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排序方式: 共有372条查询结果,搜索用时 15 毫秒
1.
目的:脉压(PP)升高一贯用来预测有心血管疾病危险患者和轻度慢性心衰(CH F)患者的心血管疾病发生率和死亡率增高。相反,PP降低与急性失代偿性心衰患者死亡率升高相关。然而,尚不清楚PP对于晚期CH F患者的预测价值。方法和结果:采用Cox比例风险回归分析研究了1901例N YH A III或IV级CH F患者(平均年龄65岁,平均射血分数26%)的资料,经校正其他危险因素后,分析PP对死亡率的影响。检测了1个亚组患者的利钠肽水平。多元Cox回归分析表明,PP降低与死亡率增高相关(每增加10m m H g的H R为0.91,95%CI0.93~0.99),这一相关性独立于平均… 相似文献
2.
Traditional and new composite endpoints in heart failure clinical trials: facilitating comprehensive efficacy assessments and improving trial efficiency 下载免费PDF全文
Stefan D. Anker Stefan Schroeder Dan Atar Jeroen J. Bax Claudio Ceconi Martin R. Cowie Adam Crisp Fabienne Dominjon Ian Ford Hossein‐Ardeschir Ghofrani Savion Gropper Gerhard Hindricks Mark A. Hlatky Richard Holcomb Narimon Honarpour J. Wouter Jukema Albert M. Kim Michael Kunz Martin Lefkowitz Chantal Le Floch Ulf Landmesser Theresa A. McDonagh John J. McMurray Bela Merkely Milton Packer Krishna Prasad James Revkin Giuseppe M.C. Rosano Ransi Somaratne Wendy Gattis Stough Adriaan A. Voors Frank Ruschitzka 《European journal of heart failure》2016,18(5):482-489
Composite endpoints are commonly used as the primary measure of efficacy in heart failure clinical trials to assess the overall treatment effect and to increase the efficiency of trials. Clinical trials still must enrol large numbers of patients to accrue a sufficient number of outcome events and have adequate power to draw conclusions about the efficacy and safety of new treatments for heart failure. Additionally, the societal and health system perspectives on heart failure have raised interest in ascertaining the effects of therapy on outcomes such as repeat hospitalization and the patient's burden of disease. Thus, novel methods for using composite endpoints in clinical trials (e.g. clinical status composite endpoints, recurrent event analyses) are being applied in current and planned trials. Endpoints that measure functional status or reflect the patient experience are important but used cautiously because heart failure treatments may improve function yet have adverse effects on mortality. This paper discusses the use of traditional and new composite endpoints, identifies qualities of robust composites, and outlines opportunities for future research. 相似文献
3.
Stuart J. Pocock João Pedro Ferreira Timothy J. Collier Christiane E. Angermann Jan Biegus Sean P. Collins Mikhail Kosiborod Michael E. Nassif Piotr Ponikowski Mitchell A. Psotka John R. Teerlink Jasper Tromp John Gregson Jonathan P. Blatchford Cordula Zeller Adriaan A. Voors 《European journal of heart failure》2023,25(5):632-641
Aims
The EMPULSE trial evaluated the clinical benefit of empagliflozin versus placebo using the stratified win ratio approach in 530 patients with acute heart failure (HF) after initial stabilization. We aim to elucidate how this method works and what it means, thereby giving guidance for use of the win ratio in future trials.Methods and results
The primary trial outcome is a hierarchical composite of death, number of HF events, time to first HF event, or a ≥5-point difference in Kansas City Cardiomyopathy Questionnaire (KCCQ) total symptom score change at 90 days. In an overall (unstratified) analysis we show how comparison of all 265 x 265 patients pairs contribute to ‘wins’ for empagliflozin and placebo at all four levels of the hierarchy, leading to an unstratified win ratio of 1.38 (95% confidence interval [CI] 1.11–1.71; p = 0.0036). How such a win ratio should (and should not) be interpreted is then described. The more complex primary analysis using a stratified win ratio is then presented in detail leading to a very similar overall result. Win ratios for de novo acute HF and decompensated chronic HF patients were 1.29 and 1.39, respectively, their weighted combination yielding an overall stratified win ratio of 1.36 (95% CI 1.09–1.68) (p = 0.0054). Alternative ways of including HF events and KCCQ scores in the clinical hierarchy are presented, leading to recommendations for their use in future trials. Specifically, inclusion of both number of HF events and time-to-first HF event appears an unnecessary complication. Also, the use of a 5-point margin for KCCQ score paired comparisons is not statistically necessary.Conclusions
The EMPULSE trial findings illustrate how deaths, clinical events and patient-reported outcomes can be integrated into a win ratio analysis strategy that yields clinically meaningful findings of patient benefit. This has implications for future trial designs that recognize the clinical priorities of patient evaluation and the need for efficient progress towards approval of new treatments. 相似文献4.
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7.
Pim van der Harst Gerrit van der Steege Rudolf A de Boer Adriaan A Voors Alistair S Hall Marcel J Mulder Wiek H van Gilst Dirk J van Veldhuisen 《Journal of the American College of Cardiology》2007,49(13):1459-1464
OBJECTIVES: This study sought to test the hypothesis that patients with chronic heart failure (CHF) have shorter telomeres compared with age-balanced and gender-balanced healthy individuals. BACKGROUND: Telomere length is considered to be a marker of biological aging. Chronic heart failure might be viewed as a condition associated with accelerated biological aging. METHODS: The telomere length ratio of leukocytes was determined prospectively by a quantitative polymerase chain reaction-based method in a case-control setting involving 803 participants: 183 healthy individuals and 620 CHF patients, ages 40 to 80 years, New York Heart Association functional class II to IV, and left ventricular ejection fraction of 0.40 or less. RESULTS: The median telomere length ratio was 0.64 (interquartile range [IQR] 0.47 to 0.88) in CHF patients compared with 1.05 (IQR 0.86 to 1.29) in control patients (p < 0.001). The telomere length ratio in CHF patients related to severity of disease (median value [IQR] of patients with New York Heart Association class II, III, or IV function was 0.67 [0.48 to 0.92], 0.63 [0.46 to 0.86], and 0.55 [0.46 to 0.75], respectively; p for trend <0.05). In addition, telomeres were shorter in patients with an ischemic compared with a nonischemic etiology of CHF. Patients with none, 1 (coronary, cerebral, or peripheral vascular disease), 2 (any combination of the previous), or 3 atherosclerotic manifestations had a median (IQR) telomere length of 0.72 (0.51 to 1.01), 0.65 (0.48 to 0.87), 0.48 (0.39 to 0.72), and 0.43 (0.27 to 0.67), respectively (p for trend <0.001). CONCLUSIONS: Telomere length is shorter in patients with CHF compared with age-balanced and gender-balanced control patients, and related to the severity of disease. In addition, telomere length was incrementally shorter according to the presence and extent of atherosclerotic disease manifestations. 相似文献
8.
Sex‐specific cardiovascular structure and function in heart failure with preserved ejection fraction
Mauro Gori Carolyn S. P. Lam Deepak K. Gupta Angela B. S. Santos Susan Cheng Amil M. Shah Brian Claggett Michael R. Zile Elisabeth Kraigher‐Krainer Burkert Pieske Adriaan A. Voors Milton Packer Toni Bransford Martin Lefkowitz John J. V. McMurray Scott D. Solomon for the PARAMOUNT Investigators 《European journal of heart failure》2014,16(5):535-542
9.
Burkert Pieske Carsten Tschpe Rudolf A. de Boer Alan G. Fraser Stefan D. Anker Erwan Donal Frank Edelmann Michael Fu Marco Guazzi Carolyn S.P. Lam Patrizio Lancellotti Vojtech Melenovsky Daniel A. Morris Eike Nagel Elisabeth Pieske-Kraigher Piotr Ponikowski Scott D. Solomon Ramachandran S. Vasan Frans H. Rutten Adriaan A. Voors Frank Ruschitzka Walter J. Paulus Petar Seferovic Gerasimos Filippatos 《European journal of heart failure》2020,22(3):391-412
Making a firm diagnosis of chronic heart failure with preserved ejection fraction (HFpEF) remains a challenge. We recommend a new stepwise diagnostic process, the ‘HFA–PEFF diagnostic algorithm’. Step 1 (P=Pre‐test assessment) is typically performed in the ambulatory setting and includes assessment for heart failure symptoms and signs, typical clinical demographics (obesity, hypertension, diabetes mellitus, elderly, atrial fibrillation), and diagnostic laboratory tests, electrocardiogram, and echocardiography. In the absence of overt non‐cardiac causes of breathlessness, HFpEF can be suspected if there is a normal left ventricular (LV) ejection fraction, no significant heart valve disease or cardiac ischaemia, and at least one typical risk factor. Elevated natriuretic peptides support, but normal levels do not exclude a diagnosis of HFpEF. The second step (E: Echocardiography and Natriuretic Peptide Score) requires comprehensive echocardiography and is typically performed by a cardiologist. Measures include mitral annular early diastolic velocity (e′), LV filling pressure estimated using E/e′, left atrial volume index, LV mass index, LV relative wall thickness, tricuspid regurgitation velocity, LV global longitudinal systolic strain, and serum natriuretic peptide levels. Major (2 points) and Minor (1 point) criteria were defined from these measures. A score ≥5 points implies definite HFpEF; ≤1 point makes HFpEF unlikely. An intermediate score (2–4 points) implies diagnostic uncertainty, in which case Step 3 (F1: Functional testing) is recommended with echocardiographic or invasive haemodynamic exercise stress tests. Step 4 (F2: Final aetiology) is recommended to establish a possible specific cause of HFpEF or alternative explanations. Further research is needed for a better classification of HFpEF. 相似文献
10.
John R. Teerlink Beth A. Davison Gad Cotter Aldo P. Maggioni Naoki Sato Ovidiu Chioncel Georg Ertl G. Michael Felker Gerasimos Filippatos Barry H. Greenberg Peter S. Pang Piotr Ponikowski Christopher Edwards Stefanie Senger Sam L. Teichman Olav Wendelboe Nielsen Adriaan A. Voors Marco Metra 《European journal of heart failure》2020,22(2):315-329