| 31. |
- Lonnebakken, Mai T., et al.
(författare)
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In-treatment stroke volume predicts cardiovascular risk in hypertension
- 2011
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Ingår i: Journal of Hypertension. - 0263-6352 .- 1473-5598. ; 29:8, s. 1508-1514
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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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| 32. |
- Mancusi, Costantino, et al.
(författare)
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Higher pulse pressure/stroke volume index is associated with impaired outcome in hypertensive patients with left ventricular hypertrophy the LIFE study
- 2017
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Ingår i: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 26:3, s. 150-155
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Tidskriftsartikel (refereegranskat)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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| 33. |
- Mancusi, Costantino, et al.
(författare)
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Impact of isolated systolic hypertension on normalization of left ventricular structure during antihypertensive treatment (the LIFE study)
- 2014
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Ingår i: Blood Pressure. - : Informa UK Limited. - 0803-7051 .- 1651-1999. ; 23:4, s. 206-212
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Tidskriftsartikel (refereegranskat)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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| 34. |
- Mancusi, Costantino, et al.
(författare)
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Management of patients with combined arterial hypertension and aortic valve stenosis : a consensus document from the Council on Hypertension and Council on Valvular Heart Disease of the European Society of Cardiology, the European Association of Cardiovascular Imaging (EACVI), the European Association of Percutaneous Cardiovascular Interventions (EAPCI)
- 2021
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Ingår i: European Heart Journal - Cardiovascular Pharmacotherapy. - : Oxford University Press. - 2055-6837 .- 2055-6845. ; 7:3, s. 242-250
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Aortic valve stenosis (AS) is the third most common cardiovascular disease. The prevalence of both AS and arterial hypertension increases with age, and the conditions therefore often co-exist. Co-existence of AS and arterial hypertension is associated with higher global left ventricular (LV) pressure overload, more abnormal LV geometry and function, and more adverse cardiovascular outcome. Arterial hypertension may also influence grading of AS, leading to underestimation of the true AS severity. Current guidelines suggest re-assessing patients once arterial hypertension is controlled. Management of arterial hypertension in AS has historically been associated with prudence and concerns, mainly related to potential adverse consequences of drug-induced peripheral vasodilatation combined with reduced stroke volume due to the fixed LV outflow obstruction. Current evidence suggests that patients should be treated with antihypertensive drugs blocking the renin-angiotensin aldosterone system, adding further drug classes when required, to achieve similar target blood pressure values as in hypertensive patients without AS. The introduction of trans-catheter aortic valve implantation has revolutionized the management of patients with AS, but requires proper blood pressure management during and following valve replacement. The purpose of this document is to review the recent evidence and provide practical expert advice on management of hypertension in patients with AS.
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| 35. |
- Minners, Jan, et al.
(författare)
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Adjusting parameters of aortic valve stenosis severity by body size
- 2014
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Ingår i: Heart. - : BMJ. - 1355-6037 .- 1468-201X. ; 100:13, s. 1024-1030
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Tidskriftsartikel (refereegranskat)abstract
- Background Adjustment of cardiac dimensions by measures of body size appears intuitively convincing and in patients with aortic stenosis, aortic valve area (AVA) is commonly adjusted by body surface area (BSA). However, there is little evidence to support such an approach. Objective To identify the adequate measure of body size for the adjustment of aortic stenosis severity. Methods Parameters of aortic stenosis severity (jet velocity, mean pressure gradient (MPG) and AVA) and measures of body size (height, weight, BSA and body mass index (BMI)) were analysed in 2843 consecutive patients with aortic stenosis (jet velocity >= 2.5 m/s) and related to outcomes in a second cohort of 1525 patients from the Simvastatin/Ezetimibe in Aortic Stenosis (SEAS) study. Results Whereas jet velocity and MPG were independent of body size, AVA was significantly correlated with height, weight, BSA and BMI (Pearson correlation coefficient (r) 0.319, 0.281, 0.317 and 0.126, respectively, all p<0.001) to the effect that larger patients presented with larger AVA (less severe stenosis). Of the anthropometric measures used for linear adjustment, BSA was most effective in eliminating the correlation between AVA and body size (r=0.007), rivalled only by allometric (non-linear) models, findings that are confirmed in 1525 prospectively followed patients from the SEAS study. Predictive accuracy for aortic valve events and cardiovascular death during 46 months of follow-up was unchanged by adjusting AVA, regardless of measure of body size (area under the receiver operating curve for AVA 0.72 (CI 0.58 to 0.87) versus, for example, AVA/BSA 0.75 (CI 0.61 to 0.88), p=0.22). Conclusions In the assessment of aortic stenosis, linear adjustment of AVA by BSA improves comparability between patients with diverging body size without, however, increasing the predictive accuracy for clinical events in a population with mild to moderate stenosis.
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| 36. |
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| 37. |
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| 38. |
- Putaala, Jukka, et al.
(författare)
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Searching for Explanations for Cryptogenic Stroke in the Young : Revealing the Triggers, Causes, and Outcome (SECRETO): Rationale and design
- 2017
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Ingår i: European Stroke Journal. - : SAGE Publications. - 2396-9873 .- 2396-9881. ; 2:2, s. 116-125
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Tidskriftsartikel (refereegranskat)abstract
- Background: Worldwide, about 1.3 million annual ischaemic strokes (IS) occur in adults aged <50 years. Of these early-onset strokes, up to 50% can be regarded as cryptogenic or associated with conditions with poorly documented causality like patent foramen ovale and coagulopathies. Key hypotheses/aims: (1) Investigate transient triggers and clinical/sub-clinical chronic risk factors associated with cryptogenic IS in the young; (2) use cardiac imaging methods exceeding state-of-the-art to reveal novel sources for embolism; (3) search for covert thrombosis and haemostasis abnormalities; (4) discover new disease pathways using next-generation sequencing and RNA gene expression studies; (5) determine patient prognosis by use of phenotypic and genetic data; and (6) adapt systems medicine approach to investigate complex risk-factor interactions. Design: Searching for Explanations for Cryptogenic Stroke in the Young: Revealing the Etiology, Triggers, and Outcome (SECRETO; NCT01934725) is a prospective multi-centre case–control study enrolling patients aged 18–49 years hospitalised due to first-ever imaging-proven IS of undetermined etiology. Patients are examined according to a standardised protocol and followed up for 10 years. Patients are 1:1 age- and sex-matched to stroke-free controls. Key study elements include centralised reading of echocardiography, electrocardiography, and neurovascular imaging, as well as blood samples for genetic, gene-expression, thrombosis and haemostasis and biomarker analysis. We aim to have 600 patient–control pairs enrolled by the end of 2018. Summary: SECRETO is aiming to establish novel mechanisms and prognosis of cryptogenic IS in the young and will provide new directions for therapy development for these patients. First results are anticipated in 2019.
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| 39. |
- Rogge, Barbara P., et al.
(författare)
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Effect of Overweight and Obesity on Cardiovascular Events in Asymptomatic Aortic Stenosis
- 2013
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Ingår i: Journal of the American College of Cardiology. - : Elsevier. - 0735-1097 .- 1558-3597. ; 62:18, s. 1683-1690
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Tidskriftsartikel (refereegranskat)abstract
- Objectives This study investigated whether overweight and obesity impacted outcome in patients with aortic valve stenosis (AS). Background Increased body mass index (BMI) is a strong predictor of higher cardiovascular (CV) morbidity and mortality in the general population but not among patients undergoing heart surgery. Methods Cardiovascular events in 1,664 patients with initially asymptomatic AS were recorded during a mean of 4.3 years of follow-up in the SEAS (Simvastatin Ezetimibe in Aortic Stenosis) study. Patients were grouped according to baseline BMI class. Results Overweight (n = 737) and obese patients (n = 334) had higher prevalence of hypertension, more abnormal left ventricular geometry, and lower stress-corrected midwall shortening throughout the study compared with normal weight patients (all p < 0.01). The AS progression rate did not differ between BMI classes. In univariate Cox regression, overweight was associated with a 17% to 22% lower rate of AS-related (p = 0.04) and ischemic CV events (p = 0.05). In multivariate analyses, adjusting for AS severity and differences in baseline characteristics, overweight had no significant influence on the rate of ischemic CV or AS-related events, whereas overweight and obesity had 46% and 67% higher rate of total mortality and 42% and 69% higher rate of combined hospital stay for heart failure and death from any cause, respectively, compared with normal weight patients (all p < 0.05). Conclusions In patients with initially asymptomatic AS participating in the SEAS study, overweight and obesity did not influence AS progression or rate of AS-related or ischemic CV events but were both associated with increased mortality. (C) 2013 by the American College of Cardiology Foundation
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| 40. |
- Rossebo, Anne B., et al.
(författare)
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Intensive lipid lowering with simvastatin and ezetimibe in aortic stenosis
- 2008
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Ingår i: New England Journal of Medicine. - 0028-4793 .- 1533-4406. ; 359:13, s. 1343-1356
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Tidskriftsartikel (refereegranskat)abstract
- Background: Hyperlipidemia has been suggested as a risk factor for stenosis of the aortic valve, but lipid-lowering studies have had conflicting results. Methods: We conducted a randomized, double-blind trial involving 1873 patients with mild-to-moderate, asymptomatic aortic stenosis. The patients received either 40 mg of simvastatin plus 10 mg of ezetimibe or placebo daily. The primary outcome was a composite of major cardiovascular events, including death from cardiovascular causes, aortic-valve replacement, nonfatal myocardial infarction, hospitalization for unstable angina pectoris, heart failure, coronary-artery bypass grafting, percutaneous coronary intervention, and nonhemorrhagic stroke. Secondary outcomes were events related to aortic-valve stenosis and ischemic cardiovascular events. Results: During a median follow-up of 52.2 months, the primary outcome occurred in 333 patients (35.3%) in the simvastatin-ezetimibe group and in 355 patients (38.2%) in the placebo group (hazard ratio in the simvastatin-ezetimibe group, 0.96; 95% confidence interval [CI], 0.83 to 1.12; P=0.59). Aortic-valve replacement was performed in 267 patients (28.3%) in the simvastatin-ezetimibe group and in 278 patients (29.9%) in the placebo group (hazard ratio, 1.00; 95% CI, 0.84 to 1.18; P=0.97). Fewer patients had ischemic cardiovascular events in the simvastatin-ezetimibe group (148 patients) than in the placebo group (187 patients) (hazard ratio, 0.78; 95% CI, 0.63 to 0.97; P=0.02), mainly because of the smaller number of patients who underwent coronary-artery bypass grafting. Cancer occurred more frequently in the simvastatin-ezetimibe group (105 vs. 70, P=0.01). Conclusions: Simvastatin and ezetimibe did not reduce the composite outcome of combined aortic-valve events and ischemic events in patients with aortic stenosis. Such therapy reduced the incidence of ischemic cardiovascular events but not events related to aortic-valve stenosis. (ClinicalTrials.gov number, NCT00092677.).
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