September 26th, 2011
Statins for Primary Prevention: The Debate Continues
Larry Husten, PHD
Several leading cardiologists have taken issue with the assertion made by Rita Redberg and the editors of the Archives of Internal Medicine that using statins for primary prevention is an example “of the widespread use of medications with known adverse effects despite the absence of data for patient benefit for these indications.”
In a research letter published in the current Archives, C. Michael Minder and colleagues (including Sanjay Kaul and Roger Blumenthal) write that they “believe there is compelling evidence to support the use of statins for primary prevention in patients at high risk… for developing coronary heart disease (CHD) over the next 10 years.” They assert that by focusing on short-term mortality, the Archives editors overlooked the substantial benefits of statin therapy for primary prevention in appropriately selected patients.
Minder and colleagues acknowledge that the evidence for a mortality benefit for statins in primary prevention is “less than robust,” but that when it comes to morbidity the “message is clear.” They cite a Cochrane meta-analysis showing a 34% reduction in revascularizations and a 30% reduction in combined fatal and nonfatal CV endpoints.
The authors argue that it is “paramount to make the distinction between low-risk and high-risk primary prevention cohorts.” They agree that primary prevention is unlikely to benefit people with a 10-year Framingham risk score of less than 10%, but that patients “without known CHD but with diabetes, hypertension, hyperlipidemia, and tobacco use … are likely to benefit from statin primary prevention.”
In response, Redberg and colleagues point out that some of the data in support of primary prevention include patients with known CHD. Furthermore, they state, the authors “do not acknowledge the commonly reported adverse effects associated with statins, including memory loss, muscle pains, weakness, and liver function abnormalities.”
8 Responses to “Statins for Primary Prevention: The Debate Continues”
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If someone can tolerate and afford high dose statin therapy it will keep their plaque load down and probably stabilized and delay any event related to that plaque.
That’s what the evidence says in plain English
I was very disappointed in Dr. Redberg’s response. She insisted that we (the authors) markedly reduce the length of our viewpoint and then she criticizes us for not mentioning statin side effects. Everyone knows that there are side effects for statins that occur initially in ~10/100 individuals. Generally 95/100 patients will eventually tolerate some dose of a statin satisfactorily. However, it is clear that statin therapy in asymptomatic persons at moderate to high risk of a CHD event over the next decade will decrease the risk of a heart attack, stroke, bypass, surgery, angioplasty/stenting. It is unbelievable that Dr. Grady and she think that the NCEP ATP III guidelines for treatment of intermediate and high risk primary prevention patients is baseless. This is basic prevention. We know that statin therapy slows the progression of atherosclerosis and helps to stabilize vulnerable plaques. To maintain that prevention of cardiovascular morbidity should not be pursued with a proven therapy is truly mind boggling and utterly ridiculous. It is amazing that that these smart clinician scientists from UCSF can take this extreme view. I feel badly for the primary prevention patients who see these members of the Archives editorial board for a cardiovascular risk assessment. Secondary prevention therapy with statins will not help the many individuals who die from their initial heart attack or stroke.
This debate is a strong argument for atherosclerosis imaging. With a simple coronary calcium score, we can accurately identify 10 year risk with much greater accuracy than all other risk factors combined. If we treat only those with a potential to benefit, we will do more good and less harm.
Competing interests pertaining specifically to this post, comment, or both:
I use calcium imaging to stratify risk prior to initiating statin therapy.
Based on robust evidence from numerous primary prevention trials, I strongly feel that the benefits of statins should not be denied to intermediate to high risk patients, especially diabetics & hypertensives for primary prevention.I’ve used statins in thousands of my patients with diabetes and hypertension, and have yet to come across any side effects !
Competing interests pertaining specifically to this post, comment, or both:
None
In a large practice focused on risk management/prevention, mainly in hypertensives, diabetics, dyslipidemics, and the potbellied, I have witnessed the near-disappearance of macro- and miscrovascular disease in the past 13 years: in nonsmokers inside the “therapeutic tent” I define, there have been two myocardial infarctions and no atherosclerotic strokes in that time, and both the heart attacks occurred in people before the anticipated stabilization of vulnerable plaque. Prior to then, I had a significant ongoing CCU census; nowadays, I am virtually never there. It cannot be chance alone. In those at risk, I use statins in low doses, niacin when the HDL is< 60, an aggressively promoted anti-oxidant diet (no refined carbohydrates, lots of plant-based foods, omega 3 oils), and abstinence from smoking. One cannot say whether the use of statins is contributory in a major way, but until data arrive to tell me they are not necessary, the fruits of this mix keep me and my patients happy, and I will continue to use them (though based on Arbiter3, low doses having fewer side effects seem good enough).
Primary vs. secondary prevention: A False Dichotomization?
Benefit-risk assessment should occur on a continuum rather than be based on the false dichotomization of primary vs. secondary prevention. I prefer a risk-based treatment paradigm. Not all patients without manifest atherothrombotic vascular disease are at low risk. For example, in JUPITER, patients with elevated CRP and =/>2 ATP III risk factors were at 2-fold higher risk, and it was in these patients that the treatment benefit with statin was most apparent. So, one could argue that the benefits of statin therapy exceed the risks in these high-risk patients. Whether one uses non-imaging or imaging variables to identify these high-risk cohorts is a matter of legitimate debate.
The benefit of statins in select higher risk primary prevention patients appears to me clear. Subclinical atherosclerosis imaging is a potentially powerful tool for selecting those at increased risk to treat. It is also helpful for selecting those patients with no obvious atherosclerosis in whom a lifestyle approach can be emphasized. This was the premise of our recent Lancet article. I agree with Sanjay that the method of risk determination can be debated – the benefit of statins cannot.
I would like to ask the editors of Archives for references supporting the “commonly reported adverse effects associated with statins, including memory loss and weakness”. This is what their argument is built on.
Agree completely with Roger, Sanjay and Michael on this issue.
The arcane view of Archives on this and other cardiovascular issues in the last several years is not a world view. Although they are clearly entitled to their assessment (although poorly grounded), I’m struggling here with the net effect of such dialogues. One does wonder about the cost to ongoing innovation that comes from alternatively devoting effort to debating decades-old concepts, which have long since been translated to guidelines followed worldwide.