| 1. |
- Wormser, David, et al.
(författare)
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Adult height and the risk of cause-specific death and vascular morbidity in 1 million people : individual participant meta-analysis
- 2012
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Ingår i: International Journal of Epidemiology. - : Oxford University Press (OUP). - 0300-5771 .- 1464-3685. ; 41:5, s. 1419-1433
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Tidskriftsartikel (refereegranskat)abstract
- BackgroundThe extent to which adult height, a biomarker of the interplay of genetic endowment and early-life experiences, is related to risk of chronic diseases in adulthood is uncertain.MethodsWe calculated hazard ratios (HRs) for height, assessed in increments of 6.5 cm, using individual-participant data on 174 374 deaths or major non-fatal vascular outcomes recorded among 1 085 949 people in 121 prospective studies.ResultsFor people born between 1900 and 1960, mean adult height increased 0.5-1 cm with each successive decade of birth. After adjustment for age, sex, smoking and year of birth, HRs per 6.5 cm greater height were 0.97 (95% confidence interval: 0.96-0.99) for death from any cause, 0.94 (0.93-0.96) for death from vascular causes, 1.04 (1.03-1.06) for death from cancer and 0.92 (0.90-0.94) for death from other causes. Height was negatively associated with death from coronary disease, stroke subtypes, heart failure, stomach and oral cancers, chronic obstructive pulmonary disease, mental disorders, liver disease and external causes. In contrast, height was positively associated with death from ruptured aortic aneurysm, pulmonary embolism, melanoma and cancers of the pancreas, endocrine and nervous systems, ovary, breast, prostate, colorectum, blood and lung. HRs per 6.5 cm greater height ranged from 1.26 (1.12-1.42) for risk of melanoma death to 0.84 (0.80-0.89) for risk of death from chronic obstructive pulmonary disease. HRs were not appreciably altered after further adjustment for adiposity, blood pressure, lipids, inflammation biomarkers, diabetes mellitus, alcohol consumption or socio-economic indicators.ConclusionAdult height has directionally opposing relationships with risk of death from several different major causes of chronic diseases.
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| 2. |
- Chinali, M., et al.
(författare)
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Mitral E wave deceleration time to peak E velocity ratio and cardiovascular outcome in hypertensive patients during antihypertensive treatment (from the LIFE echo-substudy)
- 2009
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Ingår i: The American Journal of Cardiology. - : Elsevier BV. - 1879-1913 .- 0002-9149. ; 104:8, s. 1098-104
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Tidskriftsartikel (refereegranskat)abstract
- The early mitral flow deceleration time (DTE) is a prognostically validated marker of left ventricular diastolic dysfunction. It has been reported that the DTE is influenced by the loading conditions, which can vary during antihypertensive treatment. We hypothesized that normalization of the DTE for mitral peak E-velocity (mitral deceleration index [MDI]) might better predict incident cardiovascular (CV) events in hypertensive patients during treatment compared to DTE alone or other traditional indexes of diastolic function, such as the mitral E/A ratio. We evaluated 770 hypertensive patients with electrocardiogram findings of left ventricular hypertrophy (age 66 +/- 7 years; 42% women) enrolled in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiographic substudy. Echocardiographic examinations were performed annually for 5 years during intensive antihypertensive treatment. We examined the utility of the MDI at baseline and as a time-varying predictor of incident CV events. Of the 770 patients, 70 (9%) had CV events. The baseline MDI was positively associated with age and relative wall thickness and negatively associated with gender and heart rate (all p <0.01). Unadjusted Cox regression analysis showed a positive association between the baseline MDI and CV events (hazard ratio 1.21, 95% confidence interval 1.07 to 1.37, p = 0.002). In the time-varied Cox models, a greater in-treatment MDI was associated with a greater rate of CV events (hazard ratio 1.43, 95% confidence interval 1.05 to 1.93, p = 0.022), independently of the covariates. No significant association was found for in-treatment DTE or any of the prognostically validated indexes of diastolic function. In conclusion, in our population of patients with treated hypertension with electrocardiographic findings of left ventricular hypertrophy, the MDI independently predicted future CV events. Normalization of DTE for E velocity might be preferred to other traditional diastolic function indexes in evaluating diastolic function during antihypertensive treatment.
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| 3. |
- Cicala, S., et al.
(författare)
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Are coronary revascularization and myocardial infarction a homogeneous combined endpoint in hypertension trials? The Losartan Intervention For Endpoint reduction in hypertension study
- 2010
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 28:6, s. 1134-1140
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Construction of prognostically relevant endpoints for clinical trials in hypertension has increasingly included coronary revascularization with myocardial infarction (MI) as manifestations of coronary artery disease. However, whether coronary revascularization and MI predict other cardiovascular events similarly is unknown. METHODS: We examined risks of cardiovascular death, all-cause death, and stroke following MI or coronary revascularization in hypertensive patients with left ventricular hypertrophy (LVH) enrolled in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE). We studied 9113 patients after excluding those who died within 7 days after MI or underwent coronary revascularization within 24 h after MI. RESULTS: In multivariate Cox regression adjusting for participating countries, time-varying systolic blood pressure, and Framingham risk score, hazard ratios for cardiovascular death, all-cause death, and stroke were, respectively, 4.5 (P<0.0001), 2.9 (P<0.0001), and 1.9 (P=0.003) in 321 patients with MI as first event. In similar models, coronary revascularization as first event (n=202) was not associated with increased risks of cardiovascular death, all-cause death, and stroke (P=0.06-0.86). CONCLUSION: During follow-up of hypertensive patients with LVH, occurrence of MI but not coronary revascularization as first cardiovascular event significantly increased risk of subsequent cardiovascular death, all-cause death, and stroke. In view of differences in prognostic implications, when the goal is to have a prognostically relevant composite endpoint for trials in hypertensive patients, caution should be used in combining coronary revascularization with MI.
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| 4. |
- Eijkelkamp, W. B., et al.
(författare)
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Renal function and risk for cardiovascular events in type 2 diabetic patients with hypertension: the RENAAL and LIFE studies
- 2007
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Ingår i: J Hypertens. - 0263-6352. ; 25:4, s. 871-6
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: To investigate whether a threshold exists for cardiovascular risk in type 2 diabetic patients with hypertension, the association between renal function and cardiovascular risk was examined across the entire physiological range of serum creatinine. DESIGN AND METHODS: The RENAAL and LIFE studies enrolled 1513 and 1195 patients with type 2 diabetes and hypertension, respectively. The relationship between baseline serum creatinine and the risk for a composite outcome of myocardial infarction, stroke or cardiovascular death was examined using Cox regression models. To adjust for heterogeneity between studies and treatment groups, these factors were included as strata when applicable. The analyses were conducted with adjustment for age, gender, smoking, alcohol use, blood pressure, heart rate, total and high-density lipoprotein (HDL) cholesterol, hemoglobin, albuminuria and prior cardiovascular disease. RESULTS: The hazard ratios across the baseline serum creatinine categories < 0.9 mg/dl, 0.9-1.2 mg/dl, 1.2-1.6 mg/dl, 1.6-2.8 mg/dl and >or= 2.8 mg/dl were 0.51 (95% confidence interval 0.34, 0.74), 0.74 (0.55, 1.00), 1.00 (reference), 1.24 (0.96, 1.59) and 1.67 (1.17, 2.91), respectively. Baseline serum creatinine (per mg/dl) strongly predicted the composite cardiovascular endpoint in LIFE [2.82(1.74,4.56), P < 0.001], RENAAL [1.41(1.12,1.79), P < 0.001], as well as the combined studies [1.51(1.21,1.87), P < 0.001]. CONCLUSION: A progressively higher risk for the composite cardiovascular endpoint was observed with incremental baseline serum creatinine in type 2 diabetic patients with hypertension, even within the normal range. Thus, there appears to be no serum creatinine threshold level for an increased cardiovascular risk. Baseline serum creatinine was a major independent risk factor for cardiovascular disease (www.ClinicalTrials.gov number NCT00308347).
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| 5. |
- Gerdts, E., et al.
(författare)
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Impact of overweight and obesity on cardiac benefit of antihypertensive treatment
- 2013
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Ingår i: NMCD. Nutrition Metabolism and Cardiovascular Diseases. - : Elsevier BV. - 0939-4753 .- 1590-3729. ; 23:2, s. 122-129
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Tidskriftsartikel (refereegranskat)abstract
- Background and aims: Increased body mass index (BMI) has been associated with increased cardiovascular morbidity and mortality in hypertension. Less is known about the impact of BMI on improvement in left ventricular (LV) structure and function during antihypertensive treatment. Methods and results: Annual BMI, echocardiograms and cardiovascular events were recorded in 875 hypertensive patients with LV hypertrophy during 4.8 years randomized treatment in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) echocardiography substudy. Patients were grouped by baseline BMI into normal (n = 282), overweight (n = 405), obese (n = 150) and severely obese groups (n = 38) (BMI <= 24.9, 25.0-29.9, 30.0-34.9, and >= 35.0 kg/m(2), respectively). At study end, residual LV hypertrophy was present in 54% of obese and 79% of severely obese patients compared to 31% of normal weight patients (both p < 0.01). In regression analyses, adjusting for initial LV mass/height(2.7), higher BMI predicted less LV hypertrophy reduction and more reduction in LV ejection fraction (both p < 0.05), independent of blood pressure reduction, diabetes and in-study weight change. During follow-up, 91 patients suffered cardiovascular death, myocardial infarction or stroke. In Cox regression analysis 1 kg/m(2) higher baseline BMI predicted a 5% higher rate of cardiovascular events and 10% higher cardiovascular mortality over 4.8 years (both p < 0.05). Conclusions: In hypertensive patients in the LIFE study, increased BMI was associated with less reduction of LV hypertrophy and less improvement in LV systolic function which may contribute to the observed higher cardiovascular event rate of treated hypertensive patients. (C) 2011 Elsevier B. V. All rights reserved.
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| 6. |
- Greve, Anders M., et al.
(författare)
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Resting heart rate and risk of adverse cardiovascular outcomes in asymptomatic aortic stenosis : The SEAS study
- 2015
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Ingår i: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 180, s. 122-128
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Tidskriftsartikel (refereegranskat)abstract
- Background: An elevated resting heart rate (RHR) may be an early sign of cardiac failure, but its prognostic value during watchful waiting in asymptomatic aortic stenosis (AS) is largely unknown. Methods: RHR was determined by annual ECGs in the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study of asymptomatic mild-to-moderate AS patients. Primary endpoint in this substudy was major cardiovascular events (MCEs) and secondary outcomes its individual components. Multivariable Cox-models using serially-measured RHR were used to examine the prognostic impact of RHR per se. Results: 1563 patients were followed for a mean of 4.3 years (6751 patient-years of follow-up), 553 (35%) MCEs occurred, 10% (n = 151) died, including 75 cardiovascular deaths. In multivariable analysis, baseline RHR was independently associated with MCEs (HR 1.1 per 10 min(-1) faster, 95% CI: 1.0-1.3) and cardiovascular mortality (HR 1.3 per 10 min(-1) faster, 95% CI: 1.0-1.7, both p <= 0.03). Updating RHR with annual in-study reexaminations, time-varying RHR was highly associated with excess MCEs (HR 1.1 per 10 min(-1) faster, 95% CI: 1.1-1.3) and cardiovascular mortality (HR 1.4 per 10 min(-1) faster, 95% CI: 1.2-1.7, both p <= 0.006). The association of RHR with MCEs and cardiovascular mortality was not dependent on atrial fibrillation status (both p >= 0.06 for interaction). Conclusions: RHR is independently associated with MCEs and cardiovascular death in asymptomatic AS (Clinicaltrials.gov; unique identifier NCT00092677).
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| 7. |
- Mancusi, C., et al.
(författare)
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Impact of isolated systolic hypertension on normalization of left ventricular structure during antihypertensive treatment in patients with electrocardiographic left ventricular hypertrophy (LIFE)
- 2013
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 34:Supplement: 1, s. 597-597
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Objective: Hypertension is associated with changes in left ventricular(LV) mass and geometry. We tested the impact of isolated systolichypertension (ISH) on normalization of LV structure during antihypertensive treatment.Methods: Baseline and annual echocardiograms were recorded in 875 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 inhypertension study.Results: Patients with ISH at baseline (n=128) were older, included more women, patients with diabetes or previous myocardial infarctioncompared to non-ISH patients (n=747) (all p<0.05). Baseline systolicblood pressure (BP), LV mass and ejection fraction (EF) did not differ between groups, while pulse pressure/stroke volume index (PP/SVi, an index of arterial stiffness) was higher in the ISH group (p<0.01). At the final study visit, systolic BP, LV mass, relative wall thickness (RWT) and PP/SVi were higher in the ISH group (all p<0.05). In particular, ISH patients had less reduction in LV mass and more residual LV hypertrophy compared to non-ISH patients (p<0.05). In multivariate analysis, ISH at baseline predicted higher LV mass at study end (β=0.53) independent ofhigher baseline LV mass (β=0.54) body mass index (β=0.10), atenolol-based treatment (β=0.09), and higher systolic BP (β=0.07), RWT (β=0.23) and lower LV EF (β=-0.24) at the final visit (all p<0.05), while age, historyof diabetes and PP/SVi were not significant covariates in the model.Conclusions: Antihypertensive treatment is associated with impairednormalization of LV mass and LV geometry in ISH patients with ECG LV hypertrophy. The findings may help explain the higher cardiovascular event-rate previously reported in LIFE ISH-patients.
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| 8. |
- Palmieri, V., et al.
(författare)
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Electrocardiographic characteristics and metabolic risk factors associated with inappropriately high left ventricular mass in patients with electrocardiographic left ventricular hypertrophy: the LIFE Study
- 2007
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Ingår i: J Hypertens. - 0263-6352. ; 25:5, s. 1079-85
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: To investigate electrocardiographic (ECG) and metabolic abnormalities associated with left ventricular (LV) mass inappropriately high for workload and body size (termed 'inappropriate left ventricular mass'; ILVM) in hypertensive patients with ECG left ventricular hypertrophy (LVH). METHODS: In patients enrolled in the Losartan Intervention for Endpoint Reduction (LIFE) Echocardiographic Substudy, LV structure and functions were assessed by echocardiography; Sokolow-Lyon and Cornell voltage, QRS duration, Cornell voltage-duration product and ST strain pattern in leads V5-V6 were evaluated on standard ECG tracings. ILVM was defined as observed LV mass greater than 128% of that predicted by sex, body size and stroke work. RESULTS: In univariate analysis, compared with subjects with appropriate LV mass (n = 593), ILVM (n = 348) was associated with older age, diabetes, higher body mass index, lower systolic blood pressure, higher serum creatinine and urinary albumin/creatinine levels, higher LV mass index and greater prevalence of wall motion abnormalities (all P < 0.05). ILVM was associated with higher Cornell voltage and voltage-duration product but not higher Sokolow-Lyon voltage, with longer QRS and higher prevalences of ECG ST strain and echocardiographic wall motion abnormalities, independent of covariates including echocardiographically defined LVH or LV geometry. In separate logistic models, the likelihood of ILVM was significantly related to prolonged QRS duration, higher Cornell voltage, and greater Cornell voltage-duration independently (all P < 0.01). CONCLUSION: In hypertensive patients with ECG LVH, ILVM was associated with prolonged QRS duration and higher Cornell voltage, with ECG ST strain pattern, and with echocardiographic wall motion abnormalities independent of traditionally defined LVH.
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| 9. |
- Reims, H. M., et al.
(författare)
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Alcohol consumption and cardiovascular risk in hypertensives with left ventricular hypertrophy: the LIFE study
- 2004
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Ingår i: J Hum Hypertens. - : Springer Science and Business Media LLC. - 0950-9240 .- 1476-5527. ; 18:6, s. 381-9
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Tidskriftsartikel (refereegranskat)abstract
- The Losartan Intervention For End point reduction in hypertension (LIFE) study showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke, and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios (HR) in 4287 and 685 participants who reported intakes of 1-7 and >8 drinks/week at baseline, respectively, with those in 4216 abstainers, adjusting for gender, age, smoking, exercise, and race. Within categories, clinical baseline characteristics, numbers randomized to losartan and atenolol, and blood pressure (BP) lowering were similar on the drug regimens. Overall BP control (<140/90 mmHg) at end of follow-up was similar in the categories. Composite end point rate was lower with 1-7 (24/1000 years; HR 0.87, P<0.05) and >8 drinks/week (26/1000 years; HR 0.80, NS) than in abstainers (27/1000 years). Myocardial infarction risk was reduced in both drinking categories (HR 0.76, P<0.05 and HR 0.29, P<0.001, respectively), while stroke risk tended to increase with >8 drinks/week (HR 1.21, NS). Composite risk was significantly reduced with losartan compared to atenolol only in abstainers (HR 0.81 95% confidence interval, CI (0.68, 0.96), P<0.05), while benefits for stroke risk reduction were similar among participants consuming 1-7 drinks/week (HR 0.73, P<0.05) and abstainers (HR 0.72, P<0.01). Despite different treatment benefits, alcohol-treatment interactions were nonsignificant. In conclusion, moderate alcohol consumption does not change the marked stroke risk reduction with losartan compared to atenolol in high-risk hypertensives. Alcohol reduces the risk of myocardial infarction, while the risk of stroke tends to increase with high intake.
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| 10. |
- Reims, H. M., et al.
(författare)
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Losartan benefits over atenolol in non-smoking hypertensive patients with left ventricular hypertrophy: the LIFE study
- 2004
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Ingår i: Blood Press. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 13:6, s. 376-84
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Tidskriftsartikel (refereegranskat)abstract
- We studied the impact of smoking in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study, which showed superiority of losartan over atenolol for reduction of composite risk of cardiovascular death, stroke and myocardial infarction in hypertensives with left ventricular hypertrophy. We compared hazard ratios in 4656 never-smokers, and 3033 previous and 1499 current smokers, adjusting for gender, age, alcohol intake, exercise and race. Composite endpoint rate was higher in previous (28/1000 years), as well as current (39/1000 years) smokers than in never-smokers (21/1000 years). Composite (hazard ratio 0.78, 95% CI 0.65-0.94, p < 0.01) and stroke (hazard ratio 0.61, 95% CI 0.47-0.80], p < 0.001) risks were lower with losartan than atenolol in never-smokers, but not significantly in previous smokers. Drug regimens did not differ in current smokers (composite hazard ratio 0.99, stroke hazard ratio 0.94). Smoking-treatment interactions were non-significant, but a borderline significant trend (p = 0.05) suggested decreasing benefit of losartan vs atenolol for stroke prevention from never- to previous to current smoking status. Smoking increased cardiovascular risk markedly in the LIFE study. The benefit of losartan vs atenolol is consistent with the overall conclusion of the LIFE study, although the treatment effect appeared largest in non-smokers.
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