Purpose- Much has transpired since the last scientific statement on pediatric stroke was published 10 years ago. Although stroke has long been recognized as an adult health problem causing substantial morbidity and mortality, it is also an important cause of acquired brain injury in young patients, occurring most commonly in the neonate and throughout childhood. This scientific statement represents a synthesis of data and a consensus of the leading experts in childhood cardiovascular disease and stroke. Methods- Members of the writing group were appointed by the American Heart Association Stroke Council's Scientific Statement Oversight Committee and the American Heart Association's Manuscript Oversight Committee and were chosen to reflect the expertise of the subject matter. The writers used systematic literature reviews, references to published clinical and epidemiology studies, morbidity and mortality reports, clinical and public health guidelines, authoritative statements, personal files, and expert opinion to summarize existing evidence and to indicate gaps in current knowledge. This scientific statement is based on expert consensus considerations for clinical practice. Results- Annualized pediatric stroke incidence rates, including both neonatal and later childhood stroke and both ischemic and hemorrhagic stroke, range from 3 to 25 per 100 000 children in developed countries. Newborns have the highest risk ratio: 1 in 4000 live births. Stroke is a clinical syndrome. Delays in diagnosis are common in both perinatal and childhood stroke but for different reasons. To develop new strategies for prevention and treatment, disease processes and risk factors that lead to pediatric stroke are discussed here to aid the clinician in rapid diagnosis and treatment. The many important differences that affect the pathophysiology and treatment of childhood stroke are discussed in each section. Conclusions- Here we provide updates on perinatal and childhood stroke with a focus on the subtypes, including arterial ischemic, venous thrombotic, and hemorrhagic stroke, and updates in regard to areas of childhood stroke that have not received close attention such as sickle cell disease. Each section is highlighted with considerations for clinical practice, attendant controversies, and knowledge gaps. This statement provides the practicing provider with much-needed updated information in this field.

https://escholarship.org/content/qt0sw5j7c1/qt0sw5j7c1.pdf?t=polxgl

Management of Stroke in Neonates and Children: A Scientific Statement From the American Heart Association/American Stroke Association

Use of Lipoprotein(a) in clinical practice: A biomarker whose time has come. A scientific statement from the National Lipid Association.

http://www.lipidjournal.com/article/S1933287422002446/pdf

Hypertriglyceridemia is caused by defects in triglyceride metabolism and generally manifests as abnormally high plasma triglyceride levels. Although the role of hypertriglyceridemia may not draw as much attention as that of plasma cholesterol in stroke, plasma triglycerides, especially nonfasting triglycerides, are thought to be correlated with the risk of ischemic stroke. Hypertriglyceridemia may increase the risk of ischemic stroke by promoting atherosclerosis and thrombosis and increasing blood viscosity. Moreover, hypertriglyceridemia may have some protective effects in patients who have already suffered a stroke via unclear mechanisms. Therefore, further studies are needed to elucidate the role of hypertriglyceridemia in the development and prognosis of ischemic stroke.

/pdf/hypertriglyceridemia-a-neglected-risk-factor-for-ischemic-2ok34l8l.pdf

Hypertriglyceridemia: A Neglected Risk Factor for Ischemic Stroke?

Objectives: The objective of the study is to investigate the effects of statins on the lipoprotein-associated phospholipase A2 (Lp-PLA2) mass in patients with ischemic stroke. Materials and Methods: A total number of 59 patient ages 43–69 years with cerebral stroke compared to 39 healthy controls that matching the age and body weight. The patients were divided into 32 patients on statins therapy assigned as statins users and 27 patients, not on statins therapy assigned as nonstatins users. Anthropometric and biochemical measurements were done including lipid profile and inflammatory biomarkers. Results: Stroke patients on statins therapy showed a comparable low of Lp-PLA (29.82 ± 3.19 IU/mL) to nonstatins user stroke patients (15.58 ± 5.73 IU/mL). Lp-PLA2 mass levels were positively correlated with body mass index, blood pressure changes, total cholesterol, triglyceride, and very low-density lipoprotein and stroke risk (SR) percentage. Conclusions: Patients on statins with ischemic stroke had low levels of Lp-PLA2 mass levels compared to nonstatins user with ischemic stroke. Lp-PLA2 mass levels were higher in men than women and correlated with lipid profile and SR in patients with ischemic stroke.

/pdf/lipoprotein-associated-phospholipase-a2-is-linked-with-poor-59e7nsp6of.pdf

Lipoprotein-Associated Phospholipase A2 is Linked with Poor Cardio-Metabolic Profile in Patients with Ischemic Stroke: A Study of Effects of Statins.

Dyslipidemia in Children With Arterial Ischemic Stroke: Prevalence and Risk Factors

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Dyslipidemia in Children With Arterial Ischemic Stroke: Prevalence and Risk Factors