{"id":41832,"date":"2014-02-25T18:59:57","date_gmt":"2014-02-25T23:59:57","guid":{"rendered":"http:\/\/blogs.nejm.org\/cardioexchange\/?post_type=voices&#038;p=41832"},"modified":"2014-02-25T18:59:57","modified_gmt":"2014-02-25T23:59:57","slug":"is-post-mi-statin-therapy-appropriately-intensive","status":"publish","type":"post","link":"https:\/\/blogs.nejm.org\/cardioexchange\/2014\/02\/25\/is-post-mi-statin-therapy-appropriately-intensive\/","title":{"rendered":"Is Post-MI Statin Therapy Appropriately Intensive?"},"content":{"rendered":"<p><i>CardioExchange&#8217;s<\/i><b><i> Harlan M. Krumholz<\/i><\/b><i> interviews <b>Suzanne V. Arnold<\/b> about her research group\u2019s study of statin initiation, intensification, and maximization after acute myocardial infarction. <\/i><a href=\"http:\/\/circ.ahajournals.org\/content\/early\/2014\/02\/04\/CIRCULATIONAHA.113.003589.abstract\"><i>The study is published in <\/i>Circulation<\/a><i>.<\/i><\/p>\n<p><b>THE STUDY<\/b><\/p>\n<p>Researchers assessed statin use at admission and discharge for 4340 patients with acute MI at 24 U.S. hospitals from 2005 to 2008. Maximal therapy was defined as a statin with expected LDL-cholesterol lowering of at least 50%. Among statin-naive patients, 87% without a contraindication were prescribed a statin, with almost no variability across sites (median rate ratio, 1.02). Among patients who arrived on submaximal statins, 26% had their statin therapy intensified with modest site variability (median rate ratio, 1.47). Among all patients without a contraindication, 23% were discharged on maximal statin therapy, with substantial hospital variability (median rate ratio, 2.79).<\/p>\n<p><b>THE INTERVIEW<\/b><\/p>\n<p><b><i>Krumholz: Which of your study\u2019s findings was most surprising to you?<\/i><\/b><\/p>\n<p><b><i>Arnold:<\/i><\/b> Very little of what we found was surprising. As a cardiology community, we have focused a lot on LDL numbers, to measure risk and the need for statins. I think with the MI performance measures, we at least were able to understand that all MI patients need a statin, regardless of LDL level \u2014 and our study documented high rates of statin initiation. Moving beyond just initiating statins to intensifying and maximizing statins required a deeper understanding of the statin trials, which were not as well known by clinical cardiologists. As such, physicians tended to make treatment decisions according to their perception of the patient\u2019s risk \u2014 intensifying and maximizing statins in patients with high LDL levels and those with STEMI (despite no evidence that these patients were more likely to benefit from intensive statins). We also observed a lot of site-level variability in intensification and maximization, which again was not surprising, as such clinical decisions often follow local practice patterns. We are hopeful that the new lipid guidelines will emphasize the evidence-based imperative to get all MI patients on intensive statins during the MI hospitalization.<\/p>\n<p><b><i>Krumholz: Why do you think intensification is not occurring?<\/i><\/b><\/p>\n<p><b><i>Arnold: <\/i><\/b>I think this primarily stems from a misperception about which patients are most likely to benefit from intensive statins. The prior trials showed that all MI patients were equally likely to benefit, regardless of patient characteristics. However, I think there is a misperception that patients who present with STEMI need more aggressive secondary prevention, which is why their statin regimens were more likely to be intensified. Similarly, patients with high LDL levels were thought to need more intensive statin therapy. However, LDL levels can be falsely low in a patient with acute MI, particularly in patients with severe MIs, which is one likely reason why we have not observed any association between LDL levels during MI and a differential benefit from statins. Again, I think the new guidelines will highlight the evidence for the general cardiology community.<\/p>\n<p><b><i>Krumholz: Could it be patient choice? How do you present this decision to patients?<\/i><\/b><\/p>\n<p><b><i>Arnold: <\/i><\/b>Possibly, although I suspect this matters very little in the decision to prescribe intensive statins. When I talk to patients and go over the medications I will be prescribing them to take at home, some say, \u201cBut I don\u2019t have high cholesterol. Why do I need that?\u201d What I usually then discuss is that for a patient with an MI, cholesterol is deposited in the vessels of the heart, regardless of what the blood numbers read. Statins are the best medications we have for treating those cholesterol plaques in the heart \u2014stabilizing them so they don\u2019t grow and reducing the risk that they will rupture and cause another heart attack. So for patients who have heart attacks, it is really important to be on intensive doses of these medications, regardless of the blood numbers. I try to get patients to understand that the statin is treating the <i>cholesterol plaques in the heart <\/i>\u2014 not the blood numbers. This change of focus on what the medication is targeting seems to make patients more likely to accept taking it. It is a similar conversation for beta-blockers in patients without hypertension.<\/p>\n<p><b><i>Krumholz: What is your sense of the trade-off in statin intensification (additional benefit and additional risk)?<\/i><\/b><\/p>\n<p><b><i>Arnold:<\/i><\/b> I think that intensive statins have a clear additional benefit over moderate statins in reducing the risks for recurrent MI and cardiovascular death, although to show an effect on mortality required combining the two major trials. Our pooled analysis documented an NNT of 95 patients with intensive statins to prevent 1 death \u2014 that is a fairly small NNT compared with many other secondary-prevention therapies. The more-intensive statins also increase the risk for myalgias, which cannot be ignored. The logical solution would be to start an intensive statin and, if myalgias occur, change to moderate statin therapy. However, if a patient gets myalgias with an intensive statin, he or she may be less willing to try moderate statins. Generally, I have had good luck with getting such patients to try moderate statins. However, I also admit that my personal practice is to use atorvastatin 40 mg in elderly patients who may be more likely to get a side effect (or, at least, whose mobility would be more compromised by a side effect).<\/p>\n<p>I think the decision is more difficult in a patient with a remote cardiac event. The trials studied patients just after an MI, when event rates are highest and the expected benefit of aggressive secondary prevention would probably be greatest. Is there a time period after which the benefit of intensive statin therapy does not outweigh potential risks? We have already seen a suggestion of this with beta-blockers after MI. In the first few years after an MI, I think the case for intensive statins (or at least a trial of intensive statins) is strong. After that, questions remain. Certainly, if a patient has tolerated an intensive statin for a time after an MI, there seems to be no good reason to down-titrate. The question remains as to whether or not to intensify a statin in a patient with a more remote event.<\/p>\n<p><b>JOIN THE DISCUSSION<\/b><\/p>\n<p><b>In light of Dr. Arnold\u2019s comments, share your thoughts on how well statin therapy is being delivered to patients after myocardial infarction.<\/b><\/p>\n","protected":false},"excerpt":{"rendered":"<p>Suzanne V. Arnold discusses her research group\u2019s study of statin initiation, intensification, and maximization after acute myocardial infarction.<\/p>\n","protected":false},"author":334,"featured_media":0,"comment_status":"open","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[7],"tags":[1108,1622,584],"class_list":["post-41832","post","type-post","status-publish","format-standard","hentry","category-prevention","tag-acute-myocardial-infarction","tag-quality-of-care","tag-statins"],"_links":{"self":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/41832","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/users\/334"}],"replies":[{"embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/comments?post=41832"}],"version-history":[{"count":0,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/posts\/41832\/revisions"}],"wp:attachment":[{"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/media?parent=41832"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/categories?post=41832"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/blogs.nejm.org\/cardioexchange\/wp-json\/wp\/v2\/tags?post=41832"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}