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Health Protocols

Heart Failure

Integrative Interventions

Coenzyme Q10

Coenzyme Q10 (CoQ10) has a central role in maintaining proper cardiac function and producing cellular energy in the mitochondria. It is also a potent antioxidant that helps maintain healthy blood sugar levels, preserve cognitive function, and support optimal heart health. CoQ10 is concentrated in healthy heart muscle, and CoQ10 deficiency is associated with heart failure.214,215 In one randomized controlled study, patients with moderate-to-severe heart failure who received 100 mg CoQ10 three times daily in addition to standard treatment showed improved symptoms and reduced risk of major cardiovascular events.11

In another trial that assessed circulating levels of CoQ10 in 257 cardiac patients, those with in-hospital mortalities had significantly lower levels of CoQ10.216 In a recent analysis of 14 randomized controlled trials, which included over 2,000 patients with heart failure, supplementation with CoQ10 resulted in a 31% lower mortality rate and an increased exercise capacity as compared with placebo.217

An examination of seven systematic reviews suggests CoQ10 supplementation is beneficial for heart failure patients,218 while another systematic review of 28 trials found CoQ10 enhanced exercise capacity, improved symptoms, and lowered blood pressure levels in heart failure patients.219 Other research indicates heart failure patients with lower CoQ10 levels have up to a two-fold risk of dying as compared to those with higher CoQ10 levels.220

As shown in several studies conducted by Life Extension Scientific Advisory Board Member Peter H. Langsjoen, MD, FACC, CoQ10 supplementation is especially important for individuals on cholesterol-lowering statin therapy (HMG CoA reductase inhibitors). Statin medications block the biosynthesis of both cholesterol and CoQ10, and they worsen heart muscle dysfunction in heart failure patients.12-15 In one study, diastolic dysfunction (heart muscle weakness) occurred in 70% of previously normal patients treated with 20 mg per day of Lipitor for six months. This heart muscle dysfunction was reversible with 100 mg of CoQ10 three times daily.15

Three comprehensive reviews have investigated 19 different clinical trials on the use of CoQ10 in heart failure.221-223 The results of 13 randomized controlled trials, encompassing 395 participants, revealed that CoQ10 supplementation led to a statistically significant average net increase of 3.7% in ejection fraction. For individuals with heart failure, Life Extension suggests an optimal CoQ10 blood level of 4 μg/mL.

Pycnogenol in combination with CoQ10 (PycnoQ10) may improve exercise capacity, ejection fraction, and edema in heart failure patients. In a single-blind, 12-week observational study of patients with NYHA class II or III heart failure, PycnoQ10 was well tolerated and improved systolic and diastolic function as well as heart and respiratory rate. Further research is warranted.224

Research Validates CoQ10’s Benefits

An intriguing study published in The European Journal of Heart Failure showed that CoQ10 supplementation significantly improves survival for even the most severe heart failure patients, while dramatically reducing incidence of hospitalization. This intriguing study, known as the Q-SYMBIO trial, shows CoQ10 supplementation can restore deficient CoQ10 levels in patients with moderate-to-severe heart failure, extending lifespan and improving quality of life.11

The data obtained by the Q-SYMBIO investigators revealed that heart failure patients who took 100 mg of CoQ10 three times daily were significantly less likely to:

  • die from heart failure;
  • die from any cause; and
  • have a major adverse cardiac event during the study period compared with control subjects.11

After only three months of supplementation, the researchers detected reduced levels of NT-proBNP, a marker of heart failure released from over-worked heart muscle cells.11,225 At two years, significantly more treated patients had improved their heart failure classification than placebo recipients.11

The study’s main endpoint (ie, a major adverse cardiac event [defined as unplanned hospitalization for worsening heart failure, death from a cardiovascular cause, urgent heart transplantation, or artificial mechanical heart support]) was reached by only 15% in the treatment group versus 26% in the placebo group.11


Hawthorn (Crataegus spp.) is a traditional cardiovascular tonic of plant origin that has been in use since the Middle Ages. Hawthorn extracts contain dozens of biologically active molecules, including flavonoids and polyphenols. The hawthorn-derived phytochemicals most thoroughly studied in humans are oligomeric procyanidins (OPCs). A typical hawthorn dose provides between 30 and 340 mg a day of procyanidins.226-228

Hawthorn extracts are believed to lower blood pressure by dilating coronary and peripheral blood vessels, inhibiting ACE, anti-oxidative and anti-inflammatory effects, and mild diuretic activity.229,230 Hawthorn’s efficacy in the treatment of heart failure has been demonstrated in over 4,000 patients, with significant reductions in subjective discomfort ratings, improved left ventricular ejection fraction, and increased cardiac efficiency.231 A recent meta-analysis of randomized clinical trials including over 600 subjects concluded that Hawthorn extract improves parameters such as maximal workload, left ventricle ejection fraction, and rate pressure product (a measure of the stress put on the cardiac muscle).232

The SPICE trial was a large, randomized controlled study of 2,681 NYHA class II or III patients with a left ventricular ejection fraction ≤ 35%. A 900 mg/day dose of a standardized extract from hawthorn leaves and flowers (providing 169 mg OPCs) significantly reduced cardiac mortality, and sudden cardiac death was significantly reduced for the subgroup of patients with a left ventricular ejection fraction ≥ 25%.233,234 In the HERB chronic heart failure trial, which was a placebo-controlled trial of 120 patients with NYHA class II or III heart failure, 900 mg/day standardized hawthorn extract improved left ventricular ejection fraction compared with the control group.235

Pyrroloquinoline quinone

Pyrroloquinoline quinone (PQQ), a cofactor for several energy-generating reactions in the mitochondria of the cell, may stimulate the production of new mitochondria (mitochondrial biogenesis) through interactions with mitochondrial regulatory genes.236 Impaired mitochondrial function has been implicated in heart failure development.237 In a controlled trial involving cell lines and animal models, formulations of nanocurcumin and PQQ helped modulate hypoxia-induced hypertrophy (enlargement) of human heart cells.238

In animal models of ischemic injury (depriving the heart muscle of oxygen), treatment or pretreatment with PQQ reduced the extent of ischemic damage and degree of lipid peroxidation. In addition, PQQ improved ventricular function and reduced arrhythmias (irregular heartbeats).239,240

Fish oil

Fish oil is a source of omega-3 fatty acids (eicosapentaenoic acid [EPA] and docosahexaenoic acid [DHA]), which are critical for several metabolic processes. Omega-3 fatty acids have been well studied for their prevention of cardiovascular disease and ability to reduce inflammation, hypertension, and risk of cardiovascular mortality.241-243

A recent meta-analysis of nine randomized controlled trials with 800 heart failure patients found that omega-3 polyunsaturated fatty acid (PUFA) supplementation lowered B-type natriuretic peptide (BNP) levels, an indicator of the severity of cardiac dysfunction, and serum norepinephrine levels, which are linked to increased mortality rates in heart failure patients. Supplementation increased left ventricle ejection fraction in patients with dilated cardiomyopathy. This suggests omega-3 PUFAs are beneficial in those with heart failure, although further research is needed to determine the exact dosages and mechanisms.244 A comprehensive review has investigated fish oil’s ability to improve functional capacity during heart failure. Seven trials with 825 total participants were included (dosage range of 600–4,300 mg EPA plus DHA daily); results showed left ventricular ejection fraction increased, left ventricular end-systolic volume decreased, and NYHA functional classification improved in patients with non-ischemic heart failure.245

In a study of 14 patients with NYHA class III or IV heart failure, 8 grams/day of fish oil for 18 weeks led to a statistically significant 59% reduction in the production of TNF-α (an inflammatory protein) in the seven test patients, while TNF-α levels increased 44% in the control group. 246 Patients taking fish oil also saw a trend toward a reduction in the inflammatory mediator interleukin-1 (IL-1).

In the 2018 OCEAN trial, 2 grams of fish oil (providing EPA and DHA) and 2 grams of a concentrated EPA formulation led to favorable changes in cognitive depressive symptoms and social function in people with chronic heart failure and depression. These psychological improvements corresponded with significant increases in participants’ omega-3 blood levels.247


L-carnitine is an amino acid that aids in transporting fatty acid into the mitochondria. In decompensated heart failure, L-carnitine metabolism is altered, and cardiac energy metabolism is compromised.248 Research indicates carnitine deficiency is associated with cardiomyopathy, and 1.5–6 grams of L-carnitine daily increased exercise capacity in addition to improving left ventricle ejection fraction and clinical outcomes.214 A meta-analysis of 17 randomized controlled trials, including 1,624 patients, found supplementation with L-carnitine improved clinical systems in congestive heart failure patients, including overall cardiac efficiency, left ventricle ejection fraction, and cardiac output.249 A recent literature review concluded that L-carnitine helps transport fatty acids into the mitochondria, resulting in reduced oxidative stress and inflammation. Carnitine supplementation protects against ventricular dysfunction and cardiac arrhythmias, and may help reduce hypertension, diabetes mellitus, insulin resistance, and hyperlipidemia.250

Several studies evaluating the role of L-carnitine or its analog, propionyl-L-carnitine, in heart failure have shown statistically significant increases in exercise capacity, maximum exercise time, peak heart rate, and peak oxygen consumption.251 A study that administered 30 mg/kg propionyl-L-carnitine supplementation to 30 heart failure patients demonstrated a reduced pulmonary artery pressure, improved exercise capacity, increased oxygen utilization, and reduced ventricular size.252

Improvements in ejection fraction (13.6% after 180 days) were observed in a 60-patient study of NYHA class II and III heart failure patients who received 1.5 grams propionyl-L-carnitine per day in addition to their conventional treatments (digitalis and diuretics).253 Another trial, which enrolled 80 patients with NYHA class III or IV heart failure caused by dilated cardiomyopathy (heart disease in which the ventricles become enlarged and unable to adequately pump blood), demonstrated a significantly improved 3-year survival after supplementation with L-carnitine.254


Creatine helps ensure the chemical energy supply to muscle tissue. Most research focusing on creatine has targeted its potential use in skeletal muscle metabolism, but a few studies have investigated its potential to improve heart muscle energetics in cardiovascular disease.255

A systematic review of creatine supplementation in patients with heart failure, ischemic heart disease, or acute myocardial infarction analyzed six randomized trials that collectively enrolled 1,226 patients with heart failure. Four of the trials demonstrated a significant reduction in dyspnea (breathing difficulty) in patients with heart failure receiving creatine, creatine phosphate, or phosphocreatinine.255,256

In a randomized double-blind study, 100 subjects engaged in an 8-week exercise program, followed a prepared diet regimen, and received 5 grams/day of creatine monohydrate. The control group received only the diet and exercise intervention. At the end of the study, the treatment group demonstrated reduced inflammatory markers, including IL-6, and improved endothelial functioning.257


Taurine, an amino acid found in the heart, may serve as a cardioprotective agent. In a double-blind, placebo-controlled, randomized study, 16 patients with heart failure received 500 mg of taurine three times daily for two weeks. Taurine supplementation enhanced physical function and improved cardiovascular functional capacity.258 In another randomized placebo-controlled trial, heart failure patients with an ejection fraction less than 50% were given 500 mg taurine three times daily for two weeks. The subjects exercised before and after supplementation. Inflammatory and atherogenic (arterial plaque) markers were decreased in the treatment group, suggesting taurine is a cardioprotective agent.259

In a randomized placebo-controlled clinical trial that enrolled 29 NYHA class II or III heart failure patients with a left ventricular ejection fraction < 50% (average 29.27%), subjects received 500 mg taurine three times daily or placebo. After two weeks, exercise capacity increased significantly in the taurine group compared with placebo.260 Another study that compared taurine (3 grams/day) to low-dose CoQ10 (30 mg/day) supplementation in 17 patients with congestive heart failure (ejection fraction < 50%) revealed a significant improvement in ejection fraction in the taurine group after six weeks, as shown by echocardiography.261


D-ribose, a naturally-occurring pentose sugar that is a key component in adenosine triphosphate (ATP), may aid in energy generation and functional recovery in patients with heart failure and ischemic heart disease. Multiple preclinical studies have demonstrated that supplementation with D-ribose following myocardial ischemia (when blood flow to the heart is blocked or reduced, and the heart muscle is deprived of oxygen) enhanced the regeneration of ATP.262

Research supports the use of D-ribose for optimal cardiovascular health. In a pilot study of 11 NYHA class II‒IV patients, supplementation with 5 grams/dose D-ribose for six weeks led to some improvements in tissue Doppler velocity (a measure of the heart’s velocity while beating) and the velocity ratio of diastolic filling to heart valve relaxation. Researchers conclude that D-ribose may be beneficial for patients in heart failure, but further research with larger cohort sizes is needed to substantiate these benefits.263

In another trial of 15 patients with NYHA class II or III heart failure and chronic coronary artery disease, the administration of D-ribose (5 grams, three times daily) improved cardiac functional parameters as assessed by echocardiography and quality of life scores.264 D-ribose supplementation improved respiratory parameters during exercise in 44% of patients in one study.265 Significant benefits of daily oral D-ribose in NYHA class II and III patients were reported in a double-blind, randomized, crossover trial. D-ribose supplementation significantly improved left atrial functional parameters, quality of life, and physical function activity scores in the treatment group.266

Arjuna (Terminalia arjuna)

The arjuna tree is native to India, where its bark has been used in Ayurvedic medicine for centuries, mainly as a cardiotonic. Like hawthorn, arjuna extracts contain a wide variety of bioactive molecules, especially polyphenols and flavonoids.267,268 Several studies indicate that arjuna may support optimal cardiovascular health.269

Arjuna extracts exert anti-inflammatory effects that help combat the excessive immune response that leads to arterial plaque and blood vessel occlusions.270-272 They also help modulate abnormal lipid (cholesterol) profiles that contribute to plaque formation.270,273 In addition, arjuna extracts enhance heart muscle tone, improving its “squeeze” and increasing the amount of blood it can pump each second without exhaustion.268,274,275

Arjuna extracts have modest lipid-lowering effects at the doses used in ancient Indian medicine.276 In animal studies, arjuna reduced total cholesterol, LDL cholesterol, and triglycerides; raised protective HDL; and reduced the size and number of atherosclerotic lesions in the aorta.273,277,278 Humans treated with 500 mg of arjuna tree bark powder daily experienced a total cholesterol drop of 9.7%.279 The same dose of an extract from the bark, given every eight hours, improved endothelial function (the ability of vital arteries to dilate and increase blood flow) by 9.3% in smokers.280

Vitamin D

A number of observational studies have suggested an association between low vitamin D levels and chronic heart failure,201,281 particularly among the elderly.282 For example, in a study of 548 patients re-hospitalized with heart failure, 75% were vitamin D deficient (defined as < 20 ng/mL for this study), and for each 10 ng/mL decrease in vitamin D levels, the risk of all-cause mortality increased by 10%.283

The contribution of vitamin D deficiency to the pathology of heart failure as well as its protective effects for cardiovascular health are most likely exerted by several mechanisms, including effects on the hypertensive hormone angiotensin II, influence on vascular endothelial function, effects on systemic inflammation, and impact on the risk of cardiovascular mortality.201,281,284 Vitamin D may affect BNP and parathyroid hormone levels, as well as enhance heart contractility.285 A synthetic vitamin D analog (paricalcitol) decreased inflammation and cell death in mice following experimental heart attack, while transgenic mice that lacked the vitamin D receptor showed decreased survival following a heart attack.286

Intervention trials of vitamin D for heart failure have had mixed results. In a prospective study, 100 patients with heart failure (NYHA class I‒III) received 50,000 IU vitamin D every week for eight weeks, followed by 50,000 IU every month for two months. At the end of the study, patients on supplemental vitamin D saw improvements in exercise capacity and reductions in NYHA heart failure scores.287 Another intervention showed that the administration of 2,000 IU vitamin D daily for nine months in 93 patients with heart failure had an anti-inflammatory effect.288,289

In a recent randomized double-blind trial, 40 NYHA class II‒III patients with vitamin D deficiency or insufficient vitamin D levels received either 10,000 IU vitamin D3 daily or a placebo for six months. Researchers found that in high doses, vitamin D3 replenished diminished vitamin stores, improved quality of life scores, and normalized BNP, parathyroid hormone, and C-reactive protein levels.285 More research is warranted to determine if these results occur at lower dosages.

Intervention trials using vitamin D have demonstrated modest results for lowering blood pressure. A review of 11 randomized controlled trials, including 716 subjects, found a small reduction in systolic (3.6 mmHg) and diastolic (3.1 mmHg) blood pressure at doses of 800‒2,900 IU vitamin D daily in individuals with high blood pressure.290 In another analysis of randomized controlled studies, the effect of vitamin D replacement on heart failure was mixed. It reduced the risk of mortality in one study, but did not affect heart function, exercise capacity, or quality of life in two others.201


Resveratrol, a polyphenol found in grapes, nuts, and red wine, has potent antioxidant activity. A randomized controlled study in which rats with induced post-infarction heart failure were given 15 mg/kg body weight per day of resveratrol showed that resveratrol supplementation decreased the severity of heart failure, improved left ventricular function, decreased collagen deposits in the myocardium, lowered oxidative stress, and attenuated inflammatory signaling pathways.291 A recent literature review of clinical data found that resveratrol reduces inflammation, promotes endothelial function, supports healthy blood pressure levels, and helps reduce biomarkers of cardiovascular disease.292

Resveratrol may play a role in myocardial ischemia, myocarditis, cardiac hypertrophy, and heart failure. Possible mechanism of action include reducing oxidative stress and inflammation, improving calcium handling, decreasing apoptosis, and modifying inflammatory pathways.291 Further research is warranted to fully understand resveratrol’s role in heart health.


Selenium is a cofactor necessary for a number of cellular metabolic processes. In an animal model of hypertension leading to heart failure, a selenium-free diet was associated with high mortality (70%); however, supplementation with 50 or 100 mcg/kg resulted in survival rates of 78% and 100%, respectively.293 In humans, severe selenium deficiency has been firmly linked to a reversible form of heart failure. Known as Keshan disease, the condition is potentially fatal if untreated.294,295 Several studies also suggest less severe selenium deficiency may be associated with heart failure.294

In a recent randomized, double-blind, placebo-controlled trial involving 53 patients with congestive heart failure, 200 µg selenium per day for 12 weeks reduced serum insulin levels, decreased LDL cholesterol levels, increased HDL cholesterol levels, reduced C-reactive protein levels, and elevated the plasma antioxidant capacity.296


Magnesium is a mineral found in the body that is a cofactor in over 300 enzymatic reactions, including protein synthesis and blood pressure and blood glucose regulation. It is also required for energy production and bone development, and plays a role in muscle contraction, nerve impulses, and maintaining a normal heart rhythm. Magnesium deficiency is common in people with congestive heart failure, and is believed to worsen clinical outcomes in this population.297 Recent research suggested risk factors for cardiovascular disease, including cholesterol and blood pressure levels, are associated with low serum levels and dietary intake of magnesium.298

A recent literature review focusing on epidemiological research suggests high magnesium intake is associated with lower risk of cardiovascular risk factors and cardiovascular disease, including coronary heart disease and stroke. A recent meta-analysis demonstrated a strong association between heart failure and increment of 100 mg/day of magnesium intake.299 Further randomized controlled clinical trials will help elucidate magnesium’s role in heart health.

In another trial, 300 mg magnesium citrate was found to improve heart rate variability (ie, the time variation between heartbeats) after five weeks of supplementation.300 Magnesium oxide, at a dose of 800 mg daily for three months, improved arterial elasticity compared with placebo in individuals with chronic heart failure.301 In another study, magnesium orotate (6,000 mg daily for one month, 3,000 mg daily for 11 months) or placebo was given to patients with severe congestive heart failure. The survival rate after one year of supplementation was 76% for the magnesium group vs. 52% for the placebo group. The authors concluded “Magnesium orotate may be used as adjuvant therapy in patients on optimal treatment for severe congestive heart failure, increasing survival rate and improving clinical symptoms and patient’s quality of life.302

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This information (and any accompanying material) is not intended to replace the attention or advice of a physician or other qualified health care professional. Anyone who wishes to embark on any dietary, drug, exercise, or other lifestyle change intended to prevent or treat a specific disease or condition should first consult with and seek clearance from a physician or other qualified health care professional. Pregnant women in particular should seek the advice of a physician before using any protocol listed on this website. The protocols described on this website are for adults only, unless otherwise specified. Product labels may contain important safety information and the most recent product information provided by the product manufacturers should be carefully reviewed prior to use to verify the dose, administration, and contraindications. National, state, and local laws may vary regarding the use and application of many of the treatments discussed. The reader assumes the risk of any injuries. The authors and publishers, their affiliates and assigns are not liable for any injury and/or damage to persons arising from this protocol and expressly disclaim responsibility for any adverse effects resulting from the use of the information contained herein.

The protocols raise many issues that are subject to change as new data emerge. None of our suggested protocol regimens can guarantee health benefits. The publisher has not performed independent verification of the data contained herein, and expressly disclaim responsibility for any error in literature.