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Träfflista för sökning "WFRF:(Kahan Thomas) srt2:(2005-2009)"

Sökning: WFRF:(Kahan Thomas) > (2005-2009)

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1.
  • Aspberg, Sara, et al. (författare)
  • Fetal and perinatal risk factors for inflammatory bowel disease
  • 2006
  • Ingår i: Acta Pædiatrica. - : Wiley. - 1651-2227 .- 0803-5253. ; 95:8, s. 1001-1004
  • 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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2.
  • Aspberg, Sara, et al. (författare)
  • Is neonatal phototherapy associated with an increased risk for hospitalized childhood bronchial asthma?
  • 2007
  • Ingår i: Pediatric Allergy and Immunology. - : Wiley. - 0905-6157 .- 1399-3038. ; 18:4, s. 313-319
  • 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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3.
  • Bjorkander, Inge, et al. (författare)
  • Differential Index : A Simple Time Domain Heart Rate Variability Analysis with Prognostic Implications in Stable Angina Pectoris
  • 2008
  • Ingår i: Cardiology. - : S. Karger AG. - 0008-6312 .- 1421-9751. ; 111:2, s. 126-133
  • 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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4.
  • Björkander, Inge, et al. (författare)
  • Long-term stability of heart rate variability in chronic stable angina pectoris, and the impact of an acute myocardial infarction
  • 2009
  • Ingår i: Clinical Physiology and Functional Imaging. - 1475-0961 .- 1475-097X. ; 30, s. 698-699
  • 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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5.
  • Kahan, Thomas, et al. (författare)
  • Hypertoni
  • 2005
  • Ingår i: Läkemedelsboken 2005. - 918557452X
  • Bokkapitel (populärvet., debatt m.m.)
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6.
  • Kahan, Thomas, et al. (författare)
  • Hypertoni
  • 2007
  • Ingår i: Läkemedelsboken 2007/2008. - 9185574570 ; , s. 279-294
  • Bokkapitel (övrigt vetenskapligt/konstnärligt)
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7.
  • Kurland, Lisa, 1960-, et al. (författare)
  • 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
  • Ingår i: American Journal of Hypertension. - : Oxford University Press (OUP). - 0895-7061 .- 1941-7225. ; 21:7, s. 836-839
  • 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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8.
  • Liljedahl, Stefan, et al. (författare)
  • 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
  • Ingår i: Echocardiography. - : Wiley. - 0742-2822 .- 1540-8175. ; 26:7, s. 753-758
  • 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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