Coenzyme Q10 (CoQ10) and Heart Health: Statins, Heart Failure, and the Evidence

Medical Disclaimer: This content is for educational purposes only and does not constitute medical advice, diagnosis, or treatment. Information is based on current medical literature and clinical guidelines but may not apply to your specific situation. Individual responses vary based on personal medical history and concurrent conditions. Always consult qualified healthcare providers for medical decisions. Never delay seeking medical care based on content you’ve read. If experiencing a medical emergency, seek immediate medical attention.

These articles provide education to enhance your healthcare partnership. All treatment decisions should involve your healthcare team. Use this knowledge to have informed discussions, not to replace medical care.

In brief: Coenzyme Q10 is the cardiovascular supplement with the most convincing biology and the least settled clinical case: it is essential to the cell’s energy production, and statins measurably lower its blood levels. One trial in serious heart failure (Q-SYMBIO) found fewer cardiovascular events and deaths, but no large trial has confirmed it in the decade-plus since, and the evidence that CoQ10 relieves statin-related muscle pain is inconsistent. For two narrow situations — moderate-to-severe heart failure already on full guideline therapy, and statin muscle symptoms severe enough to threaten stopping the statin — CoQ10 is a reasonable conversation to have with a clinician. For nearly everyone else taking it, including healthy adults and people using it for energy, aging, or general “heart support,” the evidence does not support it. The body makes its own CoQ10, and for most people, taking more has not been shown to prevent anything or make them feel better.

When CoQ10 Is Worth Considering

This is a long article because the topic is complicated, but the practical answer is short, so here it is first.

For most people, the evidence does not support taking CoQ10. Healthy adults make adequate amounts on their own. Statin users have measurably lower blood levels, but for most of them that drop has not been shown to cause any harm. And people who take CoQ10 for energy, aging, or “mitochondrial support” are buying a claim the research does not back up.

For two specific situations, it is reasonable to raise with a physician. The first is moderate-to-severe heart failure with a weakened heart (reduced ejection fraction) already on full guideline-directed therapy — considered as an add-on, never a replacement for proven treatments, and resting on a single unconfirmed trial. The second is statin muscle symptoms severe enough to threaten stopping a statin, after the usual causes have been checked — as a short, defined trial with clear criteria for whether it helped. Both are clinical conversations, not self-treatment decisions.

For everyone else, the evidence isn’t there. The rest of this article shows why those answers differ, and what each one is based on.

Find Your Situation

The table sums up what the research supports for different situations; each one is explained, with sources, in the sections below. It is a discussion aid, not direction for your care.

The Biology, and Its Limits

Coenzyme Q10 sits in the inner membrane of the mitochondria, shuttling electrons along the chain of protein complexes that cells use to make ATP, the molecule that powers nearly everything a cell does. (7) Heart muscle, contracting roughly 100,000 times a day without rest, is unusually dependent on that process, and concentrations of CoQ10 in heart tissue are among the highest of any organ. (7)

CoQ10 is not a vitamin. The body synthesizes it, and dietary deficiency is rare in otherwise healthy people; intake from food is not normally the limiting factor. Tissue levels do fall with age (10), and circulating levels are measurably reduced by statin therapy — the pathway covered in the next section.

Two facts complicate the leap from this biology to a reason to supplement. First, low CoQ10 in heart failure may be a result of the disease rather than a cause of it. Levels fall as heart failure gets worse, but something that drops alongside a disease is not necessarily driving it — the same “the marker is not the cause” trap that Article 3 traces through homocysteine, vitamin E, and other plausible targets that moved a number without changing outcomes. Second, no one has defined how low is too low in a statin user. Because there is no agreed point at which a low level actually causes a problem, the reasoning “your level dropped, so take more” assumes the very thing it would need to prove. Strong biology, on its own, does not show that a treatment works.

The Statin Depletion Pathway

Statins work by blocking HMG-CoA reductase, the enzyme that controls cholesterol production. That same enzyme sits upstream of a branch point that also feeds CoQ10 synthesis, so reducing one reduces the other. (5) This is not a side effect in the usual sense; it is a direct biochemical consequence of how the drugs work, and the blood-level effect is well documented. In a double-blind, placebo-controlled study, plasma CoQ10 fell by about 40% after a month of statin therapy. (5) Across studies the size of the drop varies with statin and dose, but the direction is consistent. (8)

What happens in muscle is far less settled, and this is where the depletion argument tends to overreach. Biopsy findings are genuinely mixed: some studies report modest reductions in intramuscular CoQ10, others find no clear change, and the single most-cited biopsy study of statin-myopathy patients found only a mild decrease — one that, in its authors’ words, did not produce histochemical or biochemical evidence of mitochondrial myopathy in most patients. (9)

That disconnect matters. A blood level does not reliably reflect what is happening inside cells: a person can have a reduced level in the blood while the cell’s energy machinery works fine. (8) The blood number is the easiest thing to measure and the thing supplements most reliably move, but it is the least informative about whether muscle or heart tissue is actually short of CoQ10. That is a big reason the depletion idea has been so hard to turn into a real treatment — the test that’s easy to run is not the one that tells you whether the tissue needs more.

Statins Lower CoQ10 but Still Protect the Heart

One fact should frame the whole depletion argument: statins lower CoQ10 and are, at the same time, among the most protective heart drugs in existence. The Cholesterol Treatment Trialists’ Collaboration pooled individual data from more than 170,000 patients across 26 randomized trials and found that lowering LDL cholesterol with statins reduces major vascular events by roughly a fifth for each 1 mmol/L of LDL reduction, consistently and across a wide range of patients. (19) If the CoQ10 drop did real harm to most people on statins, that benefit would not look the way it does.

Lowering CoQ10 in the blood is not the same as causing real trouble in the cell’s energy machinery. For the large majority of statin users, the LDL-lowering and anti-inflammatory benefits clearly outweigh any effect of the CoQ10 drop. It may matter more in a narrower group — people with a pre-existing mitochondrial disease, established heart failure, or genetic differences in how they handle CoQ10, where the margin is thinner — but for most people, supplementing CoQ10 is an attempt to correct a lab change that has not been shown to cause any harm. The number on the report moved. The disease did not.

The Clinical Evidence

Most supplement stories end at biological plausibility. CoQ10 is unusual because outcome data exist: at least one randomized trial measured hard endpoints — deaths and hospitalizations, not just biomarkers. That is a higher standard of evidence, even where it remains too thin to support general use. Placed side by side, the trials stop looking contradictory and start telling a clear story.

Two patterns stand out. The heart-failure evidence rests almost entirely on a single trial. And the statin-muscle trials, run in similar patients at overlapping doses, contradict one another — the signature of an inconsistent or absent effect rather than a real one.

Heart Failure: Q-SYMBIO and Its Limits

Q-SYMBIO enrolled 420 patients with moderate-to-severe heart failure (NYHA Class III–IV, meaning marked symptoms with ordinary activity or at rest) and reduced ejection fraction, all already on optimal medical therapy. They received CoQ10 100 mg three times daily (300 mg total) or placebo for two years. (1)

In absolute terms, the primary endpoint was about 11 percentage points lower over two years — a number needed to treat near 9. That magnitude reflects both the relative reduction and a high baseline event rate; in a sicker population the absolute benefit looks larger, which is part of why the result does not extend to healthier people.

Q-SYMBIO did several things well: it measured clinical endpoints rather than surrogates, ran for an appropriate two years, standardized background therapy, and used a specific, documented solubilized ubiquinone formulation. What it cannot do is stand alone. It is a single trial of 420 patients, part-funded by the company that makes the formulation, and in the more than ten years since publication no large independent trial has confirmed it. In modern cardiology a single positive trial, however striking, rarely changes the standard of care by itself — and if a supplement truly cut heart-failure mortality by this much, confirmatory trials would have followed and reshaped the guidelines. They have not. The absence of replication after a decade is as much a part of the evidence as the original result.

This is the same shape as the omega-3 story in Article 4, with a telling difference. Both rest on a single trial in a defined population. But icosapent ethyl’s REDUCE-IT led to FDA drug approval and a place in guideline therapy despite its own controversy; CoQ10’s Q-SYMBIO has produced neither. Both show that a single trial in a specific population carries real weight. Neither extends to the broad consumer market that drives most actual buying. (One contributing reason confirmation has been slow: large outcome trials are expensive and harder to fund for a non-patentable compound. That does not invalidate Q-SYMBIO, but it helps explain why a promising signal has stayed unconfirmed.)

The two supporting pieces of heart-failure evidence are weaker than they first appear. KiSel-10 gave elderly Swedes CoQ10 plus selenium for four years and reported 54% lower cardiovascular mortality (2) — but the two supplements cannot be separated, so the result cannot be attributed to CoQ10 alone, and the population was general elderly people, not heart-failure patients. The 2021 Cochrane review concluded that CoQ10 “probably reduces” all-cause mortality and heart-failure hospitalization on moderate-quality evidence, while stating there is no convincing evidence to support or refute its use. (3) The crucial detail is that the review’s mortality estimate is driven by a single study of 420 participants — Q-SYMBIO itself. The meta-analysis is not independent confirmation; it is largely the same trial, restated.

One more limit on scope: the evidence, such as it is, sits in heart failure with reduced ejection fraction. Heart failure is not one disease, and extending a reduced-EF finding to heart failure with preserved ejection fraction — where the heart pumps normally but fills poorly — is not supported by current data.

CoQ10 for Statin Muscle Symptoms

Muscle symptoms are the most common reason people stop statins, and CoQ10 is the most popular remedy for them. It is also the wrong first move. The standard approach a clinician would work through first is to confirm the statin is actually the cause — checking the timing of symptoms against starting the drug, measuring creatine kinase if indicated, and ruling out other causes such as thyroid disease, vitamin D deficiency, or drug interactions — and then to preserve LDL-lowering therapy where possible by trying a different statin or a lower dose. CoQ10 sits downstream of all of that, not ahead of it.

The trial evidence for it is genuinely inconsistent. A 2015 meta-analysis (six trials, 302 patients) found no statistically significant effect of CoQ10 on statin-associated muscle pain — a trend toward improvement that did not reach significance — and no significant effect on creatine kinase. (4) The individual trials in the table above show the same picture directly: similar patients, overlapping doses, opposite conclusions. Some later analyses find a benefit in a subset of trials; others find none. When results scatter like this across comparable studies, the honest reading is that any real effect is small, unreliable, or confined to a subgroup no one has yet defined.

Two features of statin muscle symptoms explain much of the scatter. The first is the placebo and nocebo response, which is unusually large here. In the best-designed trial, patients with a history of statin myalgia took simvastatin and placebo in blinded fashion before any CoQ10 was tested — and only about a third reproduced their muscle pain on the statin but not the placebo. (13) Two-thirds of people who believed a statin caused their muscle pain did not have pain that tracked with the actual drug under blinding. When CoQ10 was then tested in the confirmed group at 600 mg/day, it produced no benefit over placebo. (13) The second feature is that “statin myopathy” is not a single mechanism, so trials are not all studying the same thing.

The practical conclusion is narrow. Most people with statin-associated muscle symptoms will not improve meaningfully with CoQ10. Its only defensible role is a low-risk, time-limited trial in someone whose statin — a drug with strong outcome evidence — would otherwise be stopped. Any effect, if it comes, is assessed over months, not days, and symptoms that fluctuate naturally are easy to misattribute to whatever was started most recently. If there is no clear, reproducible improvement after a structured two-to-three-month trial with a quality formulation, continued use is hard to justify. And severe muscle weakness, dark urine, or a markedly elevated CK call for prompt medical evaluation, not a supplement trial.

Most CoQ10 Is Poorly Absorbed

Even where CoQ10 has evidence, a second problem sits between the label and the bloodstream: most CoQ10 is poorly absorbed. This is the product question Article 2 covers — a compound can have genuine clinical evidence and still reach a patient in a form that does not deliver it.

CoQ10 is a large (about 863 daltons), highly fat-soluble molecule that barely dissolves in water, and standard crystalline powder is absorbed at only a few percent. (6) Absorption also varies enormously between people — by several-fold for the same capsule — so one person can reach a useful blood level while another taking the identical product gains almost nothing. (6) The molecule is also chemically unstable when exposed to heat, light, and air, which is one more reason an old or poorly stored product may not contain what its label claims.

Q-SYMBIO used a specific solubilized ubiquinone with documented absorption. Whether its result carries over to other formulations is genuinely unknown — which is part of why “any CoQ10 will do” is not a safe assumption. But the bigger point is that absorption only matters where a benefit has actually been shown. A better-absorbed product can help in a situation where there is already evidence behind it. It cannot turn general wellness use into a proven treatment: the problem there is not absorption, it is that no study has shown CoQ10 helps that person in the first place. Practically, CoQ10 is absorbed better with a fat-containing meal and in divided doses, and oil-based softgels generally beat dry-powder capsules.

Where Guidelines Stand

No major medical society recommends CoQ10 for any cardiovascular indication. The 2022 AHA/ACC/HFSA heart-failure guideline builds reduced-EF treatment on four foundational drug classes — an ARNI (or ACE inhibitor or ARB), a beta-blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor, with diuretics and devices as needed — and CoQ10 is not among them. (18) Major statin-management guidance does not recommend CoQ10 for muscle symptoms, and the FDA has not approved it for any cardiovascular use. There is no CoQ10 equivalent of the authorized health claim that exists for plant sterols (Article 6) or soluble fiber (Article 7).

This is not a special verdict against CoQ10. Medical societies generally do not issue indications for supplements, because supplements are not approved drugs and most lack evidence meeting guideline thresholds — the structural reality for nearly every product in this series. The two situations where this article describes a defensible reason to discuss CoQ10 are clinical conversations, not guideline-endorsed indications: they are simply where the closest thing to supporting evidence exists. “Worth a conversation” is not “indicated,” and for most people CoQ10 has cleared neither bar.

Safety and Interactions

CoQ10’s safety profile is favorable, which is not the same as clinically irrelevant. Reported side effects are generally mild — most often digestive upset (nausea, diarrhea, appetite changes) and occasional insomnia at higher doses or with late-day dosing — and are uncommon in trials. Authoritative liver-toxicity reviews do not identify CoQ10 as a likely cause of clinically apparent liver injury. (17)

The one interaction that meaningfully affects medical management is with warfarin. CoQ10’s structure resembles vitamin K, and because warfarin works by interfering with vitamin K–dependent clotting factors, anything vitamin K–like can in theory blunt its effect. Case reports describe reduced anticoagulant response after starting CoQ10; controlled data are mixed, but the signal is real enough to act on. (15) For someone on warfarin, the sound practice is to disclose CoQ10 use and check the INR after starting, stopping, changing the dose, or switching formulations.

The broader message is not that CoQ10 is dangerous. It is that any biologically active compound is worth disclosing to the clinicians managing your care — before procedures, oncology treatment, anticoagulation, or a medication review — because an undisclosed supplement can complicate decisions that have nothing to do with whether it works.

Two Example Patients

The clearest way to see how one supplement produces opposite answers is to put two situations side by side. Both are composites built from the populations actually studied, not real patients.

Patient A is a 64-year-old woman with NYHA Class III heart failure and reduced ejection fraction, on full guideline-directed therapy — an ARNI, a beta-blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor — under a cardiologist’s care, and still symptomatic with ordinary activity. She asks whether CoQ10 might help. She matches the Q-SYMBIO profile closely, so the evidence supports a real conversation about CoQ10 as an add-on (1) — with honest expectations: one unconfirmed trial of 420 patients, a specific solubilized formulation, a 300 mg/day dose, and a few months before any effect could be judged. CoQ10 would sit alongside her four proven therapies, never in place of any of them.

Patient B is a 58-year-old man with no cardiovascular disease, no statin, normal labs, who exercises regularly and has taken 200 mg/day of CoQ10 for three years because a podcast called it essential for “mitochondrial energy.” He matches no group in which CoQ10 has been shown to reduce heart problems. His body makes enough, he has no shortage, and he has no condition it has been shown to help. The cost — often several hundred dollars a year for a quality product — buys an effect in the body with no proven benefit for someone like him, and that money would do more good spent on things with stronger evidence.

If You Decide to Try CoQ10

For the two situations where CoQ10 is defensible, the decision is not “take it” but “take it with criteria for deciding whether it worked.” A trial worth running has the same parts in either case. It starts from a specific clinical question — in heart failure, an add-on to optimal therapy under a cardiologist; in statin muscle symptoms, preserving an LDL-lowering drug that would otherwise be stopped. It uses a documented, well-absorbed formulation (solubilized ubiquinone, taken with a fat-containing meal in divided doses), because the product question from Article 2 applies directly here. It runs long enough to judge — at least two to three months. It sets stop criteria in advance: in heart failure, by the cardiologist’s assessment; in muscle symptoms, discontinuation if there is no clear, reproducible improvement by three months. And it is disclosed on the medication list, especially alongside warfarin, insulin, oncology therapy, or an upcoming procedure.

Common Misconceptions

“Statins damage my mitochondria, so I need CoQ10 to repair them.” Statins reduce CoQ10 synthesis through a shared metabolic branch point; that is not the same as damaging mitochondria. If statin-driven CoQ10 changes caused widespread mitochondrial harm, statins would not deliver the consistent protection seen across more than 170,000 patients in the Cholesterol Treatment Trialists’ meta-analysis. (19) They do.

“My CoQ10 blood level is low, so my heart muscle must be deficient.” Plasma CoQ10 does not reliably reflect intracellular or mitochondrial levels. (8) A low blood level in a statin user does not establish that heart or muscle tissue is functionally short of it, and there is no threshold at which a low plasma level predicts benefit from supplementing.

“CoQ10 gives you more energy.” No randomized trial shows improved energy, reduced fatigue, or better exercise performance in healthy adults. The pathway CoQ10 supports runs efficiently under normal conditions; the energy claim is marketing ahead of evidence.

“Any CoQ10 supplement is the same.” Formulation determines how much reaches the blood. (6) The trial with the strongest result used a specific solubilized ubiquinone, and standard crystalline products may deliver far less — so two capsules with identical labels can behave very differently.

“I felt better after starting it, so it works.” Symptoms fluctuate, placebo responses in pain and fatigue are large, and CoQ10 is often started alongside other changes — so improvement is easy to credit to the wrong thing. (13)

Practical Considerations

If, after a clinician conversation, CoQ10 is being tried for one of the two situations with evidence, a few specifics follow from the trials themselves. The doses and durations below come from the supporting studies; this is reference information, not a prescription.

For product selection, the markers worth looking for are independent third-party testing (USP, NSF, or equivalent), the specific form named on the label, an enhanced-delivery formulation with absorption data, and oil-based softgels over dry powder. A product that does not disclose its form or delivery method cannot be matched against what was studied. As Article 2 covers, certification verifies what is in the bottle, not whether what is in the bottle has cardiovascular outcome evidence behind it.

The cost is not trivial. Quality CoQ10 at therapeutic doses typically runs from tens to over a hundred dollars a month. For many households, that annual spend competes with things of clearer cardiovascular value — a blood-pressure cuff, better food, medication copays, cardiac rehabilitation, or follow-up visits — and the comparison is worth making explicitly when deciding where limited resources go.

The Bottom Line

CoQ10 has more behind it than most supplements in this series. The statin-depletion mechanism is real biochemistry, and Q-SYMBIO measured hard endpoints — fewer events and deaths — rather than biomarkers. (1) That puts it ahead of most of what is on the supplement shelf.

It is still not established therapy for most people. Q-SYMBIO is a single 420-patient trial, part-funded by the formulation’s maker, unconfirmed after more than a decade. (1) The statin-muscle evidence is inconsistent, the placebo and nocebo response in muscle-pain studies is large (4,13), and poor, variable absorption means the product many people take may not resemble what was studied. (6) Across the literature, scattered and negative results outweigh isolated positive ones — which is why CoQ10 has not become standard care.

Most people take CoQ10 to fix something that, for them, isn’t actually broken. The most likely harm isn’t a side effect; it’s wasted money and false reassurance — spending on a supplement that, for them, isn’t fixing anything. The supportable answer is narrow: for moderate-to-severe heart failure on optimal therapy, and for statin muscle symptoms threatening a statin that works, it is worth a conversation with a physician. For nearly everyone else, the body already makes what it needs, and the evidence does not support buying more.

Article 6 covers plant sterols and stanols — one of the few supplement categories with consistent LDL-lowering data and an authorized health claim, and why even reliable LDL reduction does not automatically deliver the event reduction that statins do.

Key Terms

Bioavailability. The fraction of an ingested substance that reaches the bloodstream. Standard CoQ10 is poorly absorbed, which makes formulation a clinical issue rather than a marketing one.

Coenzyme Q10 (CoQ10). A compound essential to mitochondrial energy production, made by the body. Levels fall with age and with statin therapy. Not a dietary essential the way vitamins are.

Creatine kinase (CK). A muscle enzyme that rises in the blood when muscle is injured; used to evaluate suspected statin-related muscle damage.

HFpEF (heart failure with preserved ejection fraction). Heart failure in which pumping is maintained but the heart is too stiff to fill properly. CoQ10 evidence here is lacking.

HFrEF (heart failure with reduced ejection fraction). Heart failure in which the heart muscle is weakened and pumps less effectively — the Q-SYMBIO population.

HMG-CoA reductase. The enzyme statins block to lower cholesterol; it also feeds CoQ10 synthesis, which is why statins lower CoQ10 as a direct consequence of how they work.

INR (international normalized ratio). The standardized lab value used to track warfarin dosing. Starting CoQ10 in a warfarin patient warrants an INR recheck because of a possible interaction.

NYHA class. The New York Heart Association scale for heart-failure severity. Class III–IV means marked limitation with ordinary activity, or symptoms at rest — the Q-SYMBIO range.

Statin muscle symptoms. Muscle pain, weakness, or cramping associated with statins, and the most common reason people stop them. Often attributed to muscle CoQ10 depletion, though the mechanism is debated and much of the symptom burden does not reproduce under blinding.

Ubiquinol / ubiquinone. The reduced (active) and oxidized forms of CoQ10. Most trials, including Q-SYMBIO, used ubiquinone; absorption depends heavily on formulation, and claims of ubiquinol superiority are not consistently borne out head-to-head.

References

1. Mortensen SA, Rosenfeldt F, Kumar A, et al; Q-SYMBIO Study Investigators. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. 2014;2(6):641–649.
2. Alehagen U, Johansson P, Björnstedt M, Rosén A, Dahlström U. Cardiovascular mortality and N-terminal-proBNP reduced after combined selenium and coenzyme Q10 supplementation: a 5-year prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens. Int J Cardiol. 2013;167(5):1860–1866.
3. Al Saadi T, Assaf Y, Farwati M, et al; Madmani ME. Coenzyme Q10 for heart failure. Cochrane Database Syst Rev. 2021;2:CD008684.
4. Banach M, Serban C, Sahebkar A, et al; Lipid and Blood Pressure Meta-analysis Collaboration Group. Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials. Mayo Clin Proc. 2015;90(1):24–34.
5. Ghirlanda G, Oradei A, Manto A, et al. Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study. J Clin Pharmacol. 1993;33(3):226–229.
6. Bhagavan HN, Chopra RK. Coenzyme Q10: absorption, tissue uptake, metabolism and pharmacokinetics. Free Radic Res. 2006;40(5):445–453.
7. Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr. 2001;20(6):591–598.
8. Littarru GP, Langsjoen P. Coenzyme Q10 and statins: biochemical and clinical implications. Mitochondrion. 2007;7(Suppl):S168–S174.
9. Lamperti C, Naini AB, Lucchini V, et al. Muscle coenzyme Q10 level in statin-related myopathy. Arch Neurol. 2005;62(11):1709–1712.
10. Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids. 1989;24(7):579–584.
11. Caso G, Kelly P, McNurlan MA, Lawson WE. Effect of coenzyme Q10 on myopathic symptoms in patients treated with statins. Am J Cardiol. 2007;99(10):1409–1412.
12. Young JM, Florkowski CM, Molyneux SL, et al. Effect of coenzyme Q10 supplementation on simvastatin-induced myalgia. Am J Cardiol. 2007;100(9):1400–1403.
13. Taylor BA, Lorson L, White CM, Thompson PD. A randomized trial of coenzyme Q10 in patients with confirmed statin myopathy. Atherosclerosis. 2015;238(2):329–335.
14. Skarlovnik A, Janić M, Lunder M, Turk M, Šabovič M. Coenzyme Q10 supplementation decreases statin-related mild-to-moderate muscle symptoms: a randomized clinical study. Med Sci Monit. 2014;20:2183–2188.
15. Heck AM, DeWitt BA, Lukes AL. Potential interactions between alternative therapies and warfarin. Am J Health Syst Pharm. 2000;57(13):1221–1227.
16. Langsjoen PH, Langsjoen AM. Comparison study of plasma coenzyme Q10 levels in healthy subjects supplemented with ubiquinol versus ubiquinone. Clin Pharmacol Drug Dev. 2014;3(1):13–17.
17. LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. National Institutes of Health, Bethesda, MD. Coenzyme Q10 entry. https://www.ncbi.nlm.nih.gov/books/NBK548949/
18. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. J Am Coll Cardiol. 2022;79(17):e263–e421.
19. Cholesterol Treatment Trialists’ (CTT) Collaboration; Baigent C, Blackwell L, Emberson J, et al. Efficacy and safety of more intensive lowering of LDL cholesterol: a meta-analysis of data from 170,000 participants in 26 randomised trials. Lancet. 2010;376(9753):1670–1681.

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