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, July 14, 2016

Protein-based risk score for cardiovascular outcomes in stable coronary heart disease

There are many risk calculators out there. Which one is in your doctors protocol?
Protein-based risk score for cardiovascular outcomes in stable coronary heart disease

JAMA, 07/12/2016
Researchers used large–scale analysis of circulating proteins with a goal to derive and validate a score to predict risk of cardiovascular outcomes among patients with CHD. They concluded that only modest discriminative accuracy was provided among patients with stable CHD although a risk score based on 9 proteins performed better than the refit Framingham secondary event risk score in predicting cardiovascular events. To assess whether the score is more accurate in a lower–risk population, further research is needed.

Methods

  • Design of the study is prospective cohort, in participants with stable CHD.
  • Outpatients from San Francisco were enrolled from 2000 through 2002 and followed up through November 2011 (<=11.1 years), for the derivation cohort (Heart and Soul study) and from 2006 through 2008 and followed up through April 2012 (5.6 years), for the validation cohort (HUNT3, a Norwegian population–based study).
  • 1130 proteins were measured in plasma samples, using modified aptamers
  • Derivation and validation of 9–protein risk score was done for 4–year probability of myocardial infarction, stroke, heart failure, and all–cause death.
  • Researchers used tests, including the C statistic, to assess performance of the 9–protein risk score, which was compared with the Framingham secondary event model, refit to the cohorts in this study.
  • From paired samples which were collected 4.8 years apart, evaluation of within–person change in the 9–protein risk score was done in the Heart and Soul study.

Results

  • The results demonstrated that of the 938 samples analyzed from the derivation cohort, median age of the participants enrolled was 67.0 years and 82% were men, whereas of the 971 samples analyzed from the validation cohort, participants’ median age at enrollment was 70.2 years, and 72% were men.
  • C statistics in the derivation cohort were: 0.66 for refit Framingham, 0.74 for 9–protein, and 0.75 for refit Framingham plus 9–protein models, and in the validation cohort were: 0.64 for refit Framingham, 0.70 for 9–protein, and 0.71 for refit Framingham plus 9–protein models.
  • C statistics were increased by 0.09 (95% CI, 0.06–0.12) in the derivation cohort and by 0.05 (95% CI, 0.02–0.09) in the validation cohort, by adding the 9–protein risk score to the refit Framingham model .
  • The integrated discrimination index for the 9–protein model was 0.12 (95% CI, 0.08–0.16) in the derivation cohort and 0.08 (95% CI, 0.05–0.10) in the validation cohort, compared with the refit Framingham model.
  • Researchers analysed that in paired samples among 139 participants with cardiovascular events after the second sample, absolute within–person annualized risk increased more for the 9–protein model (median, 1.86% [95% CI, 1.15%–2.54%]) than for the refit Framingham model (median, 1.00% [95% CI, 0.87%–1.19%]) (P=.002), while among 375 participants without cardiovascular events, both scores changed less and similarly (P=.30).

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