| 61. |
- Okin, Peter M, et al.
(författare)
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Incidence of atrial fibrillation in relation to changing heart rate over time in hypertensive patients : the LIFE study
- 2008
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Ingår i: Circulation - Arrhythmia and Electrophysiology. - 1941-3149. ; 1:5, s. 337-343
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Tidskriftsartikel (refereegranskat)abstract
- Background— Onset of atrial fibrillation (AF) has been linked to changes in autonomic tone, with increasing heart rate (HR) immediately before AF onset in some patients suggesting a possible role of acute increases in sympathetic activity in AF onset. Although losartan therapy and decreasing ECG left ventricular hypertrophy are associated with decreased AF incidence, the relationship of HR changes over time to development of AF has not been examined. Methods and Results— HR was evaluated in 8828 hypertensive patients without AF by history or on baseline ECG in the Losartan Intervention for End Point Reduction in Hypertension (LIFE) study. Patients were treated with losartan- or atenolol-based regimens and followed with serial ECGs annually which were used to determine HR and ECG left ventricular hypertrophy by Cornell product and Sokolow-Lyon voltage criteria. During mean follow-up of 4.7±1.1 years, new-onset AF occurred in 701 patients (7.9%). Patients with new AF had smaller decreases in HR to last in-treatment ECG or last ECG before AF (−2.7±13.5 versus −5.2±12.5 bpm), whether on losartan- (−0.4±13.5 versus −2.2±11.7 bpm) or atenolol-based treatment (−5.3±12.8 versus −8.3±12.6 bpm, all P<0.001). In univariate Cox analyses, higher HR on in-treatment ECGs was associated with an increased risk of new-onset AF, with a 15% greater risk of AF for every 10 bpm higher HR (95% CI 8% to 22%). In alternative analyses, persistence or development of a HR≥84 (upper quintile of baseline HR) was associated with a 46% greater risk of developing AF (95% CI 19% to 80%). After adjusting for treatment with losartan versus atenolol, baseline risk factors for AF, baseline and in-treatment systolic and diastolic pressure and the known predictive value of baseline and in-treatment ECG left ventricular hypertrophy for new AF, higher in-treatment HR remained strongly associated with new AF with a 19% higher risk for every 10 bpm higher HR (95% CI 10% to 28%) or a 61% increased rate of AF in patients with persistence or development of a HR≥84 (95% CI 27% to 104%, all P<0.001). Conclusion— Higher in-treatment HR on serial ECGs is associated with an increased likelihood of new-onset AF, independent of treatment modality, blood pressure lowering, and regression of ECG left ventricular hypertrophy in patients with essential hypertension.
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| 62. |
- Okin, Peter M., et al.
(författare)
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The relationship of electrocardiographic left ventricular hypertrophy to decreased serum potassium
- 2012
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Ingår i: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 21:3, s. 146-152
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Tidskriftsartikel (refereegranskat)abstract
- Background. Low serum potassium (K) is associated with increased blood pressure, impaired cardiac function and renal dysfunction. Although lower serum K is associated with cardiac hypertrophy in animal models, the relationship of low serum K to the presence and severity of electrocardiographic left ventricular hypertrophy (LVH) is unclear. Methods. Baseline and yearly Cornell product LVH levels were examined in relation to low serum K (serum K <= 3.90 mEq/l, the lowest quartile of baseline K levels) in 8586 patients with baseline K levels. Patients were randomized to losartan-vs atenolol-based treatment and additional hydrochlorothiazide (HCTZ) therapy as needed. Results. After adjusting for age, sex, race, prior antihypertensive treatment, losartan vs atenolol therapy, HCTZ use, baseline diastolic and systolic pressure, body mass index, serum creatinine and urine albumin/creatinine ratio, baseline serum K <= 3.90 was associated with significantly higher mean baseline Cornell product LVH (2898 vs 2801 mm.ms, p = 0.001) and a 24% higher risk of Cornell product LVH > 2440 mm.ms at baseline (OR 1.24, 95% CI 1.11-1.38, p < 0.001). After also adjusting for baseline Cornell product and changes in diastolic and systolic pressure between baseline and each year of measurement, in-treatment serum K <= 3.90 determined yearly was associated with significantly higher mean Cornell product LVH at years 1-3 and with statistically signifi cant 16-32% increased risks of LVH by Cornell product at years 1-4. Conclusions. A low serum K is independently associated with a greater likelihood and severity of Cornell product LVH during antihypertensive therapy.
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| 63. |
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| 64. |
- Olsen, Michael H., et al.
(författare)
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Changes in subclinical organ damage vs. in Framingham risk score for assessing cardiovascular risk reduction during continued antihypertensive treatment : a LIFE substudy
- 2011
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 29:5, s. 997-1004
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Tidskriftsartikel (refereegranskat)abstract
- Aim: To investigate whether in-treatment measurements of subclinical organ damage (SOD) assessed by elevated urine albumin/creatinine ratio (UACR) or electrocardiographic left ventricular hypertrophy improved the prediction of the composite cardiovascular endpoint of cardiovascular death, nonfatal myocardial infarction and stroke beyond in-treatment Framingham risk score (FRS).Methods: Excluding patients with a composite cardiovascular endpoint within the first year of treatment, 598 endpoints occurred in 6460 patients from the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study with baseline and 1 year values for UACR, left ventricular hypertrophy by electrocardiography and FRS available.Results: Using Cox-regression analyses, FRS1year [hazard ratio = 1.006 (0.98-1.04)] did not predict the endpoint independently of history of cardiovascular disease [hazard ratio = 1.76 (1.49-2.08)], FRSbaseline [hazard ratio = 1.07 (1.04-1.11)], UACR(baseline) [hazard ratio = 1.15 (1.07-1.23), all three P < 0.001], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.006-1.02), P < 0.01] and treatment allocation, whereas Cornell product(1yea)r [hazard ratio = 1.01 (1.006-1.02), P < 0.001] and to some degree UACR(1year) [hazard ratio = 1.05 (0.99-1.10), P = 0.09] predicted the endpoint independently of history of cardiovascular disease [hazard ratio = 1.71 (1.44-2.02)], FRSbaseline [hazard ratio = 1.08 (1.06-1.10)], Sokolow-Lyon(baseline) [hazard ratio = 1.01 (1.007-1.02), both P < 0.001], UACR(baseline) [hazard ratio = 1.11 (1.03-1.20), P < 0.01] and treatment allocation decreasing -2 Log likelihood significantly (P < 0.01).Presence of left ventricular hypertrophy by Cornell product1year or UACR(1year) at least 1 mmol/l [hazard ratio = 1.40 (1.15-1.70), P = 0.001] but not FRS1year above the median baseline value of 20 [hazard ratio = 1.22 (0.94-1.57), not significant] was associated with higher risk of subsequent endpoint after adjustment for history of cardiovascular disease [hazard ratio = 1.82 (1.54-2.15)], FRSbaseline at least 20 [hazard ratio = 1.67 (1.30-2.16)], left ventricular hypertrophy by Sokolow-Lyonbaseline or UACR(baseline) at least 1 mmol/l [hazard ratio = 1.61 (1.33-1.94), all P < 0.001] and treatment allocation [hazard ratio = 0.93 (0.79-1.09), not significant]. In contrast to FRS1year at least 20 decreased, SOD1year decreased -2Log likelihood significantly (P < 0.01).Conclusion: Cornell product(1year) and UACR(1year) improved in contrast to FRS1year risk prediction based on FRSbaseline, Sokolow-Lyon(baseline) and UACR(baseline) significantly in LIFE patients during antihypertensive treatment.
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| 65. |
- Olsen, Michael Hecht, et al.
(författare)
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Effects of losartan compared with atenolol on lipids in patients with hypertension and left ventricular hypertrophy : the losartan intervention for endpoint reduction in hypertension (LIFE) study
- 2009
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 27:3, s. 567-574
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Tidskriftsartikel (refereegranskat)abstract
- Objective: Beta-blockers and angiotensin II receptor blockers have different effects on lipids. Methods: We examined lipid levels in the Losartan Intervention For Endpoint reduction in hypertension study and their impact on the primary composite endpoint of cardiovascular death, myocardial infarction, or stroke. We measured total and high-density lipoprotein cholesterol at baseline and annually during 4.8 years of losartan-based compared with atenolol-based treatment in 8611 patients with hypertension and left ventricular hypertrophy. Results: Patients randomized to losartan-based or atenolol-based treatment had similar baseline total (6.04 ± 1.12 vs. 6.05 ± 1.13 mmol/l, NS) and high-density lipoprotein (HDL) cholesterol (1.50 ± 0.44 vs. 1.49 ± 0.44 mmol/l, NS). Total cholesterol decreased significantly but equally (-0.37 ± 1.05 vs. -0.34 ± 1.09 mmol/l, NS), whereas HDL cholesterol decreased less during the first 2 years in patients randomized to losartan compared with atenolol (-0.13 ± 0.24 vs. -0.19 ± 0.25 mmol/l) and remained higher each year (1.38, 1.37, 1.42, 1.47, and 1.48 mmol/l vs. 1.32, 1.30, 1.36, 1.40, and 1.42 mmol/l, all P < 0.001) independent of hydrochlorothiazide or statin treatment. In Cox regression analysis, baseline total cholesterol [hazard ratio (HR) = 1.08 (1.02–1.14) per mmol/l, P < 0.01], HDL cholesterol [HR = 0.56 (0.48–0.66) per mmol/l, P < 0.001], and treatment allocation [HR = 0.86 (0.76–0.98), P < 0.05] predicted composite endpoint independently. Using time-varying analyses, the predictive strength of HDL cholesterol was increased [HR = 0.36 (0.30–0.44) per mmol/l, P < 0.001], whereas that of total cholesterol [HR = 1.03 (0.97–1.09) per mmol/l, NS] and treatment allocation [HR = 0.91 (0.80–1.03), NS] were reduced. Conclusion: Losartan blunted the decrease in HDL cholesterol during antihypertensive treatment in the LIFE study. Higher intreatment HDL cholesterol was associated with fewer composite endpoints and may partly explain the better outcome of losartan-based treatment.
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| 66. |
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| 67. |
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| 68. |
- Padmanabhan, Sandosh, et al.
(författare)
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Genome-Wide Association Study of Blood Pressure Extremes Identifies Variant near UMOD Associated with Hypertension
- 2010
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Ingår i: PLoS Genetics. - : Public Library of Science (PLoS). - 1553-7404. ; 6:10
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Tidskriftsartikel (refereegranskat)abstract
- Hypertension is a heritable and major contributor to the global burden of disease. The sum of rare and common genetic variants robustly identified so far explain only 1%-2% of the population variation in BP and hypertension. This suggests the existence of more undiscovered common variants. We conducted a genome-wide association study in 1,621 hypertensive cases and 1,699 controls and follow-up validation analyses in 19,845 cases and 16,541 controls using an extreme case-control design. We identified a locus on chromosome 16 in the 59 region of Uromodulin (UMOD; rs13333226, combined P value of 3.6x10(-11)). The minor G allele is associated with a lower risk of hypertension (OR [95% CI]: 0.87 [0.84-0.91]), reduced urinary uromodulin excretion, better renal function; and each copy of the G allele is associated with a 7.7% reduction in risk of CVD events after adjusting for age, sex, BMI, and smoking status (H.R. = 0.923, 95% CI 0.860-0.991; p = 0.027). In a subset of 13,446 individuals with estimated glomerular filtration rate (eGFR) measurements, we show that rs13333226 is independently associated with hypertension (unadjusted for eGFR: 0.89 [0.83-0.96], p = 0.004; after eGFR adjustment: 0.89 [0.83-0.96], p = 0.003). In clinical functional studies, we also consistently show the minor G allele is associated with lower urinary uromodulin excretion. The exclusive expression of uromodulin in the thick portion of the ascending limb of Henle suggests a putative role of this variant in hypertension through an effect on sodium homeostasis. The newly discovered UMOD locus for hypertension has the potential to give new insights into the role of uromodulin in BP regulation and to identify novel drugable targets for reducing cardiovascular risk.
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| 69. |
- Russell, David, et al.
(författare)
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Cardiovascular Events in Subgroups of Patients During Primary Treatment of Hypertension With Candesartan or Losartan
- 2011
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Ingår i: Journal of Clinical Hypertension. - : Wiley. - 1524-6175. ; 13:3, s. 189-197
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Tidskriftsartikel (refereegranskat)abstract
- Merging data from existing electronic patient records, and electronic hospital discharge and cause of death registers, is a fast and relatively inexpensive method for comparing different treatments with regard to clinical outcome. This study compared the effects of antihypertensive treatment with candesartan or losartan on cardiovascular disease (CVD) using Swedish registers. Patients without previous CVD who were prescribed candesartan (n=7329) or losartan (n=6771) for hypertension during 1999-2007 at 72 Swedish primary care centers were followed for up to 9 years. Both medications were given according to current recommendations, and there was no difference observed in achieved blood pressures. The authors have previously shown that candesartan lowered the risk of all CVD (primary composite end point) more so than losartan (adjusted hazard ratio, 0.86; 95% confidence interval, 0.77-0.96). Candesartan also had a significantly better effect with regards to reducing the development of heart failure, cardiac arrhythmias, and peripheral arterial disease. In the present analysis, the authors found that candesartan, compared with losartan, reduced the risk of all CVD, irrespective of sex, age, previous antihypertensive treatment, baseline blood pressure, and presence of diabetes. These clinical findings may reflect differences between candesartan and losartan in their binding characteristics to the angiotensin type 1 receptor.
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| 70. |
- Ruwald, Anne Christine H., et al.
(författare)
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Losartan versus atenolol-based antihypertensive treatment reduces cardiovascular events especially well in elderly patients : the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study
- 2012
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 30:6, s. 1252-1259
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Tidskriftsartikel (refereegranskat)abstract
- Background: The Losartan Intervention For Endpoint reduction in hypertension (LIFE) study has previously demonstrated a beneficial effect of losartan compared to atenolol-based antihypertensive treatment in patients with essential hypertension and left-ventricular hypertrophy (LVH). However, patient age often influences the choice of antihypertensive drugs. Therefore, we investigated the influence of age on the effects of losartan versus atenolol-based antihypertensive treatment. Methods: A total of 9193 hypertensive patients with LVH aged 45-83 years were followed for a mean of 4.8 years. Blood pressure, high-density lipoprotein cholesterol (HDL-C), Sokolow-Lyon voltage, Cornell voltage-duration product and urine albumin-creatinine ratio (UACR) were measured yearly throughout the study. Patients were divided into two age groups according to the median age of 67 years and the effects of losartan versus atenolol-based antihypertensive treatment on the primary composite endpoint (CEP) consisting of cardiovascular death, nonfatal stroke or nonfatal myocardial infarction were investigated. Results: The beneficial effect of losartan versus atenolol-based treatment was greater in the group of patients older than 67 years [hazard ratio 0.79 (0.69-0.91), P=0.001] compared to the group of patients younger than 67 years [hazard ratio 1.03 (0.82-1.28), P=0809], P=0.045 for interaction. The beneficial effects of losartan versus atenolol-based antihypertensive treatment on pulse pressure, HDL-C, UACR, and Cornell and Sokolow-Lyon voltage were not more pronounced in patients older than 67 years compared to patients younger than 67 years. All five risk factors considered as time-varying covariates predicted CEP independently (P<0.01) with the exception of pulse pressure (P=0.37) and the interaction between age and treatment on outcome remained significant (P=0.042). Conclusions: We showed a greater beneficial effect of losartan versus atenolol-based antihypertensive treatment in the group of patients older than 67 years compared to the group of patients younger than 67 years. This difference was not explained by a more pronounced effect of losartan-based treatment on any of the cardiovascular risk factors demonstrated to have independent prognostic importance.
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