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.

Thursday, April 4, 2024

Elevated troponin levels as a predictor of mortality in patients with acute stroke: a systematic review and meta-analysis

Who approved this fucking stupidity of research that predicts death rather than doing the research that prevents death? Specific names only! They need to be drummed out of stroke!

Oops, I'm not playing by the polite rules of Dale Carnegie,  'How to Win Friends and Influence People'. 

Telling supposedly smart stroke medical persons they know nothing about stroke is a no-no even if it is true. 

Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful, I look forward to that day.

Elevated troponin levels as a predictor of mortality in patients with acute stroke: a systematic review and meta-analysis

  • Clinical Research Unit, All India Institute of Medical Sciences, New Delhi, India

Background and Aim: The prognostic potential of cardiac troponin (cTn) in acute stroke patients has been a subject of ongoing debate. Our objective was to provide a comprehensive evidence for predicting mortality in acute stroke patients by using the elevated troponin levels.

Methods: We conducted an extensive literature search, including PubMed, EMbase, and Trip Databases, covering studies published up to September 30, 2023. We computed risk ratios (RR) with 95% confidence intervals (CIs), performed sensitivity analysis, and conducted trial sequential analysis (TSA).

Results: In total, 53 studies were analyzed, with 37 focusing on acute ischemic stroke (AIS), 11 on subarachnoid hemorrhage (SAH), and 7 on Intracerebral hemorrhage (ICH). Elevated cTn levels were significantly showed a higher predictive risk for In-hospital mortality in both AIS (RR=3.80, 95% CI; 2.82 to 5.12) as well as SAH (RR=2.23, 95% CI; 1.64 to 3.02). However, no significant predictive risk between elevated cTn levels and in-hospital mortality for ICH patients (RR=1.13, 95% CI: 0.46 to 2.79). A similar pattern was observed for elevated cTn levels, indicating an increased risk of last follow-up mortality for AIS (RR=2.41, 95% CI: 1.98 to 2.93) and SAH (RR=3.08, 95% CI: 2.25 to 4.21).

Conclusion: Elevated troponin levels can serve as a promising predictive marker for both in-hospital and last follow-up mortality in AIS and SAH patients but not in ICH patients. Further prospective studies are needed to validate our findings along with exploring the preventive management of mortality in acute stroke settings.

Introduction

Acute stroke represents a critical medical condition with substantial implications for patient outcomes and healthcare systems (1). In this context, the timely and accurate identification of prognostic markers capable of predicting stroke-associated mortality emerges as a paramount imperative (2). Such markers not only facilitate risk assessment but also guide precise and targeted clinical interventions, ultimately influencing patient outcomes and optimizing healthcare resource allocation (3). Cardiac Troponin (cTn), widely recognized as a cardinal biomarker in cardiology, has recently attracted attention for its potential role as an indicator of mortality risk in patients afflicted by acute stroke (4).

In the short term, the immediate post-stroke period, in-hospital mortality rates for acute stroke patients can exhibit alarming elevations, with figures occasionally reaching a staggering 50% (5). The major driving force behind such acute fatalities often lies in cardiac-related complications. These complications manifest through the release of cardiac troponin-T (cTnT), cardiac troponin-I (cTnI), High-sensitive cardiac Troponin I (hs-cTnI) and High-sensitive cardiac Troponin T (hs-cTnT) proteins into the circulatory system. Importantly, during the acute phase of ischemic stroke (IS), a marked elevation in serum levels of cTnT or cTnI is frequently observed, establishing a robust link between cardiac injury and the stroke itself (6). The precise and timely prognosis of this cardiac involvement not only impacts therapeutic strategies but also plays a pivotal role in the monitoring and management of patient outcomes, fundamentally shaping the quality of healthcare delivery (7).

However, despite the potential of cardiac troponin as a prognostic marker, the scientific literature presents contrasting findings regarding its association with the risk of all-cause mortality in patients afflicted with acute stroke (8). Moreover, the precision of risk estimates demonstrates considerable variability across individual research studies. Troponin elevations have been reported in a substantial proportion of stroke patients, with prevalence rates ranging from 27% to 34% (9). These elevations have been consistently linked to heightened mortality in various stroke subtypes, encompassing IS, Intracerebral hemorrhage (ICH), and subarachnoid hemorrhage (SAH). Nevertheless, previous meta-analyses (6, 1017) have failed to definitively establish troponin elevation as an independent and unequivocal prognostic factor in the context of acute stroke patients. As a result, the debate concerning the predictive utility of elevated cardiac troponin levels in the stroke population continues to be a subject of scientific scrutiny. Therefore, we aimed to conduct a systematic review and meta-analysis, aptly named “Elevated Troponin Levels as a Mortality Predictor in Acute Stroke,” in order to explore the utility of cTn in predicting mortality following acute stroke.

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