Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label hs-cTnT. Show all posts
Showing posts with label hs-cTnT. Show all posts

Tuesday, May 10, 2022

EXPRESS: Elevation of cardiac biomarkers in stroke is associated with pathological findings on cardiac MRI – results of the HEBRAS study

It is your doctor's responsibility to get a cardiologist involved in your treatment, assuming that your hospital has a protocol to do this testing(bad assumption).  A 21% incidence rate should be enough to have a protocol created on testing for this, if your hospital is competent at all.

EXPRESS: Elevation of cardiac biomarkers in stroke is associated with pathological findings on cardiac MRI – results of the HEBRAS study

First Published April 11, 2022 Research Article 

Introduction

Cardiac biomarkers, such as high-sensitivity cardiac troponin T (hs-cTnT), are frequently elevated in ischemic stroke patients but the mechanisms underlying this elevation are insufficiently understood. We determined the presence of cardiac damage, assessed using cardiac MRI (CMR), in stroke patients with elevated hs-cTnT and brain natriuretic peptide (BNP).

Methods

This is a post-hoc analysis of the prospective, investigator-initiated, cross-sectional HEBRAS (HEart and BRain interfaces in Acute Stroke) study. All patients underwent measurement of hs-cTnT and BNP as well as gadolinium-enhanced CMR in the acute phase of ischemic stroke. We performed unadjusted and adjusted logistic regression models to assess the association between hs-cTnT and BNP elevation and the presence of pathological CMR findings.

Results

Two hundred and thirty three stroke patients (median age 67 years, 33% female) were included, of whom 43 (21%) had elevated hs-cTnT and 109 (47%) had elevated BNP. 100 of the 233 (43%) patients had pathological findings on CMR had focal fibrosis as detected by late-gadolinium enhancement (LGE) in 51 (23%), left-ventricular hypertrophy (LVH) in 38 (16%), reduced LVEF in 32 (14%) and left atrial dilatation in 34 (15%). After adjustment for potential confounders, both hs-cTnT (adjOR 5.0 (95%CI 2.1-11.7), p<0.001) and BNP (adjOR 4.1 (95%CI 2.3-7.3), p<0.001) were significantly associated with pathological findings on CMR. Hs-cTnT was associated with LGE, LVEF and LVH, whereas BNP was associated with left atrial dilatation and LVEF, LVH.

Conclusion

Elevated cardiac biomarkers in acute stroke including CMR are strongly associated with pathological findings on CMR. In acute stroke patients, elevation of cardiac biomarkers may identify patients who require a more thorough cardiology work-up.

 

Sunday, September 26, 2021

Cardiac troponin and recurrent major vascular events after minor stroke or TIA

 Since you don't want any major adverse cardiovascular events after your stroke you'll just have to wait to have your stroke until after your doctors and stroke hospital have initiated the research and come up with EXACT STROKE PROTOCOLS TO PREVENT THAT.  Your responsibility is to wait until then. You can't make any assumption that your stroke hospital can properly treat any type of stroke that comes in until they have defined protocols for all types. NOT GUIDELINES, guidelines are mostly worthless. The 17.2% occurrence rate is too high to not have any protocols addressing that. I wouldn't accept that risk from any medical procedure.

Cardiac troponin and recurrent major vascular events after minor stroke or TIA

First published: 25 September 2021
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi: 10.1002/ana.26225.

Abstract

Objective

To investigate whether high-sensitivity cardiac troponin T (hs-cTnT) is associated with major adverse cardiovascular events (MACE) in patients with minor stroke or transient ischemic attack (TIA), and whether this association differs after risk stratification based on the “Age, Blood pressure, Clinical features, Duration of symptoms, Diabetes” (ABCD2) score.

Methods

INSPiRE-TMS was a randomized controlled trial allocating patients with minor stroke or TIA to an intensified support program or conventional care. In this post-hoc analysis, participants were categorized using hs-cTnT levels (5th Generation, Roche, 99th percentile upper reference limit [URL] 14ng/L). Vascular risk was stratified using the ABCD2 score (lower-risk:0-5 vs. higher-risk:6-7). Cox proportional hazard regression was performed using covariate adjustment and propensity score matching (PSM) for the association between hs-cTnT and MACE (stroke/non-fatal coronary event/vascular death).

Results

Among 889 patients (mean age 70 years, 37% female), MACE occurred in 153 patients (17.2%) during a mean follow-up of 3.2 years. Hs-cTnT was associated with MACE (9.3%/year>URL vs. 4.4%/year≤URL, adjusted HR 1.63 [95%CI 1.13-2.35], adjusted HR (Q4 vs.Q1) 2.57 [95%CI 1.35-4.97], adjusted HR (log-transformed) 2.31 [95%CI 1.37-3.89]). This association remained after PSM (adjusted HR 1.76 [95%CI 1.14-2.72]). There was a significant interaction between hs-cTnT and ABCD2 category for MACE occurrence (pinteraction=0.04). In the lower-risk category, MACE rate was 9.5%/year in patients with hs-cTnT>URL, which was higher than in those ≤URL (3.8%/year) and similar to the overall rate in the higher-risk category.

Interpretation

Hs-cTnT levels are associated with incident MACE within three years after minor stroke or TIA and may help to identify high-risk individuals otherwise deemed at lower-risk based on the ABCD2 score. If confirmed in independent validation studies, this might warrant intensified secondary prevention measures and cardiac diagnostics in stroke patients with elevated hs-cTnT.

This article is protected by copyright. All rights reserved.

 

Saturday, May 29, 2021

Blood-Based Cardiac Biomarkers and the Risk of Cognitive Decline, Cerebrovascular Disease, and Clinical Events

 Useless, you describe a biomarker prediction; THEN GIVE US NOTHING TO PREVENT THAT COGNITIVE DECLINE. What the hell do you think research is for?

Blood-Based Cardiac Biomarkers and the Risk of Cognitive Decline, Cerebrovascular Disease, and Clinical Events

Originally publishedhttps://doi.org/10.1161/STROKEAHA.120.032571Stroke. ;0:STROKEAHA.120.032571

Background and Purpose:

Cardiac biomarkers, NT-proBNP (N-terminal probrain natriuretic peptide), hs-cTnT (high-sensitivity-cardiac troponin T), and GDF-15 (growth differentiation factor-15) have been proposed as important biomarkers of early vascular pathology. However, little is known of the longitudinal associations of these cardiac biomarkers with cerebrovascular disease and clinical events. We examine the association of blood-based cardiac biomarkers (NT-proBNP, hs-cTnT, and GDF-15) with cognitive decline, incident cerebrovascular disease, vascular events, and mortality.

Methods:

Four hundred thirty-four memory-clinic patients provided blood samples at baseline, underwent 3 annual neuropsychological assessments and brain magnetic resonance imaging scans at baseline and follow-up. NT-proBNP and hs-cTnT concentrations were measured by electrochemiluminescence immunoassay and GDF-15 by quantitative sandwich immunoassay. Baseline and follow-up magnetic resonance imagings were graded for white matter hyperintensities, lacunes, cerebral microbleeds, cortical infarcts, and intracranial stenosis. Data on incident vascular events and mortality were obtained.

Results:

Patients with higher levels of NT-proBNP, hs-cTnT, and GDF-15 showed greater decline in memory domain. Additionally, hs-cTnT was associated with decline in global cognition, executive function, and visuomotor speed. Higher levels of NT-proBNP were associated with incident cerebral microbleeds and hs-cTnT with incident cortical infarcts. During a mean follow-up of 3 years, 26 (5.9%) patients died and 35 (8.1%) developed vascular events. Patients with higher levels of NTpro-BNP and hs-cTnT were at increased risk of vascular events whereas those with higher levels of NT-proBNP and GDF-15 were at risk of mortality.

Conclusions:

Higher levels of blood-based cardiac biomarkers were associated with decline in memory and risk of vascular events and mortality. Moreover, NT-proBNP and hs-cTnT were associated with incident cerebral microbleeds and cortical infarcts. Thus, these biomarkers are potentially useful in identifying patients at risk of adverse vascular events and death.