Discussions that mention pravachol

High Cholesterol board


I've been taking zetia 10mg for about 10 months, and until 2.5 weeks ago I was on 80mg of Pravachol with it. Extrapolating from baseline, I should have gotten roughly a 35% decrease in LDL, and 15% from zetia. Together they should have gotten my LDL down to 95. They didn't.

I'm guessing the Lipitor and added diet changes will get me to that 95, then I anticipate having to add in a third agent, such as niacin to approach good levels. :(

I _am_ hoping to see a rise in HDL after 4 decreases in a row.

mark
I know you have FH and don't respond to statins very well....but 40 mg Lipitor is a hell of a lot more potent than 80 mg Pravachol..good luck. BTW, if the 40 mg Lipitor doesn't cut it, I would try 20 mg Crestor before going the Niacin route. The 20 Crestor has the punch of 80 Lipitor without the huge exposure to statin.

RON
I'm definately not going to be adding niacin on a whim, or without doctor discussion. And in fact, I'd definately want to see what Crestor 40 could do first.

Crestor apparently has the biggest positive effect on HDL apart from niacin, and straightlined from Pravachol 80 might give me 20% more reduction in LDL.

I won't be *****-footing around with 20mg of anything though. I'm not doing all of this to DELAY an MI, I want to prevent it.

mark
Another article:

The primary and secondary prevention and atherosclerosis regression studies below in aggregate suggest that for optimal effects, LDL cholesterol should be lowered well below 100 mg/dl, to levels around 75-80 mg/dl.

An increasing amount of data from primary prevention, secondary prevention, and atherosclerosis regression studies suggest that to provide optimal results in terms of lowering coronary heart disease events and /or stopping the progression of or reversing atherosclerotic lesions, LDL cholesterol should be lowered to well under 100 mg/dl, and optimally to <80 mg/dl.

Heart Protection Study (HPS)1

Lower LDL cholesterol is associated with a lower risk of cardiovascular disease. The purpose of the Heart Protection Study (HPS) was to investigate whether lowering LDL cholesterol with simvastatin (brand name Zocor®) reduced the development of vascular disease irrespective of initial LDL concentrations. The researchers studied 20,536 patients in the United Kingdom with coronary disease, other occlusive arterial disease, or diabetes. Patients were randomly assigned to receive either 40mg of simvastatin per day or a placebo. The average compliance was 85%, and 17% of the patients were already taking statins not related to the study.

Among the findings was that patients taking simvastatin showed in a first non-fatal or fatal stroke compared to the placebo group (444 [4.3%] vs 585 [5.7%]; p<0.0001). Additionally, patients taking simvastatin showed a lower frequency of first non-fatal or fatal heart attack (8.7% vs 11.8%, p<.0001). Overall, patients taking simvastatin had a 24% reduction in the first occurrence of any of the studied major vascular events. Importantly, patients who entered the study with LDL cholesterol < 100 mg/dl before receiving Zocor had a reduction in cardiovascular events which was essentially as great as patients whose baseline LDL cholesterol was 130 or 160 mg/dl. This focused attention on lowering LDL cholesterol to ~80 mg/dl (as in this group) for optimal prevention of cardiovascular events.

This reduction in major vascular events was not significant in the first year of the study, but it was significant in each of the following four years. Furthermore, this reduction was seen in each subcategory (based on the type of vascular disease in their history) of patients studied.

There are several important messages from this study. Adding simvastatin to an existing treatment (17% were already on statins) safely produces large additional benefits over a wide range of cholesterol ranges. Taking 40 mg of simvastatin daily reduced the rates of heart attack, stroke, and revascularization by roughly 25%.Because of 15% non-compliance in this study, the true reduction could be as large as 33%. Although treatment with simvastatin produced significant benefits, the size of the five-year benefit depends on the overall risk for vascular disease rather than only cholesterol concentrations. That is, lowering cholesterol is likely to decrease the risk of a vascular event but the amount of reduction depends largely on other factors such as smoking, obesity, and genetic predisposition, rather than cholesterol concentrations alone.

MIRACL Study2

During the early time after an acute coronary syndrome—unstable angina (chest pain due to a blockage in the heart) or sudden heart attack—patients have the highest rate of death or recurrent ischemic (blockage) events. This study investigated whether 80 mg daily of atorvastatin (brand name Lipitor®), started 1-4 days after an acute coronary event, reduced the risk of death or non-fatal ischemic events. Patients at 122 clinical centers in Europe, North America, South Africa, and Australasia (n =3086) were randomly divided into two groups, receiving either 80 mg of atorvastatin per day or a placebo. Patients were followed for 16 weeks after the occurrence of an acute coronary syndrome. The significant finding was that patients in the atorvastatin group had a lower occurrence of recurrent ischemic events in the first 16 weeks after the appearance of acute coronary syndrome.

Anglo-Scandinavian Clinical Outcomes Trial (ASCOT)3

Hypertension (high blood pressure) and elevated cholesterol are two of the most common risk factors for heart disease and stroke, which are major causes of death worldwide. Lowering blood pressure and cholesterol are important in controlling these conditions. The ASCOT study included 19,342 patients randomized into one of two antihypertensive regimens. A total of 10,305 patients were randomly selected from these groups and placed in a lipid-lowering group which consisted of 10 mg of atorvastatin daily or placebo. The atorvastatin and placebo groups of the lipid-lowering arm had identical initial cholesterol levels and blood pressure. Patients were followed for a median of 3.3 years. The atorvastatin group had a 35% relative reduction in the LDL compared to the placebo group. Fatal heart attack and fatal coronary heart disease were 36% lower in the atorvastatin group. There were also significant (29%) reductions in total coronary events and a 27% reduction in fatal and non-fatal strokes. In the atorvastatin group, LDL cholesterol levels were about 80 mg/dl on therapy, again providing emphasis on lowering LDL to well below 100 mg/dl.

Reversing Atherosclerosis with Aggressive Lipid Lowering (REVERSAL)4

This recent study compared the effectiveness of atorvastatin and pravastatin in the reversal in atherosclerosis. Five hundred and two patients diagnosed with coronary heart disease and with LDL cholesterol around 150 mg/dl were treated with either atorvastatin or pravastatin (brand name Pravachol®). Intravascular ultrasound was used to assess atherosclerotic plaque status at pre-treatment baseline and after 18 months on therapy. The group treated with atorvastatin showed a median 0.4% reduction in plaque volume (the total plaque in a given section of an artery) while the pravastatin group had a median 2.7% increase in total plaque volume. Additionally, 97% of the patients taking atorvastatin reached the recommended LDL levels (=100 mg/dL) while 67% of pravastatin patients reached this level. On atorvastatin, LDL cholesterol was lowered to around 80 mg/dl, while on pravastatin, to 110 mg/dl.
More food for thought?

"The Statins: Lipitor, Crestor, Advicor, Pravachol, and Zocor: Coronary Disease Prevention and Reversal
Not being pedantic or pompous, please allow me to ask you a question. At what cholesterol level, or as an alternative, at what LDL (the bad cholesterol) level, does the atherosclerotic (hardening of the arteries) process start or stop in a population? Castelli, discussing the work of Nobel winners Brown and Goldstein, states that this value is 150 for total cholesterol.
Another question. What is the “set point” (in milligrams percent) cholesterol at which value atherosclerosis occurs in any given person that on the other side of which atherosclerosis begins to reverse? The answer to this question is an unknowable in any given individual. In the Dean Ornish group, that value was 180. However in the absence of knowing such information concretely for each individual patient, I feel it is our obligation to view the population as a whole consistently and to understand and adhere therapeutically to those numbers where we know coronary artery disease stops in all patients: 150 or less.

Since people with hardening of the arteries are already documented to be more susceptible, in the presence of documented coronary artery disease (or diabetes) a total cholesterol value of 130 or less is safer and is, in fact, what I believe epidemiology supports as the definition for “the natural human cholesterol.” 90-130 is the cholesterol range of virtually all pre-mechanical societies and is the value where no coronary artery disease exists even in these vast populations. I realize I have not discussed cholesterol fraction ratios, other risk factors, or how to achieve this value by medication, dosage, or diet. Mimicking this as a practice pattern, I guesstimate that there has been a 98% reduction of symptomatic coronary disease in my “old” patients. Said another way, of all the cardiac patients in my practice there is an average of only one invasive cardiac procedure a month. Many, truly most, of these patients had their “last” cardiac event 20 years ago or more. To achieve this, diet plus statins such as Lipitor, Crestor, Pravachol, Zocor, and lovastatin (especially with niacin = Advicor and/or along with Zetia when taken in their maximal doses result in:

LVH (excess heart muscle thickness) regression (reversal)
Reduced arrhythmias (irregular heartbeat) and inhibition of macular degeneration
Reversed excess carotid (artery) wall thickness
Reduced death, plasty, AMI and stroke (like a whole foods diet)
Debatably reduced bone fractures
Reduced protein in the urine (microalbuminuria)
Reduced blood pressure and the frequency of diabetes
Reduced Cardiac (hs) CRP (a very important predictor of heart damage and death), tumor necrosis factor, and MMP-9 (matrix metalloproteinase)
Improved endothelial (the lining of blood vessels) function
Inhibition monocyte adhesion to the endothelium/migration
Since statins reduce the body level of CoQ10, I recommend supplementing with 60-100 mg of a highly absorbable form of CoQ1O every day that you take a statin. "



H. Robert Silverstein, M.D.
Hartford, CT
And of course no sane definition of a jury would consist of ONE person...or even a couple.
If that were so, then of course, Linus Pauling who said that VITAMIN C CURES HEART DISEASE right after he cured the cold in the '60's; Atkins cured heart disease with a high fat diet in the early 1970's;...and probably Jydia Pinkham cured it before Carter invented his Liittle Liver Pills: ALL had simple non surgical heart disease "cures" making surgery obsolete.

When I said "sane jury" I think it should be reasonable to assume that I meant a consensus of medical peers who have evaluated the total picture. When and IF it becomes clear that diet and drugs can replace surgery, percutaneous or otherwise, they will.


Do you bleed when they test your cholesterol? Do they staunch your blood? Do you consider it major surgery?


And do you honestly believe that Dean, Elena, or Peter, if faced with a 98% blockage in one of their main coronary arteries would opt for a life of "good living" instead of an overnight angioplasty?"

From an earlier post (rahod):
[quote]Intravascular ultrasound was used to assess atherosclerotic plaque status at pre-treatment baseline and after 18 months on therapy. The group treated with atorvastatin showed a median 0.4% reduction in plaque volume (the total plaque in a given section of an artery) while the pravastatin group had a median 2.7% increase in total plaque volume.
So as an alternative, facing a 98% blockage an agressive 18 month atorvastatin treatment regimen would lower a 98% blockage to ....98% but pravachol would take it UP to about 100% (whew, what a relief- dodged THAT bullet; unless you used atorvastatin...or pravachol).

To consider these as sensible treatment plans for serious reductions of existing dangerous plaques is the height of folly...and NO SANE JURY would consider them, as I implied earlier.