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- Moller, JE, et al.
(författare)
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Effects of losartan and captopril on left ventricular systolic and diastolic function after acute myocardial infarction : Results of the Optimal Trial in Myocardial Infarction with Angiotensin II Antagonist Losartan (OPTIMAAL) echocardiographic substudy
- 2004
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Ingår i: American Heart Journal. - : Elsevier BV. - 0002-8703 .- 1097-6744. ; 147:3, s. 494-501
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Tidskriftsartikel (refereegranskat)abstract
- Background Angiotensin-converting enzyme inhibitors have been shown to attenuate adverse remodeling after acute myocardial infarction (AMI), and the same has been suggested for angiotensin 11 type I receptor antagonists in animal models. Therefore the aim of the study was to compare the effects of losartan and captopril on regional systolic, diastolic, and overall left ventricular (LV) function after AMI. Methods Two hundred twenty-five patients aged 50 years with documented AMI and heart failure and/or LV dysfunction were randomly assigned treatment with either losartan (50 mg/d) or captopril (50 mg 3 times/d). Echocardiography was performed at randomization and after 3 months, echocardiograms were analyzed blinded at the core laboratory. Main outcome measures were changes in wall motion score index (WMSI), E-wave deceleration time (E-DT), and Tei index of overall LV function. Results WMSI decreased in both groups (losartan 1.58 +/- 0.23 to 1.52 +/- 0.26, P = .009, captopril 1.60 +/- 0.24 to 1.48 +/- 0.22, P < .001), although the decrease was greater in patients allocated to captopril (captopril -0.12 &PLUSMN, 0.17 vs losartan -0.05 &PLUSMN, 0.19, P = .007). In both groups E-DT increased, although the increase was significant only in patients treated with captoril (193 &PLUSMN, 61 ms to 208 &PLUSMN, 70 ms, P = .05). The change in E-DT was not different between treatment groups (captopril 14 &PLUSMN, 74 ms vs losartan 7 &PLUSMN, 80 ms, P = .52). Tei index decreased in both groups (losartan 0.59 &PLUSMN, 0.13 to 0.55 &PLUSMN, 0.15, P = .04, captopril 0.62 &PLUSMN, 0.15 to 0.55 &PLUSMN, 0.13, P < .001). However, the reduction was significantly greater in patients treated with captopril (captopril -0.08 +/- 0.14 vs losartan -0.03 +/- 0.14, P = .01). Conclusion Losartan and captopril improve systolic and overall IV function after AMI, but the benefit is greater for patients treated with captopril.
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- Aimo, Alberto, et al.
(författare)
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High-sensitivity troponin T, NT-proBNP and glomerular filtration rate : A multimarker strategy for risk stratification in chronic heart failure
- 2019
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Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 277, s. 166-172
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Tidskriftsartikel (refereegranskat)abstract
- Background: In a recent individual patient data meta-analysis, high-sensitivity troponin T (hs-TnT) emerged as robust predictor of prognosis in stable chronic heart failure (HF). In the same population, we compared the relative predictive performances of hs-TnT, N-terminal fraction of pro-B-type natriuretic peptide (NT-proBNP), hs-C-reactive protein (hs-CRP), and estimated glomerular filtration rate (eGFR) for prognosis.Methods and results: 9289 patients (66 ± 12 years, 77% men, 85% LVEF <40%, 60% ischemic HF) were evaluated over a 2.4-year median follow-up. Median eGFR was 58 mL/min/1.73 m2 (interquartile interval 46–70; n = 9220), hs-TnT 16 ng/L (8–20; n = 9289), NT-proBNP 1067 ng/L (433–2470; n = 8845), and hs-CRP 3.3 mg/L (1.4–7.8; n = 7083). In a model including all 3 biomarkers, only hs-TnT and NT-proBNP were independent predictors of all-cause and cardiovascular mortality and cardiovascular hospitalization. hs-TnT was a stronger predictor than NT-proBNP: for example, the risk for all-cause death increased by 54% per doubling of hs-TnT vs. 24% per doubling of NT-proBNP. eGFR showed independent prognostic value from both hs-TnT and NT-proBNP. The best hs-TnT and NT-proBNP cut-offs for the prediction of all-cause death increased progressively with declining renal function (eGFR ≥ 90: hs-TnT 13 ng/L and NT-proBNP 825 ng/L; eGFR < 30: hs-TnT 40 ng/L and NT-proBNP 4608 ng/L). Patient categorization according to these cut-offs effectively stratified patient prognosis across all eGFR classes.Conclusions: hs-TnT conveys independent prognostic information from NT-proBNP, while hs-CRP does not. Concomitant assessment of eGFR may further refine risk stratification. Patient classification according to hs-TnT and NT-proBNP cut-offs specific for the eGFR classes holds prognostic significance.
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- Aimo, Alberto, et al.
(författare)
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Prognostic Value of High-Sensitivity Troponin T in Chronic Heart Failure : An Individual Patient Data Meta-Analysis
- 2018
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Ingår i: Circulation. - 0009-7322 .- 1524-4539. ; 137:3, s. 286-297
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Tidskriftsartikel (refereegranskat)abstract
- Background: Most patients with chronic heart failure have detectable troponin concentrations when evaluated by high-sensitivity assays. The prognostic relevance of this finding has not been clearly established so far. We aimed to assess high-sensitivity troponin assay for risk stratification in chronic heart failure through a meta-analysis approach.Methods: Medline, EMBASE, Cochrane Library, and Scopus were searched in April 2017 by 2 independent authors. The terms were “troponin” AND “heart failure” OR “cardiac failure” OR “cardiac dysfunction” OR “cardiac insufficiency” OR “left ventricular dysfunction.” Inclusion criteria were English language, clinical stability, use of a high-sensitivity troponin assay, follow-up studies, and availability of individual patient data after request to authors. Data retrieved from articles and provided by authors were used in agreement with the PRISMA statement. The end points were all-cause death, cardiovascular death, and hospitalization for cardiovascular cause.Results: Ten studies were included, reporting data on 11 cohorts and 9289 patients (age 66±12 years, 77% men, 60% ischemic heart failure, 85% with left ventricular ejection fraction <40%). High-sensitivity troponin T data were available for all patients, whereas only 209 patients also had high-sensitivity troponin I assayed. When added to a prognostic model including established risk markers (sex, age, ischemic versus nonischemic etiology, left ventricular ejection fraction, estimated glomerular filtration rate, and N-terminal fraction of pro-B-type natriuretic peptide), high-sensitivity troponin T remained independently associated with all-cause mortality (hazard ratio, 1.48; 95% confidence interval, 1.41–1.55), cardiovascular mortality (hazard ratio, 1.40; 95% confidence interval, 1.33–1.48), and cardiovascular hospitalization (hazard ratio, 1.42; 95% confidence interval, 1.36–1.49), over a median 2.4-year follow-up (all P<0.001). High-sensitivity troponin T significantly improved risk prediction when added to a prognostic model including the variables above. It also displayed an independent prognostic value for all outcomes in almost all population subgroups. The area under the curve–derived 18 ng/L cutoff yielded independent prognostic value for the 3 end points in both men and women, patients with either ischemic or nonischemic etiology, and across categories of renal dysfunction.Conclusions: In chronic heart failure, high-sensitivity troponin T is a strong and independent predictor of all-cause and cardiovascular mortality, and of hospitalization for cardiovascular causes, as well. This biomarker then represents an additional tool for prognostic stratification.
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