Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Friday, September 9, 2016

Interpretation of the evidence for the efficacy and safety of statin therapy

This rehashing of the statin controversy just proves that these people do not understand cause and effect at all. Cholesterol does not cause plaques. Inflammation grabs the cholesterol out of the bloodstream packing it into plaque. The shortcut taken many years ago of reducing cholesterol was incorrect. The focus should have been on how to stop inflammation. But now that statins are a huge pharma business we will likely never go back and solve the real problem. I myself have been sucked into this mindset from my doctor, taking statins to reduce my cholesterol, so far I haven't noticed side effects of brain fuzziness.
You can see a video of how plaque forms here:
Inflammation In Atherosclerotic Plaque Formation  

 

Interpretation of the evidence for the efficacy and safety of statin therapy

,
Christina Reith, FRCP (Glasg.)
,
,
Prof Jane Armitage, FRCP
,
Prof Colin Baigent, FRCP
,
,
,
Prof John Danesh, FMedSci
,
,
Prof David DeMets, PhD
,
Prof Stephen Evans, MSc
,
Prof Malcolm Law, FRCP
,
Prof Stephen MacMahon, FMedSci
,
,
Prof Bruce Neal, PhD
,
Prof Neil Poulter, FMedSci
,
,
Prof Paul Ridker, MD
,
Prof Ian Roberts, PhD
,
Prof Anthony Rodgers, MBChB
,
,
Prof Kenneth Schulz, PhD
,
Prof Peter Sever, FRCP
,
Prof John Simes, MD
,
Prof Liam Smeeth, FRCGP
,
Prof Nicholas Wald, FRS
,
Prof Salim Yusuf, DPhil
,
Prof Richard Peto, FRS
This article can be found in the following collections: Ischaemic heart disease

Summary

This Review is intended to help clinicians, patients, and the public make informed decisions about statin therapy for the prevention of heart attacks and strokes. It explains how the evidence that is available from randomised controlled trials yields reliable information about both the efficacy and safety of statin therapy. In addition, it discusses how claims that statins commonly cause adverse effects reflect a failure to recognise the limitations of other sources of evidence about the effects of treatment. Large-scale evidence from randomised trials shows that statin therapy reduces the risk of major vascular events (ie, coronary deaths or myocardial infarctions, strokes, and coronary revascularisation procedures) by about one-quarter for each mmol/L reduction in LDL cholesterol during each year (after the first) that it continues to be taken. The absolute benefits of statin therapy depend on an individual's absolute risk of occlusive vascular events and the absolute reduction in LDL cholesterol that is achieved. For example, lowering LDL cholesterol by 2 mmol/L (77 mg/dL) with an effective low-cost statin regimen (eg, atorvastatin 40 mg daily, costing about £2 per month) for 5 years in 10 000 patients would typically prevent major vascular events from occurring in about 1000 patients (ie, 10% absolute benefit) with pre-existing occlusive vascular disease (secondary prevention) and in 500 patients (ie, 5% absolute benefit) who are at increased risk but have not yet had a vascular event (primary prevention). Statin therapy has been shown to reduce vascular disease risk during each year it continues to be taken, so larger absolute benefits would accrue with more prolonged therapy, and these benefits persist long term. The only serious adverse events that have been shown to be caused by long-term statin therapy—ie, adverse effects of the statin—are myopathy (defined as muscle pain or weakness combined with large increases in blood concentrations of creatine kinase), new-onset diabetes mellitus, and, probably, haemorrhagic stroke. Typically, treatment of 10 000 patients for 5 years with an effective regimen (eg, atorvastatin 40 mg daily) would cause about 5 cases of myopathy (one of which might progress, if the statin therapy is not stopped, to the more severe condition of rhabdomyolysis), 50–100 new cases of diabetes, and 5–10 haemorrhagic strokes. However, any adverse impact of these side-effects on major vascular events has already been taken into account in the estimates of the absolute benefits. Statin therapy may cause symptomatic adverse events (eg, muscle pain or weakness) in up to about 50–100 patients (ie, 0·5–1·0% absolute harm) per 10 000 treated for 5 years. However, placebo-controlled randomised trials have shown definitively that almost all of the symptomatic adverse events that are attributed to statin therapy in routine practice are not actually caused by it (ie, they represent misattribution). The large-scale evidence available from randomised trials also indicates that it is unlikely that large absolute excesses in other serious adverse events still await discovery. Consequently, any further findings that emerge about the effects of statin therapy would not be expected to alter materially the balance of benefits and harms. It is, therefore, of concern that exaggerated claims about side-effect rates with statin therapy may be responsible for its under-use among individuals at increased risk of cardiovascular events. For, whereas the rare cases of myopathy and any muscle-related symptoms that are attributed to statin therapy generally resolve rapidly when treatment is stopped, the heart attacks or strokes that may occur if statin therapy is stopped unnecessarily can be devastating.
 

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