Atrial Fibrillation:: A Common Cause of Stroke.

Atrial fibrillation is the culprit causal mechanism of twenty percent of acute ischemic strokes. As the population of Delaware ages, atrial fibrillation is a growing cause of stroke. Thus, the detection of atrial fibrillation and treatment of this cardioembolic risk factor of stroke is paramount.

Stroke: Primary Prevention.

Stroke is a leading cause of long-term disability in adults and the fifth leading cause of mortality in the United States. One of the main tasks related to stroke in the family medicine setting is assessment and management of modifiable risk factors. The American Heart Association/American Stroke Association (AHA/ASA) guidelines on primary prevention of stroke recommend that cigarette smoking, physical inactivity, overweight and obesity, dyslipidemia, hypertension, and diabetes be addressed and/or managed to decrease the risk of stroke. Obstructive sleep apnea (OSA) is an independent risk factor for stroke. Screening for OSA in patients at risk of stroke can be considered. Atrial fibrillation (AF) contributes to more than 20% of acute ischemic strokes. Guidelines recommend that some patients with AF be treated with warfarin or direct-acting oral anticoagulants for stroke prevention, as the clinical situation warrants. Other risk factors for stroke include carotid artery disease, migraine with aura, sickle cell disease, alcohol or drug use, hypercoagulable states (including COVID-19), and previous stroke or transient ischemic attack. Recent meta-analyses have found that aspirin may not be beneficial for primary prevention of stroke. Aspirin currently is not recommended for primary stroke prevention in low-risk individuals.

Stroke: Diagnostic Evaluation.

Ischemic stroke is an episode of neurologic dysfunction caused by focal cerebral, spinal, or retinal infarction. In patients with stroke symptoms, an urgent evaluation is advised. In the prehospital setting, early recognition of stroke signs allows appropriate triage of patients to hospitals that specialize in stroke management for thrombolysis or thrombectomy. In the hospital setting, evaluation of patients with suspected stroke includes clinical assessment, using the National Institutes of Health Stroke Scale (NIHSS), imaging of the head and blood vessels of the neck, and assessing for the cause of stroke. Evaluation for the etiology may include laboratory tests, cardiac imaging, and cardiac rhythm monitoring. Early measures for secondary stroke prevention can be initiated.

Stroke: Hospital Management.

Urgent evaluation of patients with acute ischemic stroke allows for a comprehensive assessment of management options. These include thrombolysis and thrombectomy, depending on symptom onset and severity, the presumed location of the occlusion, and patient comorbidities and potential for improvement. For patients who present within 4.5 hours of onset of disabling symptoms consistent with acute ischemic stroke and with no contraindications, intravenous thrombolysis is indicated. Acute mechanical thrombectomy may be indicated for patients who present within 24 hours of symptom onset and have symptoms consistent with a large vessel occlusion. After reperfusion therapy, patients require close neurologic monitoring. Patients who receive reperfusion therapy tend to have better functional outcomes than patients who do not. Secondary prevention includes use of antithrombotics and glycemic control. Common issues in the acute setting include cerebral edema, hemorrhagic transformation, and symptomatic carotid disease.

Stroke: Long-Term Poststroke Management.

It is estimated that after stroke patients live 33% fewer remaining years compared with age- and sex-matched controls. Functional recovery after stroke depends on many factors, including age, functional status before stroke, stroke severity, and comorbidities. The purpose of rehabilitation services is to improve functional status. All patients with stroke should undergo a formal assessment of rehabilitation needs before hospital discharge. Types of rehabilitation include inpatient, subacute, and home health care. Primary care of patients after stroke focuses on secondary stroke prevention, including antiplatelet therapy, hypertension and hyperlipidemia management, diet, and glycemic control. In patients with ischemic stroke and no contraindications, dual antiplatelet therapy with aspirin and clopidogrel is recommended for 21 to 90 days after stroke, but not longer. A blood pressure goal of less than 130/80 mm Hg is recommended for most patients. For most patients with diabetes, a goal A1c level of 7% or less is reasonable. Diabetes management should include a glucagon-like peptide 1 receptor agonist or sodium-dependent glucose cotransporter 2 inhibitor. Various tests, drugs, and screenings are indicated for patients with specific hypercoagulable states (eg, coagulopathies, antiphospholipid syndrome, occult malignancy, hormone therapy). Poststroke follow-up should address sequelae, such as fatigue, depression, contracture and spasticity, hemiplegic shoulder pain, and central poststroke pain.

Decreasing Stroke Code to CT Time in Patients Presenting with Stroke Symptoms.

Guided quality improvement (QI) programs present an effective means to streamline stroke code to computed tomography (CT) times in a comprehensive stroke center. Applying QI methods and a multidisciplinary team approach may decrease the stroke code to CT time in non-prenotified emergency department (ED) patients presenting with symptoms of stroke. The aim of this project was to decrease this time for non-prenotified stroke code patients from a baseline mean of 20 minutes to one less than 15 minutes during an 18-week period by applying QI methods in the context of a structured QI program. By reducing this time, it was expected that the door-to-CT time guideline of 25 minutes could be met more consistently. Through the structured QI program, we gained an understanding of the process that enabled us to effectively identify key drivers of performance to guide project interventions. As a result of these interventions, the stroke code to CT time for non-prenotified stroke code patients decreased to a mean of less than 14 minutes. This article reports these methods and results so that others can similarly improve the time it takes to perform nonenhanced CT studies in non-prenotified stroke code patients in the ED. ©RSNA, 2017.

Diagnostic Yield of Echocardiography in Transient Ischemic Attack.

BACKGROUND: Echocardiography is often performed to identify a cardiac source of embolism (CSE) causing transient ischemic attack (TIA). However, the diagnostic yield of echocardiography in TIA remains uncertain, and its role in routine evaluation of TIA is controversial. METHODS: Patients with acute TIA were prospectively enrolled at 4 stroke centers. A CSE was defined using the Causative Classification of Stroke system; patent foramen ovale was considered a relevant CSE only if the patient underwent closure or was placed on anticoagulation. Patients with a known CSE at time of admission were excluded from analysis of the yield of echocardiography. RESULTS: A total of 869 patients were enrolled at stroke centers, and 129 had a known CSE at presentation. Of the 740 remaining patients, 603 (81%) underwent echocardiography. A potential CSE was identified in 60 (10%) of these patients. The most common CSEs noted on echocardiography were complex aortic arch atherosclerosis and patent foramen ovale. History of coronary artery disease (P < .001), lack of prior stroke or TIA (P = .007), and presence of acute infarction on magnetic resonance imaging (MRI) (P < .001) were predictors of CSE on echocardiography. The yield of echocardiography was 29% in patients with both history of coronary artery disease and acute infarction on MRI, 14% with one of these features, and 5% with neither of these features (P < .0001). A CSE identified by echocardiography prompted initiation of anticoagulation in 15 of the 603 (2.5%) subjects. CONCLUSIONS: Echocardiography demonstrates a relevant CSE in a significant portion of patients with TIA. However, changes in antithrombotic therapy resulting from echocardiography are infrequent.

Lipoprotein phospholipase A2 mass and activity are not associated with the diagnosis of acute brain ischemia.

BACKGROUND: Elevated lipoprotein-associated phospholipase A2 (Lp-PLA2) levels are associated with both coronary artery and cerebrovascular diseases. The clinical diagnosis of neurovascular events, specifically transient ischemic attack can be challenging, although there is disagreement among vascular trained neurologists regarding this. Currently, there is no single accurate biomarker for the diagnosis of acute brain ischemia. AIM: We studied the relationship between Lp-PLA2 mass and activity levels and the diagnosis of acute brain ischemia in the acute phase among patients evaluated in the emergency department following transient focal neurological symptoms. METHODS: Patients evaluated in our academic center for transient neurological symptoms of possible ischemic mechanism were enrolled with informed consent. Lp-PLA2 mass and activity levels were performed by DiaDexus, Inc. RESULTS: 100 patients were enrolled: 58 were ischemic (30 stroke, 28 TIA), 10 were unknown, and 28 were non-ischemic. Blood samples were collected after a median delay of 23 h (IQR: 17, 36) after symptom onset. The median levels of Lp-PLA2 activity level for ischemic (stroke and TIA) versus non-ischemic events were 186.5 nmol/ml/min (IQR = 153, 216.3) and 169 nmol/ml/min (IQR = 137, 212.5), respectively. The median levels of Lp-PLA2 mass level for ischemic versus non-ischemic events were 202 ng/ml (IQR = 171.6, 226.1) and 192 ng/ml (167.8, 230). The differences in median Lp-PLA2 mass and activity levels were not statistically significant in the ischemic versus non-ischemic patients. Vessel imaging revealed a symptomatic stenosis in 14 patients (10 intracranial and 4 cervical). The median Lp-PLA2 mass and activity levels among patients with a symptomatic stenosis were not significantly higher than the levels measured in TIA/stroke patients without stenosis. CONCLUSION: The results of our study do not support the early measurement of Lp-PLA2 mass or activity levels for confirming an ischemic etiology in patients experiencing minor or transient focal neurological events.

What can be achieved by redesigning stroke care for a value-based world?

Stroke results in significant healthcare costs and decreased quality of life. Thoughtful healthcare delivery redesign can help solve this problem through lower-cost, higher-quality care. The dominant fee-for-service reimbursement system may not incentivize delivery systems to invest in new cost-saving delivery innovations. Furthermore, lack of transparency hinder development of new systems of care. However, emerging payment models, including bundled payments and prospective payment, promote adoption of value-based stroke care methods. Both prevention and treatment of stroke offer opportunities to improve value-for-money via adoption of a package of emerging innovations. In order to encourage such adoption, alignment of incentives is crucial.

Cost-saving innovations for acute ischemic stroke and transient ischemic attack.

Health care costs continue to rise toward unsustainable levels that will affect our nation's ability to support other key funding priorities for education, military, and infrastructure. Changing the way we deliver health care is critical to mitigating this financial crisis. This review highlights opportunities for redesigning care of acute ischemic stroke and TIA to maintain quality while substantially lowering costs. The recent innovations described are (1) adopting teleneurology networks to improve access to thrombolysis for acute ischemic stroke; (2) improving efficiency of emergency care for acute ischemic stroke; and (3) providing alternatives to inpatient care for TIA. Applying such process innovations will enable us to achieve the goal of patients and the nation-high-quality care at an affordable cost.

Sex-specific temporal trends in in-hospital mortality after stroke among middle-age individuals in the United States.

BACKGROUND AND PURPOSE: Recent studies have revealed an increase in stroke prevalence among middle-aged women in the United States. To determine whether this is due to improved survival, we assessed temporal trends in sex-specific in-hospital mortality after stroke. METHODS: Individuals aged 35 to 64 years hospitalized in 1997 to 2006 with a primary discharge diagnosis of stroke (N=2 537 097) in the United States were identified by the Nationwide Inpatient Sample. Temporal trends in sex-specific mortality after stroke and sex differences in mortality were assessed, before and after controlling for covariates. RESULTS: From 1997 to 2006, poststroke mortality decreased in both men (6.06% to 5.15%) and women (6.02% to 4.88%) aged 35 to 64 years. Unadjusted analysis revealed that women aged 35 to 44 years (odds ratio=0.89; 95% CI, 0.83 to 0.95) and 45 to 54 years (odds ratio=0.93; 95% CI, 0.89 to 0.97) had lower mortality compared with men, whereas women aged 55 to 64 years had similar mortality compared with men. After adjustment for covariates, stroke type accounted for the better survival in women aged 35 to 44 years. After adjustment for covariates, women aged 45 to 54 years persistently had better survival than did men. Women aged 55 to 64 years had better survival than did men, once race and insurance type were accounted for. CONCLUSIONS: This study revealed a decline in stroke mortality rates from 1997 to 2006 among individuals aged 35 to 64 years. Better survival among women compared with men aged 35 to 54 years may partially explain the sex disparity in stroke prevalence.