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High Cholesterol Message Board

High Cholesterol Board Index

Yes I have read the "studies" on policosanol.They concentrate on lowering cholesterol NUMBERS.Also,the claims are based on studies,as you state,on animals for any other benefit from the policosanol.
The studies clearly indicate:
Besides lowering cholesterol levels, statins are known to modify endothelial function, stabilize plaques, and reduce inflammation and thrombus formation. The MIRACL study[23] looked at the effect of atorvastatin used early in the acute coronary syndromes. A total of 3086 patients with unstable angina or non-Q wave myocardial infarction were randomly assigned to placebo or atorvastatin 80 mg daily between 24 and 96 hours of admission. After a follow-up of 16 weeks, atorvastatin therapy produced a significant reduction of primary end point, which was defined as death, nonfatal myocardial infarction, cardiac arrest, or recurrent symptomatic ischemia (RR 0.84; 95% CI 0.70-1.00). Unfortunately, there was no significant change in death, nonfatal myocardial infarction, or cardiac arrest, and the benefit is seen in the reduction of recurrent ischemia. Thus, while this study established the safety and efficacy of statins in the acute coronary setting, it also suggests that more benefit will come from other therapeutic intervention when dealing with unstable angina and myocardial infarction.[24,25] The patient with an acute coronary syndrome is facing life-threatening consequences of the sudden occlusion of coronary blood flow. For treatment to make the most impact, it must result in quick and significantly increased coronary flow; this is something hypolipidemic therapy does not do.

The value of aggressive cholesterol reduction was investigated in comparison with coronary angioplasty in the AVERT study.[26] Patients with stable angina advised for percutaneous intervention were studied. Out of 341 patients recruited, 177 had an angioplasty as advised initially; the other 164 did not have an angioplasty but were instead initiated on 80 mg per day of atorvastatin. After a follow up of 18 months, patients assigned to the aggressive lipid-lowering therapy had a significantly longer time to the first ischemic event, as well as a lower incidence of ischemic events, although the latter just failed to reach statistical significance (P = .048, not significant after adjustment for interim analysis). The safety of aggressive lipid reduction therapy was confirmed, and there is a suggestion that it may be as efficacious as percutaneous intervention in managing patients with stable angina pectoris. In fact, trials of angioplasty vs medical therapy in stable angina pectoris have shown that angioplasty does not reduce the incidence of myocardial infarction and has no effect on coronary mortality.[27,28] In fact, most myocardial infarctions are due to the sudden disruption of the mildly stenotic lesions, and not the progression of previously severely narrowed plaques.[29] Since angioplasty treats only those severely stenotic lesions and does nothing to the mildly stenotic plaques, it cannot have a big impact in reducing myocardial infarction. Moreover, there is increasing evidence that acute coronary syndromes develop in the setting of a systemic inflammatory state.[30,31] Since the statins also have an anti-inflammatory and plaque stabilization effect, it stands to reason that they would be better able to prevent plaque rupture than angioplasty, which only targets a local stenotic plaque.[32-34] Further work is needed in this area, but it does seem that drug therapy has much to offer in preventing the adverse effects of atherosclerosis.

The recent publication of the Heart Protection Study (HPS) should firmly establish the benefit of statin therapy in preventing adverse events in patients at high risk of atheromatous disease.[35] Patients recruited were defined as being at high risk of coronary mortality because of prior coronary disease (secondary prevention), presence of noncoronary atheromatous disease, or diabetes. A total of 20,536 patients were enrolled and followed up for an average of 5.5 years. Patients were randomized to receive simvastatin 40 mg per day or placebo. Simvastatin reduced the coronary mortality by 18% (P = .0005) and this resulted in a highly significant reduction in total mortality (P = .0003). Highly significant reduction was also seen in stroke, major cardiovascular events, and need for coronary and noncoronary revascularization (all P < .0001). There was no increase in nonhaemorrhagic stroke and no effect on noncardiac mortality. Benefit was seen clearly in women, in the elderly, in diabetics, and in patients with prior noncardiac atheromatous disease. This benefit extends to those patients with initially low total and LDL cholesterol levels. In fact, the proportional reduction in adverse events was found to be the same in all categories of lipid levels in the patients studied, even in those with initial LDL cholesterol below 3 mmol/L and total cholesterol below 5 mmol/L. There can now be no doubt of the strategy to take. All patients at high risk of atheromatous disease must be given statin therapy, which will reduce adverse coronary and other vascular events. Baseline cholesterol levels are just one of the many risk factors in atheromatous disease, and decision on therapy should be based on an assessment of overall risk and not just the lipid level.

With the publication of the HPS, it is hard to argue with the conclusion that statin therapy is safe. All these statin trials have now randomized well over 50,000 patients, and statin therapy has been available to clinicians for more than 2 decades. No therapy is free of adverse effects, and the cerivastatin saga highlights the importance of proper patient monitoring and the need for caution with newer formulations and in combining drugs.[36] Nevertheless, the acceptability of the statins contrasts significantly with the poor palatability and high discontinuation rates of niacin and the sequestrant formulations.[37] Although expensive, statin therapy for hyperlipidemia has been shown to be cost effective if the right patient group is targeted.[38-41] The evidence from the trials is that all patients with atheromatous disease or who are at high risk of future atheromatous disease need statin therapy. Less emphasis should be placed on the actual lipid level, and more consideration must be given to the cardiovascular risk profile of the patient. Underutilization of statin therapy is still prevalent today and is a practice that needs to be discouraged as it is far better to prevent coronary disease than to treat its consequences.[42]

It is interesting to contrast briefly the statin story with the evidence on antioxidant vitamins. The HPS also looked at the value of antioxidant vitamin supplementation in preventing adverse events in this large group of high-risk patients.[43] Patients received supplementation with 600 mg vitamin E, 250 mg vitamin C, and 2 0 mg beta-carotene daily, or matching placebo. Although vitamin supplementation significantly elevated serum vitamin levels, there was no effect on vascular or nonvascular mortality, strokes, major vascular events, and cancer incidence. The disappointing results in the antioxidant vitamin arm of the HPS means we should discourage such therapy that has been proven to carry no benefit. This need for caution with antioxidants is reinforced by a recent angiographic study.[44] A total of 160 patients with coronary artery disease were enrolled in the 3-year double-blind trial and randomly assigned to simvastatin plus niacin, antioxidants, simvastatin-niacin plus antioxidants, or placebo. The average stenosis progressed by 3.9% on placebo, 1.8% on antioxidants, 0.7% on simvastatin-niacin plus antioxidants (P = .004 compared with placebo), and it regressed by 0.4% on simvastatin-niacin alone (P < .0010). Similarly, clinical end point was 24% with placebo, 21% with antioxidants, 14% with simvastatin-niacin plus antioxidants, and only 3% with simvastatin-niacin. The clinical benefit from statin therapy and its ability to induce regression of atherosclerosis is well known.[45] The surprising result is that antioxidants appear to reduce the benefit derived from hypolipidemic therapy. The disappointing effect of vitamin E has been noted in several large studies that have concurrently shown the value of fish-oil, angiotensin-converting enzyme inhibitor, and aspirin in prevention of adverse cardiac events.[46-48] Given this poor record of antioxidants in controlled clinical trials, evidence-based clinical practice means that we should advise patients with IHD to avoid vitamin E and other antioxidants

One other thing that is brought out here.There were 50000 people in these trials with statins.Is it not logical to conclude that if there was a high incidence of adverse side effects to these drugs as has been assumed in this discussion,that it would show up in the study?The fact that there was a LOW side effect number just reinforces the fact that they do not produce side effects for the MAJORITY of the people taking them.

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