Acute and chronic effects of cigarette smoking on arterial stiffness

OBJECTIVES: Pulse wave velocity (PWV) is an indicator of arterial stiffness, especially in the aorta, and a marker for vascular damage. Smoking is reported to increase arterial stiffness. We examined the acute and chronic effects of smoking on arterial stiffness by measuring brachial--ankle PWV (baPWV) using an oscillometric method (VP 1000, Colin Co., Komaki, Japan). METHODS: All healthy male subjects (chronic smokers, n=40, 30.3 years old vs non-smokers, n=40, 28.3 years old) smoked two cigarettes (nicotine 1.5 mg) within 10 min and measured blood pressure (BP), heart rate and baPWV at baseline, 5, 15, 30, 45 and 60 min and compared with controls (n=20, 29.3 years old). RESULTS: Systolic BP was higher in chronic smokers than non-smokers or controls. Smoking increased the systolic and diastolic BP and heart rate significantly at 5 min in both chronic smokers and non-smokers as compared with baseline levels or controls (respectively, p<0.001) and returned to baseline level at 15 min. Pulse pressure did not increase significantly. baPWV increased significantly in both chronic smokers and non-smokers at 5 min (12.1--17.3 m/s vs 11.1--12.7 m/sec, respectively) and remained higher for 30 min compared with controls (p<0.001). Smoking increased baPWV to a greater extent in chronic smokers than in non-smokers (p<0.01). CONCLUSION: Acutely, cigarette smoking increased BP, heart rate and baPWV in chronic smokers and non-smokers. These effects were more prominent in chronic smokers than in non-smokers. These findings suggest that cigarette smoking have deleterious effects on cardiovascular system by stiffening arteries.     

Increased systolic ambulatory blood pressure and microalbuminuria in treated and non-treated hypertensive smokers

Objective: The primary aim of the present study was to evaluate the impact of smoking status on both clinic and ambulatory blood pressure (BP) and heart rate (HR) by using 24-h ambulatory BP monitoring in treated and non-treated hypertensive smokers and non-smokers. A secondary aim was to evaluate the interrelations between BP, smoking status and microalbuminuria. Design: Five hundred and eighty treated and non-treated hypertensive smokers and non-smokers were consecutively recruited. The patients were divided into groups of non-smokers (n = 414) and smokers (n = 166). We were able to match 115 smokers with 230 non-smokers with regard to clinic BP, gender and age. Methods: Microalbuminuria (albumin/creatinine ratio on morning spot urine sample), sitting clinic BP (mercury sphygmomanometry) and ambulatory BP (A&D TM 2421) were measured. Results: In the matched group we found a significant difference in ambulatory systolic and diastolic daytime BP between smokers and non-smokers (146.5 ± 15.0/90.6 ± 9.7 mmHg vs 142.3 ± 12.6/89.0 ± 9.0 mmHg). The smokers had significantly higher log albumin/creatinine ratio (0.51 ± 0.93 vs 0.19 ± 0.87). These results were found to be valid for treated as well as untreated patients. In both the matched and unmatched groups, the smokers had significantly higher HR. Conclusion: The higher daytime BP and HR as well as microalbuminuria in smokers may contribute to their increased cardiovascular risk. Furthermore, the higher ambulatory BP in smokers implicates that these patients tend to be underdiagnosed and undertreated if only clinic BP is used.     

Smoking is associated with increased HbA1c values and microalbuminuria in patients with diabetes--data from the National Diabetes Register in Sweden

OBJECTIVES: The aim was to examine trends in the proportion of smoking in diabetes patients, and to study associations between smoking, glycaemic control, and microalbuminuria. METHODS: Smoking habits were reported to the Swedish National Diabetes Register (NDR), with data from hospitals and primary health care. Patient characteristics included were age, gender, type of treatment, diabetes duration, HbA1c, BMI, blood pressure, antihypertensive and lipid-lowering drugs, and microalbuminuria. RESULTS: The proportion of smokers in type 1 diabetes was 12-15% during 1996-2001, it was high in females<30 years (12-16%), and was higher in the age group 30-59 years (13-17%) than in older (6-9%) patients. The corresponding proportion of smoking in type 2 diabetes was 10-12%, higher in those less than 60 years of age (17-22%) than in older (7-9%) patients. Smoking type 1 and type 2 patients in 2001 had higher mean HbA1c but lower mean BMI values than non-smokers. Smokers also had higher frequencies of microalbuminuria, in both type 1 (18 vs 14%) and type 2 (20% vs 13%) diabetes. Multiple logistic regression analyses disclosed that smoking was independently associated with elevated HbA1c levels (p<0.001) and microalbuminuria (p<0.001), but negatively with BMI (p<0.001), in both type 1 and type 2 diabetes. CONCLUSIONS: Smoking in patients with diabetes was widespread, especially in young female type 1, and in middle-aged type 1 and type 2 diabetes patients, and should be the target for smoking cessation campaigns. Smoking was associated with both poor glycaemic control and microalbuminuria, independently of other study characteristics.     

Sources of measurement variation in blood pressure in large-scale epidemiological surveys with follow-up

The Copenhagen City Heart Study (CCHS) is a longitudinal epidemiological study of 19698 subjects followed up since 1976. Variation in blood pressure (BP) measurement in the first three CCHS surveys is evaluated by assessing two components, systematic variation and random variation [daytime and seasonally variation, observer bias, non-response bias, variation with explanatory variables, such as diabetes, hypertension, body mass index (BMI), height, plasma cholesterol and smoking] for the purpose of identifying relevant errors in population surveys. BP was measured in the seated position after a 5 min rest, with the cuff around the non-dominating arm, in accordance with recommended guidelines. The participation rate fell from 74% in survey 1 to 63% in survey 3. Significant non-response bias with respect to BP values was not found. No daytime variability was noted either in systolic (SBP) or diastolic (DBP) BPs. A trend towards a lower BP was seen during the summertime. Random variation, expressed as the standard deviation of the measured values, increased with increasing BP values (SBP: 11.9-13.4 to 21.2- 25.1 mmHg; DBP: 10.6-11.2 to 11.9-13.4 mmHg). SBP was positively correlated to BMI and plasma cholesterol. SBP was 5-10 mmHg higher in diabetics ( p = 0.000-0.04) than in age- and sex-matched nondiabetics. DBP did not differ between the two groups. Smokers from the age of 50 years had a 2-4 mmHg lower SBP ( p = 0.000-0.01) and 1-3 mmHg lower DBP ( p = 0.000-0.005) than had non-smokers. In addition, significantly fewer smokers took antihypertensive medication than did non-smokers ( p = 0.000). In conclusion, judging from the degree of association with BP and/or differences between the three surveys, the most important factors to consider were seasonal variation, BMI, the use of antihypertensive drug therapy, plasma cholesterol, smoking status and diabetes. An inter-survey comparison of BP in population cohorts requires controlling for these factors.     

Relationship of systolic blood pressure with plasma homocysteine: importance of smoking status

BACKGROUND: Elevated plasma homocysteine is a risk factor for cardiovascular disease. Elevations in plasma homocysteine occur in both smokers and hypertensives, but the combined effect of smoking and hypertension on homocysteine is unknown. METHODS: Resting plasma homocysteine levels and blood pressure were determined in 56 normotensives (12 smokers) and 20 essential hypertensives (10 smokers). RESULTS: Plasma homocysteine was significantly higher in all smokers versus all non-smokers (9.46 +/- 0.5 versus 7.9 +/- 0.5 micromol/l, P = 0.041) by two-way ANOVA, and was also significantly higher in all hypertensives versus all normotensives (9.8 +/- 0.6 versus 7.6 +/- 0.4 micromol/l, P = 0.004). There was no interaction between the effects of hypertension and smoking on plasma homocysteine. Hypertensive smokers had significantly higher plasma homocysteine than either normotensive non-smokers (10.65 +/- 0.84 versus 7.05 +/- 0.26 micromol/l), hypertensive non-smokers (7.88 +/- 0.64 micromol/l) or normotensive smokers (8.36 +/- 0.5 micromol/l). In subjects overall, homocysteine levels were correlated (r = 0.306, P = 0.015) with systolic blood pressure but not with diastolic (r = 0.186). This relationship was also significant in smokers, but not non-smokers. Furthermore, subjects in the highest quintile for plasma homocysteine had significantly higher systolic BP than those in the lowest quintile. This effect was not observed when smokers were removed from the analysis. CONCLUSION: Smoking compounds the modest effect of hypertension on plasma homocysteine. The strong relationship between systolic blood pressure and homocysteine that exists only in smokers suggests that smoking-induced homocysteine elevations may raise systolic blood pressure. We speculate that smoking compounds the risk of cardiovascular disease in hypertensives, in part, by elevating homocysteine.     

Reduced nocturnal fall in blood pressure,assessed by two ambulatory blood pressure monitorings and cardiac alterations in early phases of untreated essential hypertension

To investigate whether in recently diagnosed essential hypertensives a reduced nocturnal fall in blood pressure (BP), established on the basis of two 24-h ambulatory blood pressure monitorings (ABPM) is related to a greater cardiovascular damage. In all, 355 consecutive, recently diagnosed, never-treated essential hypertensives referred for the first time to our outpatient clinic were included in the study. Each patient underwent the following procedures: (1) two 24-h ABPMs performed within 3 weeks, (2) 24-h urinary collection for microalbuminuria, (3) nonmydriatic photography of ocular fundi, (4) echocardiography, (5) carotid ultrasonography. We defined nondipping profile as a night-day systolic and diastolic fall < or =10 % (mean of two ABPMs). A dipper BP profile was found in 238 patients, whereas in 117 patients a nondipper profile was present. The two groups were similar for age, gender, body mass index, smoking habit, clinic BP, 48-h BP and heart rate, while, by definition, night-time systolic and diastolic BP were significantly higher in nondippers than in dippers (130/81 vs 121/74 mmHg, P < 0.0001).The prevalence of left ventricular hypertrophy (LVH) defined by four different criteria: (a) LV mass index (LVMI) > or = 125 g/m(2) in both genders; (b) LVMI > or = 134 gm(2) in men and > or = 110 in women; (c) LVMI> or = 125 g/m(2) in men and > or = 110 g/m(2) in women; (d) LVMI > or = 51 g/m(2.7) in men and > or = 47 g/m(2.7) in women was significantly higher in nondippers than in dippers (a: 12 vs 7%, P < 0.05; b: 16 vs 7%, P < 0.01; c: 20 vs 11%, P < 0.01; d: 35 vs 23% P < 0.02) and this finding was associated with a significant increase in aortic root and left atrium dimensions. There were no differences between the two groups in the prevalence of carotid and retinal changes and microalbuminuria. In conclusion our findings suggest that never-treated hypertensives with a reduced BP fall in the night time, defined on the basis of two ABPMs, have a higher prevalence of TOD than dippers, in terms of echocardiographic LVH. In this population setting, cardiac structural alterations are a more sensitive marker of the impact of the nocturnal BP load on cardiovascular system than other extracardiac signs of TOD.     

Relationship between smoking habits and the features of the metabolic syndrome in a non-diabetic population

INTRODUCTION: Cigarette smoking is a risk factor for type 2 diabetes mellitus. The effect of smoking on the pathogenic factors for the development of diabetes is little explored. We evaluate the relation of smoking with the features of the insulin resistance syndrome, insulin resistance, and insulin secretion. METHODS: 2412 non-diabetic men, aged 35-65 years, were studied. Smoking habit was investigated by questionnaire. Anthropometry, blood pressure, forced expiratory volume (FEV1), fasting glucose, triglycerides, total and HDL cholesterol, plasma free fatty acids (FFA), insulin and fibrinogen were measured. HOMA-IR and HOMA beta cell were calculated. The metabolic syndrome was defined according to ATP III criteria. RESULTS: The metabolic syndrome was more prevalent in smokers than non-smokers (OR: 1.34; 95% CI 1.01-1.77). This was mainly due to a higher prevalence of dyslipidemia - high triglycerides (46.1% vs 29.9%, p<0.001), or low HDL cholesterol (42.2% vs 30.4%, p<0.001), in smokers. In smokers, other features of insulin resistance - i.e. obesity, hypertension, and hyperglycemia were significantly less frequent and FFA were lower (p<0.001). Plasma insulin and HOMA beta cell were similar in the two groups (8.3 vs 8.0microU/ml and 80.7% vs 82.9%, respectively), but HOMA-IR was significantly lower in smokers (p<0.001) due to the lower glucose values observed in these people. CONCLUSIONS: Among the features of the metabolic syndrome, only dyslipidemia is associated with chronic smoking. Smoking in not associated with enhanced insulin resistance, or with impaired insulin secretion. Alternative hypotheses should be explored for the increased risk of diabetes in smokers.     

Assessment of self-monitoring of blood pressure in the diagnosis of isolated clinic hypertension

BACKGROUND: There are no studies assessing cardiovascular morbidity, morality in patients with isolated clinical hypertension (ICH) with self-blood pressure monitoring (SBPM). OBJECTIVES: To determine the value of SBPM in the diagnosis of ICH. METHODS: Cohort study. New hypertensive and normotensive patients 15-75 years, without cardiovascular events history. VARIABLES: Oriented anamnesis hypertension; blood pressure measurements (BP): clinical BP, SBPM and ambulatory BP monitoring (ABPM); evaluation of target organ damage (TOD); electrocardiogram; retinography and microalbuminuria (MA). RESULTS: One hundred and thirty-five patients, 95 hypertensive (62.1% males; mean age 59.08+/-16.8 years), 40 normotensive (37.5% males; mean are 56.32+/-10.22 years). BP measurements (mmHG) in normotensives vs hypertensives: clinical BP, 125.36/76.74 vs 149.81/87.86 mmHg (p<0.0001) and SPPM, 114.90/69.96 vs 142.06/86.31 (p<0.0001). Twenty-four-hour ABPM: 135.41/81/81.74. Prevalence of TOD in hypertensive: 23.10% left ventricular hypertrophy (LVH), sustained hypertension (SH): clinic BP, 149.88/86.34 vs 152.51/89.55 (p>0.10); SBPM: 147.895/88.95 vs 128.17/79 (p<0.0001) and ABPM, 141.72/88.22 vs 131.66/80 (p=0.053 for systolic). TOD in SH vs ICH: LVH, 24.6% vs 19.2% (p=0.814); exudates or haemorrhages, 7.7% vs 9.8% (p=0.580). The risk of an occurrence of any TOD in ICH patients is lower for 125/80 (OR=2.5). CONCLUSIONS: VAMPAHICA will provide information about value SBPM in the diagnosis of ICH. Advanced retinopathy is relative frequent in ICH patients. If TOD is accepted as a surrogate endpoint, the diagnostic values of ICH will be probably decreased.     

Losartan benefits over atenolol in non-smoking hypertensive patients with left ventricular hypertrophy: the LIFE study

We studied the impact of smoking in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios in 4656 never-smokers, and 3033 previous and 1499 current smokers, adjusting for gender, age, alcohol intake, exercise and race. Composite endpoint rate was higher in previous (28/1000 years), as well as current (39/1000 years) smokers than in never-smokers (21/1000 years). Composite (hazard ratio 0.78, 95% CI 0.65-0.94, p < 0.01) and stroke (hazard ratio 0.61, 95% CI 0.47-0.80], p < 0.001) risks were lower with losartan than atenolol in never-smokers, but not significantly in previous smokers. Drug regimens did not differ in current smokers (composite hazard ratio 0.99, stroke hazard ratio 0.94). Smoking-treatment interactions were non-significant, but a borderline significant trend (p = 0.05) suggested decreasing benefit of losartan vs atenolol for stroke prevention from never- to previous to current smoking status. Smoking increased cardiovascular risk markedly in the LIFE study. The benefit of losartan vs atenolol is consistent with the overall conclusion of the LIFE study, although the treatment effect appeared largest in non-smokers.     

Smoking is associated with impaired long-term glucose metabolism in patients with type 1 diabetes mellitus

Background and AimsSmoking is known to negatively influence glucose metabolism both in healthy subjects and in patients with diabetes. The aim of this study was to compare glycemic control in patients with type 1 diabetes mellitus who were smokers with those who did not smoke during a prospective long-term follow-up.Methods and ResultsIn a single center, 763 patients with type 1 diabetes mellitus were included, 160 (21.0%) of them were smokers. Patients were treated with intensive insulin therapy according to existing guidelines. Glucose control was monitored quarterly, diabetes related complications and cardiovascular risk factors were assessed at least once a year. Glucose control in smokers was significantly worse than in non-smokers at baseline and during follow-up (mean HbA1c during 5047 patient-years of follow-up 7.9 ± 1.3% in smokers and 7.3 ± 1.1% in non-smokers, p < 0.001) despite a higher insulin dosage in smokers (0.71 ± 0.30 U/kg vs. 0.65 ± 0.31 U/kg in non-smokers, p = 0.046). HDL cholesterol was lower in smokers at baseline (1.53 ± 0.45 vs. 1.68 ± 0.51 in non-smokers, p = 0.048). Diabetes related complications tended to occur with a higher frequency in smokers, with a significant difference in macroalbuminuria (9.8% vs. 4.8% in non-smokers, p = 0.047).ConclusionSmoking is associated with worse glucose control in patients with type 1 diabetes mellitus despite the same treatment strategies as in non-smokers. Hyperglycemia, therefore, may contribute to an earlier incidence of diabetes related complications in these patients, in addition to direct toxic effects of smoking.     

High prevalence of cardiac and extracardiac target organ damage in refractory hypertension.

OBJECTIVE : Target organ damage (TOD) in chronically treated hypertensives is related to effective blood pressure (BP) control. The aim of this study was to evaluate the prevalence of cardiac and extracardiac TOD in patients with refractory hypertension (RH) compared with well-controlled treated hypertensives (C). METHODS : Fifty-four consecutive patients with RH (57 +/- 10 years), selected according to WHO/ISH guidelines definition, and 51 essential hypertensives (55 +/- 10 years) with satisfactory BP control obtained by association therapy, underwent the following procedures: (1) clinic BP measurement; (2) blood sampling for routine chemistry examinations; (3) 24 h urine collection for microalbuminuria; (4) non-mydriatic retinography; (5) echocardiogram; (6) carotid ultrasonogram. In order to exclude 'office resistance' (defined as clinic BP > 140/90 mmHg and average 24 h BP or =1.0 mm, respectively); a higher prevalence of carotid plaques (65 versus 32%, P < 0.05), a more advanced retinal involvement (grade II and III, 73 and 5% versus 38 and 0%, P < 0.01) and a greater albumin urinary excretion (22 +/- 32 mg/24 h versus 11 +/- 13 mg/24 h, P < 0.01) were found in RH compared to C. CONCLUSIONS : Our study suggests that RH is a clinical condition associated with a high prevalence of TOD at cardiac, macro- and microvascular level and consequently with high absolute cardiovascular risk, which needs a particularly intensive therapeutic approach aimed to normalize BP levels and to induce TOD regression.     

Efficacy and safety of two treatment combinations of hypertension in very elderly patients

The study compared valsartan/amlodipine combination with irbesartan/hydrochlorothiazide (HCTZ) combination in very elderly hypertensives. After a 4-week placebo period, 94 hypertensives, aged 75-89 years were randomized to valsartan 160mg/amlodipine 5mg or irbesartan 300mg/HCTZ 12.5mg for 24 weeks according to a prospective, parallel group study. After 4 weeks amlodipine or HCTZ was doubled in non-responders. Patients were checked every 4 weeks. At each visit clinical sitting, lying and standing blood pressure (BP), systolic BP (SBP) and diastolic BP (DBP) were evaluated, and an electrocardiogram was performed. At the end of the placebo period and of the treatment period a non-invasive 24-h ambulatory BP monitoring (ABPM) was performed and electrolytes and uric acid were evaluated. Both combinations significantly reduced ambulatory BP. In the valsartan/amlodipine group the mean reduction (-29.9/-15.6 for 24h, -28.6/-14.5mmHg for day-time and -26.2/-17.4mmHg for night-time SBP/DBP) was similar to that of the irbesartan/HCTZ group (-29.6/-15.4 for 24h, -29.3/-14.9mmHg for day-time and -25.4/-16.9mmHg for night-time SBP/DBP). Both combinations significantly reduced clinical sitting and lying BP values with no difference between treatments. BP changes from lying to standing position were significantly greater in the irbesartan/HCTZ group (-17.2/-9.1mmHg) than in the valsartan/amlodipine group (-10.1/-1.9mmHg, p<0.05 for SBP and p<0.01 for DBP vs. irbesartan/HCTZ). Potassium significantly decreased and uric acid significantly increased (-0.4mmol/l, p<0.05 and +0.5mg/dl, p<0.05 vs. baseline, respectively) only in the irbesartan/HCTZ group. In conclusion, both combinations were similarly effective in reducing ambulatory and clinical BP in very elderly hypertensives. However, valsartan/amlodipine offered some advantages in terms of less pronounced BP orthostatic changes and absence of metabolic adverse effects.     

Blood pressure on arising, morning blood pressure surge and blood pressure variability in white coat hypertensives and in matched normotensives and sustained hypertensives.

INTRODUCTION: It is still controversial whether subjects with white-coat hypertension (WCHT) exhibit higher cardiovascular risk compared to normotensive subjects (NT). In subjects with WCHT it is not known whether the abnormal blood pressure (BP) reaction in the office also occurs at other times of day, particularly on arising and immediately after waking, i.e. the times at which the majority of cardiovascular events are reported to occur. OBJECTIVE AND METHODS: To evaluate with 24h ambulatory BP measurement the values of morning BP surge, BP on arising and BP variability in subjects with WCHT in comparison with age-, gender- and weight-matched normotensives (BP) and untreated sustained hypertensives (BP). RESULTS: Groups of BP, WCHT and BP were matched for age, gender and body weight: BP: n=69, age 49 +/- 7 years, 54 % female, BMI 26 +/- 1, casual BP 126/79 +/- 5/4 mmHg, daytime BP 124/80 +/- 6/6 mmHg; WCHT: n=74, age 52 +/- 8 years, 57% female, BMI 26 +/- 2, casual BP 152/95 +/- 7/7 mmHg, daytime BP 126/80 +/- 5/6 mmHg; HT: n=79, age 53 +/- 7 years, 56% female, BMI 27 +/- 2, casual BP 154/97 +/- 9/8 mmHg, daytime BP 143/89 +/- 12/10 mmHg. Of the three groups, subjects with WCHT exhibited BP on arising (121/81 +/- 13/8 mmHg) similar to that of NTs (120/80 +/- 13/9 mmHg, NS), both significantly lower than that of HTs (137/92 +/- 17/10 mmHg, p < 0.01), suggesting the absence of an alerting BP reaction in WCHT at that time. By contrast, subjects with WCHT showed higher values of systolic morning BP surge vs. NTs (25 +/- 10 vs. 22 +/- 11 mmHg, p < 0.05), both lower than that observed in hypertensives (33 +/- 11 mmHg, p < 0.01 vs. NT and WCHT) and greater daytime variability (systolic BP standard variation), i.e. 12 2 vs. 10 +/- 2 mmHg, p < 0.05, both lower than that observed in hypertensives (14 +/- 3 mmHg, p < 0.01 vs. NT and WCHT). CONCLUSIONS: Although subjects with WCHT did not show any alerting blood pressure reaction on arising, morning BP surge and BP variability were greater in these subjects than in control normotensives, although lower than sustained hypertensives. Although this is still speculative, we cannot exclude the possibility that even a slight increase in morning BP surge might in the long term constitute an additional load on the circulation that could increase cardiovascular risk in subjects with WCHT compared to matched normotensives.     

Effects of manidipine/delapril versus olmesartan/hydrochlorothiazide combination therapy in elderly hypertensive patients with type 2 diabetes mellitus.

The purpose of this study was to compare the combination treatments of manidipine/delapril and olmesartan/hydrochlorothiazide (HCTZ) in elderly diabetic hypertensives. After a 4-week placebo period, 158 hypertensive patients with type 2 diabetes (age range: 66 to 74 years) were randomized to receive combination treatment of 10 mg manidipine plus 30 mg delapril or 20 mg olmesartan plus 12.5 mg HCTZ for 48 weeks in a prospective, parallel arm trial. After 12 weeks, manidipine or HCTZ was doubled in nonresponders (systolic blood pressure [SBP] > or =130 mmHg and/or diastolic blood pressure [DBP] > or =80 mmHg). Patients were checked at the end of the placebo period and every 12 weeks thereafter. At each visit, lying, sitting and standing BP as well as fasting glycemia, glycosylated hemoglobin (HbA1c), electrolytes, uric acid, total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C) and triglycerides (TG) were evaluated. Both combinations reduced sitting SBP (-27.7 and -28.3 mmHg, respectively; both p<0.001) and DBP (-15.1 and -14.8 mmHg, respectively; both p<0.01) with no difference between the two treatments. Standing DBP was more markedly reduced by olmesartan/HCTZ (-19.5 mmHg; p<0.001) than by manidipine/delapril (-14.7 mmHg; p<0.05 vs. olmesartan/HCTZ). No changes in metabolic parameters were observed with manidipine/delapril, whereas an increase in HbA1c (+0.7%; p<0.05), uric acid (+0.4 mg/dL; p<0.05) and TG (+41.3 mg/dL; p<0.05), and a decrease in serum potassium (-0.3 mmol/L; p<0.05) and HDL-C (-3.4 mg/dL; p<0.05) were found in the olmesartan/HCTZ group. In conclusion, both combinations were similarly effective in reducing BP in elderly hypertensive diabetic patients. However, manidipine/delapril offered some advantages in terms of the less-pronounced BP orthostatic changes and absence of metabolic adverse effects.     

Diurnal Variation in Blood Pressure in Insulin-dependent Diabetic Smokers and Non-smokers with and without Microalbuminuria

In subjects with essential hypertension, loss of the normal nocturnal dip in blood pressure is associated with a greater risk of developing end-organ complications. In subjects with diabetes, smoking carries a similar association. To assess whether these factors may have an aetiological and synergistic role in the vascular complications of diabetes, 24-hour blood pressure monitoring was performed in insulin-dependent diabetic (IDDM) patients with normal albumin excretion (n = 19) and microalbuminuria (n = 21) of comparable age and duration of diabetes, and with no evidence of autonomic neuropathy or hypertension. The potential influence of smoking was examined by subdividing the groups, depending on smoking status. Ten of the microalbuminuric group and 9 of the normoalbuminuric group were current smokers, the remaining patients never having smoked. There was a significant difference between mean (±SD) daytime vs nocturnal blood pressure in patients with normal albumin excretion (114 ± 3/70 ± 4 vs 102 ± 3/62 ± 3 mmHg; p < 0.001) and microalbuminuria (109 ± 5/75 ± 5 vs 101 ± 3/65 ± 4 mmHg; p < 0.001) but mean blood pressure values did not differ significantly between the groups. A similar fall in nocturnal blood pressure was found in smokers and non-smokers with and without microalbuminuria (p < 0.001), but there was no difference between the mean blood pressure values in the different subgroups. In conclusion, normotensive IDDM patients, who do not have autonomic neuropathy, retain a significant diurnal variation in blood pressure, irrespective of smoking habit or presence of microalbuminuria. © 1997 by John Wiley & Sons, Ltd.     

Blood pressure level and relation to other cardiovascular risk factors in male hypertensive patients without clinical evidence of ischemic heart disease

Arterial hypertension is accompanied by increased morbidity and mortality and constitutes a substantial part of medical care. Antihypertensive intervention reduces the cardiovascular morbidity and mortality. The aims of the study were to evaluate the relationship between cardiovascular risk factors and the blood pressure (BP), and to evaluate the percentage of patients who had achieved a BP level as recommended by the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). BP was evaluated in relation to age, body mass index, duration of hypertension, cholesterol and triglyceride level, smoking status, information of regular exercise, a family history of ischemic heart disease (IHD) and drug treatment, in 220 men treated for arterial hypertension. In the univariate analyses we found a higher systolic blood pressure (SBP) with older age, higher SBP in smoking patients and lower SBP in patients with regular exercise. In a multivariate model age (p = 0.0004), smoking status (p = 0.01) and regular exercise (p= 0.06) were independently associated with SBP. There was a lower diastolic blood pressure (DBP) with older age, and age was independently associated with DBP. Office SBP was above 140 mmHg in 83% and above 160 mmHg in 44% of patients. During ambulatory blood pressure monitoring (AMBP), SBP was above 135 mmHg in 40% and above 155 mmHg in 15% of patients. In addition to male sex and hypertension there was a high percentage of other cardiovascular risk factors--43% was smoking, 21% had a family history of IHD, 77% had a se-cholesterol above 5.5 mmol/l and 48% had a se-triglyceride above 1.6 mmol/l. In a consecutive group of asymptomatic male treated hypertensive patients SBP is independently associated with age and smoking status, and DBP with age. A high percentage of the patients do not have a well controlled BP, and a high percentage have additional risk factors such as smoking, hypercholesterolaemia, hypertriglyceridaemia and a family history of IHD. This means that there is room for much improvement in the control of hypertension.     

Smoking and antihypertensive medication: interaction between blood pressure reduction and arterial stiffness.

To investigate how cigarette smoking and antihypertensive drug therapy may interact to affect cardiovascular disease, in this prospective study we administered amlodipine to hypertensive smokers and non-smokers and compared blood pressure reduction and indices of arterial stiffness. We measured blood pressure (BP), heart rate (HR), brachial-ankle pulse wave velocity (baPWV), and the carotid augmentation index (AIx) by using a non-invasive automated device in 101 hypertensive patients at baseline and at 1, 3, and 6 months of amlodipine administration (5.0 mg). At baseline, the AIx was significantly lower in smokers (n=27) than in non-smokers (n=74) (27.3% +/- 13.3% vs. 33.3% +/- 11.4%). After amlodipine administration, in both the groups, the mean BP, baPWV, and AIx were significantly reduced; however, the HR did not show a statistically significant difference. The reduction in the baPWV (cm/s) at 1 and 3 months was less marked in smokers than in non-smokers (mean +/- SD: -186.6 +/- 36.5 vs. -283.6 +/- 24.5 at 1 month; -136.6 +/- 42.2 vs. -280.1 +/- 29.6 at 3 months, respectively, both p<0.05). At 6 months, these intergroup differences in the reductions of baPWV disappeared. The blunted reduction of baPWV, particularly at 3 months, was significantly associated with the extent of smoking (lifetime pack-years smoked). Changes observed in the AIx and mean BP were similar between groups throughout the study period. In the short term, cigarette smoking blunts the effect of amlodipine on the reduction of arterial stiffness, independently of the mean BP level.     

Multifactorial intervention in individuals with type 2 diabetes and microalbuminuria: the Microalbuminuria Education and Medication Optimisation (MEMO) study

Aims

To determine whether tighter cardiovascular risk factor control with structured education in individuals with type 2 diabetes (T2DM) and microalbuminuria benefits cardiovascular risk factors.

Methods

Participants from a multiethnic population, recruited from primary care and specialist clinics were randomised to intensive intervention with structured patient (DESMOND model) education (n = 94) or usual care by own health professional (n = 95). Primary outcome: change in HbA1c at 18 months. Secondary outcomes: changes in blood pressure (BP), cholesterol, albuminuria, proportion reaching risk factor targets, modelled cardiovascular risk scores.

Results

Mean (SD) age and diabetes duration of participants were 61.5 (10.5) and 11.5 (9.3) years, respectively. At 18 months, intensive intervention showed significant improvements in HbA1c (7.1(1.0) vs. 7.8(1.4)%, p < 0.0001), systolic BP (129(16) vs. 139(17) mmHg, p < 0.0001), diastolic BP (70(11) vs. 76(12) mmHg, p < 0.001), total cholesterol (3.7(0.8) vs. 4.1(0.9) mmol/l, p = 0.001). Moderate and severe hypoglycaemia was 11.2 vs. 29.0%; p = 0.001 and 0 vs. 6.3%; p = 0.07, respectively. More intensive participants achieved ≥3 risk factor targets with greater reductions in cardiovascular risk scores.

Conclusions

Intensive intervention showed greater improvements in metabolic control and cardiovascular risk profile with lower rates of moderate and severe hypoglycaemia. Intensive glycaemic interventions should be underpinned by structured education promoting self-management in T2DM.     

Blood Pressure Level and Relation to other Cardiovascular Risk Factors in Male Hypertensive Patients without Clinical Evidence of Ischemic Heart Disease

Arterial hypertension is accompanied by increased morbidity and mortality and constitutes a substantial part of medical care. Antihypertensive intervention reduces the cardiovascular morbidity and mortality. The aims of the study were to evaluate the relationship between cardiovascular risk factors and the blood pressure (BP), and to evaluate the percentage of patients who had achieved a BP level as recommended by the sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC VI). BP was evaluated in relation to age, body mass index, duration of hypertension, cholesterol and triglyceride level, smoking status, information of regular exercise, a family history of ischemic heart disease (IHD) and drug treatment, in 220 men treated for arterial hypertension. In the univariate analyses we found a higher systolic blood pressure (SBP) with older age, higher SBP in smoking patients and lower SBP in patients with regular exercise. In a multivariate model age (p = 0.0004), smoking status (p = 0.01) and regular exercise (p = 0.06) were independently associated with SBP. There was a lower diastolic blood pressure (DBP) with older age, and age was independently associated with DBP. Office SBP was above 140 mmHg in 83% and above 160 mmHg in 44% of patients. During ambulatory blood pressure monitoring (AMBP), SBP was above 135 mmHg in 40% and above 155 mmHg in 15% of patients. In addition to male sex and hypertension there was a high percentage of other cardiovascular risk factors-43% was smoking, 21% had a family history of IHD, 77% had a se-cholesterol above 5.5 mmol/l and 48% had a se-triglyceride above 1.6 mmol/l. In a consecutive group of asymptomatic male treated hypertensive patients SBP is independently associated with age and smoking status, and DBP with age. A high percentage of the patients do not have a well controlled BP, and a high percentage have additional risk factors such as smoking, hypercholesterolaemia, hypertriglyceridaemia and a family history of IHD. This means that there is room for much improvement in the control of hypertension.