Background and Purpose: COVID-19 is a known risk factor for stroke. There is limited data on the influence of demographics, risk factors, and hematologic function on outcomes in COVID-19 stroke patients. Methods: All patients with acute ischemic or hemorrhagic stroke tested for COVID-19 and treated from March 13 through May 19, 2020 were retrospectively analyzed. COVID+ patients were compared to COVID- patients and a historical cohort from 2019. Results: 84 patients with radiographic acute stroke from the 2020 study period and 152 patients in the historical cohort were included. Stroke incidence in COVID+ patients was 1.5%, with a significant decline in total stroke presentations during this period compared to 2019. 37 patients were COVID+ and 47 patients were COVID-. 32% of COVID+ stroke patients were Hispanic compared to 15% and 18% in the COVID- and 2019 cohorts respectively (p = 0.069 and 0.07). COVID+ stroke patients were younger, had higher rates of hemorrhagic conversion (p = 0.034), higher initial NIHSS (p < 0.001), increased cryptogenic stroke mechanism (p = 0.02), and higher mortality independent of COVID-19 severity. COVID+ patients had higher rates of thrombocytopenia (p = 0.02), and were less likely to be on antiplatelet therapy (p = 0.025). In multivariable analysis, only COVID-19 status independently predicted mortality. Conclusions: COVID status, independent of severity, was significantly associated with higher mortality in stroke patients. COVID+ stroke patients were younger and less likely to be on antiplatelets, with higher rates of thrombocytopenia, suggesting a possible role for antiplatelet use in this population.
Background The aim of this study is to examine the relationship between time in therapeutic range (TTR) and clinical outcomes in heart failure (HF) patients in sinus rhythm (SR) treated with warfarin. Methods and Results We used data from the Warfarin vs. Aspirin in Reduced Cardiac Ejection Fraction Trial (WARCEF) to assess the relationship of TTR with the WARCEF primary outcome (ischemic stroke, intracerebral hemorrhage, or death); with death alone; ischemic stroke alone; major hemorrhage alone; and net clinical benefit (primary outcome and major hemorrhage combined). Multivariable Cox models were used to examine how the event risk changed with TTR and to compare the high TTR, low TTR, and aspirin patients, with TTR being treated as a time-dependent covariate. 2,217 patients were included in the analyses, among whom 1,067 were randomized to warfarin and 1,150 were randomized to aspirin. The median (IQR) follow-up duration was 3.6 (2.0–5.0) years. Mean (±SD) age was 61±11.3 years, with 80% being men. The mean (±SD) TTR was 57% (±28.5%). Increasing TTR was significantly associated with reduction in primary outcome (adjusted p<0.001), death alone (adjusted p=0.001), and improved net clinical benefit (adjusted p<0.001). A similar trend was observed for the other two outcomes but significance was not reached (adjusted p=0.082 for ischemic stroke, adjusted p=0.109 for major hemorrhage). Conclusions In HF patients in SR, increasing TTR is associated with better outcome and improved net clinical benefit. Patients in whom good quality anticoagulation can be achieved may benefit from the use of anticoagulants. Clinical Trial Registration URL: http://www.clinicaltrials.gov. Unique identifier: NCT00041938.
Background and Purpose: To evaluate the role of preadmission conditions, dehydration specifically, in the development of subdural hematoma in the elderly. Methods: Retrospective chart review. Results: The most prevalent pre-admission medical condition was hypertension, followed by atrial fibrillation, CAD, hyperlipidemia, diabetes, and cancer. Out of 95 patients, 69 (73%) had features of dehydration, 27% were on diuretics and 28% were on antiplatelet agents and anticoagulation. Conclusions: Elderly population is prone to dehydration. Overzealous use of diuretics especially in combination with anticoagulation or antiplatelet therapy can contribute to the development of subdural hematomas, both spontaneous and traumatic.
Neurological complications of infection by the novel H1N1 virus have been described primarily in children. In adults, patients typically present with fever and respiratory symptoms, and may develop acute respiratory distress syndrome, sepsis and stroke. We present a 45-year-old man whose presentation of aphasia and right hemiplegia were incongruent with the findings on MRI of a small acute ischemic stroke. He rapidly developed multi-organ failure and died. Nasal swab PCR obtained prior to death returned positive for influenza virus A/H1N1. At autopsy, a small acute hemorrhagic infarction in the left parietal lobe was present. We suspect that this was a cardio-embolic stroke, probably triggered by H1N1 myocarditis.Keywords: Stroke; Infection CASEIn December 2009, a 45-year-old man was awakened by his wife and was unable to speak. He fell while trying to get out of bed, and he had right sided weakness and incontinence of urine.His past medical history was significant for hypertension, diabetes mellitus, chronic renal insufficiency, and congestive heart failure due to a non-ischemic cardiomyopathy since age 19. The etiology of the cardiomyopathy was unknown. A recent ejection fraction was 40%. He also had an anterior cervical discectomy and interbody fusion at C3-4 one month prior to admission. Medications included daily enalapril, atenolol, lasix, digoxin, insulin, simvastatin, and neurontin. He had no known allergies. There was no history of alcohol, tobacco, or illicit drug use. Family history was notable for diabetes mellitus.On examination, he was afebrile. The pulse was 103 beats per minute, the blood pressure 130/70 mm Hg, the respiratory rate 16 beats per minute, and oxygen saturation 100%. Blood sugar was 267 mg/dL. Neck was supple. The remainder of the general examination was normal. On neurological exam, he was awake with right hemineglect and global aphasia. There was no definite visual field loss, and no gaze deviation. Pupils were equal, round, and reactive to light. There was a right central facial nerve palsy and a flaccid right hemiplegia. Sensory testing was unreliable.Admission laboratory values were notable for a blood urea nitrogen level of 35 mg per deciliter, creatinine level of 1.5 mg/dL, INR of 1.6 and CPK of 296 IU/L with troponin initially normal than increased to 4.8 ng/mL. Urine toxicology was normal. EKG showed sinus tachycardia with left atrial enlargement, and a left bundle branch block. Chest X-ray showed mild pulmonary venous congestion. Admission Head CT showed a small acute infarct in the left posterior parieto-occipital region, which was confirmed on the MRI of the brain (Figure 1). MRA of the brain and neck showed no significant stenosis. Transthoracic echocardiography on admission revealed a severely dilated left ventricle with an ejection fraction of less than 15%. There were multiple highly mobile densities seen at the apex consistent with thrombi. There was also evidence of severe mitral regurgitation and moderate pulmonary hypertension.The patient was admitted to t...
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