Anticoagulation in Heart Failure: a Review.
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ABSTRACT:
SUBMITTER: Zeitler EP
PROVIDER: S-EPMC5135119 | biostudies-other | 2015 Jun-Jul
REPOSITORIES: biostudies-other
Publications
Anticoagulation in Heart Failure: a Review.
Zeitler Emily P EP Eapen Zubin J ZJ
Journal of atrial fibrillation 20150630 1
Heart failure (HF) with reduced left ventricular function inflicts a large and growing burden of morbidity and mortality in the US and across the globe. One source of this burden is stroke. While it appears that HF itself may impose some risk of stroke, it is in the presence of other risk factors, like atrial fibrillation, that the greatest risks are observed. Therapeutic anticoagulation is the mainstay of risk reduction strategies in this population. While warfarin was the only available therap ...[more]
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Project description:Heart failure (HF) with reduced left ventricular function inflicts a large and growing burden of morbidity and mortality in the US and across the globe. One source of this burden is stroke. While it appears that HF itself may impose some risk of stroke, it is in the presence of other risk factors, like atrial fibrillation, that the greatest risks are observed. Therapeutic anticoagulation is the mainstay of risk reduction strategies in this population. While warfarin was the only available therapy for anticoagulation for many decades, there are now four direct oral anticoagulants available. In three of these four, outcomes in the specific subgroup of patients with heart failure have been examined. In this review, we provide some pathophysiologic basis for the risk of stroke in heart failure. In addition, the available therapeutic options for stroke risk prevention in heart failure are described in detail including how these options are incorporated into relevant professional society guidelines.
| S-EPMC4682916 | biostudies-other
Project description:Previous studies in patients with atrial fibrillation showed that a history of heart failure (HF) could negatively impact anticoagulation quality, as measured by the average time in therapeutic range (TTR). Whether additional markers of HF severity are associated with TTR has not been investigated thoroughly. We aimed to examine the potential role of HF severity in the quality of warfarin control in patients with HF with reduced ejection fraction. Data from the Warfarin versus Aspirin in Reduced Cardiac Ejection Fraction Trial were used to investigate the association between TTR and HF severity. Multivariable logistic regression models were used to examine the association of markers of HF severity, including New York Heart Association (NYHA) class, Minnesota Living with HF (MLWHF) score, and frequency of HF hospitalization, with TTR ?70% (high TTR). We included 1,067 participants (high TTR, N?=?413; low TTR, N?=?654) in the analysis. In unadjusted analysis, patients with a high TTR were older and less likely to have had strokes or receive other antiplatelet agents. Those patients also had lower NYHA class, better MLWHF scores, greater 6-minute walk distance, and lower frequency of HF hospitalizations. Multivariable analysis showed that NYHA class III and/or IV (Odds ratio [OR] 0.68 [95% confidence intervals [CIs] 0.49 to 0.94]), each 10-point increase in MLWHF score (i.e., worse health-related quality of life) (OR 0.92 [0.86 to 0.99]), and higher number of HF hospitalization per year (OR0.45 [0.30 to 0.67]) were associated with decreased likelihood of having high TTR. In HF patients with systolic dysfunction, NYHA class III and/or IV, poor health-related quality of life, and a higher rate of HF hospitalization were independently associated with suboptimal quality of warfarin anticoagulation control. These results affirm the need to assess the new approaches, such as direct oral anticoagulants, to prevent thromboembolism in this patient population.
| S-EPMC6151139 | biostudies-literature
Project description:BACKGROUND:Stroke prophylaxis in patients with atrial fibrillation (AF) and heart failure (HF) in the era of direct oral anticoagulants is not well characterized. Using data from American Heart Association Get With The Guidelines-AFIB, we sought to evaluate oral anticoagulation (OAC) use at discharge among AF patients with concomitant HF. METHODS AND RESULTS:AF patients with a diagnosis of HF hospitalized from January 2013 to March 2017 were included. We compared patient characteristics and use of OAC at discharge among patients with reduced (redundant ejection fraction [EF], EF?40%), borderline (40%<EF<50%), and preserved (EF?50%) EF using multivariable mixed logistic regression models. Among 10?883 patients with AF and HF, 1790 (16.4%) had a reported contraindication to anticoagulation and were excluded from further analysis. Among 9093 patients eligible for OAC, 3499 (38.5%) had HF with reduced EF, 1062 (11.7%) had HF with borderline EF, and 4532 (49.8%) had HF with preserved EF. The median CHA2DS2-VASc score was 5 (Q1, Q3; 3, 6) among all patients and higher among those with HF with preserved EF than HF with reduced EF (5 [4, 6] versus 4 [3, 5]; P<0.0001). The proportion of eligible patients discharged on OAC was 94.9%, with 43.6% discharged on warfarin and 50.7% discharged on direct oral anticoagulants. A higher proportion of patients with HF with reduced EF and HF with borderline EF were discharged on direct oral anticoagulants than with HF with preserved EF, but the difference was small (52.8%, 53.1% versus 48.5%, respectively; P=0.0002). EF group was not significantly associated with a patient's OAC use at discharge. CONCLUSIONS:In the context of American Heart Association Get With The Guidelines-AFIB, a quality improvement program, the rate of use of OAC at discharge in eligible AF patients with HF was almost 95%. To our knowledge, these rates represent some of the highest use of appropriate anticoagulation for patients in a national registry to date.
| S-EPMC6319668 | biostudies-literature
Project description:BackgroundIn non-valvular atrial fibrillation (NVAF) patients, congestive heart failure (CHF) confers an increased risk of stroke or systemic thromboembolism. This risk is present in both heart failure (HF) with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). It is unclear if clinicians account for both types of CHF in their NVAF anticoagulation practices. Accordingly, we characterized current outpatient anticoagulation trends in NVAF patients with HFpEF compared to patients with HFrEF.MethodsThe outpatient NCDR PINNACLE-AF registry was analyzed to identify patients with NVAF and CHF. The study population was subdivided into HFpEF (ie, LVEF???40%) and HFrEF (LVEF?<?40%). Anticoagulation rates by CHF group were compared and stratified by CHA2 DS2 -VASc score.ResultsA total of 340?127 patients with NVAF and CHF were identified, of whom 248?136 (73.0%) were classified as HFpEF and 91?991 (27.0%) as HFrEF. Patients with HFpEF had higher mean CHA2 DS2 -VASc scores and were more likely to be female, older, and have hypertension (P <?0.001). Unadjusted anticoagulation rates were significantly lower in patients with HFpEF compared to those with HFrEF (60.6% vs 64.2%, respectively). Lower rates of anticoagulation in the HFpEF group persisted after risk adjustment (RR: 0.93 [95% CI: 0.91, 0.94]). Stratification by CHA2 DS2 -VASc score demonstrated that lower rates of anticoagulation in patients with HFpEF persisted until a score of ?5.ConclusionsPatients with NVAF and HFpEF have significantly lower anticoagulation rates when compared to their HFrEF counterparts. These findings suggest a potential underappreciation of HFpEF as a risk factor in patients with NVAF.
| S-EPMC6712307 | biostudies-literature
Project description:Background and purposeAtrial fibrillation and heart failure with reduced ejection fraction (HFrEF) are common sources of cardioembolism. While oral anticoagulation is strongly recommended for atrial fibrillation, there are marked variations in guideline recommendations for HFrEF due to uncertainty about net clinical benefit. This systematic review and meta-analysis evaluates the comparative association of oral anticoagulation with stroke and other cardiovascular risk in populations with atrial fibrillation or HFrEF in sinus rhythm and identify factors mediating different estimates of net clinical benefit.MethodsPubMed and Embase were searched from database inception to November 20, 2019 for randomized clinical trials comparing oral anticoagulation to control. A random-effects meta-analysis was used to estimate a pooled treatment-effect overall and within atrial fibrillation and HFrEF trials. Differences in treatment effect were assessed by estimating I2 among all trials and testing the between-trial-population P-interaction. The primary outcome measure was all stroke. Secondary outcome measures were ischemic stroke, hemorrhagic stroke, mortality, myocardial infarction, and major hemorrhage.ResultsTwenty-one trials were eligible for inclusion, 15 (n=19 332) in atrial fibrillation (mean follow-up: 23.1 months), and 6 (n=9866) in HFrEF (mean follow-up: 23.9 months). There were differences in primary outcomes between trial populations, with all-cause mortality included for 95.2% of HFrEF trial population versus 0.38% for atrial fibrillation. Mortality was higher in controls groups of HFrEF populations (19.0% versus 9.6%) but rates of stroke lower (3.1% versus 7.0%) compared with atrial fibrillation. The association of oral anticoagulation with all stroke was consistent for atrial fibrillation (odds ratio, 0.51 [95% CI, 0.42–0.63]) and HFrEF (odds ratio, 0.61 [95% CI, 0.47–0.79]; I2=12.4%; P interaction=0.31). There were no statistically significant differences in the association of oral anticoagulation with cardiovascular events, mortality or bleeding between populations.ConclusionsThe relative association of oral anticoagulation with stroke risk, and other cardiovascular outcomes, is similar for patients with atrial fibrillation and HFrEF. Differences in the primary outcomes employed by trials in HFrEF, compared with atrial fibrillation, may have contributed to differing conclusions of the relative efficacy of oral anticoagulation.
| S-EPMC8478106 | biostudies-literature
Project description:AimsTo review maternal and foetal outcomes in women with mechanical heart valves (MHVs) treated with vitamin-K antagonists (VKAs), first-trimester heparin followed by VKAs (sequential treatment), low molecular weight heparin (LMWH) and unfractionated heparin (UFH) during pregnancy, in order to inform practice.Methods and resultsMedline, Embase and Central were searched from inception until February 2016. Two reviewers independently screened 1786 titles, reviewed 110 full-texts and extracted data and assessed risk-of-bias from 46 articles. Pooled incidence (95% confidence intervals) was calculated for maternal and foetal outcomes. Included studies had a moderate or high risk-of-bias. With VKAs, sequential treatment and LMWH, maternal mortality occurred in 0.9% (0.4-1.4), 2.0% (0.8-3.1) and 2.9% (0.2-5.7), thromboembolic complications in 2.7% (1.4-4.0), 5.8% (3.8-7.7) and 8.7% (3.9-13.4), livebirths in 64.5% (48.8-80.2), 79.9% (74.3-85.6) and 92.0% (86.1-98.0) and anticoagulant-related foetal/neonatal adverse events (embryopathy or foetopathy) in 2.0% (0.3-3.7), 1.4% (0.3-2.5) and 0%, respectively. When UFH is used throughout pregnancy, 11.2% (2.8-19.6) suffered thromboembolic complications. Foetal loss and adverse events occurred with first-trimester warfarin doses ≤ 5 mg/day, although there were more livebirths [83.6% (75.8-91.4) vs. 43.9% (32.8-55.0)] and fewer foetal anomalies [2.3% (0.7-4.0) vs. 12.4% (3.3-21.6)] with lower doses than with warfarin > 5 mg/day.ConclusionsVKAs are associated with fewest maternal complications but also with fewest livebirths. Sequential treatment does not eliminate anticoagulant-related foetal/neonatal adverse events. LMWH is associated with the highest number of livebirths. The safety of UFH throughout pregnancy and first-trimester warfarin ≤ 5 mg/day remains unconfirmed.
| S-EPMC5429939 | biostudies-literature
Project description:BackgroundCardiovascular diseases contribute substantially to the poor health and reduced life expectancy of Indigenous Australians. Heart failure is a common, disabling, progressive and costly complication of these disorders. The epidemiology of heart failure and the adequacy of relevant health service provision in Indigenous Australians are not well delineated.MethodsA systematic search of the electronic databases PubMed, Embase, Web of Science, Cinahl Plus, Informit and Google Scholar was undertaken in April 2012 for peer-reviewed journal articles relevant to the topic of heart failure in Indigenous Australians. Additionally, a website search was done to identify other pertinent publications, particularly government reports.ResultsThere was a paucity of relevant peer-reviewed research, and government reports dominated the results. Ten journal articles, 1 published conference abstract and 10 reports were eligible for inclusion. Indigenous Australians reportedly have higher morbidity and mortality from heart failure than their non-Indigenous counterparts (age-standardised prevalence ratio 1.7; age-standardised hospital separation ratio ?3; crude per capita hospital expenditure ratio 1.58; age-adjusted mortality ratio >2). Despite the evident disproportionate burden of heart failure in Indigenous Australians, the accuracy of estimation from administrative data is limited by poor indigenous identification, inadequate case ascertainment and exclusion of younger subjects from mortality statistics. A recent journal article specifically documented a high prevalence of heart failure in Central Australian Aboriginal adults (5.3%), noting frequent undiagnosed disease. One study examined barriers to health service provision for Indigenous Australians in the context of heart failure.ConclusionsDespite the shortcomings of available published data, it is clear that Indigenous Australians have an excess burden of heart failure. Emerging data suggest that undiagnosed cases may be common in this population. In order to optimise management and to inform policy, high quality research on heart failure in Indigenous Australians is required to delineate accurate epidemiological indicators and to appraise health service provision.
| S-EPMC3521206 | biostudies-literature
Project description:ObjectiveTo determine the impact of multidisciplinary interventions on hospital admission and mortality in heart failure.DesignSystematic review. Thirteen databases were searched and reference lists from included trials and related reviews were checked. Trial authors were contacted if further information was required.SettingRandomised controlled trials conducted in both hospital and community settings.PatientsTrials were included if all, or a defined subgroup of patients, had a diagnosis of heart failure.InterventionsMultidisciplinary interventions were defined as those in which heart failure management was the responsibility of a multidisciplinary team including medical input plus one or more of the following: specialist nurse, pharmacist, dietician, or social worker. Interventions were separated into four mutually exclusive groups: provision of home visits; home physiological monitoring or televideo link; telephone follow up but no home visits; and hospital or clinic interventions alone. Pharmaceutical and exercise based interventions were excluded.Main outcome measuresAll cause hospital admission, all cause mortality, and heart failure hospital admission.Results74 trials were identified, of which 30 contained relevant data for inclusion in meta-analyses. Multidisciplinary interventions reduced all cause admission (relative risk (RR) 0.87, 95% confidence interval (CI) 0.79 to 0.95, p = 0.002), although significant heterogeneity was found (p = 0.002). All cause mortality was also reduced (RR 0.79, 95% CI 0.69 to 0.92, p = 0.002) as was heart failure admission (RR 0.70, 95% CI 0.61 to 0.81, p < 0.001). These results varied little with sensitivity analyses.ConclusionMultidisciplinary interventions for heart failure reduce both hospital admission and all cause mortality. The most effective interventions were delivered at least partly in the home.
| S-EPMC1769009 | biostudies-literature
Project description:PURPOSE OF REVIEW:Heart failure with preserved ejection fraction (HFpEF) is a relatively new disease entity used in medical terminology; however, both the number of patients and its clinical significance are growing. HFpEF used to be seen as a mild condition; however, the symptoms and quality of life of the patients are comparable to those with reduced ejection fraction. The disease is much more complex than previously thought. In this article, information surrounding the etiology, diagnosis, prognosis, and possible therapeutic options of HFpEF are reviewed and summarized. RECENT FINDINGS:It has recently been proposed that heart failure (HF) is rather a heterogeneous syndrome with a spectrum of overlapping and distinct characteristics. HFpEF itself can be distilled into different phenotypes based on the underlying biology. The etiological factors of HFpEF are unclear; however, systemic low-grade inflammation and microvascular damage as a consequence of comorbidities associated with endothelial dysfunction, oxidative stress, myocardial remodeling, and fibrosis are considered to play a crucial role in the pathogenesis of a disease. The H2FPEF score and the HFpEF nomogram are recently validated highly sensitive tools employed for risk assessment of subclinical heart failure. Despite numerous studies, there is still no evidence-based pharmacotherapy for HFpEF and the mortality and morbidity associated with HFpEF remain high. A better understanding of the etiological factors, the impact of comorbidities, the phenotypes of the disease, and implementation of machine learning algorithms may play a key role in the development of future therapeutic strategies.
| S-EPMC7347676 | biostudies-literature
Project description:To review possible associations reported between genetic variants and the risk, therapeutic response and prognosis of heart failure.Electronic databases (PubMed, Web of Science and CNKI) were systematically searched for relevant papers, published between January 1995 and February 2015.Eighty-two articles covering 29 genes and 39 polymorphisms were identified.Genetic association studies of heart failure have been highly controversial. There may be interaction or synergism of several genetic variants that together result in the ultimate pathological phenotype for heart failure.
| S-EPMC5536573 | biostudies-literature