PubMed Health⌕ Search

Biomedical subjects

Kurt Boman

Publications and source records attributed to Kurt Boman.

36 records · Page 2Linked to original sources
PubMed2004

Estimated intake of milk fat is negatively associated with cardiovascular risk factors and does not increase the risk of a first acute myocardial infarction. A prospective case-control study.

Milk fat is high in saturated fatty acids (SFA) and high intakes of SFA are associated with cardiovascular diseases. The aim of the present study was to prospectively evaluate the potential risk of a first-ever acute myocardial infarction (AMI) in relation to the estimated milk-fat intake, reflected as the proportions of pentadecanoic acid (15 : 0) and heptadecanoic acid (17 : 0) in serum lipid esters. This was evaluated in a study population selected within the Västerbotten Intervention Program and the northern Sweden 'Monitoring of Trends and Determinants in Cardiovascular disease' survey populations. A prospective case-control design was used. The proportions of the biomarkers were lower in the cases (n 78) than in the controls (n 156), who were matched for age, sex, sampling time and geographical region. The standardised odds ratios of becoming an AMI case were between 0.7 and 0.8 for the biomarkers. The proportions of 15 : 0 and 17 : 0 in serum phospholipids were significantly and negatively correlated to serum concentrations of plasminogen activator inhibitor-1, tissue-type plasminogen activator, triacylglycerols, insulin, specific insulin, pro-insulin and leptin (all P<0.0001), suggesting a negative relationship to the insulin-resistance syndrome and the risk of CHD. Adjustment for BMI did not materially change the relationships. Although there seems to be a negative association between milk-fat intake as mirrored by the proportions of 15 : 0 and 17 : 0 in serum lipid esters and a first-ever AMI, adjustment for clinical risk factors removed this relationship.

Adult↗
PubMed2004

Interactions between fibrinolysis, lipoproteins and leptin related to a first myocardial infarction.

BACKGROUND: The summarized importance of haemostatic and metabolic variables (insulin, lipids including lipoprotein (a) [Lp(a)] and leptin) in predicting first myocardial infarction, as well as possible interactions among these variables, have not been reported. DESIGN: A prospective case-control study nested within the Northern Sweden Health and Disease Cohort. METHODS: Sixty-two men diagnosed with a first myocardial infarction were sex- and age-matched with 124 controls. Conditional logistic regression was conducted including established risk factors, plasma levels of plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (tPA) mass concentration, von Willebrand factor, insulin, proinsulin, specific insulin, apolipoprotein A-I (apo A-I), Lp(a), and leptin. Interaction analysis was also performed for tPA, apo A-I, Lp(a), leptin and proinsulin. RESULTS: Smoking, low plasma levels of apo A-I and high plasma levels of cholesterol, Lp(a), tPA, PAI-1, proinsulin and leptin were associated with myocardial infarction in univariate conditional logistic regression analysis. High tPA [odds ratio (OR), 21.3; 95% confidence interval (CI), 2.04-222] and Lp(a) (OR, 7.21; 95% CI, 1.31-39.8) and low apo A-I (OR, 0.15; 95% CI, 0.02-0.93) remained significant risk determinants in multivariate analysis with smoking habits, body mass index, hypertension, cholesterol, and diabetes included as covariates. There were non-significant synergic interactions between high Lp(a) and leptin and tPA, respectively, and between high Lp(a) and low apo A-I. CONCLUSION: Plasma levels of tPA, Lp(a), and apo A-I are independently associated with subsequent development of a first myocardial infarction in men.

Apolipoproteins B↗
PubMed2003

Left ventricular mass regression in the LIFE study: effect of previous antihypertensive treatment.

BACKGROUND: Whether to include only those patients who have not had prior hypertension treatment in clinical trials of left ventricular (LV) mass reduction is controversial. Accordingly, our aim was to study the relationship between prior treatment and both baseline and 1-year echocardiographic LV mass in subjects enrolled in the Losartan Intervention For Endpoint reduction (LIFE) study. METHODS: We studied clinical and baseline echocardiographic data on 960 patients with electrocardiographically confirmed left ventricular hypertrophy enrolled in the electrocardiographic substudy of the LIFE study, 847 of whom had LV mass remeasured after 1 year of blinded treatment. The majority (75%) of these patients had prior medical treatment for hypertension. RESULTS: In multivariable regression analysis, controlling for age, sex, blood pressure (BP), body mass index, and indices of pump and myocardial function, prior antihypertensive treatment was not associated with either greater LV mass or relative wall thickness on the baseline study. Moreover, there was no significant difference between the 637 subjects who were previously treated and the 210 who were not treated with regard to the mean reduction in systolic or diastolic pressures (-25 +/- 17 v -24 +/- -16 and -13 +/- 9 mm Hg v -12 +/- 9 mm Hg), LV mass (-27 +/- 38 v -29 +/- 34 g), or LV mass/body surface area (-14 +/- 20 v -15 +/- 18 g/m(2)), all P >.05. CONCLUSIONS: Prior treatment is not associated with either greater LV mass or greater relative wall thickness when age, body mass index, sex, systolic BP, heart rate, or indices of LV volume load and systolic function are taken into account. In addition, prior treatment is not associated with lesser degrees of LV mass reduction. For design of future clinical trials, restriction of inclusion criteria to only previously untreated patients does not appear to be necessary when the selection criterion is electrocardiographically determined left ventricular hypertrophy.

Aged↗
PubMed2003

Trends in blood pressure, lipids, lipoproteins and glucose metabolism in the Northern Sweden MONICA project 1986-99.

AIM: The authors present an analysis of time trends in blood pressure, hypertension, and lipids in the adult population of Northern Sweden over the period 1986-99. METHOD: Four population surveys were undertaken with new and independent cohorts, 25-64 years old. RESULTS: Small changes in blood pressure were observed during the study period with increased systolic blood pressure in men and decreased diastolic blood pressure in women. The proportion with high blood pressure was found to be constant over time and only 50% were prescribed antihypertensive drugs and of these only a minority were normotensive. Total serum cholesterol decreased from 6.4 to 5.7 mmol/l in men and from 6.3 to 5.7 mmol/l in women over the study period, and this was accompanied by an increase in HDL cholesterol by about 10% in both sexes. The proportion with high cholesterol decreased from 41% to 26%. Triglycerides increased between 1986 and 1990 and no further changes were found in the following surveys. CONCLUSION: In the Northern Sweden MONICA population total cholesterol has declined and HDL cholesterol has increased during the past 13 years and small changes in blood pressure have been observed for both men and women.

Adult↗
PubMed2002

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study.

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.

Aged↗
PubMed2002

Correlates of pulse pressure reduction during antihypertensive treatment (losartan or atenolol) in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study).

In hypertensive patients, pulse pressure has been related to hypertension-induced target organ damage and risk of cardiovascular events. However, correlates of pulse pressure reduction during antihypertensive treatment have been less extensively investigated. We related pulse pressure changes to clinical and echocardiographic findings before and after 2 years of antihypertensive treatment in 767 patients aged 55 to 80 years (mean 66) in the Losartan Intervention For End point reduction in hypertension study. Over 2 years, blood pressure and pulse pressure were reduced from 173/98 to 147/84 mm Hg and from 75 to 63 mm Hg, respectively, both p <0.001. In linear multivariate analysis controlling for initial pulse pressure, 2-year reduction in pulse pressure correlated negatively with age and concomitant diabetes mellitus, and positively with body height and 2-year reduction in mean blood pressure (multiple R(2) = 0.42, p <0.01). When dividing the study population into 2 groups using a prognostically validated partition for pulse pressure, patients with pulse pressure > or =63 mm Hg after 2 years of antihypertensive treatment (n = 349) were older and shorter, included more women and patients with isolated systolic hypertension, diabetes mellitus, albuminuria, and echocardiographic left ventricular hypertrophy at baseline, and also had a smaller decrease in mean blood pressure and the urinary albumin/creatinine ratio over 2 years (all p <0.05). Thus, in hypertensive patients with electrocardiographic left ventricular hypertrophy, older age, less reduction in mean blood pressure, concomitant diabetes mellitus, and shorter stature are associated with attenuated pulse pressure reduction during antihypertensive treatment.

Aged↗
PubMed2002

Change of left ventricular geometric pattern after 1 year of antihypertensive treatment: the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study.

BACKGROUND: Patients with hypertension have different types of left ventricular (LV) geometry, but the impact of blood pressure (BP) reduction on LV geometry change during antihypertensive treatment remains unclear. METHODS: Two-dimensional and M-mode echocardiograms were recorded at baseline in 853 unmedicated patients with stage II to III hypertension and LV hypertrophy determined by electrocardiography (Cornell voltage duration > or =2440 mV x ms or modified Sokolow-Lyon criteria: SV1 + RV5/RV6 >38 mV) after 14 days of placebo treatment. Follow-up echocardiography was done after 1 year of blinded treatment with either losartan or atenolol, in some cases supplemented with thiazide and calcium antagonist to reach target a BP of 140/90 mm Hg. RESULTS: Baseline systolic/diastolic BP were reduced from 174 +/- 20/95 +/- 11 to 151 +/- 19/84 +/- 11 mm Hg. LV mass was reduced from 234 +/- 56 to 207 +/- 51 g and relative wall thickness from 0.41 +/- 0.07 to 0.38 +/- 0.06 (all P <.001). Prevalence of concentric LV hypertrophy decreased from 24% to 6%, eccentric LV hypertrophy from 46% to 37%, and concentric LV remodeling from 10% to 6%; normal geometry increased from 20% to 51%. A shift toward lower LV mass and relative wall thickness was found, as approximately 73% of those with concentric LV remodeling at baseline shifted to normal geometric pattern, whereas only 7% of those with normal pattern at baseline shifted to concentric LV remodeling. Of patients with concentric LV hypertrophy at baseline, 34% shifted to eccentric LV hypertrophy, whereas only 3% with eccentric LV hypertrophy at baseline had concentric LV hypertrophy. Furthermore, multiple regression analysis showed that Doppler stroke volume reduction was a significant correlate of LV mass reduction (beta = 0.108, P <.001) independent of BP, heart rate change, and assigned drug treatment. CONCLUSIONS: Antihypertensive treatment reduces LV mass and decreases the prevalence of LV hypertrophy and concentric LV remodeling. Additional control of Doppler stroke volume potentiates the effect of BP reduction on LV mass regression independent of the BP reduction per se.

Aged↗
PubMed2002

Progressive hypertrophy regression with sustained pressure reduction in hypertension: the Losartan Intervention For Endpoint Reduction study.

OBJECTIVE: To examine the time course of left ventricular (LV) geometric response to blood pressure (BP) control during 2 years of systematic antihypertensive treatment. DESIGN: A total of 754 hypertensive patients with left ventricular hypertrophy (LVH) by Cornell voltage-duration product or Sokolow-Lyon voltage criteria on a screening electrocardiogram had their LV mass measured by echocardiogram at enrolment in the Losartan Intervention For Endpoint Reduction (LIFE) trial, and after 12 and 24 months of blinded therapy with losartan-based or atenolol-based regimens. SETTING: The LIFE trial, in which hypertensive patients with electrocardiographic LVH (Cornell voltage-duration product > 2440 mm x ms and/or Sokolow-Lyon voltage criteria SV1 + RV5-6 > 38 mm) were randomized to >or= 4 years double-blinded treatment with losartan or atenolol. PARTICIPANTS: A total of 754 LIFE participants with serial echocardiographic measurements of LV geometry. INTERVENTIONS: None. MAIN OUTCOME MEASURES: LV wall thicknesses, diameter and mass, and its indices. RESULTS: Mean systolic/diastolic BP fell from 173/95 to 150/84 mmHg after 1 year (P < 0.001) and to 148/83 mmHg at year 2 (P = not significant). Mean echocardiographic LV mass fell from 233 g at baseline to 206 g after 1 year (P < 0.001, adjusted for change in systolic BP) and to 195 g at year 2 (P < 0.001 versus year 1), with a parallel decrease in indexed LV mass [from 56.1 to 49.7 g/m2.7 (P < 0.001), to 47.1 g/m2.7 (P < 0.001 versus year 1)]. Relative wall thickness decreased from 0.41 at baseline to 0.37 at year 1 (P < 0.001), to 0.36 at year 2 (P < 0.001 versus year 1). As a result, there were serial decreases in prevalences of eccentric LVH [44 to 38%, and to 30% (P < 0.001 versus year 1)] and concentric LVH [24 to 7% (P < 0.001), to 2% (P < 0.05 versus year 1)], and increases in the proportion with normal LV geometry [22 to 50% (P < 0.001), and to 64% (P < 0.01 versus year 1)]. CONCLUSIONS: Sustained BP reduction in hypertensive patients with target organ damage causes continued decrease in echocardiographic LV mass and prevalence of anatomic LVH for at least 2 years despite only small BP decreases after the first year of blinded therapy. These data document cardiac benefit of sustained BP control and suggest that maximum LVH regression with effective antihypertensive treatment requires at least 2 years.

Aged↗
PubMed2002

High remaining risk in poorly treated hypertension: the 'rule of halves' still exists.

OBJECTIVES: To estimate risk factors for stroke, to examine how different categories of patients with increased blood pressure are associated with risk for first-ever stroke event, and to estimate the proportions of these categories in a geographically defined population in northern Sweden. SETTING: The study was nested within the Västerbotten Intervention Program and the Northern Sweden MONICA cohorts. DESIGN AND PARTICIPANTS: A population-based cross-sectional study and an incident case-control study were carried out. The incident case-control study comprised 129 cases of first-ever stroke diagnosed during 1985-96, with two randomly selected controls per case, chosen from the same geographically defined population. The cross-sectional study was based on 59,735 participants. Blood pressure status was categorized as: normotensive [systolic blood pressure (SBP) <140 mmHg and diastolic blood pressure (DBP) <90 mmHg]; treated and adequately controlled hypertension (SBP <140 mmHg and DBP <90 mmHg); treated but poorly controlled hypertension (SBP > or = 140 mmHg or DBP > or = 90 mmHg, or both); untreated hypertension (SBP > or = 140 mmHg or DBP > or = 90 mmHg, or both); newly detected increased blood pressure (SBP > or = 140 mmHg or DBP > or = 90 mmHg, or both). MAIN OUTCOME MEASURE: Risk for first-ever stroke. RESULTS: In the cross-sectional study, 68% of individuals were normotensive, 3% had treated and adequately controlled hypertension, 6% had treated but poorly controlled hypertension, 7% had untreated hypertension, and 16% had newly detected increased blood pressure. In univariate analysis of the case-control study, history of diabetes, daily smoking, obesity, increased blood pressure and the hypertension categories 'treated but poorly controlled' and 'untreated' were associated with an increased stroke risk. In multivariate logistic regression analysis, only diabetes and the hypertension categories treated but poorly controlled and untreated remained significant, with odds ratios 6.1 (95% confidence interval 2.4 to 15.3) and 4.3 (95% confidence interval 1.7 to 10.5), respectively. Only one of the 129 individuals who suffered stroke had treated and adequately controlled hypertension. CONCLUSIONS: The study illustrates the importance of adequate blood pressure control and, at the same time, that the vast majority in the population with increased blood pressure did not receive optimal care. Thus the 'rule of halves' still exists, and the high remaining risk in poorly treated hypertensive individuals in Sweden is remarkable and requires attention from the medical profession.

Adult↗
PubMed2002

Quantitative measurement of carotid atherosclerosis in relation to levels of von Willebrand factor and fibrinolytic variables in plasma--a 2-year follow-up study.

BACKGROUND: It has been proposed that the mechanism of action of the new risk factors for myocardial infarction and stroke, von Willebrand factor (vWF), tissue plasminogen activator (tPA) and tissue plasminogen activator inhibitor-1 (PAI-1) could possibly be mediated via a primary effect on atherogenesis but there is little data to substantiate this. DESIGN: A prospective single-centre cohort study of progression of atherosclerosis. METHODS: Carotid plaque area was quantitated by two-dimensional (2D) ultrasound in 258 subjects at entry and after 1 and 2 years. Plasma and serum samples were drawn at baseline and serum lipids and plasma levels of haemostatic factors were measured. RESULTS: The traditional risk factors, smoking, total cholesterol, hypertension and male gender explained 51% of the variance in plaque area at baseline and 48% at 1-year follow-up. There were small positive associations of plaque area with vWF, tPA and tPA/PAI-1 complex and a tendency to negative associations with PAI-1 levels, independent from the traditional risk factors. The additional explanatory power of the haemostatic factors did not exceed 3%. CONCLUSION: The data accord with a marginal role in atherogenesis of vWF and tPA, and underline the major impact of smoking, hypertension and cholesterol on carotid plaque area progression.

Adult↗
PubMed2002

Tissue-type plasminogen activator -7,351C/T enhancer polymorphism is associated with a first myocardial infarction.

We recently identified a polymorphic Sp1 binding site in an enhancer at the tissue-type plasminogen activator (tPA) locus (tPA -7,351C/T), which was associated with vascular tPA release. Subjects homozygous for the -7,351C allele had twice the tPA release rate compared to subjects carrying the -7,351T allele. In this study we tested the hypothesis that the tPA -7,351C/T polymorphism is associated with myocardial infarction (MI). In a population-based prospective nested case-control study within northern Sweden, genotypes were determined among 61 MI cases and 120 controls. In a multivariate model, the tPA -7,351C/T polymorphism (OR 2.68 for T allele carriers; 95% CI 1.31-5.50), tPA antigen (OR 1.16; 95% CI 1.07-1.25) and apo A-I (OR, 0.997; 95% CI 0.995-0.999) were independently associated with a first MI. These findings suggest that genetic markers of local tPA release and circulating steady-state tPA levels carry independent prognostic information.

Apolipoprotein A-I↗
PubMed2002

Prospective study on soluble thrombomodulin and von Willebrand factor and the risk of ischemic and hemorrhagic stroke.

The aim of the present study was to examine if soluble thrombomodulin (sTM) and von Willebrand factor (VWF) could predict a first-ever ischemic or hemorrhagic stroke. This study was an incident case-referent study from within a population-based cohort in northern Sweden. Up to 1996 about 44,000 subjects had been screened and stroke cases were classified according to the WHO MONICA criteria. A first-ever stroke occurred in 108 cases. A total of 216 controls were selected from the same cohort. This prospective study found no association with sTM or VWF and the development of a first-ever ischemic stroke (n = 87) in the logistic regression model. For the hemorrhagic stroke cases (n = 18), the multivariate logistic regression model revealed a significant negative association with sTM. When dichotomized, the upper level (>17.3 microg/L) of sTM, as compared with the lower level (<17.3 microg/L), showed one fifth of the risk for hemorrhagic stroke (OR, 0.18; CI, 0.05 to 0.69). No significant association was found for VWF. We suggest that the novel finding of an inverse relation between sTM and hemorrhagic stroke should be investigated in a larger study.

Brain Ischemia↗