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Träfflista för sökning "WFRF:(Lonnebakken Mai T.) "

Sökning: WFRF:(Lonnebakken Mai T.)

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1.
  • Greve, Anders M., et al. (författare)
  • Contrasting Hemodynamic Mechanisms of Losartan- vs. Atenolol-Based Antihypertensive Treatment : A LIFE Study
  • 2012
  • Ingår i: American Journal of Hypertension. - 0895-7061. ; 25:9, s. 1017-1023
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND Pharmaceutical differences in central hemodynamics might influence cardiac response to antihypertensive treatment despite similar lowering of brachial blood pressure (BP). METHODS Data from all patients with at least two echocardiographic examinations in the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) echocardiographic substudy (n = 801); high-risk patients on losartan- vs. atenolol-based antihypertensive therapy. Echocardiography was performed annually for 4 years to measure stroke index (SI), heart rate, cardiac index (CI), conduit artery stiffness assessed as pulse pressure/stroke index (PP/SI) and total peripheral resistance index (TPRI). RESULTS Atenolol- and losartan-based therapy reduced BP similarly (cumulative difference in mean brachial blood pressure 0.3 mm Hg, P = 0.65). After 4 years the cumulative means of SI and heart rate were 1.8 ml/m(2) higher and 5.7 beats/min lower on atenolol-based treatment, respectively (both P < 0.001). This kept CI below baseline in atenolol-treated patients, whereas in the losartan group CI was unchanged from baseline throughout the study. TPRI was decreased more and remained lower in the losartan group (cumulative difference in mean TPRI 287 dynes/sec(-5)/cm/m(2), P < 0.001). These findings partly explained univariate differences in systolic- and diastolic function indices between the two treatments; fully adjusted losartan was only associated with a smaller left atrial diameter (cumulative mean difference 0.07 cm; 95% confidence intervals, -0.13 to -0.01, P = 0.03). CONCLUSIONS Contrasting hemodynamics impacted cardiac response to similar reductions in brachial BP on losartan- vs. atenolol-based therapy. The similar reduction of PP/SI suggests that the antihypertensive regimens used in the LIFE study had comparable effects on arterial stiffness (LIFE study; NCT00338260)
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2.
  • Lonnebakken, Mai T., et al. (författare)
  • In-treatment stroke volume predicts cardiovascular risk in hypertension
  • 2011
  • Ingår i: Journal of Hypertension. - 0263-6352. ; 29:8, s. 1508-1514
  • Tidskriftsartikel (refereegranskat)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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