Specific risk of atrial fibrillation and stroke in oncology patients

Atrial fibrillation (AF) is the most common sustained arrhythmia being present in 1.5–2% of the population and has been found to occur more frequently in oncology patients.1 Cancer and cancer therapy may seem to be a risk factor for the development of AF and both share common risk factors, such as ageing. The occurrence of AF in cancer may be due to comorbid states or a direct tumour effect, but it also may represent a complication of cancer therapy,2 whereby inflammation is present for both conditions (Table 1).1,3 The increasing survival of cancer patients may further raise the incidence of the arrhythmia. There are specific types of cancer (pancreatic, ovarian, lung, and primary hepatic) which have in themselves an increased embolic risk. In addition, there are many cancer treatments that also increase that risk (cisplatin, gemcitabine, 5-fluorouracil, erythropoietin, and granulocyte colony stimulating factors).2 Epidemiological evidence of AF in patients with cancer AF, atrial fibrillation. Source: Farmakis D, Parissis J, Filippatos G. Insights into onco-cardiology: atrial fibrillation in cancer. J Am Coll Cardiol 2014;63:945–53. Epidemiological evidence of AF in patients with cancer AF, atrial fibrillation. Source: Farmakis D, Parissis J, Filippatos G. Insights into onco-cardiology: atrial fibrillation in cancer. J Am Coll Cardiol 2014;63:945–53. On the other hand, in oncology patients, there is an increased bleeding risk, especially when the location of the tumour is intracranial, or in haematologic malignancies with coagulation defects. Some cancer therapy induces thrombocytopenia, which further increases the risk of bleeding. Severe metastatic hepatic disease also worsens the situation. Atrial fibrillation affects the prognosis of cancer patients. The presence of cancer in addition to AF significantly increases the risk of stroke. Cancer may be related to hypercoagulability, but it also increases the bleeding risk. Treating AF in patients with malignancies is a challenge, especially in terms of antithrombotic therapy, because cancer may result in an increased risk of either thrombosis or haemorrhage and an unpredictable anticoagulation response. Thromboembolic risk prediction scores such as CHADS2 may not be applicable (risk assessment scales are not validated for oncology patients). The general lack of evidence imposes an individualized approach. Because of the lack of evidence, the prevention of stroke in patients with cancer and AF is generally done as in non-cancer patients, and there no dedicated trials. However, they are special patients and it should be important to pay attention to cancer stage, prognosis, and potential interactions with cancer therapies. Patients with malignancies and AF require multidisciplinary care by cardiologists and oncologists including a careful planning of antithrombotic therapy. There is controversy about which anticoagulant would be the best. Vitamin K antagonists (VKA) may interact with many cancer therapies (Figure 1).4 For this reason, when the patient has an active cancer or is in treatment with chemotherapy, oncologists prefer using low-molecular-weight heparins. Furthermore, weak evidence suggests beneficial effects in cancer patients (potential antitumor effect because of anti-angiogenesis).5,6 Mechanisms of warfarin–cancer drugs interactions. Source: Pangilinan JM, Pangilinan PH Jr, Worden FP. Use of warfarin in the patient with cancer. J Support Oncol 2007;5:131–136. Regarding new oral anticoagulants (NOACs), cancer patients were excluded from NOAC AF trials. However, data from venous thromboembolism in cancer patients’ trials showed preliminary evidence of efficacy and safety of the NOACs in the patients that developed AF later. In the general population, they are safer than VKA and effective for stroke prevention. If a patient with cancer and AF is going to receive an NOAC, specific monitoring modalities should be considered. In addition to careful clinical examination for bleeding signs and regular monitoring of liver and renal function, repetitive full blood counts including platelets should be evaluated. New oral anticoagulants may not be suitable for use in patients with some cancer therapies, because they share metabolic pathways. Further research is needed to find out more about the impact of the interaction. It is very important to adjust the dose in special situations that occur frequently in these patients, e.g. the loss of weight, inability to take oral medication, the nausea, vomiting, and diarrhoea after chemotherapy. NOACs have many other advantages, such us comfortable dosing scheme. This is important in patients with concomitant medications and comorbidities like cancer patients.7,8 When anticoagulant therapy needs to be newly initiated in a patient with malignancy developing AF, therapy with VKAs or heparins is usually considered over NOACs, because of the wider clinical experience with these drugs, the possibility of close monitoring and the reversal options. However, if the patient was previously taking an NOAC before the diagnosis of the cancer, continuation of prior NOAC therapy may be possible.9 There are still many questions with no answers regarding NOACs. At this moment, available evidence is not enough for clinical practice recommendations, and further studies are needed. This is a promising field for the near future of the antithrombotic treatment in oncology patients. References are available as supplementary materialat European Heart Journal online.