Increase in the Size of an Intracardiac Thrombus during Dabigatran Therapy (110 mg b.i.d.) in an Acute Cardioembolic Stroke Patient

We report a case of atrial fibrillation in a patient in whom a mobile thrombus in the left atrial appendage increased in size after low-dose dabigatran therapy. A 74-year-old man was admitted to our hospital because of sudden onset of right hemiplasia and dysarthria. On admission, his National Institutes of Health Stroke Scale score was three. Axial diffusion-weighted magnetic resonance images and magnetic resonance angiography images showed hyperintense signals in the left front-parietal cerebral cortex without any intracranial stenotic lesions, and acute cardioembolic stroke associated with nonvalvular atrial fibrillation was diagnosed. Transesophageal echocardiography revealed a mobile thrombosis (1.0 × 2.2 cm) in the left atrial appendage, and dabigatran therapy (110 mg b.i.d.) was initiated to prevent stroke recurrence. Transesophageal echocardiography performed 6 days later revealed that the size of the thrombus had increased to 1.5 × 3.0 cm. Medication was changed to warfarin, and the thrombosis subsequently decreased in size. The patient did not have a recurrent stroke and was discharged with a National Institutes of Health Stroke Scale score of zero. This case demonstrates that low-dose dabigatran may not be effective in reducing the size of a thrombus

Empagliflozin in Patients with Chronic Kidney Disease

Background The effects of empagliflozin in patients with chronic kidney disease who are at risk for disease progression are not well understood. The EMPA-KIDNEY trial was designed to assess the effects of treatment with empagliflozin in a broad range of such patients. Methods We enrolled patients with chronic kidney disease who had an estimated glomerular filtration rate (eGFR) of at least 20 but less than 45 ml per minute per 1.73 m(2) of body-surface area, or who had an eGFR of at least 45 but less than 90 ml per minute per 1.73 m(2) with a urinary albumin-to-creatinine ratio (with albumin measured in milligrams and creatinine measured in grams) of at least 200. Patients were randomly assigned to receive empagliflozin (10 mg once daily) or matching placebo. The primary outcome was a composite of progression of kidney disease (defined as end-stage kidney disease, a sustained decrease in eGFR to < 10 ml per minute per 1.73 m(2), a sustained decrease in eGFR of & GE;40% from baseline, or death from renal causes) or death from cardiovascular causes. Results A total of 6609 patients underwent randomization. During a median of 2.0 years of follow-up, progression of kidney disease or death from cardiovascular causes occurred in 432 of 3304 patients (13.1%) in the empagliflozin group and in 558 of 3305 patients (16.9%) in the placebo group (hazard ratio, 0.72; 95% confidence interval [CI], 0.64 to 0.82; P < 0.001). Results were consistent among patients with or without diabetes and across subgroups defined according to eGFR ranges. The rate of hospitalization from any cause was lower in the empagliflozin group than in the placebo group (hazard ratio, 0.86; 95% CI, 0.78 to 0.95; P=0.003), but there were no significant between-group differences with respect to the composite outcome of hospitalization for heart failure or death from cardiovascular causes (which occurred in 4.0% in the empagliflozin group and 4.6% in the placebo group) or death from any cause (in 4.5% and 5.1%, respectively). The rates of serious adverse events were similar in the two groups. Conclusions Among a wide range of patients with chronic kidney disease who were at risk for disease progression, empagliflozin therapy led to a lower risk of progression of kidney disease or death from cardiovascular causes than placebo