk for cardiovascular events.

Acute Effects of Cigarette Smoking on Arterial Stiffness and Blood Pressure in Male Smokers With Hypertension

Although the acute increase of arterial stiffness and blood pressure (BP) after cigarette smoking in healthy smokers is considered a possible mechanism of increased cardiovascular risk, the acute effect of smoking on arterial stiffness in hypertensive smokers is unknown. We investigated the acute effects of cigarette smoking on arterial stiffness and BP in hypertensive male smokers. Heart rate (HR), brachial and ankle BP, and pulse-wave velocity (PWV) were measured in 22 hypertensive male smokers (HTs) and in 30 normotensive male smokers (NTs) before and 5, 10, and 15 min after smoking one cigarette (nicotine content, 0.9 mg). Smoking induced acute increases of HR, brachial BP, and heart-femoral PWV (hfPWV) in NTs and HTs (P < .05). Ankle systolic BP and femoral-ankle PWV were acutely increased in HTs (P < .05), but not in NTs. In HTs, brachial systolic BP and hfPWV at 15 min were higher than at baseline (P < .05). An acute increase of hfPWV in the HTs was significant (P = .025) after adjustment for total cholesterol, time-dependent HR, and brachial mean arterial pressure, but acute changes of other PWVs lost statistical significance. Cigarette smoking acutely increases aortic stiffness and BP in male smokers with hypertension, and the effects persist longer than in male smokers without hypertension.

The association of exposure to cadmium through cigarette smoke with pregnancy-induced hypertension in a selenium deficient population

Oxidative stress has been postulated as major contributor to endothelial dysfunction and pregnancy-induced hypertension. We have examined the association of exposure to cadmium through cigarette smoke with hypertension disorders during pregnancy in the selenium deficient population. Markers of lipid peroxidation and antioxidative defense were measured and correlated with cadmium blood concentration in normotensive and hypertensive pregnant smokers and nonsmokers. We have observed significantly higher blood Cd in hypertensive smokers and significant differences in all other parameters. Se concentrations were lower in smokers, both in normotensive and hypertensive group as well as values of nonenzymatic (Zn, Cu, and glutathione) and enzymatic (superoxide dismutase, glutathione peroxidase, and glutathione reductase) parameters of antioxidative defense. Results of the study indicate that exposure to cadmium through cigarette smoke in pregnant women, living in Se deficient areas is associated with significantly higher cadmium concentrations and lower levels of enzymatic and nonenzymatic antioxidants and that it can be considered as a risk factor for pregnancy-induced hypertension. Selenium supplementation should be considered for recommendation in such condition.

Renal vascular sclerosis is associated with inherited thrombophilias

Vascular sclerosis is often seen in renal biopsies. It is usually associated with diabetes mellitus, hypertension, smoking, etc. However, whether inherited thrombophilic states such as factor V gene mutation, prothrombin gene mutation, and methylenetetrahydrofolate reductase (MTHFR) gene mutation are associated with the vascular sclerosis is not known. Renal biopsies that showed vascular disease were grouped into five groups: (1) diabetic patients, (2) hypertensive patients, (3) diabetic and hypertensive patients, (4) smokers, and (5) vascular sclerosis of unknown etiology (idiopathic renal disease). Renal biopsies with no vascular sclerosis were used as controls. Frozen tissue was analyzed for factor V Leiden mutation, prothrombin G20210A mutation, and MTHFR C677T. Factor V Leiden mutation and prothrombin G20210A mutation was not seen in patients with diabetes, hypertension, or smoking, whereas MTHFR C677T polymorphism in these groups was not significant, compared to the controls. In the idiopathic renal disease group, three of the 17 patients (17.6%) had prothrombin G20210A mutation, two of the 17 patients (11.8%) had the factor V Leiden mutation, and five of the 17 (29.4%) were homozygous for the MTHFR C677T polymorphism. When the data were evaluated as a whole, 10 mutations were found in 17 patients (P<0.0005 compared to controls) or eight of the 17 patients (47%) were observed to have at least one of the three forms of inherited thrombophilia (P<0.001 compared to controls). These findings indicate that renal vascular lesions, in the absence of diabetes, hypertension, or smoking appears to be associated with inherited thrombophilias.

Estudo de prevalência e multiplicidade de fatores de risco cardiovascular em hipertensos do Município de Brusque, SC

To investigate the prevalence and multiplicity of additional risk factors (RF) in a population sample of hypertensive smokers, diagnosed and enrolled at the Hiperdia Program of the Ministry of Health, in the city of Brusque, SC, Brazil. Determination of the anthropometrical parameters and laboratory variables recognized as cardiovascular risk factors. Elevated prevalence of RF in addition to systemic arterial hypertension (SAH) and smoking, configuring the multiplicity that concurs with a marked elevation of the risk of cardiovascular events in this population sample. In hypertensive populations, the prevention, identification and RF control measures must be implemented; computerized programs such as the Hiperdia/MS can help in patients follow-up, allowing a more stringent multidisciplinary approach, especially regarding the analysis of the attainment of treatment goals and the subsequent decrease of cardiovascular risk.

Angiotensin II type-1 receptor A1166C polymorphism is associated with increased risk of ischemic stroke in hypertensive smokers.

Recent observations revealed a novel role of angiotensin-converting enzyme 2 and the angiotensin II type-1 receptor (AT1R) in lung injury, thereby extending knowledge about the functions of the angiotensin system. Angiotensin II, whose target is the AT1R, is a potent vasoconstrictor. Accordingly, an imbalance leading to enhanced activity of the angiotensin II-AT1R axis is postulated to contribute to both circulatory disturbances and lung injury. In this context, a functional single-nucleotide polymorphism, AT1R A1166C, which leads to enhanced responsiveness of the AT1R, has been postulated as a candidate susceptibility factor for ischemic stroke. The aim of our study was to investigate its occurrence in ischemic stroke and to analyze its possible synergistic associations with clinical risk factors. Genetic and clinical data on 308 consecutive patients with acutely developing ischemic stroke were analyzed. A total of 272 stroke and neuroimaging alteration-free subjects served as a control group. Univariate and logistic regression statistical approaches were used. Alone, the AT1R 1166C allele did not pose a risk of stroke. In hypertensive smokers, however, it was associated with an increased risk of ischemic stroke (OR 22.3, 95% CI 5.8–110.2, p<0.001). Further subgroup analysis revealed the same association for both small-vessel (OR 24.3, 95% CI 6.1–121.1, p<0.001) and large-vessel (OR 21.3, 95% CI 4.6–81.1, p<0.001) infarction. On a pathophysiological basis, our results suggest the possibility that the AT1R A1166C polymorphism might give rise to ischemic stroke indirectly via an unfavorable effect on the cardiorespiratory function.

Disparity in frequency of normal coronary artery in black and white patients undergoing cardiac catheterization.

Normal epicardial coronary arteries (NCA) based on angiography have been reported to occur more frequently in Blacks than in Whites, but these studies have suffered from the limitation of being retrospective, reporting on relatively small numbers of subjects, or lacking a systematic angiogram interpretation. Angiograms of 560 consecutive patients (226 Black and 334 White) enrolled in the Harlem-Bassett Study were reviewed. The presence of coronary artery disease risk factors was documented. A coronary artery was defined as normal if no segment contained a luminal diameter stenosis > 24%. Overall, NCA were found in 39.1% of patients (Blacks 42.9% and Whites 36.5%) and were present most frequently in White women (53.7%). Black men were two times more likely than White men to have NCA (odds ratio [OR] 2.09, P < .002). More Blacks than Whites with NCA were hypertensive (OR 3.30, P < .001) and cigarette smokers (OR 5.18, P < .001), whereas more Whites had hypercholesterolemia (OR .29, P < .001). Significant racial differences exist between the Black and White populations in regard to the presence of NCA. The traditional risk factors of age, diabetes, cigarette smoking, and hypercholesterolemia are present in both groups. However, a racial disparity exists in the frequency of some risk factors (hypertension, cigarette smoking, hypercholesterolemia) in patients with NCA.

Renal plasma flow, filtration fraction and microalbuminuria in hypertensive patients: Effects of chronic smoking

Albumin excretion rate is usually increased in people who smoke, but the physiological basis of this phenomenon is not fully understood. The effect of chronic smoking on renal haemodynamics was studied in a cohort of 66 men. Twenty-seven were smokers and 36 were hypertensive. In all subjects, the albumin excretion rate was evaluated; in hypertensive patients, a renoscintigraphic evaluation of renal plasma flow and glomerular filtration were carried out and the filtration fraction was calculated. The hypertensive smoking population presented an increased urinary albumin excretion rate in comparison with hypertensive non-smoking patients. No significant differences were found for the mean values of renal plasma flow, the glomerular filtration rate and the filtration fraction between hypertensive smokers and hypertensive non-smoking patients. In hypertensive patients, smoking does not modify typical renal haemodynamic changes of arterial hypertension; however, it significantly increases the albumin excretion rate.

Hypertensive smokers have a worse cardiovascular risk profile than non‐smokers in spite of treatment – A national study in Sweden

Smoking is a well‐established risk factor for cardiovascular disease. Studies have indicated that smoking may outweigh the benefit of blood pressure (BP) control. Our aim was to compare cardiovascular risk factors in smokers vs non‐smokers from a national sample of treated hypertensives. Data were collected on smoking habits, BP control, total and low‐density lipoprotein (LDL) cholesterol, diabetes, left ventricular hypertrophy (LVH), and microalbuminuria (MA), from records of 4424 consecutive patients by 189 physicians. All technical methods were local. Treated hypertensives who smoked had microalbuminuria significantly more often than non‐smokers, 26.2% vs 20.5% (p<0.05), and a higher proportion of smokers were suboptimally controlled (DBP⩾90 mmHg), 32.7% vs 25.0% (p<0.01). Smoking males had a higher prevalence of LVH (25.7% vs 20.1; p<0.05), microalbuminuria (29.7% vs 24.7%; p<0.01), and a higher proportion of subjects with uncontrolled systolic BP (⩾140 mmHg) (72.8% vs 68.9%; p<0.01). Both DBP and total cholesterol were higher in smoking vs non‐smoking females. An increased prevalence of LVH and microalbuminuria was independently associated with smoking. In summary, smokers with treated hypertension show a higher proportion of LVH (men), microalbuminuria and worse diastolic BP control than non‐smokers. This may hypothetically reflect either less compliance with drug treatment in smokers or that smoking impairs the pharmacological effects of antihypertensive drugs.

Acute and Chronic Effects of Smoking on the Arterial Wall Properties and the Hemodynamics in Smokers with Hypertension

Background and Objectives：Smoking increases cardiovascular risk and it is known to acutely increase arterial stiffness in healthy smokers. We investigated the acute and chronic effects of smoking on the arterial mechanics in smokers with hypertension. Subjects and Methods：To evaluate the acute effects of smoking, the heart rate (HR), brachial blood pressure (BP), ankle systolic BP, heart-carotid pulse wave velocity (hcPWV), heartfemoral PWV (hfPWV), femoral-ankle PWV (faPWV), heart-brachial PWV (hbPWV), and the ankle-brachial index (ABI) were measured in male hypertensive smokers (n=22, 42±2 years, mean±SEM) and in normotensive smokers (n=30, 39±1 years) before and 5, 10 and 15 minutes after smoking 1 cigarette (nicotine content: 0.9 mg). To evaluate the chronic effects of smoking, we compared the HR, brachial BP, PWVs, ABI and carotid intima-media thickness (IMT) between the normotensive smokers and nonsmokers (n=32, 37±1 years), and also between the hypertensive smokers and nonsmokers (n=21, 48±2 years). Results：Smoking induced significant acute increases of the HR, brachial BP and hfPWV in the normotensive and hypertensive smokers (p 0.05). The magnitude of the increase in the HR, brachial BP and hfPWV after smoking were not different between the hypertensive and normotensive smokers. There was no significant differences (p>0.05) between the chronic normotensive smokers and the nonsmokers, and also between the hypertensive smokers and the non-smokers. Conclusion：Smoking acutely increased the HR, brachial BP and aortic stiffness in hypertensive smokers and normotensive smokers, and it had a more significant impact on the femoral arterial stiffness in the hypertensive smokers than in the normotensive smokers. However there were no significant chronic effects of smoking on the hemodynamics, arterial stiffness and carotid IMT. Our findings suggest that the acute increase in aortic and femoral arterial stiffness after smoking may contribute to the increased incidence of adverse cardiovascular events in smokers with hypertension. (Korean Circulation J 2005;35:493-499)