Miscellaneous
I've found that I can often increase compliance with statins by having pt take them 3x/week or QOD. I try this often especially in my secondary prevention group. I understand "any statin is better than none", but do data support this approach? -- any is better than none! No rct with this but yes data supports every other day but that is observational..what about vascepa in reducing CAD risk both primary and secondary risk? Vascepa is now the first and only drug approved by the FDA as an adjunct to maximally tolerated statin therapy to reduce the risk of myocardial infarction, stroke, coronary revascularization, and unstable angina requiring hospitalization in adult patients with elevated triglyceride (TG) levels (≥150 mg/dL) and established cardiovascular disease or diabetes mellitus and two or more additional risk factors for cardiovascular diseaseReduce it trial---The big trial which showed all the promise used mineral oil as a placeboAND then we have evaporate trial—which showed steady plaqueThe groups didn’t start off the same!When you do an RCT- everything is random and therefor EVERYTHING IS EQUAL—but that idnt happen. And yes the people were blinded but they don’t say that the people reading the CT was blindedThe placebo group had higher CRP and dramatically worse cholesterol panels after taking mineral oilThen most recently we have the strength it trial- which showed no difference and should have had high bioavailability! Like LDL that went up 50 points in the placebo group!! That shouldn’t happen!What about fibrates for triglycerides > 400 or 500 to prevent complications like pancreatitis? No – no- no- no evidence for fibrates, period, throw them away. DRUGECTOMY for everyoneGiven evidence is only for patient to age 79, what do you recommend for patients over 79 with high lipids or on who are on a statin if concern for risk of negative cognitive effects of statins in this group? Remember 5 years or less to live. stop the statin. And the cognitive declinePlease comment on lipophilic vs hydrophilic statins and possible detrimental effects on cognition.If cognitive risk is so small, why is there a black-box warning? It makes it difficult to convince the patient to take a statin when they read this warning.ano M, Bell KL, Galasko D, et al. A randomized, double-blind, placebo-controlled trial of simvastatin to treat Alzheimer disease. Neurology 2011;77(6):556-563.In this multicenter trial, the authors gave simvastatin or placebo to 406 patients with mild to moderate Alzheimer disease, aged at least 50 years, with a Mini-Mental State Examination score between 12 and 26, who otherwise would not have been taking a statin. Simvastatin was no better than placebo in slowing cognitive deterioration in patients with mild to moderate Alzheimer disease. (LOE = 1b)Steenland K, Zhao L, Goldstein FC, Levey AI. Statins and cognitive decline in older adults with normal cognition or mild cognitive impairment. J Am Geriatr Soc 2013;61(9):1449-55.These researchers serially assessed approximately 3500 elderly patients for 3.4 years. The elders did not have dementia at baseline and approximately one third were using a statin. After 3.4 years of follow-up, the rate of cognitive decline among statin users was comparable with that of nonusers. https://www.ahajournals.org/doi/10.1161/circ.128.suppl_22.A10589Results: Significantly higher proportional reporting ratios (PRRs) were observed for lipophilic statins, which more readily cross the blood-brain barrier, (range: 1.48-3.50) compared to hydrophilic statins (range: 0.68-1.60). However, fluvastatin, lovastatin, and pitavastatin (lipophilic) had relatively few adverse reports in the AERS database. The signal of higher risk of cognitive dysfunction was observed for the lipophilic statin atorvastatin (PRR = 2.68, 95% confidence interval: 2.52-2.85) followed by simvastatin (PRR = 2.20, 95% confidence interval: 2.02-2.40).Conclusions: Inconsistent with the FDA class warning, highly lipophilic statins with specific pharmacokinetic properties (atorvastatin and simvastatin) appear to confer a significantly greater risk of adverse cognitive effects compared to other lipophilic statins and those with hydrophilic solubility properties.“Keep in mind that cohort studies are unable to account for 2 important phenomena: the healthy-user effect and reverse causality. The healthy-user effect, the primary explanation for older theories of the "benefits" of hormone replacement, refers to the observation that healthy people are more likely to use preventive measures and that the outcomes are due to good health, not the intervention. In reverse causality, we find that patients in declining health stop using treatments because they no longer perceive a potential benefit. It takes a randomized trial to overcome these phenomena.”Last but not leastZhou Z et al. Effect of statin therapy on cognitive decline and incident dementia in older adults. J Am Coll Cardiol 2021 Jun 29; 77:3145. (https://doi.org/10.1016/j.jacc.2021.04.075)They followed 18,846 study participants for a median of 4.7 years. Participants' median age was 74 years, and 56% were women. With 85,557 person-years of follow-up, the investigators identified 566 incident cases of dementia. Statin use was associated with nonsignificant increases in all-cause dementia (hazard ratio, 1.16) and probable Alzheimer disease (HR, 1.33; 95% CI 1.00 to 1.77). Statin use was not associated with mild cognitive impairment, but there was a nonsignificant increase in association with Alzheimer disease (HR, 1.44).Any thoughts on coronary CTA (rather than calcium score) or carotid intimal medial thickness as a tool for risk assessment? No—no prospective RCT—all retrospective. And the people are baseline high risk to begin with. if you would choose one single best statin for primary and secondary prevention, which one would you pick? The one the pt will takeshould take a statin if it increases LFT?? YES remember we are decreasing heart attacks and strokes!! We have no evidence on was a smell increase in your LFT does long term but we have evidence that long term these drugs have a 30% RR reduction in heart attacks and strokes!Some patients like to take Co Q10 with their statin. What is your experience with this? Taking it for muscle aches and remember there is no real difference in muscle aches compared to placebo. If you don't check cholesterol but every 10 years, how do you know that further risk reduction is needed for secondary prevention or additional medication to statin is needed -- you do it based on their risk reduction! There are 3 criteria – 1. 1 event in last 12 months. 2. 2 eents in their life. 3. An event with 3 or more risk factors. what are the real risks of statins increasing risks of DM? depends where you read—cocochane has the HR at 1.18 but that is a 2 yr study. For our calculation of the risk of diabetes the answer likely lies between 0.4% and 4%, and we have chosen what we believe to be a conservative estimate of 2% as a midway point in this credible interval.The raw numbers of 270 and 216 new onset diabetes cases from 24 months of exposure to a statin and a placebo (respectively) can be extrapolated, assuming that increased diabetes risk is likely to continue linearly with exposure. This yields 675 and 540 cases at 5 years. How long do you do washout between statin? No hard science to this they have not randomized different months of wash out as far as I am aware of so 3-6 months and you will be fine. Anything to say about Nexletol?Is there any benefit in obtaining lipoprotein profiles? NO—not for the events we care about. There is evidence that you can get this panels and then you could add a drug or increase a dose and decrease a lab value but we treat patients not lab values and there is no evidence It improves patient orientated outcomes. WHATPCSK9 DO YOU USE? Whatever insurance will pay for and remember they are still really really really expensive and IV only so this should be dead last line and only in the highest of the highest of the highest risk.