Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm

Abstract

H eart failure (HF) represents a major and growing public health problem because of its prevalence, incidence, morbidity, mortality, and economic costs. The prevalence of HF is 2% to 3% of the general population. 1 Five million Americans are affected, with Ͼ550 000 cases diagnosed each year. 2 The mortality rate from severe HF remains Ͼ60% within 5 years of diagnosis, and 50% of hospitalized patients with HF require readmission within 6 months of discharge. In the US estimated costs amount to Ͼ $35 billion per year. 3 Although several therapies (eg, ␤-blockers, angiotensinconverting enzyme [ACE] inhibitors, and cardiac resynchronization therapy) have been proven effective in improving HF outcomes, many unanswered questions about optimal treatment remain. One area of ongoing uncertainty is the appropriate role for antithrombotic therapy in patients with HF. Observational data suggest that patients with HF have an increased venous thromboembolism (VTE) risk (deep venous thromboembolism [DVT], pulmonary embolism [PE], peripheral arterial thromboembolism, and stroke). 4 These epidemiological findings are supported by multiple mechanisms that can contribute to a hypercoagulable state in patients with HF. Despite this increased risk of VTE, the role of antithrombotic therapy remains unclear. In this article, we provide an overview of epidemiology, pathophysiology, clinical trial data, and therapeutic recommendations for prevention of thromboembolism in HF. Search StrategyWe searched PubMed for articles published between 1958 and 2010 using the following search terms: epidemiology of heart failure, thromboembolism and heart failure, thrombogenesis and heart failure, anticoagulation in heart failure, antiplatelet agent and heart failure, aspirin and heart failure, bleeding risk and anticoagulation, and aspirin and angiotensin-converting enzyme inhibitors. We also studied abstracts from national and international cardiovascular meetings to identify unpublished studies using the key words anticoagulation and dilated cardiomyopathy. EpidemiologyData from published observational studies and secondary analyses of randomized controlled trials (RCTs) indicate that patients with HF patients have a higher risk for VTE than the general population. Observational CohortsDVT and PE Several case-cohort studies have shown that HF is associated with a 2-to 3-fold increased risk of DVT and PE compared with other medical conditions. 5 Retrospective analyses report an annual VTE incidence of 1.0% to 4.5% in patients with HF. 6 In RCTs of thromboprophylaxis in hospitalized patients with HF followed for 90 days, DVT rates ranged from 4.0% to 14.6%. 7,8 The Prophylaxis in Medical Patients With Enoxaparin trial evaluated VTE incidence in hospitalized patients with (nϭ353) and without (nϭ749) HF during a follow-up of 14 days after discharge and found that 15% of patients with HF not treated with enoxaparin developed VTE. 9 Beemath et al, 4 using data from the National Hospital Discharge Survey, found an increased risk of VTE in hospitalized p...

Is There a Rationale for Antiplatelet Therapy in Acute Heart Failure?

“…In contrast, conflicting data have been observed with regard to the association of platelet biomarkers with prognosis. 7,9,21,23,24 Notably, the small size of these previous studies underscores the need for ongoing exploration of the biology of platelet activation in HF. n/a n/a n/a n/a Kandis et al 10 Acute vs chronic HF Acute>chronic HF Yes n/a n/a n/a n/a n/a n/a n/a No differences between groups; decrease at followup for acute HF n/a n/a n/a n/a …”

“…Several mechanisms that are activated in chronic HF and further enhanced during acute decompensation may promote a prothrombotic state 9 and may explain, in part, the observed increased platelet reactivity. 5 Endothelial damage and dysfunction along with imbalances in nitric oxide production and increased expression of adhesion molecules may lead to enhanced platelet adhesion and activation.…”

“…One such potential mechanism is platelet activation. 5,6 The activation of neurohormonal, inflammatory, and thrombotic pathways [7][8][9] is known to be associated with enhanced platelet reactivity in AHF. [10][11][12][13][14] However, whether increased platelet activity is simply a marker of this systemic imbalance or an actual contributor to acute decompensation is incompletely understood.…”

The Year in Heart Failure

“…Disappointment continued with publication of the randomized controlled ASCEND-HF (Acute Study of Clinical Effectiveness of Nesiritide in Decompensated Heart Failure). In this study of 7,000 patients, nesiritide was not associated with a change in the rate of rehospitalization or State-of-the-Art Reviews Table 2 State-of-the-Art Reviews "Cirrhotic Cardiomyopathy" (10) "Update 2011: Clinical and Genetic Issues in Familial Dilated Cardiomyopathy" (11) "Exercise Training in Heart Failure: Practical Guidance" (12) "The Role of Exercise Training in Heart Failure" (13) "Heart Failure and Chronic Obstructive Pulmonary Disease" (14) "Heart Failure With Preserved Ejection Fraction: Pathophysiology, Diagnosis, and Treatment" (15) "Medical and Surgical Treatment of Acute Right Ventricular Failure" (16) "Obstructive Sleep Apnea and Heart Failure" (17) "Pregnancy in Patients With Pre-Existing Cardiomyopathies" (18) "Thromboembolism and Antithrombotic Therapy in Patients With Heart Failure in Sinus Rhythm: Current Status and Future Directions" (19) "Troponin Elevation in Heart Failure" (20) death and had a nonsignificant effect on dyspnea (21). Moreover, the DOSE (Diuretic Optimization Strategies Evaluation) trial showed no significant difference in symptoms or renal function when loop diuretic therapy was administered by continuous infusion or bolus and no significant difference in outcomes at low versus high dose (23).…”

Anticoagulación para pacientes con insuficiencia cardiaca en ritmo sinusal: habitual en la práctica clínica, pero aún no basada en la evidencia

“…Sin embargo, en la evaluació n inicial deberían utilizarse siempre las escalas CHA 2 DS 2 -VASc y HAS-BLED para establecer la relació n riesgo-beneficio entre iniciar y no iniciar el tratamiento con ACO 15 . En la prá ctica clínica, sin embargo, los ACO se administran con mayor asiduidad: entre el 10 y el 30% de los pacientes con IC sin FA reciben este tratamiento 16 . En la prá ctica clínica, sin embargo, los ACO se administran con mayor asiduidad: entre el 10 y el 30% de los pacientes con IC sin FA reciben este tratamiento 16 .…”