Anticoagulation for Heart Failure Patients in Sinus Rhythm: Common in Clinical Practice But Still Not Evidence-based Anticoagulacion para pacientes con insuficiencia cardiaca en ritmo sinusal: habitual en la practica clinica, pero aun no basada en la evidencia

Heart failure (HF) remains a challenging medical problem with growing numbers of cases and dramatically increasing costs of medical care. Despite indisputable progress in the modern management of HF patients, morbidity and mortality are still unacceptably high, which fully justifies a search for novel therapies. In parallel, some drugs, already very well known, are commonly used in everyday practice despite a lack of evidence from large clinical trials, due to physicians’ strong belief that they may simply work in HF patients. Oral anticoagulants (OAC) constitute one of the best examples of ancillary treatment of HF, and their use has a more than 60-year history. In the most recent European observational studies, OAC were used in 43% of all patients with stable chronic HF, 1 and in 39% of those discharged from hospital after an episode of decompensation. 2 In fact, the statement that ‘‘patients with congestive HF are prone to develop thromboembolic (TE) complications which increase the morbidity and mortality of the disease,’’ made in 1950, 3 forms a background for the first attempts to introduce OAC into the treatment of HF patients, but also sounds very timely today. Since then, we have accumulated strong evidence from epidemiological and pathophysiological studies linking HF syndrome to an increased risk of TE events seen in a broad clinical perspective as ischemic stroke, pulmonary embolism, other venous or arterial TE complications including acute myocardial infarction and sudden cardiac death. 4,5 The epidemiological studies rather uniformly confirm increased risk of stroke among HF patients compared with the general population and a recent meta-analysis of 26 studies reported the incidence of ischemic stroke was 18 per 1000 persons in the first year of HF diagnosis and increased to 47 per 1000 persons at 5 years. 6 Other studies also seem to confirm particularly high risk of stroke in the early phase after HF diagnosis. 4 It is estimated that HF ranks second as a cause of ischemic stroke, just after atrial fibrillation (AF), and is responsible for more than 60 000 strokes per year in the United States. 4 According to actual etiological classification of ischemic stroke, symptomatic HF with low left ventricular ejection fraction (LVEF), previous myocardial infarction with low LVEF, and dilated cardiomyopathy are considered as primary high risk sources of embolic stroke (with annual risk >2%). 7 Stroke is always associated with an ominous outcome in these populations and HF also increases risk of venous TE complications. Deep venous thrombosis may be present in 10% to 20% of hospitalized patients with HF not receiving prophylaxis. Up to 10% of HF-related deaths are due to pulmonary embolism. 8 Interestingly, many HF deaths initially classified as sudden and unexpected may be due to new coronary occlusion due to TE. In the ATLAS (Assessment of Treatment with Lisinopril and Survival) study, myocardial infarction confirmed at autopsy accounted for 40% of all sudden deaths. 9 Although risk of TE complications is linked with severity of HF (in particular with impaired LVEF), recent analyses from clinical trials that recruited the whole spectrum of HF patients seem to show that the rate of stroke and stroke-related mortality may be independent of the magnitude of LVEF impairment. 10 Whether patients with so-called HF with preserved LVEF are also at high risk for TE complications needs to be established in future studies. Pathophysiology of increased risk of TE events in HF is traditionally linked with 3 elements comprising the ‘‘Virchow triad’’: abnormalities in blood flow, vessel wall, and blood constituents. 5 Neuroendocrine activation typical of HF syndrome may also contribute to rheological abnormalities. 5 Recently, high