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  • Result 31-40 of 53
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31.
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33.
  • Lonnebakken, Mai T., et al. (author)
  • In-treatment stroke volume predicts cardiovascular risk in hypertension
  • 2011
  • In: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 29:8, s. 1508-1514
  • Journal article (peer-reviewed)abstract
    • Objective To evaluate whether lower stroke volume during antihypertensive treatment is a predictor of cardiovascular events independent of left ventricular geometric pattern. Methods The association between left ventricular stroke volume and combined cardiovascular death, stroke and myocardial infarction, the prespecified primary study endpoint, was assessed in Cox regression analysis using data from baseline and annual follow-up visits in 855 patients during 4.8 years of randomized losartan-based or atenolol-based treatment in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy. Results During follow-up, a total of 91 primary endpoints occurred. At baseline, lower left ventricular stroke volume was associated with smaller body size, female sex, lower left ventricular mass and stress-corrected midwall shortening, higher relative wall thickness and total peripheral resistance, more concentric left ventricular geometry and impaired diastolic relaxation (all P<0.01). Baseline stroke volume did not predict outcome. However, in time-varying multivariable Cox regression analysis, lower in-treatment left ventricular stroke volume indexed for height(2.04) was associated with higher risk of cardiovascular events {hazard ratio 1.69 per 1 SD (6 ml/m(2.04)) lower stroke volume [95% confidence interval (CI) 1.35-2.11], P<0.001} independent of in-treatment left ventricular mass and concentric geometry and in a secondary model also independent of stress-corrected midwall shortening, impaired diastolic relaxation, heart rate, new-onset atrial fibrillation and study treatment [hazard ratio 1.46 per 1 SD (6 ml/m(2.04)) lower stroke volume (95% CI 1.13-1.88)]. Conclusion Assessment of in-treatment left ventricular stroke volume may reflect cardiac and vascular remodeling and impairment and, hence, adds information on cardiovascular risk in treated hypertensive patients beyond assessment of left ventricular structure alone. 
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34.
  • Mancusi, Costantino, et al. (author)
  • Higher pulse pressure/stroke volume index is associated with impaired outcome in hypertensive patients with left ventricular hypertrophy the LIFE study
  • 2017
  • In: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 26:3, s. 150-155
  • Journal article (peer-reviewed)abstract
    • We tested the prognostic impact of a marker of arterial stiffness, pulse pressure/stroke volume index (PP/SVi), in patients with hypertension and left ventricular (LV) hypertrophy. We used data from 866 patients randomized to losartan or atenolol-based antihypertensive treatment, over a median of 4.8 years, in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. The association of PP/SVi with outcomes was tested in Cox regression analyses and reported as hazard ratio (HR) and 95% confidence intervals (CI). In multivariate regression, reduction of PP/SVi was independently associated with male gender, reduction in systolic blood pressure (BP) and relative wall thickness and with an increase in left ventricular ejection fraction (all p < .05). After adjusting for confounders, higher baseline PP/SVi predicted a 38% higher hazard of combined major fatal and non-fatal cardiovascular events (95% CI 1.04-1.84), and higher hazard of cardiovascular mortality (HR 2.35 (95% CI 1.59-3.48) and stroke (HR 1.45 (95% CI 1.06-1.99) (all p < .05). Higher PP/SVi also predicts higher rate of hospitalization for HF (HR 2.15 (95% CI 1.48-3.12) and a 52% higher hazard of all-cause mortality (95% CI 1.10-2.09) (both p < .05). In hypertensive patients with electrocardiographic LV hypertrophy, higher PP/SVi was associated with increased cardiovascular morbidity and mortality.
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35.
  • Mancusi, Costantino, et al. (author)
  • Impact of isolated systolic hypertension on normalization of left ventricular structure during antihypertensive treatment (the LIFE study)
  • 2014
  • In: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 23:4, s. 206-212
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: We tested the impact of isolated systolic hypertension (ISH) on normalization of left ventricular (LV) structure during antihypertensive treatment.METHODS: Baseline and annual echocardiograms were recorded in 873 hypertensive patients with electrocardiographic signs of LV hypertrophy during 4.8 years randomized losartan- or atenolol-based antihypertensive treatment in the Losartan Intervention For Endpoint (LIFE) reduction in hypertension study and classified as having ISH (n = 128) if systolic BP ≥ 160 mmHg and diastolic BP < 90 mmHg, or non-ISH divided into two groups by systolic BP ≥ 160 mmHg (non-ISH ≥ 160 mmHg) (n = 645) and systolic BP < 160 mm Hg (n = 100) (non-ISH < 160 mmHg), respectively.RESULTS: Patients with ISH were older, with higher prevalence of diabetes than non-ISH groups and higher pulse pressure/stroke volume index (all p < 0.05). Baseline systolic blood pressure (BP) differed between groups and was highest in the non-ISH ≥ 160 mmHg group (p < 0.05). Systolic BP reduction was less in the ISH group (p < 0.05). LV geometry did not differ between ISH and non-ISH ≥ 160 mmHg groups at baseline, but ISH had more residual LV hypertrophy of concentric type at the last study visit (p < 0.05). In multivariate analysis, less reduction of LV mass was predicted by ISH (β = - 0.07) independent of significant associations with baseline LVMi (β = 0.52) and atenolol-based treatment (β = - 0.08) and clinical confounders (all p < 0.05).CONCLUSIONS: ISH is associated with impaired normalization of LV mass during systematic antihypertensive treatment. The findings may help explain the higher cardiovascular event rate previously reported in ISH patients.
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39.
  • Okin, Peter M, et al. (author)
  • Competing effects of hypokalemia and hydrochlororothiazide treatment  on regression of Cornell product left ventricular hypertrophy  in hypertensive patients : implications for the development of potassium-sparing diuretics
  • 2009
  • In: Circulation. - 0009-7322 .- 1524-4539. ; 120:Suppl. 18, s. s1015-s1015
  • Journal article (other academic/artistic)abstract
    • Background: Hydrochlorothiazide (HCTZ) treatment is associated with blood pressure reduction and regression of left ventricular hypertrophy (LVH). HCTZ is also associated with hypokalemia (hypoK), which increases blood pressure and is associated with a greater likelihood and severity of electrocardiographic (ECG) LVH. However, the competing effects of HCTZ use and concomitant hypoK on LVH regression have not been examined. Methods: Baseline and yearly Cornell product (CP) ECG LVH levels were examined in relation to hypoK (serum K 3.90, the lowest quartile) and HCTZ use in 7816 patients in the LIFE study with baseline and year-1 K levels. Patients were randomized to losartan vs atenolol-based treatment and additional HCTZ as needed. Results: Patients on HCTZ had lower serum K levels at year 1 (4.05 ± 0.38 vs 4.24 ± 0.38), year 2 (4.04 ± 0.38 vs 4.25 ± 0.38), year 3 (4.04 ± 0.39 vs 4.27 ± 0.39) and year 4 (4.05 ± 0.41 vs 4.26 ± 0.38) of the study (all p < 0.001). In 2-way analysis of covariance adjusting for age, sex, race, prior and randomized treatment, yearly body mass index, serum glucose and creatinine, and for baseline and change in diastolic and systolic pressure, hypoK was associated with less mean reduction of CP LVH whereas HCTZ use was associated with greater regression of CP LVH between baseline and years 1 to 4. Multivariate logistic regression analyses with the same covariates revealed that hypoK was associated with a statistically significant 15 to 19% lower likelihood of median (236 mm·ms) reduction in CP LVH while HCTZ use was associated with an 18 to 33% greater likelihood of CP LVH regression of 236 mm·ms between baseline and years 1 to 4. Conclusions: HCTZ therapy is independently associated with a greater likelihood and magnitude of LVH regression whereas concomitant hypoK is associated with a competing lower likelihood and magnitude of LVH regression during antihypertensive therapy. These findings suggest that hypoK may blunt regression of LVH during treatment.
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40.
  • Okin, Peter M., et al. (author)
  • Digoxin use and risk of mortality in hypertensive patients with atrial fibrillation
  • 2015
  • In: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 33:7, s. 1480-1486
  • Journal article (peer-reviewed)abstract
    • Background: Digoxin is widely used for rate control of atrial fibrillation. However, recent studies have reported conflicting results on the association of digoxin with mortality when used in patients with atrial fibrillation. Moreover, the relationship of digoxin use to mortality in hypertensive patients with atrial fibrillation has not been examined.Methods and results: All-cause mortality was examined in relation to in-treatment digoxin use in 937 hypertensive patients with ECG left ventricular hypertrophy in atrial fibrillation at baseline (n = 134) or who developed atrial fibrillation during follow-up (n = 803), randomly assigned to losartan or atenolol-based treatment, in post-hoc analysis of a substudy of the Losartan Intervention For Endpoint Reduction in hypertension (LIFE) trial. During 4.7 ± 1.1 years of mean follow-up, 167 patients died (17.8%) and 372 (39.7%) were treated with digoxin. In univariate Cox analyses, in-treatment digoxin use, entered as a time-varying covariate, was associated with a 61% higher risk of dying (hazard ratio 1.61, 95% confidence interval 1.18–2.19, P = 0.003). After adjusting for other univariate predictors of death in this population, including age, diabetes, history of ischemic heart disease, stroke, or heart failure, baseline Cornell product, QRS duration, heart rate, serum glucose, creatinine and high-density lipoprotein cholesterol, and a propensity score for digoxin use entered as standard covariates, and for in-treatment heart rate, pulse pressure, and Sokolow–Lyon voltage treated as time-varying covariates, digoxin use was no longer a significant predictor of mortality (hazard ratio 1.04, 95% confidence interval 0.73–1.48, P = 0.839).Conclusion: In hypertensive patients with ECG left ventricular hypertrophy with existing or new atrial fibrillation, digoxin use is not associated with a significantly increased risk of all-cause mortality after adjusting for other independent predictors of death and for the factors associated with the propensity to use digoxin in this population. These findings suggest that factors other than digoxin use may account for the increased mortality found with digoxin use in some studies.
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  • Result 31-40 of 53

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