This site uses cookies to improve your experience. To help us insure we adhere to various privacy regulations, please select your country/region of residence. If you do not select a country, we will assume you are from the United States. Select your Cookie Settings or view our Privacy Policy and Terms of Use.
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Used for the proper function of the website
Used for monitoring website traffic and interactions
Cookie Settings
Cookies and similar technologies are used on this website for proper function of the website, for tracking performance analytics and for marketing purposes. We and some of our third-party providers may use cookie data for various purposes. Please review the cookie settings below and choose your preference.
Strictly Necessary: Used for the proper function of the website
Performance/Analytics: Used for monitoring website traffic and interactions
Brain arteriovenous malformations (AVMs), cerebral cavernous malformations (CCMs), and intracranial aneurysms are major causes of hemorrhagic stroke, yet noninvasive therapies to prevent growth or rupture are lacking. Due to the genetic overlap, these advancements may also offer future therapeutic strategies for intracranial aneurysms.
A cerebral aneurysm (CA) is an abnormal artery deformation in the brain that may lead to hemorrhagic stroke, brain damage, coma, and even death when a CA ruptures. We hypothesized that increasing CA sample size will allow more robust biomarker identification. Stroke, Volume 56, Issue Suppl_1 , Page ATMP1-ATMP1, February 1, 2025.
In this study, our hypothesis was that markers of NETs are higher in aneurysmal SAH patients developing DCI compared to SAH patients not developing DCI. Using aneurysmal SAH patient blood collected at 1, 2, 4, 7, and 10 days post-SAH, we used ELISA kits to measure three markers of NETs: neutrophil elastase, citrullinated histone H3, and H3.1
Introduction:Intracranial aneurysms (IAs) are weak outpouchings on cerebral vessels that can rupture, causing subarachnoid hemorrhage. Timely and accurate risk stratification of IAs is paramount.Objective:Aneurysm wall enhancement (AWE) is a potential imaging biomarker for risk stratification. The LOO accuracy improved to 85.7% (66.6%
The rate of incidentally discovered unruptured intracranial aneurysms has increased with the broad availability of neuroimaging. The determination of the risk of rupture of brain aneurysms is challenging. Several clinical scales for aneurysm rupture prediction have been developed.
Aneurysms are localized dilations of blood vessels, which can expand to 50% of the original diameter. The pathophysiology of aneurysms is complex and diverse, often associated with progressive vessel wall dysfunction resulting from vascular smooth muscle cell (VSMC) death and abnormal extracellular matrix synthesis and degradation.
Introduction:Early brain injury (EBI), a complex collection of pathophysiological processes occurring within 72 hours aneurysmal subarachnoid hemorrhage (aSAH), is the key link connecting the initial event to the delayed and long-term complications.
Background:Small extracellular vesicles (sEVs) from blood samples of patients with cerebral aneurysms (CA) have been used as a biomarker for CA. Stroke, Volume 56, Issue Suppl_1 , Page AWP384-AWP384, February 1, 2025. However, biological function of sEVs in CA has not been studied.
Approximately 30% of aneurysmal subarachnoid hemorrhage (aSAH) patients who survive the rupture develop delayed cerebral ischemia (DCI) 4 to 10 days following aSAH. Thus, we sought to investigate various biomarkers of platelets to identify which factors are predictive of patients at-risk for DCI.
The expression of GPBAR1 in the human endothelium correlated with the expression of inflammatory biomarkers. Mice lackingFxrandGpbar1−/−/Fxr−/−display hypotension and aortic inflammation, along with altered intestinal permeability that deteriorates with age, and severe dysbiosis, along with dysregulated bile acid synthesis.
1,2 ASCVD causes or contributes to conditions that include coronary artery disease (CAD), cerebrovascular disease, and peripheral vascular disease (inclusive of aortic aneurysm).3 Atherosclerotic cardiovascular disease (ASCVD), caused by plaque buildup in arterial walls, is one of the leading causes of disability and death worldwide.1,2
Kawasaki Disease Case : Angela Khidhir, DO, MSc (USA) presented a compelling case on ACS and tamponade potentially linked to Kawasaki disease-related Coronary Artery Aneurysm. This debate underscored the growing role of CSP despite the current limited evidence supporting it. REVERSE-FLOW Trial: Prof.
Cerebral aneurysms (CA) arise from the sites of weakened artery walls in the brain, and they may cause hemorrhagic stroke, coma, and death when they rupture. It is believed that mechanisms of CA formation in women may differ from those in men; however, sex-specific CA biomarkers are poorly identified.
It looks like anterior LV aneurysm. In acute STEMI, the T-wave is large, whereas in LV aneurysm , the T-wave is not so large. In this study of "aborted" STEMI , 11% of patients with a 5 hours symptom onset to PCI time had no significant biomarker elevation. The pain was partly relieved with sublingual nitroglycerin.
BACKGROUND:Many studies have explored whether individual plasma protein biomarkers improve cardiovascular disease risk prediction. CONCLUSIONS:Measurement of targeted protein biomarkers produced superior prediction of aggregated and disaggregated cardiovascular events. Circulation, Ahead of Print.
ObjectiveAbdominal aortic aneurysm (AAA) is a life-threatening vascular condition. These genes are linked to immune cell activity and the inflammatory microenvironment, providing potential biomarkers for early detection and a basis for further research into AAA progression.
ObjectiveRobust evidence has demonstrated that inflammation plays an important role in the occurrence and development of abdominal aortic aneurysms (AAA). However, whether UHR is associated with AAA remains unclear.
When there are QS-waves, one should always think about LV aneurysm, but ST to QRS ratio and T-wave to QRS ratio are far too large and not compatible with left ventricular aneurysm. There is some R wave in the lateral precordial leads. Leads V3 and V4 both have 6mm ST elevation. This ECG shows a lot of "acuity".
We organize all of the trending information in your field so you don't have to. Join thousands of users and stay up to date on the latest articles your peers are reading.
You know about us, now we want to get to know you!
Let's personalize your content
Let's get even more personalized
We recognize your account from another site in our network, please click 'Send Email' below to continue with verifying your account and setting a password.
Let's personalize your content