Statin therapy

Statin therapy underused for treating severe hypercholesterolemia

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The number of adults with severe hypercholesterolemia prescribed general and high-intensity statins in a Kentucky health system falls below recommended guidelines, according to a study published in The American Journal of Cardiology.

Wael Eid

“Individuals with severe hypercholesterolemia have a fivefold higher long-term risk for coronary heart disease and atherosclerotic cardiovascular disease compared with individuals with average LDL-C levels,” Wael Eid, MD, an endocrinologist and lipid specialist at St. Elizabeth Physicians Regional Diabetes Center in Covington, Kentucky, the University of Kentucky College of Medicine in Lexington, the University of South Dakota Sanford School of Medicine in Sioux Falls and Alexandria University in Egypt, told Healio. “There are distinct rigorous guidelines to support aggressive treatment for severe hypercholesterolemia with high-intensity statins and other lipid-lowering therapies, if needed. However, there is a general feeling that these guidelines are not yet fully implemented. The value of this study was to assess the extent of use of these guidelines in the population we serve, to identify potential areas of gaps in care, and to be able to identify these individual patients and optimize their treatment.”

Source: Adobe Stock

Eid and colleagues conducted a cross-sectional study of every patient who had LDL cholesterol measured in the St. Elizabeth Health Care system from 2009 to April 2020. Severe hypercholesterolemia was defined as having LDL cholesterol levels of at least 190 mg/dL. Those with severe hypercholesterolemia were placed in one group (n = 19,695) while those without severe hypercholesterolemia were placed into a second group (n = 245,525).

The severe hypercholesterolemia group had a higher prevalence of hypertension and higher mean blood pressure, systolic BP, diastolic BP and cholesterol values than those with nonsevere hypercholesterolemia.

Most patients with no comorbidities in the severe hypercholesterolemia group were treated by primary care providers (43.2% to 45.7%) — who mostly prescribed low- or moderate-intensity statin therapy — whereas 3.4% to 4.4% were treated by an endocrinologist and 2.5% to 3.3% by a cardiologist.

In the severe hypercholesterolemia group, 77% were prescribed general statins and 27% high-intensity statin therapy. Of the severe hypercholesterolemia group, 83% had persistently elevated LDL cholesterol levels, and 22% of these were prescribed a high-intensity statin.

Patients with comorbidities were more likely to be prescribed statins, regardless of hypercholesterolemia severity. Adults with severe hypercholesterolemia aged 40 to 75 years (74% to 76.3%) and those older than 75 years (65.6% to 73.6%) were more likely to receive a statin prescription than those younger than 40 years (50% to 58.3%).

“There was evidence of treatment paradox where those with highest risk for CVD are not treated as aggressively as they should,” Eid said. “Less than one-third of patients with severe hypercholesterolemia are treated by high-intensity statins. Younger patients with severe hypercholesterolemia are being less aggressively treated than those who are middle-aged, even though both have high risk for CVD. Most of these patients are being cared for at primary care offices rather than specialty medicine, and that is where most of the efforts in optimizing care should be targeted.”

Eid said support is needed from quality improvement and clinical utilization departments to have initiatives for optimizing risk for patients with severe hypercholesterolemia. He added that greater awareness of severe hypercholesterolemia in primary care practices and identifying barriers for statin therapy optimization are other important issues to address.

Bempedoic acid may further reduce LDL when added to high-intensity statin therapy

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Patients treated with bempedoic acid in addition to high-intensity statin therapy had a further reduction in LDL, according to results presented in a late-breaker session at the National Lipid Association Scientific Sessions.

“Bempedoic acid, or ETC-1002, is a pro-drug, and it needs to be converted into its active form by a very specific Acyl-CoA synthetase that is almost exclusively found in the liver and to a much lesser extent in the kidneys, but not in the muscle cell,” Mary McGowan, MD, chief medical officer at Esperion Therapeutics and co-director of the Lipid Clinic at Dartmouth-Hitchcock Medical Center in Lebanon, New Hampshire, said in the presentation. “By [converting] ETC-1002, you get ETC-1002 CoA, and this is an inhibitor of ATP citrate lyase. ATP citrate lyase is an enzyme upstream from the HMG-CoA reductase enzyme, and as such, inhibition here does exactly what statins do.”

McGowan added that the enzyme decreases intercellular cholesterol production, which upregulates LDL receptors which in turn increases the removal of LDL from the bloodstream, lowering serum LDL levels.

Mary McGowan, MD

Mary McGowan

Previous studies

Other phase 2 studies were completed, in which a total of 1,045 patients were treated with bempedoic acid or placebo. When bempedoic acid was used as monotherapy, patients saw a 30% reduction in LDL. The combination of bempedoic acid and ezetimibe (Zetia, Merck) lowered LDL by 48%. The addition of bempedoic acid to low- and moderate-dose statins lowered LDL by an additional 20% to 24%.

In the present study, researchers assessed the LDL-lowering efficacy of 180 mg of bempedoic acid when added onto a background of 80 mg of atorvastatin. Also analyzed were “the pharmacokinetics of steady-state of atorvastatin and its active metabolite, ortho-hydroxy atorvastatin, alone and in combination with steady-state bempedoic acid,” McGowan said.

This study enrolled a total of 64 patients who were on either low- and moderate-intensity statins with LDL > 115 mg/dL or high-intensity statins with LDL > 100 mg/dL. All patients in the first treatment period received 80 mg of atorvastatin.

After 28 days of receiving daily atorvastatin, patients were randomly assigned to either receive bempedoic acid (n = 41; mean age, 58 years; 51% women) or placebo (n = 23; mean age, 58; 44% women) in addition to the atorvastatin 80 mg treatment.

LDL reduction

At 28 days after randomization, the least-squares mean percentage change on LDL from baseline was +9% in the placebo group and –13% in the bempedoic acid group (difference, –22%; 95% CI, –36.4 to –7.96; P = .0028), which “was consistent with what we saw in our previous studies,” McGowan said. Bempedoic acid also significantly lowered apolipoprotein B, non-HDL, total cholesterol and high-sensitivity C-reactive protein, she said.

Researchers also analyzed the pharmacokinetics, in which maximum concentration did not change.

“Atorvastatin [pharmacokinetics], the [area under the curve] increased by 29%, and the ortho-hydroxy atorvastatin, a primary metabolite of atorvastatin, increased by 22%,” McGowan said.

Patients did not experience serious adverse events. Four unique patients had myalgia (n = 2) or elevated creatine kinase (n = 2). Myalgia symptoms improved while patients remained on the study drug, and [creatine kinase] elevations were not confirmed on repeat measurement, McGowan said.

“In this study, utilizing 80 mg of atorvastatin in combination with bempedoic acid, we had no [alanine aminotransaminase] or [aspartate aminotransferase] greater than three times the upper limit of normal either in the placebo group or the bempedoic acid group, and we had no patients with repeated and confirmed [creatine kinase] elevations of greater than five times the upper limit of normal,” McGowan said.

“We presented these data to the FDA for review. Subsequently, the FDA concurred with our proposal to use high-intensity atorvastatin 40 [mg and] 80 mg in our phase 3 program, which is ongoing now,” McGowan said. “We have four large clinical trials ongoing now for LDL reduction. One is completely enrolled, 2,230 patients, and we have a large [CV] outcome trial ongoing in patients at high CV risk, including those with statin intolerance.” – by Darlene Dobkowski

Reference:

McGowan M, et al. Late Breakers. Presented at: National Lipid Association Scientific Sessions; May 18-21, 2017; Philadelphia.

Statins Increase Diabetes Risk by up to 50% in Older Women

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Statin therapy increases the risk of new-onset diabetes in elderly women by 33%, and the higher the dose, the greater the risk, a new analysis of the observational Australian Longitudinal Study on Women’s Health shows.

“Clearly, statins have beneficial effects, including a reduction in the risk of cardiovascular events; however, the dose-response effect we observed suggests that it may be wise to avoid using higher doses of statins in older women,” lead author Mark Jones, MD, senior lecturer, school of public health, the University of Queensland, Brisbane, Queensland, told Medscape Medical Newsin an email.

 “GPs and their elderly female patients should be aware of the risks,” Dr Jones added in a University of Queensland statement, noting that those elderly women taking statins “should be carefully and regularly monitored for increased blood glucose to ensure early detection and management of diabetes.”

And, he and his colleagues suggest, it may be the case that statins could be stopped altogether in some elderly women.

Women Take Statins on Average, for 6.5 Years

The new analysis included 8372 Australian women aged between 76 and 82 years at baseline who were followed for 10 years; it ispublished in the March issue of Drugs and Aging.

Dr Jones and colleagues note that the majority of participants in statin trials have been males and that females, especially elderly ones, have been underrepresented.

 “Our group has expertise and experience in women’s health, including being involved with the Australian Longitudinal Study on Women’s Health for the past 20 years, and we focused on the older cohort of women [in this study] because we thought this is a population that has generally not been included in clinical trials,” Dr Jones explained to Medscape Medical News.

Previous studies have also shown an association between use and onset of diabetes, he and his colleagues add, and while often the benefits of statins are said to outweigh the risk of diabetes, this depends on the indication for statins in the first place. For example, statin use in primary prevention of cardiovascular disease remains controversial, they say.

The primary outcome of their analysis, new-onset diabetes, was based on a new prescription for insulin, insulin analogues, or other glucose-lowering agents. And statin exposure was determined based on prescriptions dispensed between July 1, 2002 and August 31, 2013.

 “We found that almost 50% [49%] of women in their late seventies and eighties in the study took statins, and 5% were diagnosed with new-onset diabetes,” Dr Jones noted.

The mean interval for which women took a statin was 6.5 years.

While women could have taken different statins at different doses over the 10-year follow-up interval, the greatest proportion of participants received atorvastatin followed by simvastatin, the researchers explain.

And when there was a change in the dose of a statin, it tended to be toward a higher dose over time.

Risk of Diabetes Ranged From 17% to 51%

The risk of new-onset diabetes went from a low of 17% with the lowest doses of a statin to a high of 51% for those taking the highest doses.

 At an adjusted hazard ratio (HR) of 1.33% for the overall cohort, this risk translates into a number-needed-to-harm of 131 patients for every 5 years of treatment with a statin.

New-Onset Diabetes by Statin Dose*

Statin dose Hazard ratio P
Low dose 1.17 0.35
Mid dose 1.26 0.077
High dose 1.46 0.005
Very high dose 1.51 0.004
*Compared with no statin use

“What’s most concerning was that we found a ‘dose effect,’ where the risk of diabetes increased as the dosage of statins increased, [and] over the 10 years of the study, most of the women progressed to higher doses of statins,” Dr Jones observed.

 He and his colleagues therefore recommend that ongoing risk assessment is “critical” to ensure optimal health outcomes and quality of life in older women.

Deprescribe Statins in Older Women

The results suggest “elderly women should not be exposed to higher doses of statins,” they add.

Indeed, in some cases, it may be wiser to stop statins altogether in this patient group, they note, adding that, in their study, around one-third of users didn’t fill a prescription for statins in the last 6 months prior to death or end of follow-up.

 “The women in our study would have been aged 86 to 92 at the end of follow-up and, depending upon reason for initial prescribing—primary or secondary prevention—serious consideration could perhaps now be recommended for statin deprescribing in women of this age,” they conclude.
Source: medscape.com

Statin therapy reduces MACE, mortality in asymptomatic PAD

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Patients with a low ankle-brachial index, but without clinically recognized CVD, may experience lower major adverse CV events and mortality rates while on statin therapy, according to study findings published in the Journal of the American College of Cardiology.

Rafel Ramos, MD, PhD, of the Jordi Gol Institute for Primary Care Research in Girona, Spain, and researchers categorized 5,480 patients from the Catalan primary care system’s clinical database into two groups: statins nonusers or new users (first prescription or re-prescribed after at least 6 months). All of the patients had an ankle-brachial index of 0.95 or lower and no diagnosis of CVD. The patients’ mean age was 67 years and 44% were women. Diabetes and hypertension were prevalent diagnoses in this population. The median follow-up was 3.6 years.

The primary outcomes were all-cause mortality and MACE, which includedMI, cardiac revascularization and ischemic stroke. Angina and CHD were secondary outcomes.

The incidence of MACE was 19.7 events/1,000 person-years in new statin users and 24.7 events/1,000 person-years in nonusers. The rate of all-cause mortality was 24.8 in new users and 30.3 in nonusers. The HRs for MACE decreased by 20% and all-cause mortality by 19%.

According to the researchers, up to 85% of patients with asymptomatic peripheral artery disease could be identified with ankle-brachial screening. This suggests that an ankle-brachial index of 0.95 or lower may be useful in identifying good candidates for statin therapy, regardless of the lack of other risk factors, they wrote.

“Recent American College of Cardiology/American Heart Association guidelines on the treatment of blood cholesterol to reduce atherosclerotic [CV] risk in adults suggest that [ankle-brachial index] can be assessed as an additional factor to support statin therapy in patients at low 10-year [CHD] risk and with moderate LDL cholesterol blood level,” the researchers wrote.

Due to the observational design of the study, there may not be enough evidence to establish clinical recommendations, but the researchers called for randomized controlled trials to evaluate this further.

In a related editorial, Mary McGrae McDermott, MD, from Northwestern University Feinberg School of Medicine, andMichael H. Criqui, MD, MPH, from the University of California, San Diego School of Medicine, noted that “the AHA/ACC guidelines on cholesterol treatment already suggest that people with PAD should be treated with cholesterol-lowering therapy. This recommendation is not limited to people who have symptoms.”

“Widespread [ankle-brachial index] screening could be potentially useful if it identified a large number of individuals with a low [ankle-brachial index] who would otherwise not qualify for cholesterol-lowering therapy,” McDermott and Criqui wrote. “However, the results reported by Ramos et al suggest that most patients in their study qualified for statin therapy even before the [ankle-brachial index] measurement.”

Instead, McDermott and Criqui suggested the focus should be on patients with a low ankle-brachial index, but no other indications for statins. They wrote, however, that because this would be a small population, there was no justification for universal ankle-brachial index screening. – by Tracey Romero

Coronary CT Angiography Can Track Regression of Noncalcified Plaques by Statin Therapy

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Moderate and intensive statin treatment can retard or even bring about regression of noncalcified coronary plaque as shown by coronary CT angiography (CCTA), according to new research from China[1].

“Clinicians should know the potential usage of CT scans for high-risk patients, and if noncalcified plaques are found, strengthened statin therapy should be considered,” lead author Dr Bin Lu (Fuwai Hospital, Beijing) told heartwire from Medscape by email. “If clinicians know patients have positive coronary noncalcified plaques based on CT images, they should recommend to their patients to take statins regularly and follow up the disease after 1 or 2 years.”

Extensive clinical trial evidence points to serial coronary intravascular ultrasound (IVUS) as an imaging method to show that statin therapy can stop progression of coronary plaque or induce regression, but IVUS is invasive and unsuitable for nonischemic patients. However, CCTA has emerged as an imaging tool that can accurately and noninvasively measure luminal narrowing and characterize coronary plaques, according to the researchers.

They conducted a prospective multicenter observational study involving 206 consecutive patients with mild noncalcified plaque and undergoing CCTA.

The results were published online July 13, 2016 in the American Heart Journal.

The researchers divided patients into three groups: intensive statin therapy (n=55), moderate statin therapy (n=85), or no statin therapy (n=66). Patients in the intensive group took 20 to 40 mg/d atorvastatin or 10 to 20 mg/d rosuvastatin. Patients in the moderate group took 10 to 20 mg/d atorvastatin, 5 to 10 mg/d rosuvastatin, 20 to 40 mg/d fluvastatin, or 10 to 20 mg/d simvastatin.

The researchers performed serial scans after a median interval of 18 months to measure low-attenuation plaque (LAP) volume, total plaque volume, and percent plaque volume.
Patients in the intensive group experienced significantly improved lipid profiles during follow-up: total cholesterol, LDL-C, and triglycerides significantly decreased (P<0.001 all), while HDL-C increased nonsignificantly. Patients in the moderate-therapy group also experienced decreases in total cholesterol, LDL-C, and triglycerides (P<0.05), while HDL-C slightly increased.

Patients in the no-treatment group experienced no lipid-profile change.

On CCTA, the researchers observed significant regression of LAP volume, total plaque volume, and percent plaque volume in the intensive group compared with the no-treatment group (-7.1 vs. 0.9, -16.4 vs 12.3, -6.2 vs 3.5, respectively, P<0.001 all). They observed retarded progression of LAP, total plaque volume, and percent plaque volume in the moderate-treatment group.

Using a multivariable prediction model, the researchers found that total plaque volume, higher baseline LAP volume, and moderate and intensive therapy each predicted plaque regression (P<0.001, 0.004, and <0.001, respectively).

Based on their study results, they concluded, “This further confirms the feasibility of using serial CCTA to assess changes in plaque characteristics, allowing this method to potentially track atherosclerosis noninvasively.

“After this study, we are now full of confidence to treat our patients who have positive coronary plaques with statins. However, we need to do more about following up the patients for major adverse cardiac events after early detection and treatment of noncalcified coronary artery plaques,” Lu said.

Statin Therapy and Acute Memory Impairment

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TAKE-HOME MESSAGE

  • People taking statins were compared with nonusers of lipid-lowering drugs (LLDs) and users of non-statin LLDs to assess the association between statin use and memory impairment. A strong association was seen between initial statin use and diagnosis of acute memory loss within 30 days when compared with nonusers of LLDs but the association was not seen when comparing statin users with users of non-statin LLDs. However, there was an association seen between use of non-statin LLDs and acute memory loss when compared with controls not taking LLDs.
  • The results show that the use of statins and non-statin LLDs both increased the risk of acute memory loss in 30 days compared with nonuse. These results may indicate that all LLDs cause acute memory loss, or they may reflect detection bias.

This is an elegant epidemiologic analysis that addresses the ongoing concern that statins could potentially contribute to memory loss. Our view is that the conclusions of this provocative study are reassuring, consistent with those of other recent high-quality studies. The results show nothing special about statins, but rather that all lipid-lowering drugs are potentially associated with acute small amounts of memory loss in a small segment of adults. We agree with the authors’ view that the association is best explained by a “detection bias.” Patients who take statins or other lipid-lowering drugs may have more medical contact than others, giving more opportunities to report memory complaints, which can create a signal between lipid-lowering medications and memory even without a causal connection.

Therefore, when clinicians see patients with memory complaints on statin therapy, it is prudent to cast a wide net in line with the advice of the 2013 ACC/AHA guidelines: “evaluate the patient for nonstatin causes, such as exposure to other drugs, as well as for systemic and neuropsychiatric causes, in addition to the possibility of adverse effects associated with statin drug therapy.”

This retrospective study looked at new statin users in comparison with non-users and with users of non-statin lipid-lowering medications. These data from 1987 to 2013 were based on a database gathered by clinicians in the United Kingdom. It appears that patients on lipid-lowering drugs see their doctors more often and may thus report mild memory issues more often. Our group previously published a meta-analysis in theMayo Clinic Proceedings that statins tend to have a modest protective view against long-term memory problems.

High-Sensitivity Cardiac Troponin I and B-Type Natriuretic Peptide as Predictors of Vascular Events in Primary Prevention Impact of Statin Therapy

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Abstract

Background—Cardiac troponin and B-type natriuretic peptide (BNP) concentrations are associated with adverse cardiovascular outcome in primary prevention populations. Whether statin therapy modifies this association is poorly understood.

Methods and Results—We measured high-sensitivity cardiac troponin I (hsTnI) in 12 956 and BNP in 11 076 participants without cardiovascular disease in the Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating Rosuvastatin (JUPITER) trial before randomization to rosuvastatin 20 mg/d or placebo. Nearly 92% of participants had detectable circulating hsTnI, and 2.9% of men and 4.1% of women had levels above proposed sex-specific reference limits of 36 and 15 ng/L, respectively. hsTnI concentrations in the highest tertile were associated with a first major cardiovascular event (adjusted hazard ratio [aHR], 2.19; 95% confidence interval, 1.56–3.06; P for trend <0.001). BNP levels in the highest tertile were also associated a first cardiovascular event (aHR, 1.94; 95% confidence interval, 1.41–2.68; P for trend <0.001). The risk of all-cause mortality was elevated for the highest versus the lowest tertiles of hsTnI (aHR, 2.61; 95% confidence interval, 1.81–3.78; P for trend <0.001) and BNP (aHR, 1.45; 95% confidence interval, 1.03–2.04; P for trend 0.02). Rosuvastatin was equally effective in preventing a first cardiovascular event across categories of hsTnI (aHR range, 0.50–0.60) and BNP (aHR range, 0.42–0.67) with no statistically significant evidence of interaction (P for interaction=0.53 and 0.20, respectively).

Conclusions—In a contemporary primary prevention population, baseline cardiac troponin I and BNP were associated with the risk of vascular events and all-cause mortality. The benefits of rosuvastatin were substantial and consistent regardless of baseline hsTnI or BNP concentrations.

Cholesterol Guidelines May Underestimate Cardiovascular Risk in HIV-Infected Patients – See more at: http://www.jwatch.org/na35651/2014/09/09/cholesterol-guidelines-may-underestimate-cardiovascular#sthash.fanWUptz.dpuf

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Although new guidelines recommend statin use in more HIV-infected patients, most of those with evidence of coronary plaque are still not flagged as needing therapy.

 Cholesterol guidelines released in 2013 recommend statin therapy for, among others, patients aged 40 to 75 with a 10-year atherosclerotic cardiovascular disease (CVD) risk ≥7.5%, as estimated by a new calculator. Whether this recent guideline, which was designed for the general population, is better than the 2004 Adult Treatment Panel III guidelines at predicting CVD — or at appropriately recommending statin use — in HIV-infected patients is not known. Now, investigators have examined the performance of the new and old guidelines in a cohort of HIV-infected patients.

A total of 108 patients without known CVD underwent coronary computed-tomography angiography (CCTA). The median age was 46 years, 50% were current smokers, and 20% were receiving antihypertensive medications. Despite the relatively low overall 10-year atherosclerotic CVD risk score (3.3%), 36% of participants had high-risk–morphology plaque detected on angiography. When the new and old guidelines were applied, several striking findings emerged:

  • In the overall study population, statins would be recommended for 21% by the 2013 guidelines versus 8% by the 2004 guidelines.

  • Among patients with high-risk–morphology coronary plaque, statins would be recommended for 26% by the 2013 guidelines and 10% by the 2004 guidelines.

  • Among patients without coronary plaque, statins would be recommended for 15% by the 2013 guidelines versus 5% by the 2004 guidelines.

COMMENT

The main limitation of this study is that detection of high-risk–morphology plaque on CCTA is not yet known to be predictive of CVD risk — or statin benefit — in HIV-infected patients. Nevertheless, the finding that 74% of HIV-infected patients with high-risk–morphology plaque would not qualify for statins even by the more-encompassing 2013 guidelines is alarming. Would HIV-infected patients who do not meet current guidelines benefit from statin use? A randomized clinical trial to address this question is in the offing.

– See more at: http://www.jwatch.org/na35651/2014/09/09/cholesterol-guidelines-may-underestimate-cardiovascular#sthash.fanWUptz.dpuf

Statin therapy for the prevention of atrial fibrillation: a meta-analysis of randomized controlled trials.

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OBJECTIVES: To assess the efficacy of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) for primary and secondary prevention of atrial fibrillation, and to evaluate the efficacy of individual statins and their dosages.
DESIGN: Meta-analysis of 20 randomized controlled trials. PATIENTS: A total of 32,311 patients who received either a statin (16,203 patients) or a placebo or active control regimen (16,108 patients) for either primary or secondary prevention of atrial fibrillation as part of a research study. MEASUREMENTS AND
MAIN RESULTS: A systemic literature search of MEDLINE, EMBASE, and the Cochrane Controlled Trials Register was performed to identify randomized controlled trials involving the prevention of atrial fibrillation with statin therapy. Effect size was expressed as odds ratio (OR) with 95% confidence interval (CI). Subgroup analysis was performed to explore the reasons for heterogeneity. Of the 20 trials, atorvastatin was studied in 11, pravastatin in five, rosuvastatin in three, and simvastatin in one. Overall, among the 32,311 patients in these trials, the risk of atrial fibrillation was significantly reduced by statins (OR 0.59, 95% CI 0.45-0.76), and the drugs were effective for both primary prevention (OR 0.67, 95% CI 0.51-0.88) and secondary prevention (OR 0.40, 95% CI 0.20-0.83). Secondary prevention was not superior to primary prevention, however. A significant benefit was observed in the atorvastatin-treated subgroup (OR 0.43, 95% CI 0.27-0.66), especially in the dose range of 10-40 mg/day (OR 0.29, 95% CI 0.19-0.45). No protective effect was observed in the pravastatin subgroup (OR 1.03, 95% CI 0.77-1.37).
CONCLUSION: This meta-analysis suggests that statin therapy is useful for the prevention of atrial fibrillation. The benefit of statins in secondary prevention was significant but not superior to primary prevention. Atorvastatin was more effective than pravastatin, and its effects were dose related, with lower doses being more effective. The number of trials focusing on individual drugs is still insufficient, and more randomized controlled trials are necessary to further support these conclusions.

Source: Pharmacotherapy.