BackgroundLarge clinical trials are lack of data on non‐vitamin K antagonist oral anticoagulants for acute stroke patients.AimTo evaluate the choice of oral anticoagulants at acute hospital discharge in stroke patients with nonvalvular atrial fibrillation and clarify the underlying characteristics potentially affecting that choice using the multicenter Stroke Acute Management with Urgent Risk‐factor Assessment and Improvement‐NVAF registry (ClinicalTrials.gov NCT01581502).MethodThe study included 1192 acute ischemic stroke/transient ischemic attack patients with nonvalvular atrial fibrillation (527 women, 77·7 ± 9·9 years old) between September 2011 and March 2014, during which three nonvitamin K antagonist oral anticoagulant oral anticoagulants were approved for clinical use. Oral anticoagulant choice at hospital discharge (median 23‐day stay) was assessed.ResultsWarfarin was chosen for 650 patients, dabigatran for 203, rivaroxaban for 238, and apixaban for 25. Over the three 10‐month observation periods, patients taking warfarin gradually decreased to 46·5% and those taking nonvitamin K antagonist oral anticoagulants increased to 48·0%. As compared with warfarin users, patients taking nonvitamin K antagonist oral anticoagulants included more men, were younger, more frequently had small infarcts, and had lower scores for poststroke CHADS 2, CHA 2 DS 2‐VASc, and HAS‐BLED, admission National Institutes of Health stroke scale, and discharge modified Rankin Scale. Nonvitamin K antagonist oral anticoagulants were started at a median of four‐days after stroke onset without early intracranial hemorrhage. Patients starting nonvitamin K antagonist oral anticoagulants earlier had smaller infarcts and lower scores for the admission National Institutes of Health stroke scale and the discharge modified Rankin Scale than those starting later. Choice of nonvitamin K antagonist oral anticoagulants was independently associated with 20‐day or shorter hospitalization (OR 2·46, 95% CI 1·87–3·24).ConclusionsWarfarin use at acute hospital discharge was still common in the initial years after approval of nonvitamin K antagonist oral anticoagulants, although nonvitamin K antagonist oral anticoagulant users increased gradually. The index stroke was milder and ischemia‐risk indices were lower in nonvitamin K antagonist oral anticoagulant users than in warfarin users. Early initiation of nonvitamin K antagonist oral anticoagulants seemed safe.

This is the first description of the unique clinical features of SCA36, a relatively pure cerebellar ataxia with progressive motor neuron involvement. Thus, SCA36 is a disease that stands at the crossroads of SCA and motor neuron disease.

Stroke or systemic embolism during the initial three-month anticoagulation period after stroke/transient ischemic attack was not frequent as compared to previous findings regardless of warfarin or non-vitamin K antagonist oral anticoagulants were used. Intracranial hemorrhage was relatively uncommon in non-vitamin K antagonist oral anticoagulant users, although treatment assignment was not randomized. Early initiation of non-vitamin K antagonist oral anticoagulants during the acute stage of stroke/transient ischemic attack in real-world clinical settings seems safe in bleeding-susceptible Japanese population.

Stroke/TIA patients receiving DOACs for secondary prevention were younger and had lower stroke severity and risk indices than those receiving warfarin. Estimated cumulative incidences of stroke and systemic embolism within 2 years were similar between warfarin and DOACs users, but those of death and intracranial hemorrhage were significantly lower among DOAC users.

To evaluate the effect of exercise on left ventricular diastolic filling, the following were measured at rest and during exercise in 14 control subjects and 15 athletes, using digitized M-mode echocardiography: the peak early diastolic lengthening rate of the left ventricular dimension and the filling volume and the filling fraction during the first 0.10 s of diastole. During ergometer exercise performed at a level that increased the heart rate to 100 beats/min, there were significant increases in the peak normalized lengthening rate of the left ventricular dimension (control subjects, 4.2 +/- 1.3 vs. 6.1 +/- 1.1 s-1, mean +/- SD, P less than 0.001; athletes, 5.3 +/- 0.9 vs. 7.4 +/- 1.1 s-1, P less than 0.001), filling volume (control subjects, 15 +/- 12 vs. 33 +/- 10 ml, P less than 0.001; athletes, 21 +/- 12 vs. 63 +/- 18 ml, P less than 0.001), and filling fraction (control subjects, 21 +/- 14 vs. 42 +/- 17%, P less than 0.005; athletes, 21 +/- 13 vs. 54 +/- 12%, P less than 0.01). The peak lengthening rate of the left ventricular dimension, the filling volume, and the filling fraction were significantly greater in athletes than in control subjects during exercise (P less than 0.005, P less than 0.001, and P less than 0.05, respectively). Augmented early diastolic filling may be a mechanism to provide adequate filling for the ventricle at high heart rates produced by exercise, especially in athletes.