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Showing papers by "Sverre E. Kjeldsen published in 2004"


Journal ArticleDOI
TL;DR: Blood pressure was reduced by both treatments, but the effects of the amlodipine-based regimen were more pronounced, especially in the early period, which emphasise the importance of prompt blood-pressure control in hypertensive patients at high cardiovascular risk.

2,432 citations


Journal ArticleDOI
01 Jan 2004-Drugs
TL;DR: The reductions in major cardiovascular events with atorvastatin are large, given the short follow-up time, and may have implications for future lipid-lowering guidelines.
Abstract: Background The lowering of cholesterol concentrations in individuals at high risk of cardiovascular disease improves outcome. No study, however, has assessed benefits of cholesterol lowering in the primary prevention of coronary heart disease (CHD) in hypertensive patients who are not conventionally deemed dyslipidaemic.

1,087 citations


Journal ArticleDOI
17 Nov 2004-JAMA
TL;DR: Less-severe electrocardiographic LVH by Cornell product and SokolowLyon voltage criteria during antihypertensive therapy is associated with lower likelihoods of CV morbidity and mortality, independent of blood pressure lowering and treatment modality in persons with essential hypertension.
Abstract: 0.80; 95% CI, 0.73-0.87; P.001, respectively), MI (HR, 0.90; 95% CI, 0.82-0.98; P=.01; and HR, 0.90; 95% CI, 0.81-1.00; P=.04), and stroke (HR, 0.90; 95% CI, 0.840.96; P=.002; and HR, 0.81; 95% CI, 0.75-0.89; P.001). Conclusions Less-severe electrocardiographic LVH by Cornell product and SokolowLyon voltage criteria during antihypertensive therapy is associated with lower likelihoods of CV morbidity and mortality, independent of blood pressure lowering and treatment modality in persons with essential hypertension. Antihypertensive therapy targeted at regression or prevention of electrocardiographic LVH may improve prognosis.

599 citations


Journal ArticleDOI
TL;DR: Reaching blood pressure control by 6 months, independent of drug type, was associated with significant benefits for subsequent major outcomes; the blood pressure response after just 1 month of treatment predicted events and survival.

594 citations


Journal ArticleDOI
TL;DR: The increase in SUA over 4.8years in the LIFE study was attenuated by losartan compared with atenolol treatment, appearing to explain 29% of the treatment effect on the primary composite end point.

466 citations



Journal ArticleDOI
TL;DR: Baseline albuminuria is a powerful risk factor for CV events and one-fifth of the difference in favor of losartan on the primary CEP was explained by the greater reduction inalbuminuria onLosartan.
Abstract: ObjectivesTo examine a possible relationship between baseline albuminuria and effect of losartan versus atenolol on cardiovascular (CV) events in hypertensive patients with left ventricular hypertrophy, the effect of losartan versus atenolol on albuminuria, and whether the benefits of losartan versu

137 citations


Journal ArticleDOI
TL;DR: Results of the subanalysis are sufficient to generate the hypothesis that black patients with hypertension and LVH might not respond as favorably to losartan-based treatment as non-black patients with respect to cardiovascular outcomes, and do not support a recommendation forLosartan as a first-line treatment for this purpose.

132 citations


Journal ArticleDOI
TL;DR: ECG strain is a marker of increased CV risk in hypertensive patients in the setting of aggressive blood pressure lowering, independent of baseline severity of ECG LVH.
Abstract: The ECG strain pattern of lateral ST depression and T-wave inversion is a marker for left ventricular hypertrophy (LVH) and adverse prognosis in population studies. However, whether ECG strain is an independent predictor of cardiovascular (CV) morbidity and mortality in the setting of aggressive antihypertensive therapy is unclear. ECGs were examined at study baseline in 8854 hypertensive patients with ECG LVH who were treated in a blinded manner with atenolol- or losartan-based regimens. Strain was defined by the presence of a downsloping convex ST segment with an inverted asymmetrical T wave opposite to the QRS axis in leads V5 and/or V6 and was present in 971 patients (11.0%). The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study composite end point of CV death or nonfatal myocardial infarction or stroke occurred in 1035 patients (11.7%). In Cox analyses adjusting only for treatment effect, ECG strain was a significant predictor of CV death (hazard ratio [HR] 2.26, 95% confidence interval [CI] 1.78 to 2.86), fatal/nonfatal myocardial infarction (HR 2.16, 95% CI 1.67 to 2.80), fatal/nonfatal stroke (HR 1.76, 95% CI 1.39 to 2.21), and the composite CV end point (HR 1.99, 95% CI 1.70 to 2.33). After further adjusting for standard CV risk factors, baseline blood pressure, and severity of ECG LVH, ECG strain remained a significant predictor of CV mortality (HR 1.53, 95% CI 1.18 to 2.00), myocardial infarction (HR 1.55, 95% CI 1.16 to 2.06), and the composite CV end point (HR 1.33, 95% CI 1.11 to 1.59). Thus, ECG strain is a marker of increased CV risk in hypertensive patients in the setting of aggressive blood pressure lowering, independent of baseline severity of ECG LVH.

123 citations


Journal ArticleDOI
TL;DR: Analysis of recently reported and ongoing mega-trials of renin-angiotensin-aldosterone system inhibitors may support the notion that their vasculoprotective properties confer greater benefit by virtue of their effects beyond blood-pressure reduction.

63 citations


Journal ArticleDOI
TL;DR: It is hypothesized that insulin sensitivity and vagal cardiac control are independently related in young men after adjustment for fitness and other confounding variables and are related independently of physical fitness in youngMen.
Abstract: OBJECTIVES We hypothesized that insulin sensitivity and vagal cardiac control are independently related in young men after adjustment for fitness and other confounding variables. DESIGN Male volunteers aged 21-24 years with high (borderline hypertensive; n = 20) and low-normal (normotensive; n = 21) screening blood pressure (BP) were studied cross-sectionally. METHODS Mean R-R interval (RR) and heart rate variability (HRV) were computed from 30-min ECGs, and baroreflex sensitivity (BRS) and latency (phase shift) from 15-min beat-to-beat finger blood pressure (BP) and heart rate recordings. Insulin-adjusted glucose disposal rate (GDR/I) was measured with a 90-min hyperinsulinaemic glucose clamp and fitness by peak oxygen uptake (VO2peak) during a treadmill test. RESULTS HRV, baroreflex function, GDR/I, and VO2peak did not differ between the groups. GDR/I correlated positively with time and frequency domain HRV, including high-frequency power (HF) (r = 0.40, P = 0.01) and root-mean squared successive differences (RMSSD) (r = 0.43, P = 0.005), but not BRS or phase shift. GDR/I correlated with VO2peak (r = 0.70, P < 0.0001) and was explained (R = 0.56) by VO2peak (beta = 0.57, P < 0.0001) and RR (beta = 0.29, P = 0.03), independently of HRV and measures of obesity. Conversely, RR (beta = 0.55, P = 0.0004) and HRV, including HF (beta = 0.44, P = 0.006) and RMSSD (beta = 0.46, P = 0.004) were explained by GDR/I, independently of VO2peak. CONCLUSIONS Insulin sensitivity and autonomic cardiac control are related independently of physical fitness in young men.

Journal ArticleDOI
TL;DR: Plasma catecholamine responses are related to BP responses and carryover effects, and reflect perceived stress in young men, and are associated with impaired BP recovery after mental stress.
Abstract: We assessed plasma noradrenaline (NA) and adrenaline (A) at rest during a hyperinsulinaemic glucose clamp and responses to a mental arithmetic stress test (MST) in relation to blood pressure (BP) responses (Finapres) and distress in 20 men with high (> or =140/90 mmHg) and 21 men with normal ( or =6) than in the low-stress category, independently of BP status (p < 005) High screening BP is associated with impaired BP recovery after mental stress Plasma catecholamine responses are related to BP responses and carryover effects, and reflect perceived stress in young men

Journal ArticleDOI
TL;DR: Moderate alcohol consumption does not change the marked stroke risk reduction with losartan compared to atenolol in high-risk hypertensives, while the risk of stroke tends to increase with high intake.
Abstract: Alcohol consumption and cardiovascular risk in hypertensives with left ventricular hypertrophy : the LIFE study.

Journal ArticleDOI
TL;DR: It is suggested that adrenal medullary activation in borderline hypertension mainly characterizes lean subjects, but measures of overweight are independently related to lower plasma E and HR responses.

Journal ArticleDOI
TL;DR: It is shown that one single screening BP measurement predicts insulin resistance and elevated fasting glucose in this cohort and young healthy men with elevated screening BP are characterized by increased sympathetic activity and insulin resistance.
Abstract: The cardiovascular metabolic syndrome is characterized by the presence of several cardiovascular risk factors, including blood pressure (BP) elevation. We aimed to study the relation between mental stress, plasma catecholamines, BP and BP responses to mental stress in healthy young Caucasian men selected from different levels of screening BP. We included 98 men with high and 22 men with normal screening BP. They were examined at baseline in the laboratory, during a hyperinsulinemic, isoglycemic glucose clamp and during mental stress. At baseline in the laboratory, the men with high screening BP were characterized by elevated BP (p < 0.005) and plasma catecholamines (p < 0.05), but unaltered serum lipid levels compared to men with normal screening BP. After 2 h rest the differences almost disappeared, but could be reproduced during a mental arithmetic stress test. The men with elevated screening BP had significantly higher fasting glucose (p = 0.01) and lower insulin sensitivity (p < 0.005). In a multiple ...

Journal ArticleDOI
TL;DR: 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, and a borderline significant trend suggested decreasing benefit ofLosartan Vs atanolol for stroke prevention from never‐ to previous to current smoking status.
Abstract: 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.

Journal ArticleDOI
TL;DR: The largest randomized trial of antihypertensives ever, designed specifically to have sufficient power to examine cardiac outcome, concluded that thiazide-type diuretics are superior to newer drugs in preventing CVD.
Abstract: The clinical trial evidence, which established the cardiovascular protective effects of drug treatment for hypertension, comes mainly from studies with therapy based on thiazide diuretics [1]. However, prevention of cardiac events was lower than expected [2], perhaps as a consequence of the adverse metabolic effects of diuretics [3–7]. Beta-blockers, despite powerful evidence of cardioprotective properties [8], appear no better and may be inferior [9, 10]. Newer antihypertensives should avoid metabolic complications and might provide advantages beyond blood pressure reduction. Comparative outcome trials with angiotensin-converting enzyme (ACE) inhibitors [11, 12] and calcium-channel blockers [13, 14] have failed to demonstrate convincing advantages over diuretics. Individual trials were underpowered and hence uninformative. Even meta-analysis of the accumulated data could not exclude a clinically relevant difference in cause-specific outcomes including cardiac events [15]. A bigger trial was needed and ALLHAT offered the welcome prospect of a definitive comparison between diuretic-based therapy and treatment based on newer drugs [16]. ALLHAT (Antihypertensive and Lipid Lowering to prevent Heart Attack Trial), the largest randomized trial of antihypertensives ever, was designed specifically to have sufficient power to examine cardiac outcome (fatal and non-fatal myocardial infarction) as the primary endpoint. The trial randomized 42,418 patients, aged 55 years or older with mild to moderate hypertension and at least one additional cardiovascular risk factor, to doubleblind therapy based on chlorthalidone 12.5–25 mg daily (n = 15,255) or one of three other antihypertensive treatments: amlodipine 2.5–10 mg daily ( n = 9048), lisinopril 10–40 mg daily ( n = 9054) or doxazosin 1–8 mg daily (n = 9061). Add-on drugs were at the discretion of local investigators: atenolol, clonidine, reserpine and hydralazine (step 3). The alpha-blocker arm was stopped prematurely, leaving 33,357 participants who were followed up for a mean of 4.9 years on diuretic, calcium-channel blocker or ACE inhibitor. The primary outcome occurred in 2956 participants with no difference between the rates with the reference drug chlorthalidone (11.5%) and amlodipine (11.5%) or lisinopril (11.4%). Relative risks (RR) were 0.98 (95% CI 0.90–1.07) for amlodipine and 0.99 (95% CI 0.91–1.08) for lisinopril. The investigators pre-specified four secondary endpoints – all-cause mortality, fatal and non-fatal stroke, combined coronary heart disease (CHD) (primary outcome plus coronary revascularization or angina with hospitalization), and combined cardiovascular disease (CVD) (combined CHD plus stroke, treated angina without hospitalization, heart failure and peripheral arterial disease). All-cause mortality and combined CHD did not differ between the groups. However, lisinopril was associated with higher rates of combined CVD (RR 1.10, 95% CI 1.05–1.16) and stroke (RR 1.15, 95% CI 1.02–1.30). Heart failure was reported significantly more often in patients randomized to amlodipine (RR 1.38, 95% CI 1.25–1.52) and lisinopril (RR 1.19, 95% CI 1.07–1.31). The results were generally consistent across the range of pre-specified subgroups (according to age, gender, ethnicity and diabetes). The authors concluded that thiazide-type diuretics are superior to newer drugs in preventing CVD and are less expensive, and that these drugs should be the preferred first-line antihypertensive therapy. The findings from such a large trial are likely to be hugely influential but require careful critical scrutiny before changes in clinical practice are adopted. The ALLHAT results were achieved only at enormous cost. Was the price worthwhile? Size is not everything. A large sample size gives power but this is only relevant if participants continue on randomized therapy. The study report makes it very difficult to assess this critical information with certainty. By year 5, it appears that 28–39% of participants had discontinued randomized study drugs. Some 5–10% provided no drug data at year 5 and such individuals have a high probability of protocol deviation, suggesting that the true continuation with randomized therapy was 50–60%. In addition, 13–17% of randomized patients were taking a comparator drug and a further 7–9% were taking a comparator drug without

Journal Article
TL;DR: Echocardiography can reveal subclinical heart disease as well as serve as a guide to correct diagnosis and treatment in hypertensives.
Abstract: Hypertension commonly leads to heart disease, in particular left ventricular hypertrophy, heart failure and coronary artery disease. Left ventricular hypertrophy and coronary artery disease are both often subclinical diseases in hypertensives. Symptomatic coronary artery disease in hypertension may be due to atherosclerosis in epicardial arteries, microvascular dysfunction, reduced fibrinolytic capacity, or left ventricular hypertrophy; the latter is present in 20-50% of patients with mild to moderate and in up to 90% of patients with severe hypertension. Left ventricular hypertrophy in hypertension is associated with a twofold increase in risk of myocardial infarction, sudden death and stroke, and a fourfold increase in risk of heart failure. While coronary artery disease is the most common cause of heart failure in men, hypertension and in particular untreated isolated systolic hypertension is the most common cause in women. Heart failure symptoms may be subtle in hypertension, like tiredness or reduced physical capacity. Echocardiography can reveal subclinical heart disease as well as serve as a guide to correct diagnosis and treatment.


Journal ArticleDOI
TL;DR: 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, and a borderline significant trend suggested decreasing benefit ofLosartan Vs atanolol for stroke prevention from never- to previous to current smoking status.

Journal ArticleDOI
TL;DR: Losartan had an effect on plasma catecholamines comparable to that with the beta-blocker atenolol in patients with hypertension and left ventricular hypertrophy at rest and during hyperinsulinaemia, finding it unlikely that a difference in sympathetic activity explains the outcome benefits of losartan over atenorol in the LIFE study.
Abstract: Hypertension is a major risk factor for morbidity and mortality. Plasma catecholamines are linked to the pathogenesis of hypertension. Pharmacological intervention, including treatment with beta-blockers, reduces cardiovascular mortality and morbidity. In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, the angiotensin receptor blocker losartan significantly reduced cardiovascular end points compared to the beta-blocker atenolol. Thus, for the first time, one drug was shown to be superior to another in hypertension. The present substudy examined the effects of atenolol vs losartan treatment on plasma catecholamines at rest and during hyperinsulinaemia in a cohort of 86 LIFE patients. Plasma adrenaline increased significantly from placebo treatment at baseline to year 1 of treatment (P<0.0001), and also during hyperinsulinaemia (P<0.0001). Plasma noradrenaline did not change significantly from placebo treatment at baseline to year 1, but increased significantly during hyperinsulinaemia both at baseline and at year 1 (P<0.0001 for both). There were no differences in plasma catecholamines or the relative changes between the two treatment arms at any stage. In a subset of 42 patients examined also at years 2 and 3, these findings were confirmed during long-term treatment. Thus, losartan had an effect on plasma catecholamines comparable to that with the beta-blocker atenolol in patients with hypertension and left ventricular hypertrophy at rest and during hyperinsulinaemia. We find it unlikely that a difference in sympathetic activity explains the outcome benefits of losartan over atenolol in the LIFE study.

Journal ArticleDOI
TL;DR: Abstract P-406 Key Words: Left Bundle Branch Block, Hypertensive, left Ventricle Hypertrophy, Left Ventricled Hypertension, and Left Bundles Branch Block are studied.

Journal ArticleDOI
TL;DR: Nt-proBNP, more than Nt- ProANP, strongly predicts cardiovascular events in patients with hypertension and LV hypertrophy, especially in patients without diabetes or clinically overt cardiovascular disease.


Journal Article
TL;DR: Treatment with 10 mg atorvastatin o.d. in hypertensive patients at moderate risk gives a significant risk reduction of coronary heart disease, independent of baseline level of total cholesterol.
Abstract: Background The majority of cardiovascular events and deaths attributable to both raised blood pressure and dyslipidaemia occur in subjects with relatively "normal" blood pressure and lipid levels respectively. The study was designed to evaluate the potential benefits of cholesterol lowering in the primary prevention of coronary heart disease in hypertensive subjects with average and below average levels of serum cholesterol. Material and methods Out of 19 342 hypertensive subjects (aged 40-79) who were initially randomized to one of two antihypertensive treatment strategies in the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT), 10 305 subjects with total cholesterol levels Results The lipid arm of the study was prematurely stopped after a median follow-up period of 3.3 years. One hundred events occurred in those randomized to atorvastatin compared to 154 events in those receiving placebo, a 36 % relative risk reduction (p = 0.0005) in the primary endpoint. Among secondary and tertiary endpoints, stroke was reduced with 27% (p = 0.02). There was a non-significant 13% reduction in total mortality. Non-cardiovascular mortality was similar in the two treatment limbs of the trial. After three years of follow-up, atorvastatin lowered total serum cholesterol by 1.1 mmol/L compared with placebo. Interpretation Treatment with 10 mg atorvastatin o.d. in hypertensive patients at moderate risk gives a significant risk reduction of coronary heart disease, independent of baseline level of total cholesterol.


Journal Article
TL;DR: Losartan prevented more cardiovascular complications than atenolol for the same reduction in blood pressure and have positive additional effects beyond blood pressure control in patients with hypertension and left ventricular hypertrophy.
Abstract: BACKGROUND: The LIFE study (Losartan Intervention For Endpoint reduction in hypertension) is a randomized, double-blind comparison of losartan and atenolol-based treatment. The study hypothesis was that losartan would reduce cardiovascular morbidity and mortality more than traditional antihypertensive treatment with atenolol. MATERIAL AND METHODS: The study included 9193 patients in seven countries. RESULTS: By the end of the study, the mean dose was losartan 82 mg and atenonol 79 mg, whereas 94% of patients in both groups received additional hydrochlorothiazide. Blood pressure was reduced 30/17 mmHg by losartan and 29/17 mm Hg by atenolol. Despite the same reduction in blood pressure, the primary combined endpoint (cardiovascular mortality, non-fatal stroke and myocardial infarction) was reduced by 13.0% (p = 0.021) in the losartan group. Non-fatal and fatal strokes were reduced by 24.9% (p = 0.001). In two pre-specified subgroup analyses, cardiovascular mortality was reduced by 46% (p = 0.01) in patients with isolated systolic hypertension (n = 1326), and total mortality was reduced by 39% (p = 0.002) in patients with diabetes (n = 1159). INTERPRETATION: Losartan prevented more cardiovascular complications than atenolol for the same reduction in blood pressure and have positive additional effects beyond blood pressure control in patients with hypertension and left ventricular hypertrophy.

01 Jan 2004
TL;DR: The VALUE trial was designed to test the hypothesis that for the same degree of blood pressure lowering, the angiotensin receptor blocker, valsartan, would reduce cardiac morbidity and mortality more than the calcium channel blocker, amlodipine, in highrisk hypertensive patients.
Abstract: Several classes of antihypertensive agents have been shown to reduce cardiovascular morbidity and mortality in the high-risk hypertensive population, however, large hypertension trials have yet to demonstrate significant differences between treatments. The question that remains to be answered is ‐ do the different mechanisms of action of the antihypertensive drugs possess different cardiovascular protective properties beyond blood pressure lowering? The Valsartan Antihypertensive Long-term Use Evaluation (VALUE) trial was designed to test the hypothesis that for the same degree of blood pressure (BP) lowering, the angiotensin receptor blocker (ARB), valsartan, would reduce cardiac morbidity and mortality more than the calcium channel blocker, amlodipine, in highrisk hypertensive patients. The majority of enrolled patients were previously on antihypertensive therapy and were directly rolled over to randomized therapy consisting of a gradual up-titration of valsartan or amlodipine, with the addition of diuretics to achieve target BP. The late-breaking results of VALUE, as well as the clinical implications of the results, are the subject of this Cardiology Scientific Update.

Journal ArticleDOI
TL;DR: Recent data from a large-scale follow-up study of apparently healthy subjects indicate that three repeated measurements of urinary albumin–creatinine ratio are superior to predict all-cause mortality compared to one or two measurements, and current European guidelines recommend that erum creat inine, preferably with estimation of creatinine clearance, and serum urea be assessed, and urinaryalbumin excretion be measured in all hypertensive patients.
Abstract: The diagnosis of hypertension-induced renal damage is based on elevated serum creatinine, decreased creatinine clearance or elevated urinary excretion of albumin according to the 2003 Guidelines of the European Society of Hypertension and the European Society of Cardiology [1]. Thus, slight elevation of serum creatinine concentration (107–133 mol/l) is taken as sign of target organ damage. According to the same guidelines, the presence of mild renal insufficiency, defined as serum creatinine 133 mol/l (1.5 mg/dl) in men and 124 mol/l (1.4 mg/dl) in women [2, 3] or by estimated creatinine clearance values below 60–70 ml/min [4], is classified as an associated clinical condition, i.e. a very high added risk in the high normal or hypertensive blood pressure range. Increased urinary albumin excretion is a sign of a derangement in the glomerular filtration barrier [5]. Microalbuminuria [usually defined as albumin concentration 20 mg/l or albumin–creatinine ratio 2.5 mg/mmol (in men) or 3.5 mg/mmol (in women)] predicts development of overt diabetic nephropathy in subjects with type 1 as well as type 2 diabetes [6], while the presence of proteinuria or albuminuria indicate the existence of established renal parenchymatous disease [7]. Microalbuminuria and in particular overt albuminuria is associated with significant increase in cardiovascular risk [8]. In non-diabetic hypertensive patients, microalbuminuria predicts cardiovascular events, even below the threshold values currently considered pathological [9]. There is a continuous relationship between urinary albumin excretion and cardiovascular as well as noncardiovascular mortality in the general population [10]. Recent data from a large-scale follow-up study of apparently healthy subjects indicate that three repeated measurements of urinary albumin–creatinine ratio are superior to predict all-cause mortality compared to one or two measurements [11]. Such a procedure lowers the albumin–creatinine ratio cut-off level to the 60th percentile ( 0.76 mg/mmol or 6.7 g/mg) allowing improved outcome prediction [11]. The finding of an impaired renal function in a hypertensive patient, i.e. elevated serum creatinine, reduced creatinine clearance or microalbuminuria, is commonly encountered in clinical practice and constitutes a potent predictor of future cardiovascular events or death [4, 12]. Current European guidelines therefore recommend that erum creatinine, preferably with estimation of creatinine clearance, and serum urea be assessed, and urinary albumin excretion be measured in all hypertensive patients [1]. This issue of Blood Pressure contains interesting papers in this respect. Firstly, the short review by Leoo & Odar-Cederlo ̈f [13] review the importance of repeated testing for microalbuminuria in patients with diabetes [13]. The goal of treatment is to reduce urinary output of albumin as well as blood pressure. Thus, urinary albumin excretion needs to be assessed regularly as does blood pressure, in order to ensure that the therapeutic measures are effective [13]. Secondly, Reims and co-workers report from the LIFE Study [14] that hypertensive patients with left ventricular hypertrophy who smoke have higher urinary albumin excretion and serum creatinine than nonsmokers, while previous smokers have an intermediate urinary albumin excretion and serum creatinine level. Increased albumin excretion was an important predictor of cardiovascular endpoints in the LIFE study patients [15] and both elevated urinary albumin excretion and increased serum creatinine may contribute to the increased risk imposed by smoking [14]. Thirdly, Sørensen and co-workers [16] report from a Danish study of 115 hypertensive smokers and 230 hypertensive non-smokers, carefully matched for clinic blood pressure, age and gender, that smokers have higher ambulatory systolic blood pressure and urinary albumin–creatinine ratio. The authors suggest that the higher daytime blood pressure as well as microalbuminuria in smokers may contribute to their increased cardiovascular risk [16]. The overall picture, thus, is that urinary albumin excretion, a measure of altered glomerular barrier and indicative of increased risk of cardiovascular disease and mortality, should be assessed in all hypertensives. This is particularly relevant in patients with diabetes and in smokers. Furthermore, threshold levels of urinary albumin excretion associated with increased risk need to be established, and randomized clinical trials are warranted to determine whether lowering of albumin excretion confers reduced cardiovascular risk.