Showing papers by "Sverre E. Kjeldsen published in 2005"
TL;DR: The amlodipine-based regimen prevented more major cardiovascular events and induced less diabetes than the atenolol- based regimen, and these effects might not be entirely explained by better control of blood pressure.
2,595 citations
TL;DR: The novel finding is that new-onset AF and associated stroke were significantly reduced by losartan- compared to atenolol-based antihypertensive treatment with similar blood pressure reduction.
791 citations
University of Copenhagen1, Novo Nordisk2, Umeå University3, Aarhus University4, University of Gothenburg5, Cornell University6, Karolinska Institutet7, University of Helsinki8, University of Michigan9, University of Oslo10, University of Bergen11, University of Alabama at Birmingham12, Merck & Co.13
TL;DR: Monitoring of albuminuria should be an integrated part of the management of hypertension if it is not decreased by the patient’s current antihypertensive and other treatment, and further intervention directed toward blood pressure control and other modifiable risks should be considered.
Abstract: Few data are available to clarify whether changes in albuminuria over time translate to changes in cardiovascular risk. The aim of the present study was to examine whether changes in albuminuria during 4.8 years of antihypertensive treatment were related to changes in risk in 8206 patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. Urinary albumin/creatinine ratio (UACR) was measured at baseline and annually. Time-varying albuminuria was closely related to risk for the primary composite end point (ie, when UACR decreased during treatment, risk was reduced accordingly). When the population was divided according to median baseline value (1.21 mg/mmol) and median year 1 UACR (0.67 mg/mmol), risk increased stepwise and significantly for the primary composite end point from those with low baseline/low year 1 (5.5%), to low baseline/high year 1 (8.6%), to high baseline/low year 1 (9.4%), and to high baseline/high year 1 (13.5%) values. Similar significant, stepwise increases in risk were seen for the components of the primary composite end point (cardiovascular mortality, stroke, and myocardial infarction). The observation that changes in UACR during antihypertensive treatment over time translated to changes in risk for cardiovascular morbidity and mortality was not explained by in-treatment level of blood pressure. We propose that monitoring of albuminuria should be an integrated part of the management of hypertension. If albuminuria is not decreased by the patient's current antihypertensive and other treatment, further intervention directed toward blood pressure control and other modifiable risks should be considered.
579 citations
TL;DR: Atorvastatin significantly reduced the risk of major cardiovascular events and procedures among diabetic patients with well-controlled hypertension and without a history of CHD or markedly elevated cholesterol concentrations.
Abstract: OBJECTIVE — This study aims to establish the benefits of lowering cholesterol in diabetic patients with well-controlled hypertension and average/below-average cholesterol concentrations, but without established coronary disease. RESEARCH DESIGN AND METHODS — In the lipid-lowering arm of the AngloScandinavian Cardiac Outcomes Trial (ASCOT-LLA), 10,305 hypertensive patients with no history of coronary heart disease (CHD) but at least three cardiovascular risk factors were randomly assigned to receive 10 mg atorvastatin or placebo. Effects on total cardiovascular outcomes in 2,532 patients who had type 2 diabetes at randomization were compared. RESULTS — During a median follow-up of 3.3 years, concentrations of total and LDL cholesterol among diabetic participants included in ASCOT-LLA were 1 mmol/l lower in those allocated atorvastatin compared with placebo. There were 116 (9.2%) major cardiovascular events or procedures in the atorvastatin group and 151 (11.9%) events in the placebo group (hazard ratio 0.77, 95% CI 0.61– 0.98; P 0.036). For the individual components of this composite end point, the number of events occurring in the diabetes subgroup was small. Therefore, although fewer coronary events (0.84, 0.55–1.29;P 0.14) and strokes (0.67, 0.41–1.09; P 0.66) were observed among the patients allocated atorvastatin, these reductions were not statistically significant. CONCLUSIONS — Atorvastatin significantly reduced the risk of major cardiovascular events and procedures among diabetic patients with well-controlled hypertension and without a history of CHD or markedly elevated cholesterol concentrations. The proportional reduction in risk was similar to that among participants who did not have diagnosed diabetes. Allocation to atorvastatin prevented9 diabetic participants from suffering a first major cardiovascular event or procedure for every 1,000 treated for 1 year. Diabetes Care 28:1151–1157, 2005
365 citations
TL;DR: Serial mean matching for differences in systolic blood-pressure attenuated HRs for coronary and stroke events to a similar extent as did adjustments for systols in Cox-regression analyses, which noted no temporal link between size of differences in blood pressure and different event rates.
324 citations
TL;DR: Losartan is more effective than atenolol-based therapy in reducing the risk of the primary composite end point of cardiovascular morbidity and mortality as well as stroke and cardiovascular death in hypertensive patients with ECG LV hypertrophy and AF.
248 citations
TL;DR: ECG strain identifies hypertensive patients at increased risk of developing CHF and dying as a result of CHF, even in the setting of aggressive blood pressure lowering.
Abstract: Background— The ECG strain pattern of ST depression and T-wave inversion is strongly associated with left ventricular hypertrophy (LVH) independently of coronary heart disease and with an increased risk of cardiovascular morbidity and mortality in hypertensive patients. However, whether ECG strain is an independent predictor of new-onset congestive heart failure (CHF) in the setting of aggressive antihypertensive therapy in unclear. Methods and Results— The relationship of ECG strain at study baseline to the development of CHF was examined in 8696 patients with no history of CHF who were enrolled in the Losartan Intervention for Endpoint Reduction in Hypertension (LIFE) study. All patients had ECG LVH by Cornell product and/or Sokolow-Lyon voltage criteria on a screening ECG, were treated in a blinded manner with atenolol- or losartan-based regimens, and were followed up for a mean of 4.7±1.1 years. Strain was defined as a downsloping convex ST segment with inverted asymmetrical T-wave opposite the QRS ax...
101 citations
101 citations
TL;DR: Substantial cerebrovascular benefit could be realized with the institution of losartan-based therapy over conventional therapy among hypertensive patients with left ventricular hypertrophy across the spectrum of cardiovascular risk.
Abstract: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study showed that treatment with the angiotensin II type-1 receptor antagonist losartan reduces overall stroke risk compared with conventional therapy with the beta-blocker atenolol. We conducted secondary analyses in LIFE to determine the extent to which the cerebrovascular benefits of losartan apply to different clinical subgroups and stroke subtypes and to assess the dependence of these benefits on baseline and time-varying covariates. Among 9193 hypertensive patients with electrocardiographic evidence of left ventricular hypertrophy, random allocation to losartan-based treatment lowered the risk of fatal (hazard ratio [HR], 0.65; 95% confidence interval [CI], 0.43 to 0.96; P=0.032) and atherothrombotic stroke (HR, 0.72; 95% CI, 0.59 to 0.88; P=0.001) compared with atenolol-based therapy. Although comparable risk reductions occurred for hemorrhagic and embolic stroke, these were not statistically significant. The number of neurological deficits per stroke was similar, but there were fewer strokes in the losartan group for nearly every level of stroke severity. Effects were consistent in all clinical subgroups except for those defined by age and ethnicity. The benefits of losartan on all strokes were independent of baseline and time-varying risk factors, including blood pressure. The number needed to treat for 5 years to prevent 1 stroke was 54 for the average participant, declining to 25, 24, and 9 for patients with cerebrovascular disease, isolated systolic hypertension, and atrial fibrillation, respectively. In conclusion, substantial cerebrovascular benefit could be realized with the institution of losartan-based therapy over conventional therapy among hypertensive patients with left ventricular hypertrophy across the spectrum of cardiovascular risk.
99 citations
TL;DR: It is demonstrated that smoking-related increase in brachial-ankle pulse wave was evident even when blood pressure returned to baseline values, and the acute increase in arterial stiffness in chronic smokers was surprisingly greater than that in non-smokers.
Abstract: (2005). Is smoking a causative factor of hypertension? Blood Pressure: Vol. 14, No. 2, pp. 69-71.
63 citations
TL;DR: Losartan treatment was associated with less peripheral vascular hypertrophy/rarefaction and higher insulin sensitivity, supporting the hypothesis that peripheral vascular changes in hypertension may induce insulin resistance.
Abstract: ObjectiveHypertension and insulin resistance might be associated through peripheral vascular hypertrophy/rarefaction which compromises skeletal muscle blood flow and decreases glucose uptake, inducing insulin resistance. We hypothesized that treatment with losartan as compared to atenolol would impr
TL;DR: Fixed combination ARB/hydrochlorothiazide agents make sense as initial therapy for patients in whom BP is >20/ 10mm Hg above goal and outcome trials in patients with hypertension are reviewed.
Abstract: We discuss combination therapy with angiotensin receptor antagonists (angiotensin receptor blockers; ARBs) and thiazide diuretics in light of the independent actions of both types of agents, and the adverse effects of both agents independently and in the context of the physiologic synergy achieved in using these agents together. ARBs counteract many of the adverse events associated with the use of thiazide diuretics and have been shown to reduce the occurrence of new-onset diabetes mellitus. We also review outcome trials in patients with hypertension (such as LIFE [Losartan Intervention For Endpoint reduction in hypertension], VALUE [Valsartan Antihypertensive Long-term Use Evaluation], and SCOPE [Study on COgnition and Prognosis in the Elderly]), in which losartan, valsartan, and candesartan cilexetil were used in combination with hydrochlorothiazide. Fixed combination ARB/hydrochlorothiazide agents make sense as initial therapy for patients in whom BP is >20/ 10mm Hg above goal.
University of Copenhagen1, Cornell University2, University of Naples Federico II3, Merck & Co.4, University of Gothenburg5, Karolinska Institutet6, University of Helsinki7, University of Michigan8, University of Oslo9, Aarhus University10, Umeå University11, University of Bergen12, University of Alabama13
TL;DR: Body build and risk of cardiovascular events in hypertension and left ventricular hypertrophy: the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study as mentioned in this paper, which was conducted in the UK.
Abstract: Body build and risk of cardiovascular events in hypertension and left ventricular hypertrophy : the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study.
TL;DR: Data suggest that losartan‐based treatment is more effective than an atenolol‐ based treatment for patients with ISH and a high risk for stroke.
Abstract: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study reported that a losartan-based antihypertensive regimen reduced cardiovascular morbidity and mortality (composite of cardiovascular death, stroke, and myocardial infarction) more than therapy based on atenolol in patients with left ventricular hypertrophy and isolated systolic hypertension (ISH). Patients aged 55-80 years with blood pressures 160-200/<90 mm Hg were followed for a mean of 4.7 years. Blood pressure was similarly reduced in the losartan (n=660) and atenolol (n=666) ISH groups. There were 88 (6.6%) patients who experienced a stroke, 18 of which were fatal. Of patients experiencing strokes, 72.7% had an ischemic stroke. ISH patients in LIFE compared to the non-ISH group had a higher incidence of any stroke and embolic stroke, and similar incidences of fatal, atherosclerotic, and hemorrhagic/other strokes. The incidence of any stroke (40% risk reduction [RR], p=0.02), fatal stroke (70% RR, p=0.035), and atherothrombotic stroke (45% RR, p=0.022) was significantly lower in losartan-treated compared to the atenolol-treated patients. The 36% RR for embolic strokes in the losartan group was not statistically significantly (p=0.33) different from the atenolol group. These data suggest that losartan-based treatment is more effective than an atenolol-based treatment for patients with ISH and a high risk for stroke.
TL;DR: In patients with hypertension and left ventricular hypertrophy in the LIFE study, there were significantly higher risks, adjusted for the Framingham risk score, for the primary composite end point, stroke, and total mortality in the highest versus lowest quartile of pulse pressure with atenolol-based treatment.
Abstract: In the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, the primary composite end point of cardiovascular death, stroke, and myocardial infarction was reduced by losartan versus atenolol in patients with hypertension and left ventricular hypertrophy. The objective of this post hoc analysis was to determine the influence of pulse pressure on outcome. Patients were divided into quartiles of baseline pulse pressure. Cox regression, including baseline Framingham risk score as a covariate, was used to compare risk in the quartiles. In the atenolol group, there were significantly higher risks in the highest versus lowest quartile for the composite end point 28% (confidence interval [CI], 2% to 62%; P=0.035), stroke 84% (CI, 32% to 157%; P 0.2), stroke -5% (CI, -34% to 37%; P>0.2), myocardial infarction 30% (CI, -13% to 94%; P>0.2), and total mortality 32% (CI, -1% to 76%; P=0.062). In patients with hypertension and left ventricular hypertrophy in the LIFE study, there were significantly higher risks, adjusted for the Framingham risk score, for the primary composite end point, stroke, and total mortality in the highest versus lowest quartile of pulse pressure with atenolol-based treatment. The risks in the losartan group also increased with increasing pulse pressure quartile, but were lower than those in the atenolol group, and were not significant.
TL;DR: Collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.
Abstract: Cardiac fibrosis and high levels of circulating collagen markers has been associated with left ventricular (LV) hypertrophy. However, the relationship to vascular hypertrophy and blood pressure (BP) load is unclear. In 204 patients with essential hypertension and electrocardiographic LV hypertrophy, we measured sitting BP, serum collagen type I carboxy-terminal telopeptide (ICTP) reflecting degradation, procollagen type I carboxy-terminal propeptide (PICP) reflecting synthesis and LV mass by echocardiography after 2 weeks of placebo treatment and after 1 year of antihypertensive treatment with a losartan- or an atenolol-based regimen. Furthermore, we measured intima–media thickness of the common carotid arteries (IMT), minimal forearm vascular resistance (MFVR) by plethysmography and ambulatory 24-h BP in around half of the patients. At baseline, PICP/ICTP was positively related to IMT (r=0.24, P<0.05), MFVRmen (r=0.35, P<0.01), 24-h systolic BP (r=0.24, P<0.05) and 24-h diastolic BP (r=0.22, P<0.05), but not to LV mass. After 1 year of treatment with reduction in systolic BP (175±15 vs 151±17 mmHg, P<0.001) and diastolic BP (99±8 vs 88±9 mmHg, P<0.001), ICTP was unchanged (3.7±1.4 vs 3.8±1.4 μg/l, NS) while PICP (121±39 vs 102±29 μg/l, P<0.001) decreased. The reduction in PICP/ICTP was related to the reduction in sitting diastolic BP (r=0.31, P<0.01) and regression of IMT (r=0.37, P<0.05) in patients receiving atenolol and to reduction in heart rate in patients receiving losartan (r=0.30, P<0.01). In conclusion, collagen markers reflecting net synthesis of type I collagen were positively related to vascular hypertrophy and BP load, suggesting that collagen synthesis in the vascular wall is increased in relation to high haemodynamic load in a reversible manner.
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01 Jan 2005
TL;DR: It is hypothesized that losartan was superior to atenolol in reducing cardiovascular events in a lower-risk group (LRG) versus a higher- risk group (HRG) of patients in a Losartan Intervention For Endpoint reduction (LIFE) substudy, independently of blood pressure (BP) reduction.
Abstract: We hypothesized that losartan was superior to atenolol in reducing cardiovascular events in a lower-risk group (LRG) versus a higher-risk group (HRG) of patients in a Losartan Intervention For Endpoint reduction (LIFE) substudy, independently of blood pressure (BP) reduction. In a post hoc analysis, we designated 4282 patients as LRG on the basis of: (1) no previous cardiovascular disease (coronary, cerebral, peripheral vascular disease); (2) no diabetes; (3) no isolated systolic hypertension; and (4) inclusion of the lowest 3 quartiles of electrocardiographically documented left ventricular hypertrophy. The HRG consisted of 4911 remaining patients who did not qualify for the LRG. In the LRG, losartan was superior to atenolol in reducing stroke: hazard ratio (HR), 0.72 (95% confidence interval [CI], 0.53 to 0.98); new-onset diabetes (HR, 0.74 [95% CI, 0.58 to 0.93]; and new-onset atrial fibrillation: HR, 0.69 (95% CI, 0.51 to 0.92), all P<0.05 but not composite end points or cardiovascular mortality (both P=NS). In the HRG, losartan was superior to atenolol in reducing composite end points: HR, 0.82 (95% CI, 0.71 to 0.94), P<0.01; cardiovascular mortality: HR, 0.77 (95% CI, 0.62 to 0.95), P<0.05; stroke: HR, 0.75 (95% CI, 0.61 to 0.92), P<0.01; new-onset diabetes: HR, 0.76 (95% CI, 0.60 to 0.96), P<0.05; and new-onset atrial fibrillation: HR, 0.71 (95% CI, 0.58 to 88), P<0.05. Test for interaction of treatment with LRG versus HRG was not significant for composite end point, stroke, or atrial fibrillation, but was for cardiovascular mortality (P=0.018). Achieved systolic BP reduction favored losartan over atenolol by -1.8 mm Hg in LRG (P=NS) and -0.7 mm Hg (P=0.001) in HRG, but no significant differences occurred in diastolic or mean BP in either group. In conclusion, losartan compared with atenolol reduces the risk of stroke, new-onset diabetes, and new-onset atrial fibrillation in the LRG and the HRG.
TL;DR: There was a statistical interaction between treatment and aspirin in the LIFE study, with significantly greater reductions for the CEP and MI with losartan in patients using aspirin than in patients not using aspirin at baseline.
TL;DR: In patients following an acute myocardial infarction, no difference in either global or regional LVEF was observed between baseline and 12 months when treatment with carvedilol was compared with atenolol.
Abstract: Background: β-Blockers have been found to reduce mortality and morbidity in postmyocardial infarction patients. However, it is not fully understood whether all β-blockers have simil
TL;DR: The haemorheological effect of mental stress is increased in young men with high screening BP and may be mediated by the acute increase in BP.
Abstract: We studied effects of mental stress on whole-blood viscosity (WBV) and blood pressure (BP), and relations between WBV and autonomic nervous system activity and insulin sensitivity. We measured WBV (rotational rheometer), plasma noradrenaline (NA), finger BP, heart rate variability (HRV) and baroreflex sensitivity (BRS; transfer technique) during hyperinsulinaemic glucose clamp and mental arithmetic stress test (MST) in 20 men with high ( > or =140/90 mmHg) and 21 men with normal (< or =115/75 mmHg) screening BP, and 10 women regardless of screening BP (all normotensive). WBV and NA increased during the MST, while HRV and BRS decreased. During the MST, WBV (all shear rates) and the response ((delta)WBV) (low shear) were higher in men with high compared to normal screening BP (p<0.05). In men, WBV correlated positively with NA and negatively with HRV, BRS and insulin sensitivity. The diastolic BP response ((delta)DBP) was independently explained by high-shear (delta)WBV (p<0.05) and (delta)NA (p<0.0001), and (delta)WBV independently by (delta)DBP (p<0.05). WBV is related to increased sympathetic activity, impaired vagal cardiac control and low insulin sensitivity in young adults. The haemorheological effect of mental stress is increased in young men with high screening BP and may be mediated by the acute increase in BP.
TL;DR: Losartan is more effective than atenolol-based therapy in reducing the risk of the primary composite end point of cardiovascular morbidity and mortality as well as stroke and cardiovascular death in hypertensive patients with ECG LV hypertrophy and AF.
TL;DR: Increased adrenaline secretion may be related to high BP, but may at the same time be associated with a beneficial metabolic profile, as determined by Amst in multiple regression models.
Abstract: We studied plasma adrenaline (A) in relation to physical fitness, metabolic cardiovascular risk factors and cardiovascular responses. Men (age 21–24 years) with high and normal (both n = 19) screening blood pressure (BP) were studied cross‐sectionally. We measured peak oxygen uptake (VO2peak) (treadmill exercise), and plasma catecholamines, heart rate (HR), finger systolic (SBP) and diastolic (DBP) BP, and insulin‐adjusted glucose disposal rate (GDR/I) during a hyperinsulinaemic glucose clamp (rest) and mental arithmetic stress test (MST). By multiple regression, A at rest (Arest) (β = 0.37, p<0.05) and during MST (Amst) (β = 0.40, p<0.01) were associated with high screening BP. In the respective models, Arest was negatively related to body mass index (BMI) (β = −0.56, p<0.001) and Amst positively to VO2peak (β = 0.54, p<0.001). BP and HR responses correlated positively with VO2peak, but were determined by Amst in multiple regression models. Independently of BMI and VO2peak, serum high‐density lipoprotein...
TL;DR: Use of ARBs alone or in combination with other classes of antihypertensive agents to lower blood pressure and/or medications to control other conditions reduces risk of cardiovascular disease outcomes and Type 2 diabetes with excellent tolerability.
Abstract: Targeting the renin-angiotensin system for the reduction of cardiovascular outcomes in hypertension : angiotensin-converting enzyme inhibitors and angiotensin receptor blockers.
TL;DR: The increasing prevalence of hypertension worldwide will put further strain on the present cardiovascular pandemic, and prevention, detection, treatment and control of hypertension play an even more crucial role in future protection of cardiovascular disease.
Abstract: Current estimates [1] reveal that more than a quarter of the adult world population has hypertension. An approximate one billion of people with diagnosed and undiagnosed hypertension is estimated t...
TL;DR: The growing prevalence of hypertension, diabetes and hyperlipidemia will further extend cardiovascular pandemic, and recent estimates indicate that the metabolic syndrome will become a greater population burden in developing countries compared to developed ones.
Abstract: Worldwide estimates (1) reveal that more than 25% of the adult population has diagnosed or undiagnosed hypertension. The current approximate of one billion hypertensive males and females in the world is estimated to increase to more than 1.5 billion by 2025. The growing prevalence of hypertension, diabetes and hyperlipidemia will further extend cardiovascular pandemic, and recent estimates (1) indicate that the metabolic syndrome will become a greater population burden in developing countries compared to developed ones. Moreover, in the hypertensive patient population from the developing countries, the onset of cardiovascular disease is also predicted to occur at an earlier age (2). Over the past century, cardiovascular disease and stroke has changed from a being a minor cause of global death and disability to become one of the major contributors to the global burden of disease and disability (3–7). Today, cardiovascular diseases account for 30% of all worldwide deaths because there is an ongoing epidemiological transition manifested as a decline in communicable disease and an increase in non-communicable disease. Owing to the cardiovascular complications of stroke and myocardial infarction, the current estimated hypertension-attributable mortality of almost 3 million deaths worldwide (5.8% of total deaths), represents more than 17.5 million years of life lost (YLLs). Moreover, there is an estimated more than 19 million disability adjusted life years (DALYs) (1) related to non-fatal cardiovascular disease. Hypertension is one of the three leading causes of visits to primary healthcare physicians in most Western European countries (8), where the average of all-cause annual consultation per person reaches 6.1 (9). In fact, individuals with hypertension and hypertension-related morbidity use medical services approximately 50% more than normotensive persons (10). Most of the hypertension-related medical risks and the corresponding economic cost estimates are very conservative, since they are based only on the costs of hypertension care and do not incorporate the substantial costs of treating hypertension-related complications. When analyzing the cost of a disease, two main categories of costs are considered: direct and indirect costs. Direct costs usually involve the screening, diagnosis and lifelong management costs (clinic visits, laboratory tests, acquisition of drugs, adverse effects of medications, and transport/time), as well as reduced future healthcare costs and increased healthcare costs due to longer life expectation (the last two categories are controversial). Indirect costs on the other hand mainly include the costs of morbidity/disability and mortality (11). Currently, direct costs represent around 50 to 70% of the total cost of hypertension. In the USA in 1995 they were estimated at $US 18.7 billion (12), in Sweden in 1991 these costs were estimated at $US425 per person (13) and in New Zealand in 1988 direct costs amounted to $NZ430 per person (14). Indirect costs are much more difficult to estimate and currently there is no agreement between experts on whether or not they should be incorporated into the economic analysis (11,15). Murray & López (16) calculated that hypertension accounts for 17.6 million YLLs worldwide (1.9% of total YLLs), 1.4 million years lived with disability (YLDs; 0.3 % of total YLDs) and 19 million DALYs (1.4% of total DALYs). Drug treatment accounts for 60–70% of the direct costs of hypertension (17,18), mostly because of the number of people receiving treatment for hypertension and inflation of antihypertensive drug prices. Then, are the resources spent related to the direct costs spent wisely by society and individuals? Whether a particular treatment is cost effective depend on the answers to the following questions (19): (i) is the treatment effective, (ii) how much does the treatment cost, and (iii) do the benefits compare with the costs? Relating to the first point, there should today be no doubt that the treatment of hypertension is highly effective based on the evidence from major mortality/morbidity outcome trials. In short, data from different therapeutic trials (20) demonstrates that a reduction in cardiovascular morbidity and mortality with antihypertensive treatment occurs in malignant hypertension, but also in severe hypertension, mildto-moderate hypertension, hypertension in patients Blood Pressure. 2005; 14: 131–132
TL;DR: Clinical trials in elderly patients show good efficacy and high responder rates with the same doses as in younger patients of valsartan, and the tolerability profile is similar to placebo.
Abstract: Valsartan is a widely used, efficacious and very well-tolerated antihypertensive agent. By specifically blocking the action of angiotensin II on the angiotensin Type 1 receptor, valsartan reduces unwanted effects of angiotensin II, such as aldosterone, vasopressin and endothelin secretion, vasoconstriction, diuresis, endothelial cell hyperplasia, mitogenesis, induction of growth factors and production of collagen. Valsartan has a simple pharmacokinetic profile and requires no metabolism to become active. The dose-related efficacy of valsartan has been clearly demonstrated and the tolerability profile is similar to placebo. Clinical trials in elderly patients show good efficacy and high responder rates with the same doses as in younger patients. Valsartan is available as 80-, 160- and 320-mg tablets, and also in the same doses in combination with hydrochlorothiazide, 12.5 or 25 mg. Availability varies between countries. Beyond the reduction of blood pressure, valsartan is indicated for use in several count...
Journal Article•
TL;DR: The hypothesis that uric acid is an independent cardiovascular risk factor is supported, at least in women, and further studies are warranted.
Abstract: Background Hyperuricaemia is associated with reduced renal function and increased cardiovascular risk. It is still disputed, however, whether hyperuricaemia is an independent cardiovascular risk factor or just a marker of increased cardiovascular risk. Material and methods A review of the literature based on Medline is presented and data from the LIFE (Losartan Intervention For Endpoint reduction in hypertension) study discussed in relation to the association between uric acid and cardiovascular events. Results Epidemiological data have shown an independent relationship between serum uric acid and cardiovascular risk, at least in women. In LIFE, uric acid at baseline corresponded positively with cardiovascular risk in women, though not in men. Differences in serum uric acid during the study could statistically explain 29% of the reduction in cardiovascular events in the losartan group compared to atenolol. Interpretation These findings support the hypothesis that uric acid is an independent cardiovascular risk factor. Further studies are warranted.
TL;DR: The European Meeting on Hypertension has established itself as the most important hypertension congress in the world, and it has occurred that false abstracts have twice been submitted and, in one case, accepted for poster presentation.
Abstract: The European Meeting on Hypertension was organized for the 15th time in Milan in June 2005. Every second meeting takes place in Milan; after the record turnout of more than 8000 delegates at the 14...
TL;DR: Three trials have evaluated the effects of ARB treatment in patients with hypertension and manifestations of cardiovascular disease and/or diabetes, and used different comparator agents (eg, placebo, β-blocker, calcium antagonist), and had different primary end points.
Abstract: Introduction Hypertension increases the risk for major cardiovascular events and progression of cardiovascular disease. Even modest reductions in blood pressure confer substantial reductions in risk for events. The renin-angiotensinaldosterone system (RAAS) and its principal mediator, angiotensin II, have pivotal roles in the shortand longterm regulation of blood pressure and in the prognosis of hypertension. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARB), which interfere with the vasoconstrictive and trophic effects of angiotensin II, have blood pressure-lowering effects similar to other antihypertensive agents but also have vasculoprotective properties and preserve renal function in patients with nephropathy due to diabetes and from other causes. Three trials have evaluated the effects of ARB treatment in patients with hypertension and manifestations of cardiovascular disease and/or diabetes. These trials focused on various patient populations based on age and cardiovascular risk level, used different comparator agents (eg, placebo, β-blocker, calcium antagonist), and had different primary end points.