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- 2019
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Tidskriftsartikel (refereegranskat)
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| 6. |
- Andersson, Tobias, 1976, et al.
(författare)
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Country of birth and mortality risk in hypertension with and without diabetes: the Swedish primary care cardiovascular database.
- 2021
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Ingår i: Journal of hypertension. - 1473-5598. ; 39:6, s. 1155-1162
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Tidskriftsartikel (refereegranskat)abstract
- Hypertension and diabetes are common and are both associated with high cardiovascular morbidity and mortality. We aimed to investigate associations between mortality risk and country of birth among hypertensive individuals in primary care with and without concomitant diabetes, which has not been studied previously. In addition, we aimed to study the corresponding risks of myocardial infarction and ischemic stroke.This observational cohort study of 62557 individuals with hypertension diagnosed 2001-2008 in the Swedish Primary Care Cardiovascular Database assessed mortality by the Swedish Cause of Death Register, and myocardial infarction and ischemic stroke by the National Patient Register. Cox regression models were used to estimate study outcome hazard ratios by country of birth and time updated diabetes status, with adjustments for multiple confounders.During follow-up time without diabetes using Swedish-born as reference, adjusted mortality hazard ratios per country of birth category were Finland: 1.26 (95% confidence interval 1.15-1.38), high-income European countries: 0.84 (0.74-0.95), low-income European countries: 0.84 (0.71-1.00) and non-European countries: 0.65 (0.56-0.76). The corresponding adjusted mortality hazard ratios during follow-up time with diabetes were high-income European countries: 0.78 (0.63-0.98), low-income European countries: 0.74 (0.57-0.96) and non-European countries: 0.56 (0.44-0.71). During follow-up without diabetes, the corresponding adjusted hazard ratio of myocardial infarction was increased for Finland: 1.16 (1.01-1.34), whereas the results for ischemic stroke were inconclusive.In Sweden, hypertensive immigrants (with the exception for Finnish-born) with and without diabetes have a mortality advantage, as compared to Swedish-born.
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| 7. |
- Andersson, Tobias, 1976, et al.
(författare)
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The impact of diabetes, education and income on mortality and cardiovascular events in hypertensive patients: A cohort study from the Swedish Primary Care Cardiovascular Database (SPCCD).
- 2020
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Ingår i: PloS one. - : Public Library of Science (PLoS). - 1932-6203. ; 15:8
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Tidskriftsartikel (refereegranskat)abstract
- In this study we aimed to estimate the effect of diabetes, educational level and income on the risk of mortality and cardiovascular events in primary care patients with hypertension.We followed 62,557 individuals with hypertension diagnosed 2001-2008, in the Swedish Primary Care Cardiovascular Database. Study outcomes were death, myocardial infarction, and ischemic stroke, assessed using national registers until 2012. Cox regression models were used to estimate adjusted hazard ratios of outcomes according to diabetes status, educational level, and income.During follow-up, 13,231 individuals died, 9981 were diagnosed with diabetes, 4431 with myocardial infarction, and 4433 with ischemic stroke. Hazard ratios (95% confidence intervals) for diabetes versus no diabetes: mortality 1.57 (1.50-1.65), myocardial infarction 1.24 (1.14-1.34), and ischemic stroke 1.17 (1.07-1.27). Hazard ratios for diabetes and ≤9 years of school versus no diabetes and >12 years of school: mortality 1.56 (1.41-1.73), myocardial infarction 1.36 (1.17-1.59), and ischemic stroke 1.27 (1.08-1.50). Hazard ratios for diabetes and income in the lowest fifth group versus no diabetes and income in the highest fifth group: mortality 3.82 (3.36-4.34), myocardial infarction 2.00 (1.66-2.42), and ischemic stroke 1.91 (1.58-2.31).Diabetes combined with low income was associated with substantial excess risk of mortality, myocardial infarction and ischemic stroke among primary care patients with hypertension.
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| 8. |
- Aspberg, Sara, et al.
(författare)
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Confirmed association between neonatal phototherapy or neonatal icterus and risk of childhood asthma
- 2010
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Ingår i: Pediatric Allergy and Immunology. - : Wiley. - 0905-6157 .- 1399-3038. ; 21:4, s. 733-739
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Tidskriftsartikel (refereegranskat)abstract
- We have previously demonstrated an association between neonatal phototherapy and/or neonatal icterus and risk of hospitalization for childhood asthma. This study included children who were prescribed anti-asthmatic medication on a population basis to study exposures during the foetal and neonatal period and risk of childhood asthma. The Swedish Medical Birth Register was linked to the Swedish Prescribed Drug Register. Perinatal data for singleton children who were prescribed anti-asthmatic medication (n = 61 256) were compared with corresponding data for all singleton children born in Sweden from 1 January 1990 to 30 June 2003 and surviving to 1 July 2005 (n = 1 338 319). Mantel-Haenszel's odds ratios were calculated after adjustment for various known confounders. Being the first-born child, maternal age above 44 yr, involuntary childlessness for more than 1 yr, maternal smoking during pregnancy, maternal diabetes mellitus of any kind, pre-eclampsia, caesarean section, and instrumental vaginal delivery were all associated with an increased prescription of anti-asthmatic medication during childhood. Preterm birth, low birth weight, being small for gestational age, respiratory problems, mechanical ventilation, and sepsis and/or pneumonia were also associated with increased drug prescriptions. Neonatal phototherapy and/or icterus were risk determinants for children who developed asthma before the age of 12. After controlling for confounders, the odds ratio for phototherapy and/or icterus remained at 1.30 (95% confidence interval 1.16-1.47). In conclusion, this large population-based study confirms an association between some maternal and perinatal factors and childhood asthma, including neonatal phototherapy and/or icterus.
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| 9. |
- Aspberg, Sara, et al.
(författare)
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Fetal and perinatal risk factors for inflammatory bowel disease
- 2006
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Ingår i: Acta Pædiatrica. - : Wiley. - 1651-2227 .- 0803-5253. ; 95:8, s. 1001-1004
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Tidskriftsartikel (refereegranskat)abstract
- Aim: To study the influence of specific factors and events during pregnancy and the perinatal period on the risk of children developing inflammatory bowel disease. Methods: Population-based national register study. Linkage between the Swedish Medical Birth Register and the Swedish Hospital Discharge Register during the period 1987 to 2000 identified 455 singleton infants who later developed inflammatory bowel disease. Data for these children were compared with data for all children born in Sweden during the same period. Results: Smoking during early pregnancy reduced the risk of inflammatory bowel disease ( odds ratio ( OR) 0.71, 95% CI 0.55-0.91). For ulcerative colitis the odds ratio was 0.70 ( 95% CI 0.56-0.86), and for Crohn's disease 0.73 ( 95% CI 0.58 - 0.94). Infections during the neonatal period seemed to increase the risk of inflammatory bowel disease ( OR 17.6, 95% CI 3.6 - 51.6), but the number of observed events was small. The other factors examined did not influence the risk of inflammatory bowel disease. Conclusion: Maternal smoking during early pregnancy reduces the risk for the child to be hospitalized with a diagnosis of inflammatory bowel disease. Severe neonatal infections may increase the risk. Thus, some exposures during the fetal and neonatal period seem to affect the risk of inflammatory bowel disease later in life.
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| 10. |
- Aspberg, Sara, et al.
(författare)
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Is neonatal phototherapy associated with an increased risk for hospitalized childhood bronchial asthma?
- 2007
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Ingår i: Pediatric Allergy and Immunology. - : Wiley. - 0905-6157 .- 1399-3038. ; 18:4, s. 313-319
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Tidskriftsartikel (refereegranskat)abstract
- This population-based register study examined if factors during the fetal and neonatal period influence the risk for the child to develop bronchial asthma (asthma). From the Swedish Hospital Discharge Register we identified children, born between 1987 and 1999, who had been hospitalized for asthma up to 2001. Thus, the outcome measure contains only hospitalized cases, not all children with asthma. Children younger than 2 yr at admission were excluded because of the uncertainty about the diagnosis of asthma in younger children. The remaining 14,803 children were compared with all children born the same years, recorded in the Swedish Medical Birth Registry, for information on pre- and perinatal characteristics. Odds ratios (ORs) were calculated with Mantel-Haenszel technique and 95% confidence intervals (CIs) with Miettinen's test-based method. The presence of various maternal and neonatal confounders were identified and adjusted for in the analyses. The association between some known factors and childhood asthma were confirmed: young maternal age, maternal smoking, period of unwanted childlessness, low maternal level of education, maternal diabetes, preterm birth, low birth weight, small-for-gestational age, caesarean section, and instrumental vaginal delivery. A number of neonatal characteristics were shown to be independent risk factors: sepsis or pneumonia, neonatal respiratory problems and treatments, neonatal icterus, and/or neonatal phototherapy. The association with icterus and phototherapy remained after exclusion of cases showing other neonatal risk factors and after adjustment for maternal factors (OR 1.27, 95% CI: 1.08-1.50), and increased to 1.5 if the children had been hospitalized for asthma more than once. In conclusion, our results suggest an association between neonatal icterus and/or treatment with neonatal phototherapy and hospitalized childhood asthma. This association needs further exploration.
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| 11. |
- Aspberg, Sara, et al.
(författare)
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Large differences between patients with acute myocardial infarction included in two Swedish health registers
- 2013
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Ingår i: Scandinavian Journal of Public Health. - : SAGE Publications (UK and US). - 1403-4948 .- 1651-1905. ; 41:6, s. 637-643
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Tidskriftsartikel (refereegranskat)abstract
- Background: Acute myocardial infarction (MI) is a leading cause for morbidity and mortality in Sweden. We aimed to compare patients with an acute MI included in the Register of information and knowledge about Swedish heart intensive care admissions (RIKS-HIA, now included in the register Swedeheart) and in the Swedish statistics of acute myocardial infarctions (S-AMI). Methods: Population based register study including RIKS-HIA, S-AMI, the National patient register and the Cause of death register. Odds ratios were determined by logistic regression analysis. Results: From 2001 to 2007, 114,311 cases in RIKS-HIA and 198,693 cases in S-AMI were included with a discharge diagnosis of an acute MI. Linkage was possible for 110,958 cases. These cases were younger, more often males, had fewer concomitant diseases and were more often treated with invasive coronary artery procedures than patients included in S-AMI only. There were substantial regional differences in proportions of patients reported to RIKS-HIA. Conclusions: Approximately half of all patients with an acute MI were included in RIKS-HIA. They represented a relatively more healthy population than patients included in S-AMI only. S-AMI covered almost all patients with an acute MI but had limited information about the patients. Used in combination, these two registers can give better prerequisites for improved quality of care of all patients with acute coronary syndromes.
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| 12. |
- Bager, Johan-Emil, et al.
(författare)
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Blood pressure levels and risk of haemorrhagic stroke in patients with atrial fibrillation and oral anticoagulants: results from The Swedish Primary Care Cardiovascular Database of Skaraborg.
- 2021
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Ingår i: Journal of hypertension. - 1473-5598. ; 39:8, s. 1670-1677
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Tidskriftsartikel (refereegranskat)abstract
- To assess the risk of haemorrhagic stroke at different baseline SBP levels in a primary care population with hypertension, atrial fibrillation and newly initiated oral anticoagulants (OACs).We identified 3972 patients with hypertension, atrial fibrillation and newly initiated OAC in The Swedish Primary Care Cardiovascular Database of Skaraborg. Patients were followed from 1 January 2006 until a first event of haemorrhagic stroke, death, cessation of OAC or 31 December 2016. We analysed the association between continuous SBP and haemorrhagic stroke with a multivariable Cox regression model and plotted the hazard ratio as a function of SBP with a restricted cubic spline with 130mmHg as reference.There were 40 cases of haemorrhagic stroke during follow-up. Baseline SBP in the 145-180mmHg range was associated with a more than doubled risk of haemorrhagic stroke, compared with a SBP of 130mmHg.In this cohort of primary care patients with hypertension and atrial fibrillation, we found that baseline SBP in the 145-180mmHg range, prior to initiation of OAC, was associated with a more than doubled risk of haemorrhagic stroke, as compared with an SBP of 130mmHg. This suggests that lowering SBP to below 145mmHg, prior to initiation of OAC, may decrease the risk of haemorrhagic stroke in patients with hypertension and atrial fibrillation.
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| 13. |
- Bartels-Rausch, T., et al.
(författare)
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A review of air-ice chemical and physical interactions (AICI): Liquids, quasi-liquids, and solids in snow
- 2014
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Ingår i: Atmospheric Chemistry And Physics. - : Copernicus GmbH. - 1680-7316 .- 1680-7324. ; 14:3, s. 1587-1633
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Tidskriftsartikel (refereegranskat)abstract
- Snow in the environment acts as a host to rich chemistry and provides a matrix for physical exchange of contaminants within the ecosystem. The goal of this review is to summarise the current state of knowledge of physical processes and chemical reactivity in surface snow with relevance to polar regions. It focuses on a description of impurities in distinct compartments present in surface snow, such as snow crystals, grain boundaries, crystal surfaces, and liquid parts. It emphasises the microscopic description of the ice surface and its link with the environment. Distinct differences between the disordered air-ice interface, often termed quasi-liquid layer, and a liquid phase are highlighted. The reactivity in these different compartments of surface snow is discussed using many experimental studies, simulations, and selected snow models from the molecular to the macro-scale. Although new experimental techniques have extended our knowledge of the surface properties of ice and their impact on some single reactions and processes, others occurring on, at or within snow grains remain unquantified. The presence of liquid or liquid-like compartments either due to the formation of brine or disorder at surfaces of snow crystals below the freezing point may strongly modify reaction rates. Therefore, future experiments should include a detailed characterisation of the surface properties of the ice matrices. A further point that remains largely unresolved is the distribution of impurities between the different domains of the condensed phase inside the snowpack, i.e. in the bulk solid, in liquid at the surface or trapped in confined pockets within or between grains, or at the surface. While surface-sensitive laboratory techniques may in the future help to resolve this point for equilibrium conditions, additional uncertainty for the environmental snowpack may be caused by the highly dynamic nature of the snowpack due to the fast metamorphism occurring under certain environmental conditions. Due to these gaps in knowledge the first snow chemistry models have attempted to reproduce certain processes like the long-term incorporation of volatile compounds in snow and firn or the release of reactive species from the snowpack. Although so far none of the models offers a coupled approach of physical and chemical processes or a detailed representation of the different compartments, they have successfully been used to reproduce some field experiments. A fully coupled snow chemistry and physics model remains to be developed. © Author(s) 2014.
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| 14. |
- Bentzel, Sara, et al.
(författare)
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Long-term secondary prevention and outcome following acute coronary syndrome: Real-world results from the Swedish Primary Care Cardiovascular Database (SPCCD)
- 2024
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Ingår i: European journal of preventive cardiology. - 2047-4881. ; 31:7, s. 812-821
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Tidskriftsartikel (refereegranskat)abstract
- Most studies of treatment adherence after acute coronary syndrome (ACS) are based on prescribed drugs and lack long-term follow-up or consecutive data on risk factor control. We studied the long-term treatment adherence, risk factor control and its association to recurrent ACS and death.We retrospectively included 3765 patients (mean age 75 years, 40% women) with incident ACS from 1 January 2006 until 31 December 2010 from the SPCCD-SKA database. All patients were followed until 31 December 2014 or death. We recorded blood pressure (BP), low density lipoprotein-cholesterol (LDL-C), recurrent ACS and death. We used data on dispensed drugs to calculate proportion of days covered for secondary prevention medications. Cox regressions were used to analyse the association of achieved BP and LDL-C to recurrent ACS and death.The median follow-up time was 4.8 years. Proportion of patients that reached BP <140/90mmHg was 58% year 1 and 66% year 8. 65% of the patients reached LDL-C<2.5mmol/L at year 1 and 56% at year 8, however adherence to statins varied from 43% to 60%. Only 62% of the patients had yearly measured BP, and only 28% yearly measured LDL-C. SBP was not associated with a higher risk of recurrent ACS or death. LDL-C of 3.0mmol/L were associated with a higher risk of recurrent ACS [HR 1.19 (95% CI 1.00-1.40)] and death HR 1.26 [(95% CI 1.08-1.47)] compared to an LDL-C 1.8mmol/L.This observational long-term real-world study demonstrates low drug adherence and potential for improvement of risk factors after ACS. Furthermore, the study confirms that uncontrolled LDL-C is associated with adverse outcome even in this older population.
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| 15. |
- Berg, Jenny, et al.
(författare)
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Determinants of Utility Based on the EuroQol Five-Dimensional Questionnaire in Patients with Chronic Heart Failure and Their Change Over Time: Results from the Swedish Heart Failure Registry
- 2015
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Ingår i: Value in Health. - : Wiley: No OnlineOpen / Elsevier. - 1098-3015 .- 1524-4733. ; 18:4, s. 439-448
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Tidskriftsartikel (refereegranskat)abstract
- Background: There is limited information on drivers of utilities in patients with chronic heart failure (CHF). Objectives: To analyze determinants of utility in CHF and drivers of change over 1 year in a large sample from clinical practice. Methods: We included 5334 patients from the Swedish Heart Failure Registry with EuroQol five-dimensional questionnaire information available following inpatient or outpatient care during 2008 to 2010; 3495 had 1-year follow-up data Utilities based on Swedish and UK value sets were derived. We applied ordinary least squares (OLS) and two-part models for utility at inclusion and OLS regression for change over 1 year, all with robust standard errors. We assessed the predictive accuracy of both models using cross-validation. Results: Patients mean age was 73 years, 65% were men, 19% had a left ventricular ejection fraction of 50% or more, 23% had 40% to 49%, 27% had 30% to 39%, and 31% had less than 30%. For both models and value sets, utility at inclusion was affected by sex, age, New York Heart Association class, ejection fraction, hemoglobin, blood pressure, lung disease, diabetes, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, nitrates, antiplatelets, and diuretics. The OLS model performed slightly better than did the two-part model on a population level and for capturing utility ranges. Change in utility over 1 year was influenced by age, sex, and (measured at inclusion) disease duration, New York Heart Association class, blood pressure, ischemic heart disease, lung disease, angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and antiplatelets. Conclusions: Utilities in CHF and their change over time are influenced by diverse demographic and clinical factors. Our findings can be used to target clinical interventions and for economic evaluations of new therapies.
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| 16. |
- Bjorkander, Inge, et al.
(författare)
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Differential Index : A Simple Time Domain Heart Rate Variability Analysis with Prognostic Implications in Stable Angina Pectoris
- 2008
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Ingår i: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 111:2, s. 126-133
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To examine the usefulness of time domain heart rate variability (HRV) measurements by a simple graphical method, the differential index (DI), in prognostic assessments of patients with chronic stable angina pectoris. METHODS: HRV measurements in the time domain by DI were compared to conventional measurements of standard deviation of all normal-to-normal intervals (SDNN), percent of differences between adjacent normal RR intervals >50 ms (PNN50) and square root of the mean of the sum of squares of differences between adjacent normal RR intervals (RMSSD) from 24-hour ambulatory electrocardiographic recordings in 678 patients in the Angina Prognosis Study in Stockholm. The patients received double-blind treatment with metoprolol or verapamil. Main outcome measures were cardiovascular death or non-fatal myocardial infarction during follow-up (median 40 months). RESULTS: Patients suffering cardiovascular death (n = 30) had lower DI, SDNN and PNN50 (all p < 0.001). In a multivariate Cox model, DI below median independently predicted cardiovascular death (p = 0.002), as did SDNN (p = 0.016) and PNN50 (p = 0.030), but not RMSSD (p = 0.10). The separation of survival curves was most pronounced and specificity was slightly better with DI. DI and PNN50 increased with metoprolol but not verapamil treatment. Short-term treatment effects were not related to prognosis. CONCLUSIONS: Low time domain HRV carries independent prognostic information regarding cardiovascular death in stable angina pectoris. The simple DI method provided equally good or better prognostic information than conventional, more laborious HRV methods.
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| 17. |
- Björkander, Inge, et al.
(författare)
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Long-term stability of heart rate variability in chronic stable angina pectoris, and the impact of an acute myocardial infarction
- 2009
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Ingår i: Clinical Physiology and Functional Imaging. - 1475-0961 .- 1475-097X. ; 30, s. 698-699
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Heart rate variability (HRV) reflects the balance between cardiac parasympathetic and sympathetic autonomic influences. Reduced HRV has adverse prognostic implications. The time course for changes in HRV over prolonged periods of time and the influence of an acute coronary event on HRV are not well established. METHODS: Heart rate variability was assessed in patients with chronic stable angina pectoris, who were followed for 3 years within the Angina Prognosis Study in Stockholm. Patients who suffered an acute myocardial infarction after the study were re-examined after this event. We assessed HRV by the simple geometric method differential index, and traditional time- and frequency-domain measurements of HRV. RESULTS: The differential index was essentially unchanged during the study (i.e. the ratio month 36/month 1 was 1.00 +/- 0.06, n = 261). Also most other time and frequency indices of HRV (SDNN, r-MSSD, SDNNIDX, total power, and VLF, LF, HF respectively; n = 63) remained largely unchanged; pNN50 and LF/HF were, however, less reproducible. In 21 patients with a subsequent acute myocardial infarction, SDNN, SDNNIDX, total power, LF and LF/HF were reduced following the event, whereas differential index, pNN50 and HF remained unchanged. CONCLUSIONS: Differential index and other indices of HRV are stable and reproducible in patients with chronic stable angina pectoris. High-frequency HRV (reflecting cardiac parasympathetic activity) and the differential index changed little following an acute coronary event, and may be suitable for predictions of the future risk of sudden death even in the presence of a recent acute coronary event.
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| 18. |
- Bokrantz, Tove, et al.
(författare)
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Antihypertensive drug classes and the risk of hip fracture: results from the Swedish primary care cardiovascular database.
- 2020
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Ingår i: Journal of hypertension. - 1473-5598. ; 38:1, s. 167-175
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Tidskriftsartikel (refereegranskat)abstract
- Hypertension and fractures related to osteoporosis are major public health problems that often coexist. This study examined the associations between exposure to different antihypertensive drug classes and the risk of hip fracture in hypertensive patients.We included 59246 individuals, 50 years and older, diagnosed with hypertension during 2001-2008 in the Swedish Primary Care Cardiovascular Database. Patients were followed from 1 January 2006 (or the date of diagnosis of hypertension) until they had their first hip fracture, died, or reached the end of the study on 31 December 2012. Cox proportional hazards models were used to calculate the risk of hip fracture across types of antihypertensive medications, adjusted for age, sex, comorbidity, medications, and socioeconomic factors.In total, 2593 hip fractures occurred. Compared to nonusers, current use of bendroflumethiazide or hydrochlorothiazide was associated with a reduced risk of hip fracture (hazard ratio 0.86; 95% CI 0.75-0.98 and hazard ratio 0.84; 95% CI 0.74-0.96, respectively), as was use of fixed drug combinations containing a thiazide (hazard ratio 0.69; 95% CI 0.57-0.83). Current use of loop diuretics was associated with an increased risk of hip fracture (hazard ratio 1.23; 95% CI 1.11-1.35). No significant associations were found between the risk of hip fracture and current exposure to beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, aldosterone-receptor blockers or calcium channel blockers.In this large observational study of hypertensive patients, the risk of hip fracture differed across users of different antihypertensive drugs, results that could have practical implications when choosing antihypertensive drug therapy.
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| 20. |
- Brändström, Helena, et al.
(författare)
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A single nucleotide polymorphism in the promoter region of the human gene for osteoprotegerin is related to vascular morphology and function
- 2002
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Ingår i: Biochemical and Biophysical Research Communications - BBRC. - 0006-291X .- 1090-2104. ; 293:1, s. 13-17
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Tidskriftsartikel (refereegranskat)abstract
- Osteoprotegerin (OPG) is a secreted member of the tumor necrosis factor receptor family, and has previously been shown to regulate bone mass by inhibiting osteoclast differentiation and activation. Recent evidence indicates that OPG also plays a role in the vascular system, since ablation of the OPG gene in mice results in calcification of the aorta and renal arteries, and association has been found between serum levels of OPG and cardiovascular mortality. This study presents a novel single nucleotide polymorphism, a T/C transition located 129 bp upstream the TATA-box of the human OPG gene, detected by sequence analysis. The OPG genotype was determined by restriction fragment length polymorphism in a cohort consisting of 59 healthy subjects. The intima-media thickness (IMT) in the common carotid artery and maximal post-ischemic forearm blood flow (FBF) were investigated. Subjects with the CC genotype showed a significantly increased IMT (p<0.05) and a concommitantly reduced maximal FBF (p<0.01) as compared to those with the T allele. Thus, our results show that the polymorphism in the promoter region of OPG is associated with both vascular morphology and function in apparently healthy subjects.
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| 21. |
- Brändström, Helena, et al.
(författare)
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A single nucleotide polymorphism in the promoter region of the osteoprotegerin gene is related to intima-media thickness of the carotid artery in hypertensive patients : The Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA)
- 2004
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Ingår i: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 13:3, s. 152-157
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Tidskriftsartikel (refereegranskat)abstract
- Osteoprotegerin (OPG) is a secreted member of the tumor necrosis factor receptor family, and in previous studies has been shown to regulate osteoclast activity and differentiation. Ablation of the OPG gene in mice results in calcification of the aorta and renal arteries. We have previously reported an association between a single nucleotide polymorphism in the promoter region of OPG and vascular morphology and function in healthy humans. The objective with this study was to confirm our previous results in a larger population, and in addition, to study subjects with hypertension. The OPG genotype was determined by restriction fragment length and the intima-media thickness (IMT) of the common carotid artery was measured by ultrasound in 100 patients with hypertension and left ventricular hypertrophy, and 75 healthy normotensive control subjects. In the hypertensive group subjects with the CC genotype (n=24) showed a significantly increased IMT compared to those with the TC (n=52, p=0.007) and TT (n=24, p=0.009) genotype, in the hypertensive group only (mean +/- SD for TT=0.88 +/- 0.21 mm, TC=0.90 +/- 0.16 mm, CC=1.05 +/- 0.31 mm). The allele distribution did not differ between hypertensive and control individuals. The present study confirms our previous finding and shows that polymorphism in the promoter region of OPG is associated with vascular morphology in hypertensive subjects.
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| 22. |
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| 23. |
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| 24. |
- Hallberg, Pär, et al.
(författare)
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Adipocyte-derived leucine aminopeptidase genotype and response to antihypertensive therapy
- 2003
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Ingår i: BMC Cardiovascular Disorders. - : Springer Science and Business Media LLC. - 1471-2261 .- 1471-2261. ; 18:3, s. 11-
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundAdipocyte-derived leucine aminopeptidase (ALAP) is a recently identified member of the M1 family of zinc-metallopeptidases and is thought to play a role in blood pressure control through inactivation of angiotensin II and/or generation of bradykinin. The enzyme seems to be particularly abundant in the heart. Recently, the Arg528-encoding allele of the ALAP gene was shown to be associated with essential hypertension.MethodsWe evaluated the influence of this polymorphism on the change in left ventricular mass index in 90 patients with essential hypertension and echocardiographically diagnosed left ventricular hypertrophy, randomised in a double-blind study to receive treatment with either the angiotensin II type I receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol for 48 weeks. Genyotyping was performed using minisequencing.ResultsAfter adjustment for potential covariates (blood pressure and left ventricular mass index at baseline, blood pressure change, age, sex, dose and added antihypertensive treatment), there was a marked difference between the Arg/Arg and Lys/Arg genotypes in patients treated with irbesartan; those with the Arg/Arg genotype responded on average with an almost two-fold greater regression of left ventricular mass index than patients with the Lys/Arg genotype (-30.1 g/m2 [3.6] vs -16.7 [4.5], p = 0.03).ConclusionsThe ALAP genotype seems to determine the degree of regression of left ventricular hypertrophy during antihypertensive treatment with the angiotensin II type I receptor antagonist irbesartan in patients with essential hypertension and left ventricular hypertrophy. This is the first report of a role for ALAP/aminopeptidases in left ventricular mass regulation, and suggests a new potential target for antihypertensive drugs.
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| 25. |
- 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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| 26. |
- Hallberg, Pär, et al.
(författare)
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Gender-specific association between preproendothelin-1 genotype and reduction of systolic blood pressure during antihypertensive treatment : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)
- 2004
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Ingår i: Clinical Cardiology. - : Wiley. - 0160-9289 .- 1932-8737. ; 27:5, s. 287-290
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Studies suggest that endothelin-1 contributes to the pathogenesis of hypertension. A G5665T gene polymorphism of preproendothelin-1 has been shown to be associated with higher blood pressure in overweight patients. No study has yet determined the effect of this polymorphism on the change in blood pressure during antihypertensive treatment.HYPOTHESIS:This study aimed to determine this effect in hypertensive patients with left ventricular (LV) hypertrophy during antihypertensive treatment with either irbesartan or atenolol.METHODS: We determined the preproendothelin-1 genotype using minisequencing in 102 patients with essential hypertension and LV hypertrophy verified by echocardiography, randomized in a double-blind fashion to treatment with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor antagonist atenolol.RESULTS:The change in systolic blood pressure (SBP) after 12 weeks of treatment was related to the preproendothelin-1 genotype in men; after adjustment for potential covariates (age, blood pressure, and LV mass index at study entry, dose of irbesartan/atenolol, and type of treatment), those carrying the T-allele responded on average with a more than two-fold greater reduction than those with the G/G genotype (-21.9 mmHg [13.9] vs. -8.9 [2.3], p = 0.007). No significant differences in blood pressure change between G/G and carriers of the T-allele were seen among women.CONCLUSIONS:Our finding suggests a gender-specific relationship between the G5665T preproendothelin-1 polymorphism and change in SBP in response to antihypertensive treatment with irbesartan or atenolol, suggesting the endothelin pathway to be a common mechanism included in the hypertensive action of the drugs.
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| 27. |
- 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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| 28. |
- Hallberg, Pär, et al.
(författare)
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Transforming growth factor beta1 genotype and change in left ventricular mass during antihypertensive treatment : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA)
- 2004
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Ingår i: Clinical Cardiology. - : Wiley. - 0160-9289 .- 1932-8737. ; 27:3, s. 169-73
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Angiotensin II, via the angiotensin II type 1 (AT1) receptor, may mediate myocardial fibrosis and myocyte hypertrophy seen in hypertensive left ventricular (LV) hypertrophy through production of transforming growth factor beta1 (TGF-beta1); AT1-receptor antagonists reverse these changes. The TGF-beta1 G + 915C polymorphism is associated with interindividual variation in TGF-beta1 production. No study has yet determined the impact of this polymorphism on the response to antihypertensive treatment. HYPOTHESIS: We aimed to determine whether the TGF-beta1 G + 915C polymorphism was related to change in LV mass during antihypertensive treatment with either an AT1-receptor antagonists or a beta1-adrenoceptor blocker. The polymorphism was hypothesized to have an impact mainly on the irbesartan group. METHODS: We determined the association between the TGF-beta1 genotype and regression of LV mass in 90 patients with essential hypertension and echocardiographically diagnosed LV hypertrophy, randomized in a double-blind study to receive treatment for 48 weeks with either the AT1-receptor antagonist irbesartan or the beta1-adrenoceptor blocker atenolol. RESULTS: Irbesartan-treated patients who were carriers of the C-allele, which is associated with low expression of TGF-beta1, responded with a markedly greater decrease in LV mass index (LVMI) than subjects with the G/G genotype (adjusted mean change in LVMI -44.7 g/m2 vs. -22.2 g/m2, p = 0.007), independent of blood pressure reduction. No association between genotype and change in LVMI was observed in the atenolol group. CONCLUSIONS: The TGF-beta1 G + 915C polymorphism is related to the change in LVMI in response to antihypertensive treatment with the AT1-receptor antagonist irbesartan.
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| 29. |
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| 30. |
- Hellqvist, Henrik, et al.
(författare)
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Estimation of aortic stiffness by finger photoplethysmography using enhanced pulse wave analysis and machine learning
- 2024
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Ingår i: Frontiers in Cardiovascular Medicine. - : Frontiers Media SA. - 2297-055X. ; 11
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Aortic stiffness plays a critical role in the evolution of cardiovascular diseases, but the assessment requires specialized equipment. Photoplethysmography (PPG) and single-lead electrocardiogram (ECG) are readily available in healthcare and wearable devices. We studied whether a brief PPG registration, alone or in combination with single-lead ECG, could be used to reliably estimate aortic stiffness. Methods: A proof-of-concept study with simultaneous high-resolution index finger recordings of infrared PPG, single-lead ECG, and finger blood pressure (Finapres) was performed in 33 participants [median age 44 (range 21–66) years, 19 men] and repeated within 2 weeks. Carotid–femoral pulse wave velocity (cfPWV; two-site tonometry with SphygmoCor) was used as a reference. A brachial single-cuff oscillometric device assessed aortic pulse wave velocity (aoPWV; Arteriograph) for further comparisons. We extracted 136 established PPG waveform features and engineered 13 new with improved coupling to the finger blood pressure curve. Height-normalized pulse arrival time (NPAT) was derived using ECG. Machine learning methods were used to develop prediction models. Results: The best PPG-based models predicted cfPWV and aoPWV well (root-mean-square errors of 0.70 and 0.52 m/s, respectively), with minor improvements by adding NPAT. Repeatability and agreement were on par with the reference equipment. A new PPG feature, an amplitude ratio from the early phase of the waveform, was most important in modelling, showing strong correlations with cfPWV and aoPWV (r = −0.81 and −0.75, respectively, both P < 0.001). Conclusion: Using new features and machine learning methods, a brief finger PPG registration can estimate aortic stiffness without requiring additional information on age, anthropometry, or blood pressure. Repeatability and agreement were comparable to those obtained using non-invasive reference equipment. Provided further validation, this readily available simple method could improve cardiovascular risk evaluation, treatment, and prognosis.
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| 31. |
- Holmlund, A., et al.
(författare)
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Soluble intercellular adhesion molecule-1 is related to endothelial vasodilatory function in healthy individuals
- 2002
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Ingår i: Atherosclerosis. - 0021-9150 .- 1879-1484. ; 165:2, s. 271-276
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate the associations between markers of systemic and vascular inflammation, and indicators of vascular morphology and function. METHODS: In 59 apparently healthy individuals, we measured serum levels of highly sensitive C-reactive protein (hsCRP), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin. Endothelium-dependent (EDV) and -independent (EIDV) vasodilatation was evaluated in the forearm by venous occlusion plethysmography and local infusions of methacholine and sodium nitroprussid. Endothelial function index (EFI) was expressed as the EDV/EIDV ratio. The intima-media thickness (IMT) of the common carotid artery was investigated with ultrasound (far wall). RESULTS: EFI was inversely related only to ICAM-1 (r=-0.31, P<0.02) by univariate analysis. This association remained significant after adjustment for age, sex, blood pressure, smoking and serum cholesterol. EFI did not relate to hsCRP, VCAM-1 or E-selectin. Neither hsCRP, nor the adhesion molecules were significantly related to carotid artery IMT. CONCLUSION: ICAM-1 was related to endothelial vasodilatory function, but not to IMT, suggesting that endothelial inflammatory activation is related to an impaired vascular relaxation in apparently healthy individuals.
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| 32. |
- Holmqvist, Lina, et al.
(författare)
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Cardiovascular outcome in treatment-resistant hypertension: results from the Swedish Primary Care Cardiovascular Database (SPCCD).
- 2018
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Ingår i: Journal of hypertension. - 1473-5598. ; 36:2, s. 402-409
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Tidskriftsartikel (refereegranskat)abstract
- To assess cardiovascular outcome in patients with treatment-resistant hypertension (TRH) compared with patients with nontreatment-resistant hypertension (HTN).Cohort study with data from 2006 to 2012 derived from the Swedish Primary Care Cardiovascular Database with hypertensive patients aged at least 30 years. TRH was defined as blood pressure at least 140/90mmHg despite medication adherence to three or more dispensed antihypertensive drug classes. Patients with cardiovascular comorbidity were excluded. The association between TRH and cardiovascular events with adjustment for important confounders was analyzed.We included 4317 TRH patients and 32282 HTN patients. TRH patients (61% women) were older (70 vs. 66 years), had higher SBP (152 vs. 141mmHg) and more diabetes (30 vs. 20%) (P<0.001 for all) compared with HTN patients. Mean follow-up time was 4.3 years. In the adjusted analysis, TRH patients had an increased risk for total mortality [hazard ratio 1.12; 95% confidence interval (CI), 1.03-1.23], cardiovascular mortality (hazard ratio 1.20; 95% CI, 1.03-1.40) and incident heart failure (hazard ratio 1.34; 95% CI, 1.17-1.54) but not for incident stroke (hazard ratio 1.03; 95% CI, 0.90-1.19) or transitoric ischemic attack (hazard ratio 1.12; 95% CI, 0.86-1.46) compared with HTN patients.Patients with TRH have a poor prognosis beyond blood pressure level, compared with hypertensive patients without TRH. In particular, the high risk for heart failure is of clinical importance and merits further investigation.
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| 33. |
- Holmqvist, Lina, et al.
(författare)
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Prevalence of treatment-resistant hypertension and important associated factors—results from the Swedish Primary Care Cardiovascular Database
- 2016
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Ingår i: Journal of the American Society of Hypertension. - : Elsevier BV. - 1933-1711 .- 1878-7436. ; 10:11, s. 838-846
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Tidskriftsartikel (refereegranskat)abstract
- © 2016 American Society of HypertensionWe aimed to describe the prevalence, treatment, and associated comorbidity of treatment-resistant hypertension (TRH). This registry-based cohort study from The Swedish Primary Care Cardiovascular Database assessed 53,090 hypertensive patients attending primary care. Patients adherent to antihypertensive treatment measured by pharmacy fills and with proportion of days covered ≥80% were included. The prevalence of TRH was 17% when considering all current TRH definitions. Adherence to mineralocorticoid receptor antagonists differed between TRH- and non-TRH patients (8 vs. 4%). Higher frequencies (prevalence ratio and 95% confidence intervals) of diabetes mellitus (1.59, 1.53–1.66), heart failure (1.55, 1.48–1.64), atrial fibrillation (1.33, 1.27–1.40), ischemic heart disease (1.25, 1.20–1.30), and chronic kidney disease (1.38, 1.23–1.54) were seen in patients with TRH compared to patients without TRH. These findings, in a population with valid data on medication adherence, emphasize a broad preventive approach for these high-risk patients.
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| 34. |
- Jekell, Andreas, et al.
(författare)
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Markers of inflammation, endothelial activation, and arterial stiffness in hypertensive heart disease and the effects of treatment : results from the SILVHIA study
- 2013
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Ingår i: Journal of Cardiovascular Pharmacology. - 0160-2446 .- 1533-4023. ; 62:6, s. 559-566
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Tidskriftsartikel (refereegranskat)abstract
- We assessed the contribution of blood pressure (BP), inflammation, and endothelial activation to the development of structural vascular and cardiac changes in hypertension. Furthermore, the effects of antihypertensive therapy were studied. We studied 114 patients with hypertension and left ventricular hypertrophy and 38 matched hypertensive subjects without cardiac hypertrophy and 38 normotensive subjects. The group with hypertension and cardiac hypertrophy were randomized to treatment with an angiotensin receptor blocker (irbesartan) or a beta-adrenergic receptor blocker (atenolol) for 48 weeks. Markers of inflammation (high-sensitive C-reactive protein, interleukin-6, leukocyte counts), vascular function (ambulatory aortic stiffness index, arterial compliance, and pulse pressure), and endothelial activation (E-selectin, intracellular adhesion molecule-1, vascular adhesion molecule-1) were assessed. Markers of inflammation and arterial stiffness were lowest in the normotensive group and highest in patients with hypertensive heart disease; endothelial markers were similar between groups. Inflammation was independently related to BP. Markers of arterial stiffness were independently related to BP and to a lesser extent to left ventricular mass. Antihypertensive treatment improved arterial compliance; inflammatory and endothelial markers remained unchanged. In conclusion, markers of inflammation and arterial stiffness are independently related to BP. Antihypertensive therapy seems to improve arterial stiffness, but effects on markers of inflammation and endothelial activation are small.
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| 35. |
- Jekell, Andreas, et al.
(författare)
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Treatment of hypertensive left ventricular hypertrophy
- 2018
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Ingår i: Current Pharmaceutical Design. - : Bentham Science Publishers Ltd.. - 1381-6128 .- 1873-4286. ; 24:37, s. 4391-4396
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Forskningsöversikt (refereegranskat)abstract
- Background: The development and risk potential of hypertension-induced left ventricular (LV) hypertrophy has been well described in epidemiological studies. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. However, the best treatment strategy is still debated, as well as the appropriate blood pressure target in these patients. Objective: We here review the treatment of LV hypertrophy and the potential benefit on clinical outcomes, against a background of the epidemiology and pathophysiology. Results: Both hemodynamic and non-hemodynamic mechanisms contribute to hypertensive LV hypertrophy, which is characterized by an inappropriate myocardial fibrosis. Stringent blood pressure control reduces LV hypertrophy. Blockers of the renin-angiotensin-aldosterone system may have valuable effects on cardiac and electrophysiological remodelling beyond the effects of blood pressure reduction. Thus, they represent a cornerstone in the treatment of hypertensive LV hypertrophy, but most often other antihypertensive drug classes need to be added. Current guidelines indicate a blood pressure target in most patients with hypertensive LV hypertrophy of 120–130/80 mmHg. Conclusions: LV hypertrophy and myocardial fibrosis are important characteristics of hypertensive heart disease and associated with untoward prognosis. Regression of LV hypertrophy reduces cardiovascular morbidity and mortality. New drugs under development may add additional benefit.
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| 36. |
- Johansson, Jonathan S M, et al.
(författare)
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Prediabetes and incident heart failure in hypertensive patients: Results from the Swedish Primary Care Cardiovascular Database.
- 2022
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Ingår i: Nutrition, metabolism, and cardiovascular diseases : NMCD. - : Elsevier BV. - 1590-3729 .- 0939-4753. ; 32:12, s. 2803-2810
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Tidskriftsartikel (refereegranskat)abstract
- The cardiovascular risk conferred by concomitant prediabetes in hypertension is unclear. We aimed to examine the impact of prediabetes on incident heart failure (HF) and all-cause mortality, and to describe time in therapeutic blood pressure range (TTR) in a hypertensive real-world primary care population.In this retrospective cohort study, 9628 hypertensive individuals with a fasting plasma glucose (FPG) in 2006-2010 but no diabetes, cardiovascular or renal disease were followed to 2016; median follow-up was 9 years. Prediabetes was defined as FPG 5.6-6.9mmol/L, and in a secondary analysis as 6.1-6.9mmol/L. Study outcomes were HF and all-cause mortality. Hazard ratios (HR) were compared for prediabetes with normoglycemia using Cox regression. All blood pressure values from 2001 to the index date (first FPG in 2006-2010) were used to calculate TTR. At baseline, 51.4% had prediabetes. The multivariable-adjusted HR (95% confidence intervals) was 0.86 (0.67-1.09) for HF and 1.06 (0.90-1.26) for all-cause mortality. For FPG defined as 6.1-6.9mmol/L, the multivariable-adjusted HR were 1.05 (0.80-1.39) and 1.42 (1.19-1.70), respectively. The prediabetic group had a lower TTR (p<0.05).Prediabetes was not independently associated with incident HF in hypertensive patients without diabetes, cardiovascular or renal disease. However, prediabetes was associated with all-cause mortality when defined as FPG 6.1-6.9mmol/L (but not as 5.6-6.9mmol/L). TTR was lower in the prediabetic group, suggesting room for improved blood pressure to reduce incident heart failure in prediabetes.
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| 37. |
- Kahan, Thomas, et al.
(författare)
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Hypertoni
- 2005
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Ingår i: Läkemedelsboken 2005. - 918557452X
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Bokkapitel (populärvet., debatt m.m.)
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| 38. |
- Kahan, Thomas, et al.
(författare)
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Hypertoni
- 2003
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Ingår i: Läkemedelsboken 2003/2004. - 9185574457
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 39. |
- Kahan, Thomas, et al.
(författare)
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Hypertoni
- 2007
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Ingår i: Läkemedelsboken 2007/2008. - 9185574570 ; , s. 279-294
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Bokkapitel (övrigt vetenskapligt/konstnärligt)
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| 40. |
- Kahan, Thomas, et al.
(författare)
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Hypertoni är största hotet mot global hälsa : ger ökad risk för framför allt hjärt–kärlsjukdom, demens och njursjukdom
- 2013
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Ingår i: Läkartidningen. - : Läkartidningen förlag AB. - 0023-7205 .- 1652-7518. ; 110:22, s. 1088-1089
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Tidskriftsartikel (refereegranskat)abstract
- Förhöjt blodtryck är i dag den viktigaste riskfaktorn av global betydelse för den totala sjukdomsbördan. Medelblodtrycket (åldersjusterat) sjunker i västerländska befolkningar. I Sverige beräknas omkring 2 miljoner individer ha hypertoni, och andelen ökar med en åldrande befolkning. Behandling av hypertoni ger stora behandlingsvinster. Trots detta når bara en av tre behandlade patienter i svensk sjukvård målblodtryck (lägre än 140/90 mm Hg).
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| 41. |
- Kahan, Thomas, et al.
(författare)
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Risk prediction in stable angina pectoris
- 2013
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Ingår i: European Journal of Clinical Investigation. - : Wiley. - 0014-2972 .- 1365-2362. ; 43:2, s. 141-151
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND:Although stable angina pectoris often carries a favourable prognosis, it remains important to identify patients with an increased risk of cardiovascular (CV) complications. Many new markers of disease activity and prognosis have been described. We evaluated whether common and easily accessible markers in everyday care provide sufficient prognostic information.MATERIALS AND METHODS:The Angina Pectoris Prognosis Study in Stockholm treated 809 patients (248 women) with stable angina pectoris with metoprolol or verapamil double blind during a median follow-up of 3·4 years, with a registry-based extended follow-up after 9·1 years. Clinical and mechanistic variables, including lipids and glucose, renal function, ambulatory and exercise-induced ischaemia, heart rate variability, cardiac and vascular ultrasonography, and psychosocial variables were included in an integrated analysis. Main outcome measures were nonfatal myocardial infarction (MI) and CV death combined.RESULTS: In all, 139 patients (18 women) suffered a main outcome. Independent predictive variables were (odds ratio [95% confidence intervals]), age (1·04 per year [1·00;1·08], P = 0·041), female sex (0·33 [0·16;0·69], P = 0·001), fasting blood glucose (1.29 per mM [1.14; 1.46], P < 0·001), serum creatinine (1·02 per μM [1·00;1·03], P < 0·001) and leucocyte counts (1·21 per 106 cells/L [1·06;1·40], P = 0·008). Smoking habits, lipids and hypertension or a previous MI provided limited additional information. Impaired fasting glucose was as predictive as manifest diabetes and interacted adversely with serum creatinine. Sexual problems were predictive among men.CONCLUSIONS:Easily accessible clinical and demographic variables provide a good risk prediction in stable angina pectoris. Impaired glucose tolerance and an elevated serum creatinine are particularly important.
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| 42. |
- Kurland, Lisa, et al.
(författare)
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Aldosterone synthase (CYP11B2) -344 C/T polymorphism is related to antihypertensive response : result from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial
- 2002
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Ingår i: American Journal of Hypertension. - : Elsevier. - 0895-7061 .- 1941-7225. ; 15:5, s. 389-93
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Our aim was to determine whether the aldosterone synthase (CYP11B2) -344 C/T polymorphism was associated with the blood pressure (BP)-lowering response to antihypertensive treatment. METHODS: Patients with mild-to-moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind study to receive treatment with either the angiotensin II type 1 (AT1) receptor antagonist irbesartan (n = 43), or the beta1-adrenergic receptor blocker atenolol (n = 43). The aldosterone synthase (CYP11B2) -344 C/T polymorphism was analyzed using solid-phase minisequencing and related to BP reduction after 3 months treatment. Serum aldosterone levels were measured. RESULTS: After 3 months treatment the mean reductions in BP were similar for both treatment groups. When assessing the systolic BP reduction in the irbesartan group, patients with the TT variant had a more pronounced reduction (-21 +/- 19 SD mm Hg, n = 17) than both the TC (-14 +/- 18 mm Hg, n= 18) and CC (0 +/- 17 mm Hg, n = 8) genotypes (P = .04). There was no association between this polymorphism and the diastolic BP response. The -344 C/T polymorphism was not associated with the BP response to atenolol. Nor was it related to the baseline serum aldosterone level. CONCLUSIONS: The aldosterone synthase -344 C/T polymorphism was related to the BP-lowering response in hypertensive patients treated with the AT1-receptor antagonist irbesartan.
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| 43. |
- Kurland, Lisa, et al.
(författare)
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Angiotensin converting enzyme gene polymorphism predicts blood pressure response to angiotensin II receptor type 1 antagonist treatment in hypertensive patients
- 2001
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Ingår i: Journal of Hypertension. - : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 19:10, s. 1783-1787
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To determine whether polymorphisms in the renin-angiotensin system can predict blood pressure-lowering response to antihypertensive treatment; more specifically, in response to treatment with irbesartan or atenolol. DESIGN AND METHODS: Eighty-six patients with hypertension were randomized to double-blind treatment with either the angiotensin II type 1 receptor antagonist irbesartan or the beta1 adrenergic receptor blocker atenolol and followed for 3 months. We analysed angiotensinogen T174M and M235T, angiotensin converting enzyme (ACE) I/D and angiotensin II type 1 receptor A1166C polymorphisms and related them to blood pressure reduction. RESULTS: The mean reductions in blood pressure were similar for both treatments. In the irbesartan group, individuals homozygous for the ACE gene I allele showed a greater reduction in diastolic blood pressure, exceeding those with the D allele (-18 +/- 11 SD versus -7 +/- 10 mmHg, P = 0.0096). This was not the case during treatment with atenolol, and the interaction term between type of treatment and ACE II genotype was significant (P = 0.0176). The angiotensinogen and angiotensin II type 1 receptor polymorhisms were not related to the response to treatment. CONCLUSIONS: ACE genotyping predicted the blood pressure-lowering response to antihypertensive treatment with irbesartan but not atenolol. Thus, specific genotypes might predict the response to specific antihypertensive treatment.
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| 44. |
- Kurland, Lisa, 1960-, et al.
(författare)
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Angiotensinogen gene polymorphisms : relationship to blood pressure response to antihypertensive treatment. Results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs Atenolol (SILVHIA) trial
- 2004
-
Ingår i: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225. ; 17:1, s. 8-13
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: The renin-angiotensin-aldosterone system (RAAS) is important for the development of hypertension, and several antihypertensive drugs target this system. Our aim was to determine whether specific single nucleotide polymorphisms (SNPs) in RAAS genes were related to the blood pressure (BP) lowering effect of antihypertensive treatment. METHODS: Patients with mild to moderate primary hypertension and left ventricular hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta(1)-adrenergic receptor blocker atenolol (n = 49) as monotherapy. A microarray-based minisequencing system was used to genotype 30 SNPs in seven genes in the RAAS. These polymorphisms were related to the antihypertensive response after 12 weeks treatment. RESULTS: The BP reductions were similar in the atenolol and the irbesartan groups. Presence of the angiotensinogen (AGT) -6A allele or the AGT 235T allele were both associated with the most pronounced systolic BP response to atenolol treatment (P =.001 when -6 AA+AG was compared with GG and P =.008 for presence of the 235T variant compared with 235 MM). CONCLUSIONS: We found that SNPs in the angiotensinogen gene were associated with the BP lowering response to atenolol. This study is limited by a relatively small sample size, and the results should therefore be viewed as preliminary. Despite this limitation, these results illustrate the potential of using SNP genotyping as a pharmacogenetic tool in antihypertensive treatment.
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| 45. |
- Kurland, Lisa, 1960-, et al.
(författare)
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Polymorphisms in the angiotensinogen and angiotensin II type 1 receptor gene are related to change in left ventricular mass during antihypertensive treatment : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation versus Atenolol (SILVHIA) trial
- 2002
-
Ingår i: Journal of Hypertension. - : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 20:4, s. 657-663
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Our aim was to determine if gene polymorphisms in the renin-angiotensin-aldosterone system (RAAS) were related to the degree of change in left ventricular hypertrophy (LVH) during antihypertensive treatment. METHODS AND RESULTS: Patients with essential hypertension and echocardiographically diagnosed LVH were included in a double-blind study to receive treatment with either the angiotensin II type 1 receptor (AT1-receptor) antagonist irbesartan (n = 41), or the beta-1 adrenergic receptor blocker atenolol (n = 43) as monotherapy for 3 months. The angiotensinogen T174M and M235T, the angiotensin-converting enzyme I/D, the AT1-receptor A1166C and the aldosterone synthase (CYP11B2) -344 C/T polymorphisms were analysed and related to the change in left ventricular mass (LVM). Patients with the angiotensinogen 174 TM genotype treated with irbesartan responded with the greatest reduction in LVM (-23 +/- 31SD g/m2 for TM and +0.5 +/- 18 g/m2 for TT, P = 0.005), independent of blood pressure reduction. Both the angiotensinogen 235 T-allele (P = 0.02) and the AT1-receptor 1166 AC genotype responded with the greatest reduction in LVM when treated with irbesartan (-0.1 +/- 19 g/m2 for AA and -18 +/- 30 g/m2 for AC, P = 0.02), independent of blood pressure reduction. These polymorphisms were not associated with the change in LVM during treatment with atenolol. DISCUSSION: The angiotensinogen T174M and M235T and the AT1-receptor A1166C polymorphisms were related to the change in LVH during antihypertensive treatment with an AT1-receptor antagonist; of these angiotensinogen T174M was the most powerful. This highlights the role of the RAAS for left ventricular hypertrophy and the potential of pharmacogenetics as a tool for guidance of antihypertensive therapy.
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| 46. |
- Kurland, Lisa, 1960-, et al.
(författare)
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The relationship between the plasma concentration of irbesartan and the antihypertensive response is disclosed by an angiotensin II type 1 receptor polymorphism : results from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs. Atenolol (SILVHIA) Trial
- 2008
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Ingår i: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225. ; 21:7, s. 836-839
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Tidskriftsartikel (refereegranskat)abstract
- Background The aim of this study was to investigate the effect of the plasma concentration of irbesartan, a specific angiotensin II type 1 receptor (AT1R) antagonist, and the blood pressure response in relation to AT1R gene polymorphisms. Methods Plasma irbesartan was analyzed in 42 patients with mild-to-moderate hypertension and left ventricular hypertrophy from the Swedish Irbesartan Left Ventricular Hypertrophy Investigation vs. Atenolol (SILVHIA) trial, who were treated with irbesartan as monotherapy for 12 weeks. Blood pressure and irbesartan concentration were measured at trough, i.e., 24 ± 3 h after the last dose. Five AT1R gene polymorphisms were analyzed by minisequencing. Results Neither the plasma concentration of irbesartan, nor any of the AT1R polymorphisms were associated with the blood pressure response to irbesartan treatment. However, the interaction term between the plasma concentration of irbesartan and the AT1R C5245T polymorphism was related to the reduction in systolic blood pressure after 12 weeks of treatment (P = 0.025). Furthermore, the plasma concentration of irbesartan was related to the change in systolic blood pressure in individuals homozygous for the AT1R 5245 T allele (r = -0.56, P = 0.030), but not for other genotypes. Conclusions There was an association between plasma concentrations of irbesartan and the blood pressure response for hypertensive patients with AT1R 5245 TT. Because of the small sample size, this study needs to be viewed as hypothesis generating. This is the first study, to our knowledge, indicating that the concentration–response relationship of an antihypertensive drug may be genotype dependent.
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| 47. |
- Liljedahl, Stefan, et al.
(författare)
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The effects of antihypertensive treatment on the doppler-derived myocardial performance index in patients with hypertensive left ventricular hypertrophy : results from the Swedish irbesartan in left ventricular hypertrophy investigation versus atenolol (SILVHIA)
- 2009
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Ingår i: Echocardiography. - : Wiley. - 0742-2822 .- 1540-8175. ; 26:7, s. 753-758
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. METHODS: The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. RESULTS: Antihypertensive treatment lowered MPI (mean difference -0.03 +/- 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (beta-coefficient -0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, beta-coefficient -0.39 P < 0.001) and peripheral vascular resistance (beta-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, beta-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. CONCLUSION: The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure.
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| 48. |
- Liljedahl, Ulrika, et al.
(författare)
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A microarray minisequencing system for pharmacogenetic profiling of antihypertensive drug response
- 2003
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Ingår i: Pharmacogenetics. - : Ovid Technologies (Wolters Kluwer Health). - 0960-314X .- 1473-561X. ; 13:1, s. 7-17
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Tidskriftsartikel (refereegranskat)abstract
- We aimed to develop a microarray genotyping system for multiplex analysis of a panel of single nucleotide polymorphisms (SNPs) in genes encoding proteins involved in blood pressure regulation, and to apply this system in a pilot study demonstrating its feasibility in the pharmacogenetics of hypertension. A panel of 74 SNPs in 25 genes involved in blood pressure regulation was selected from the SNP databases, and genotyped in DNA samples of 97 hypertensive patients. The patients had been randomized to double-blind treatment with either the angiotensin II type 1 receptor blocker irbesartan or the beta 1-adrenergic receptor blocker atenolol. Genotyping was performed using a microarray based DNA polymerase assisted 'minisequencing' single nucleotide primer extension assay with fluorescence detection. The observed genotypes were related to the blood pressure reduction using stepwise multiple regression analysis. The allele frequencies of the selected SNPs were determined in the Swedish population. The established microarray-based genotyping system was validated and allowed unequivocal multiplex genotyping of the panel of 74 SNPs in every patient. Almost 7200 SNP genotypes were generated in the study. Profiles of four or five SNP-genotypes that may be useful as predictors of blood pressure reduction after antihypertensive treatment were identified. Our results highlight the potential of microarray-based technology for SNP genotyping in pharmacogenetics.
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| 49. |
- Liljedahl, Ulrika, et al.
(författare)
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Single nucleotide polymorphisms in the apolipoprotein B and low density lipoprotein receptor genes affect response to antihypertensive treatment
- 2004
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Ingår i: BMC Cardiovascular Disorders. - : Springer Science and Business Media LLC. - 1471-2261 .- 1471-2261. ; 4:1, s. 16-
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Dyslipidemia has been associated with hypertension. The present study explored if polymorphisms in genes encoding proteins in lipid metabolism could be used as predictors for the individual response to antihypertensive treatment. METHODS: Ten single nucleotide polymorphisms (SNP) in genes related to lipid metabolism were analysed by a microarray based minisequencing system in DNA samples from ninety-seven hypertensive subjects randomised to treatment with either 150 mg of the angiotensin II type 1 receptor blocker irbesartan or 50 mg of the beta1-adrenergic receptor blocker atenolol for twelve weeks. RESULTS: The reduction in blood pressure was similar in both treatment groups. The SNP C711T in the apolipoprotein B gene was associated with the blood pressure response to irbesartan with an average reduction of 19 mmHg in the individuals carrying the C-allele, but not to atenolol. The C16730T polymorphism in the low density lipoprotein receptor gene predicted the change in systolic blood pressure in the atenolol group with an average reduction of 14 mmHg in the individuals carrying the C-allele. CONCLUSIONS: Polymorphisms in genes encoding proteins in the lipid metabolism are associated with the response to antihypertensive treatment in a drug specific pattern. These results highlight the potential use of pharmacogenetics as a guide for individualised antihypertensive treatment, and also the role of lipids in blood pressure control.
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| 50. |
- Liljedahl, Ulrika, et al.
(författare)
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Single nucleotide polymorphisms predict the change in left ventricular mass in response to antihypertensive treatment
- 2004
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Ingår i: Journal of Hypertension. - : Lippincott Williams & Wilkins. - 0263-6352 .- 1473-5598. ; 22:12, s. 2321-8
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Our aim was to determine whether the change in left ventricular (LV) mass in response to antihypertensive treatment could be predicted by multivariate analysis of single nucleotide polymorphisms (SNPs) in candidate genes reflecting pathways likely to be involved in blood pressure control. METHODS: Patients with mild to moderate primary hypertension and LV hypertrophy were randomized in a double-blind fashion to treatment with either the angiotensin II type 1 receptor antagonist irbesartan (n = 48) or the beta1 adrenoreceptor blocker atenolol (n = 49). A microarray-based minisequencing system was used for genotyping 74 SNPs in 25 genes. These genotypes were related to the change in LV mass index by echocardiography, after 12 weeks treatment as monotherapy, using stepwise multiple regression analysis. RESULTS: The blood pressure reductions were similar and significant in both treatment groups. Two SNPs in two separate genes (the angiotensinogen T1198C polymorphism, corresponding to the M235T variant and the apolipoprotein B G10108A polymorphism) for those treated with irbesartan, and the adrenoreceptor alpha2A A1817G for those treated with atenolol, significantly predicted the change in LV mass. The predictive power of these SNPs was independent of the degree of blood pressure reduction. CONCLUSION: SNPs in the angiotensinogen, apolipoprotein B, and the alpha2 adrenoreceptor gene predicted the change in LV mass during antihypertensive therapy. These results illustrate the potential of using microarray-based technology for SNP genotyping in predicting individual drug responses.
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