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- Emmelin, Maria, et al.
(författare)
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Self-rated ill-health strengthens the effect of biomedical risk factors in predicting stroke especially for men : An incident case referent study
- 2003
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 21:5, s. 887-896
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To examine how self-rated ill-health interacts with biomedical stroke risk factors in predicting stroke and to explore differences between men and women and educational groups. DESIGN: An incident case-referent study where the study subjects had participated in a prior health survey. SETTING: Nested within the Västerbotten Intervention Program (VIP) and the Northern Sweden MONICA cohorts. SUBJECTS: The 473 stroke cases had two referents per case, matched for age, sex and residence, from the same study cohorts. RESULTS: Self-rated ill-health independently increased the risk of stroke, specifically for men. The interaction effect between self-rated health and biomedical risk factor load was greater for men than for women. The attributable proportion due to interaction between having a risk factor load of 2+ and self-rated ill-health was 42% for men and 15% for women. Better-educated individuals with self-rated ill-health and two or more of the biomedical risk factors had a higher risk of stroke than the less educated. Calculations of the respective contribution to the stroke cases of self-rated health, hypertension and smoking showed that self-rated ill-health had a role in 20% of the cases and could alone explain more than one-third of the cases among those who rated their health as bad, more so for men than for women. CONCLUSIONS: The results underscore the importance of including both a gender and a social perspective in discussing the role of self-rated health as a predictor of disease outcome. Physicians must be more gender sensitive when discussing their patient's own evaluation of health in relation to biomedical risk factors.
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- Hallberg, Pär, et al.
(författare)
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B2 bradykinin receptor (B2BKR) polymorphism and change in left ventricular mass in response to antihypertensive treatment : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial
- 2003
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Ingår i: Journal of Hypertension. - : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 21:3, s. 621-4
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Hypertension is associated with a number of adverse morphologic and functional changes in the cardiovascular system, including left ventricular (LV) hypertrophy. Studies have demonstrated that bradykinin, through the B2 bradykinin receptor (B2BKR), mediates important cardiovascular effects that may protect against LV hypertrophy. Recently, a +9/-9 exon 1 polymorphism of the B2BKR was shown to be strongly associated with LV growth response among normotensive males undergoing physical training. We aimed to clarify whether the processes found in exercise-induced LV growth in normotensive people also occur in pathological LV hypertrophy. DESIGN AND METHODS: We determined the B2BKR genotype of 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, included in a double-blind study to receive treatment for 48 weeks with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol. RESULTS: B2BKR +9/+9 genotypes responded poorly in LV mass regression, independent of blood pressure reduction or treatment, as compared to the other genotypes (adjusted mean change in LV mass index = -10.0 +/- 4.6 versus -21.6 +/- 2.2 g/m2, P = 0.03). CONCLUSIONS: Our results suggest an impact of the B2BKR polymorphism on LV mass regression during antihypertensive treatment.
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- Hallberg, Pär, et al.
(författare)
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The CYP2C9 genotype predicts the blood pressure response to irbesartan : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial
- 2002
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Ingår i: Journal of Hypertension. - : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 20:10, s. 2089-2093
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The cytochrome P450 CYP2C9 enzyme (CYP2C9) metabolizes many clinically important drugs, for example, phenytoin, warfarin and the angiotensin II type 1 (AT(1)) receptor antagonists, losartan and irbesartan. Single nucleotide polymorphisms in the CYP2C9 gene result in the expression of three important variants, CYP2C9*1(wild-type), CYP2C9*2 and CYP2C9*3, the last two exhibiting reduced catalytic activity compared with the wild-type. The CYP2C9 genotype is known to determine sensitivity to and dose requirements for both warfarin and phenytoin, and also the rate of metabolism of losartan. However, its influence on clinical response to treatment with the AT(1) receptor antagonist, irbesartan, has not been investigated. OBJECTIVE: To determine whether the CYP2C9genotype influences the blood pressure-decreasing response to antihypertensive treatment with irbesartan. DESIGN AND METHODS: One hundred and two patients with essential hypertension and left ventricular hypertrophy were allocated randomly to groups to receive double-blind treatment with either irbesartan (n = 49) or the beta(1)-adrenergic receptor blocker, atenolol ( n= 53). Blood pressure was measured before and after 12 weeks of treatment. genotyping was performed using solid-phase minisequencing. RESULTS: The diastolic blood pressure (DBP) response differed in relation to the CYP2C9 genotype in patients given irbesartan: the reduction in patients with genotype CYP2C9*1/CYP2C9*1 (n = 33) was 7.5% and that with CYP2C9*1/CYP2C9*2 (n = 12) was 14.4% ( P= 0.036). A similar trend was seen for systolic blood pressure. In contrast, no relation was seen between the CYP2C9 genotype and blood pressure response to atenolol, a drug not metabolized via CYP2C9. CONCLUSIONS: The CYP2C9 genotype seems to predict the DBP response to irbesartan, but not to atenolol, in patients with essential hypertension.
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- Khalili, Payam, et al.
(författare)
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Smoking as a modifier of the systolic blood pressure-induced risk of cardiovascular events and mortality : a population-based prospective study of middle-aged men
- 2002
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Ingår i: Journal of Hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0263-6352 .- 1473-5598. ; 20:9, s. 1759-1764
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Tidskriftsartikel (refereegranskat)abstract
- Objective To examine to what degree smoking habits modulate the relationship between systolic blood pressure (SBP) and risk for cardiovascular morbidity (first event) and mortality in middle-aged men. Design and methods In all, 22 444 middle-aged men were recruited from a population-based screening study (mean attendance rate 71%). Risk factor intervention was offered to about 20% of participants. Subjects were followed in local and national registers for cardiovascular morbidity and mortality during more than 17 years of follow-up. Lifestyle variables were investigated at baseline, including smoking habits. Event rates were calculated in relation to quintiles (Q1-Q5) of baseline SBP in untreated subjects, subdivided into categories of smoking habits, but also for 915 previously known, treated hypertensive (tHT) patients at baseline. Results We found an increasing incidence of first cardiovascular event (CE) with increasing SBP levels, ranging from 63.5 CE/10 000 person-years (Q1) to 62.3, 70.5,82.3 and 115.1 CE/10 000 person-years (Q2-Q5). The corresponding figure in tHTs; was 153 CE/10 000 person-years. If further subdivided into smokers/ex-smokers/non-smokers, the relative risks (RR) of smokers were 1.9 [95% confidence interval (Cl): 1.5-2.4], 2.1 (1.8-2.5), 2.3 (1.8-2.9), 1.8 (1.5-2.1), and 1.7 (1.5-2.0) compared to present non-smokers, in relation to SBP (Q1-Q5). In tHTs; the RR was 1.4 (1.1-1.8). Cardiovascular mortality rates differed in relation to SBP and smoking habits, from 40.3 (present non-smokers) and 70.7 (smokers) deaths/10 000 person-years in Q1, to 54.2 and 134.0 deaths/10 000 person-years in Q5. In tHTs the corresponding figures were 81.6 and 149.4 deaths/10 000 person-years, respectively. No difference in risk was found for never-smokers compared to ex-smokers in relation to SBP. The risk in moderate/heavy smokers (> 10 cigarettes/day) compared to other smokers (less than or equal to 10 cigarettes/day) was significantly (P < 0.005) increased only in Q5. Conclusion Increasing systolic blood pressure levels in middle-aged men is associated with an increasing risk of future cardiovascular events and mortality, an association modified by smoking habits. Patients with treated hypertension in the 1970-1980s were also at an increased risk in spite of healthcare efforts. This calls for a more comprehensive multiple risk factor approach for the management and reduction of cardiovascular risk in these patients. (C) 2002 Lippincott Williams Wilkins.
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- Kjeldsen, SE, et al.
(författare)
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Influence of age, sex and blood pressure on the principal endpoints of the Nordic Diltiazem (NORDIL) Study
- 2002
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Ingår i: Journal of Hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0263-6352 .- 1473-5598. ; 20:6, s. 1231-1237
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Tidskriftsartikel (refereegranskat)abstract
- Background The aim of the Nordic Diltiazem (NORDIL) Study was to compare patients with essential hypertension receiving calcium-antagonist-based treatment with diltiazem and similar patients receiving conventional diuretic/beta-blocker-based treatment, with respect to cardiovascular morbidity and mortality. Objective To assess the influence of age, sex, severity of hypertension and heart rate on treatment effects, in a sub-analysis. Methods The NORDIL study was prospective, randomized, open and endpoint-blinded. It enrolled, at health centres in Norway and Sweden, 10881 patients aged 50-74 years who had diastolic blood pressure (DBP) of 100 mmHg or more. Systolic blood pressure (SBP) and DBP were decreased by 20.3/18.7 mmHg in the diltiazem group and by 23.3/18.7 mmHg in the diuretic/beta-blocker group - a significant difference in SBP (P < 0.001). Results The incidence of the primary endpoint - a composite of cardiovascular death, cerebral stroke and myocardial infarction - was similar for the two treatments. Fatal and non-fatal stroke occurred in 159 patients in the diltiazem group and in 196 patients in the conventional treatment group [relative risk MR) 0.80, 95% confidence interval (CO 0.65 to 0.99, P = 0.0401, whereas there was a non-significant inverse tendency with respect to all myocardial infarction. Three Were significantly fewer cerebral strokes ip atiepts receiving diltiazem in the subgroups with baseline SBP > 170 mmHg (n = 5420, RR 0.75,95% CI 0.58 to 0.98, P = 0.032), DBP 105 mmHg (n = 5881, RR 0.74,95% Cl 0.57 to 0.97, P = 0.030) and pulse pressure greater than or equal to 66 mmHg (n = 5461, RR 0.76, 95% Cl 0.58 to 0.99, P = 0.041), and more myocardial infarctions in those with heart rate less than 74 beats/min (n = 5303, RR 1.13, 95% Cl 1.01 to 1.87, P = 0.040). However, the tendencies for fewer strokes and greater incidence of myocardial infarction were present across subgroups when results were analysed for age, sex, severity of hypertension and heart rate, and treatment-subgroup interaction analyses were not statistically significant. Conclusions Compared with a conventional diuretic/beta-blocker-based anti hypertensive regimen, there were additional 25% reductions in stroke in the diltiazem-treated patients with blood pressure or pulse pressure greater than the medians, and an increase in myocardial infarction in those with heart rate less than the median. Such findings may be attributable to chance, but the consistency of, in particular, the stroke findings may also suggest an ability of diltiazem, beyond conventional treatment, to prevent cerebral stroke in hypertensive patients with the greatest cardiovascular risk. (C) 2002 Lippincott Williams Wilkins.
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