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.

Sunday, December 9, 2018

Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study

I don't have enough medical brain power to understand so ask your doctor for it in understandable terms.  So you can ask whether better stroke recovery is more important than calcifying your arteries.

Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons  Oct. 2012

Or these competing narratives;

Statins associated with improved heart structure and function May 2017 

Stroke Rounds: Statin Users Have Better Outcomes February 2016

Statins induce angiogenesis, neurogenesis, and synaptogenesis after stroke

September 2011 

New study strengthens evidence of the connection between statin use and cataracts  December 2014 

Stroke Patients Boost Survival by Getting Statins in Hospital    October 2014

 

 

 

 

Statin Medication Enhances Progression of Coronary Artery Calcification: The Heinz Nixdorf Recall Study

Under an Elsevier user license
open archive

Statins are suggested to stabilize plaque by decreasing lipid-rich and necrotic plaque components and increasing plaque calcification 1, 2. However, to date the relationship between statin administration and progression of coronary artery calcification (CAC) is poorly understood, and existing data are limited to patient cohorts and relatively short follow-up times. Therefore, in this study, we aimed to investigate whether the use of statins influences the progression of CAC during >5 years of follow-up in an observational study based on participants from the general population cohort of the Heinz Nixdorf Recall Study, free from clinical cardiovascular disease at baseline (3). CAC score was assessed using electron-beam computed tomography at baseline and after 5 years using an identical scanning protocol and quantified by the Agatston score. Regression analysis was used to determine the association of CAC progression with statin intake, with log transformation of CAC to normalize for its distribution.
We included 3,483 participants (mean age 59 ± 8 years, 47% men) in this analysis. Overall, 230 subjects received statin medications at baseline. Median CAC scores at baseline were 58.8 (interquartile range [IQR]: 2.6 to 273.3) for subjects with statin intake and 5.9 (IQR: 0 to 80.2) for subjects without. Median follow-up CAC scores were 141.3 (IQR: 19.6 to 554.7) for subjects with statin intake and 21.2 (IQR: 0.0 to 174.6) for those without.
In unadjusted regression analysis, taking a statin was associated with 39% higher progression in CAC+1 (Table 1). This relationship was slightly attenuated after adjustment for cardiovascular risk factors but remained statistically significant, with approximately 31% higher progression of CAC+1, attributable to statin intake. Likewise, subjects with statin intake had almost 2-fold odds for CAC progression greater than the expected range compared with subjects without statin medication in unadjusted and adjusted regression analyses.

Tables and more at link. 

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