Publications by authors named "Per Omvik"

Background: Pharmaceutical differences in central hemodynamics might influence cardiac response to antihypertensive treatment despite similar lowering of brachial blood pressure (BP).

Methods: Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs. atenolol-based antihypertensive therapy.

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Aim: To investigate whether in-treatment measurements of subclinical organ damage (SOD) assessed by elevated urine albumin/creatinine ratio (UACR) or electrocardiographic left ventricular hypertrophy improved the prediction of the composite cardiovascular endpoint of cardiovascular death, nonfatal myocardial infarction and stroke beyond in-treatment Framingham risk score (FRS).

Methods: Excluding patients with a composite cardiovascular endpoint within the first year of treatment, 598 endpoints occurred in 6460 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study with baseline and 1 year values for UACR, left ventricular hypertrophy by electrocardiography and FRS available.

Results: Using Cox-regression analyses, FRS(1year) [hazard ratio=1.

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Objective: We assessed readily available patient characteristics, including albuminuria (not included in traditional cardiovascular risk scores), as predictors of cardiovascular events in hypertension with left ventricular hypertrophy (LVH) and developed risk algorithms/scores for outcomes.

Methods: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study compared effects of losartan-based versus atenolol-based therapy on cardiovascular events in 9193 patients with hypertension and LVH. Univariate and multivariate analyses identified baseline variables with significant impact on development of the primary composite endpoint (cardiovascular death, stroke and myocardial infarction) and its components.

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Objective: Beta-blockers and angiotensin II receptor blockers have different effects on lipids.

Methods: We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke. We measured total and high-density lipoprotein cholesterol at baseline and annually during 4.

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Background: The prognostic importance of hemoglobin is controversial. We investigated the prognostic importance of baseline and in-treatment hemoglobin in the LIFE study.

Methods: Eight thousand one hundred ninety-four LIFE patients with hypertension and left ventricular hypertrophy with available baseline hemoglobin measurements were randomized to losartan- or atenolol-based treatment and followed for 4.

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We recently demonstrated reduced exercise capacity in treated genetic haemochromatosis, in spite of normal radial left ventricular (LV) systolic function assessed by 2-dimensional echocardiography at rest. It remains unknown if haemochromatosis-related impairment of LV long-axis function can be demonstrated also at rest. LV long-axis function was assessed by echocardiography including spectral tissue Doppler of systolic (S') and early (E') diastolic velocities in 105 treated haemochromatosis patients and 50 controls.

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Objectives: We recently demonstrated reduced exercise capacity in phlebotomy treated genetic haemochromatosis in spite of normal systolic function. The present objective was to investigate diastolic function at rest.

Design: Diastolic function was echocardiographically assessed in 132 phlebotomy treated genetic haemochromatosis patients and 50 controls.

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There has been a lot of interest about new-onset diabetes mellitus in recent hypertension trials, but the implications of diabetes development on cardiac outcomes have not been known. In the Valsartan Antihypertensive Long-Term Use Evaluation trial, 15 245 high-risk patients were followed for an average of 4.2 years.

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Background: Many patients with genetic haemochromatosis complain about fatigue and reduced physical capacity. Exercise capacity, however, has not been evaluated in larger series of haemochromatosis patients treated with repeated phlebotomy.

Design And Methods: We performed exercise echocardiography in 152 treated haemochromatosis patients (48+/-13 years, 26% women) and 50 healthy blood donors (49+/-13 years, 30% women), who served as controls.

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Objective: To compare blood pressure response and antihypertensive medication use visit-by-visit from baseline in patients receiving losartan-based or atenolol-based therapy in the LIFE study.

Research Design: LIFE was a randomized, double-blind trial comparing losartan-based and atenolol-based treatment regimens on the primary composite endpoint of death, myocardial infarction (MI), or stroke in 9193 patients aged 55-80 years with hypertension and left ventricular hypertrophy. Systolic and diastolic, pulse, and mean arterial pressures, blood pressure responder rates, distribution of open-label antihypertensive agents utilized, and the proportion of patients on randomized treatment were determined for each group at each clinic visit over a follow-up period of at least 4 years.

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The influence of left atrial size on cardiovascular events during antihypertensive treatment has not been reported previously from a long-term, prospective, randomized hypertension treatment trial. We recorded left atrial diameter by annual echocardiography and cardiovascular events in 881 hypertensive patients (41% women) with electrocardiographic left ventricular hypertrophy aged 55 to 80 (mean: 66) years during a mean of 4.8 years of randomized losartan- or atenolol-based treatment in the Losartan Intervention for Endpoint Reduction in Hypertension Study.

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The objective of the study was to assess the influence of left ventricular (LV) hypertrophy regression on exercise capacity in hypertensive patients. Doppler echocardiography was performed at rest and during exercise in 51 patients with electrocardiographic LV hypertrophy before and after 1 year of randomized blinded losartan- or atenolol-based antihypertensive treatment. After 1 year, blood pressure was comparably reduced by 32/14 and 27/13 mmHg, respectively, in the losartan and atenolol groups, but the atenolol group had higher mean LV mass index (118 vs 103 g/m2) and lower LV ejection fraction (61% vs 67%) and midwall shortening (15.

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Agents that counteract the negative impact of the renin-angiotensin-aldosterone system (RAAS) are effective antihypertensives and reduce the risk of developing Type 2 diabetes. Contrary to common perception, angiotensin-converting enzyme inhibitors do not share the apparent benefit of angiotensin II receptor blockers (ARBs) in reducing risk of cardiovascular-disease outcomes, particularly stroke, in randomised clinical trials. RAAS agents, especially ARBs, are well tolerated.

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Objectives: We conducted a subgroup analysis in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study to determine whether aspirin interacted with the properties of losartan, an angiotensin-II receptor antagonist.

Background: Negative interactions between angiotensin-converting enzyme inhibitors and aspirin have been reported. There are no data reported from clinical trials about possible interactions between angiotensin-II receptor antagonists and aspirin.

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Background: Obesity may independently increase the risk of adverse events in hypertension with target-organ damage. We investigated whether body build was independently associated with higher cardiovascular risk and whether treatment with losartan relative to atenolol influenced the impact of body build on the primary composite end point of cardiovascular death, stroke, and myocardial infarction and on cardiovascular death in patients with hypertension and left ventricular hypertrophy in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.

Methods And Results: The population of 9079 patients was divided as follows: thin (body mass index [BMI] <20 kg/m2, 2%), normal weight (BMI 20 to 24.

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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.

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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.

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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).

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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.

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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.

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Objectives: To 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 versus atenolol could be explained by influence of losartan on albuminuria.

Design: Double-blind, randomized, controlled trial of 4.8 years.

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Background: The Keito machine offers automatic measurements of blood pressure (BP), height and weight on insertion of coins and has been introduced in pharmacies.

Design: Cross-sectional study comparing automatic BP measurements by the Keito machine to office BP measurements by physicians.

Methods: Patients scheduled for pre-catheterisation screening participated in the study.

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Background: New guidelines adopted in Norway for antihypertensive medication implies prescription of a thiazide diuretic as the drug of first choice. The background for the change in the rules for prescription drugs paid for by the National Insurance system with a capped co-payment is a resolution of the Norwegian parliament as part of a budget compromise for 2004. The resolution was supported by results from the ALLHAT study (antihypertensive and lipid-lowering treatment to prevent heart attack trial).

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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.

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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.

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