Direct oral anticoagulants for stroke prevention in patients with device-detected atrial fibrillation: assessing net clinical benefit.

Subclinical, device-detected atrial fibrillation (AF) is frequently recorded by pacemakers and other implanted cardiac rhythm devices. Patients with device-detected AF have an elevated risk of stroke, but a lower risk of stroke than similar patients with clinical AF captured with surface electrocardiogram. Two randomized clinical trials (NOAH-AFNET 6 and ARTESiA) have tested a direct oral anticoagulant (DOAC) against aspirin or placebo. A study-level meta-analysis of the two trials found that treatment with a DOAC resulted in a 32% reduction in ischaemic stroke and a 62% increase in major bleeding; the results of the two trials were consistent. The annualized rate of stroke in the control arms was ∼1%. Several factors point towards overall net benefit from DOAC treatment for patients with device-detected AF. Strokes in ARTESiA were frequently fatal or disabling and bleeds were rarely lethal. The higher absolute rates of major bleeding compared with ischaemic stroke while on treatment with a DOAC in the two trials are consistent with the ratio of bleeds to strokes seen in the pivotal DOAC vs. warfarin trials in patients with clinical AF. Prior research has concluded that patients place a higher emphasis on stroke prevention than on bleeding. Further research is needed to identify the characteristics that will help identify patients with device-detected AF who will receive the greatest benefit from DOAC treatment.

Clinical challenges in the treatment of a patient with decompensated heart failure and glucose-6-phosphate dehydrogenase deficiency (G6PDd).

We present a case of a man in his 60s, known with glucose-6-phosphate dehydrogenase deficiency (G6PDd) and cor pulmonale, admitted to the department of cardiology due to cardiac decompensation and anaemia. The main complaint was dyspnoea. Echocardiography confirmed severe cor pulmonale with compression of the left ventricle. G6PDd has been linked with pulmonary hypertension which could contribute to aforementioned echocardiographic findings. Diuretics are the first line of treatment when it comes to cardiac decompensation, but sulfonamide diuretics can induce or exacerbate haemolysis in patients with G6PDd. Due to the respiratory distress of the patient, a treatment plan including sulfonamide diuretics was initiated in collaboration with the haematologists. Unfortunately, the patient died 2 days after admission. This case emphasises that not all cardiac patients can tolerate standard treatment with sulfonamide diuretics; despite this, they remain essential in the acute setting, and they are associated with foreseeable but only partly manageable complications in susceptible patients.