Statins health benefit is the lowering of thrombi the same way aspirin does.  Lowering cholesterol doesn’t get at the root cause—oxidative damage of VLDL, unstable plaque (fresh), and atherosclerosis.  We recommend if you wish to lower your cholesterol profile, to use extended release niacin, 1,500 mgs. Niacin has been used for over 50 years with proven result, and extended release avoid the unpleasant flush which occurs short after taking a 500 mgs or more.  Current literature is of course less than supportive given the financial benefits of pushing statins.  

AZ's Crestor flubs key heart failure trial

November 5, 2007

AstraZeneca didn't get its coveted results from the long-awaited CORONA trial. Crestor failed to show any statistically significant benefit in heart failure patients. So Crestor lacks a competitive edge enjoyed by rival Lipitor and generic statins: Trials that show a clear reduction in deaths and heart disease.

It was a long shot, really; heart failure isn't generally considered to be relieved by statins like Crestor. But AZ wanted something different from the old, tried-and-true data that shows the drugs stave off complications from heart disease. A head-to-head trial against Lipitor would have cost beaucoups, and it would have been risky to boot. What if Lipitor had come out ahead?

Statins show in major study a 20-25% reduction in MI, however, aspirin does as well.  Moreover those on statins are more likely to have earlier intervention if experience a heart attack.  This is a confounding variable when comparing mortality rates—jk.

Association of Statin Therapy with Outcomes of Acute Coronary Syndromes: The GRACE Study

Frederick A. Spencer, MD; Jeanna Allegrone, BA; Robert J. Goldberg, PhD; Joel M. Gore, MD; Keith A.A. Fox, MB, ChB, FRCP; Christopher B. Granger, MD; Rajendra H. Mehta, MD; David Brieger, MD, the GRACE Investigators*

1 June 2004 | Volume 140 Issue 11 | Pages 857-866

Background: Statins administered early in patients with acute coronary syndromes may lead to modest reductions in recurrent ischemic events.

Objective: To examine the association between previous and early in-hospital statin therapy and the presentation and outcomes of an acute coronary syndrome.

Design: Cohort study.

Setting: 94 hospitals in 14 countries participating in the Global Registry of Acute Coronary Events (GRACE).

Patients: 19 537 patients with an acute coronary syndrome who were enrolled from April 1999 to September 2002.

Measurements: Statin use before and after presentation with an acute coronary syndrome and associated rates of myocardial infarction, hospital complications, and hospital mortality. The composite end point included death, in-hospital myocardial infarction, and stroke.

Results: Patients who were already taking statins when they presented to the hospital were less likely to have ST-segment elevation (odds ratio [OR], 0.79 [95% CI, 0.71 to 0.88]) or myocardial infarction (OR, 0.78 [CI, 0.70 to 0.86]). Patients who continued to take statins in the hospital were less likely to experience complications or die than patients who never received statins (OR, 0.66 [CI, 0.56 to 0.77]). Patients not previously taking statins who began statin therapy in the hospital were less likely to die than patients who never received statin therapy (OR, 0.38 [CI, 0.30 to 0.48]). However, adjustment for the hospital of admission attenuated the association between initiation of statin therapy and the composite end point (OR, 0.84 [CI, 0.65 to 1.10]).

Limitations: This observational study cannot exclude confounding by clinical and hospital factors.

Conclusions: These data support the hypothesis that statin therapy can modulate early pathophysiologic processes in patients with acute coronary syndromes. A randomized trial of statin therapy in acute myocardial infarction is warranted.

American Heart Association at http://www.americanheart.org/presenter.jhtml?identifier=3035946

Another major study shows statins are at best no better than aspirin. 

After Myocardial Infarction: The IDEAL Study: A Randomized Controlled Trial

Date: November 16, 2005

Summary: Aggressively reducing the levels of “bad cholesterol” or low density lipoprotein (LDL) in patients who had already had a heart attack did not reduce the percentage of deaths from heart disease, the occurrence of heart attacks or sudden heart stoppages in patients who had had to be resuscitated.

This is particularly telling, for if as big PhARMA maintains the more you lower LDL the slower is the development of atherosclerosis.  However when comparing high dose statins to low dose usage, there was a negative result.  This conclusion supports the conclusion which I—and others maintain—that statins benefits is rather through the same mechanism as aspirin, that of reducing thrombus; and like aspirin, there is little if any reduction in the rate of  thrombus with a higher does of either aspirin or statins, nor is their combination superior--jk.

The Grace Study Results

The very choice of two different statins rather than two doses of the same statin is suspect, since for to test the benefits of a higher does, normally it is compared directly to a lower does, rather than a lower dose of a another drug of the same family of drugs.  Given the big PhARMA bias, the reasonable conclusion is that they have stacked the test protocol so as to favor the high dose treatment.  However, the results showed a very minor benefit. There were 8,888 subject followed for approximately 2 years.  The low dose group had 4% coronary deaths and the high dose a 3.9%.  For nonfatal myocardial infractions the difference was 6% versus 7.2%.  Given the greater expense and side effects there is scant reason for taking the higher does statin.  Moreover is one factors in the difference in deaths from cancer (a know risk of statins), it turns out that the higher dose had a higher death rate.  There were 112 death from cancer in the high does and 99 in the low does group, or a difference of 13.  Subtract the coronary deaths difference of 3 (178 versus 175 for the high does) and there is a net loss of life of 10 for the higher dose group.        

The entire study is available on the internet at http://jama.ama-assn.org/cgi/content/full/294/19/2437  or in the JAMA at Vol. 294 No. 18, November 16, 2005

There are a number of troubling gaps in statin studies.  In particular (1) the failure to do a proper follow-up on the animal studies which confirm that they are carcinogens (a twenty year follow-up would be required, which is about the time it takes for cigarettes to significantly increase the incidence of cancer),  They could gather this information from the records of insurance companies.  (2) The fact that those with normal levels of LDL and LDL:HDL does not show significant benefit from statins.  (3) The failure to elucidate how statins reduce the incidence (like aspirin) of thrombi.  Possible the positive results for the high-risk group are because of this mechanism rather than an improved LDL:HDL ratio.  If it reduced the rate of plaque formation it should benefit everyone.  For example aspirin reduces the risk of colon cancer nearly 50%.  This benefit is for all people who take an aspirin per day—higher dose produces greater protection and the longer the better.  Why doesn’t this pattern of benefits apply to statins?  If lowering the LDL:HDL ratio by statins worked then we all should be taking them along with our vitamins, and start by the age of 30 for men.  (4) A good ratio without statins indicates a lower risk of MI, but a good ratio with statins confers little benefit (once the thrombi effect is adjusted for). This is glossed over in studies.  All too often there are various conditions for enrollment, testing, tracking of events, etc. in a study which are manipulated in a way so as to produce positive results.  (4) Failure to examine other serious side effects such as cognitive impairment & fatigue (effect up muscles and Q-10).  To quote Shakespeare, there is something rotten in Denmark--jk.