|Nutritional Treatments for Cardiomyopathy, Congestive
Heart Failure, and Ventricular Arrhythmias
Report 2A - Revision 3 - October 15, 2003
Jeff Gold, Senior Scientist, Advanced Research Programs
World Environmental Organization; Ph: (706) 769-1000; Email: JGold@World.Org
This report will review evidence published primarily in peer-reviewed medical journals outlining the use of nutritional supplements and other dietary modifications to treat cardiomyopathy, congestive heart failure (CHF), and ventricular arrhythmias. Some nutritional supplements presented in this report (e.g. Coenzyme Q10, magnesium) have proven so effective they should be considered a mandatory part of any treatment protocol for cardiomyopathy, congestive heart failure, and/or arrhythmias.
In humans, cardiomyopathy is often the underlying cause when a young athlete, seemingly in the peak of health, collapses while playing a sport and dies.(1) Cardiomyopathy is also common in some dog breeds, particularly boxers and dobermans.
There are two primary types of cardiomyopathy, hypertrophic and dilated. Hypertrophic cardiomyopathy causes the walls of the lower heart chambers or ventricles to thicken. Dilated cardiomyopathy is indicated when the ventricle walls thicken somewhat but most of the heart enlargement is caused by expansion of the ventricle chambers.(1) Dilated cardiomyopathy, which accounts for more than 90% of all cases, is also distinguished by diminished myocardial contractility, and disproportionately thinner septal and free wall thickness.(2)
Cardiomyopathy often results in ventricular premature complexes (VPCs), ventricular tachycardia (VT) and other arrhythmias.(3) A common cause of death in cardiomyopathy is sudden death from a long episode of VT or other arrhythmia from which the heart does not recover.(1) Death usually occurs within 6 months to a few years after first symptoms appear.
If one is able to control the arrhythmias associated with cardiomyopathy, the eventual cause of death is usually CHF due to significant enlargement of the heart and its deterioration to the point where it can no longer pump blood effectively.(1) The course of treatment therefore becomes two fold, i.e. trying to prevent and control arrhythmias while also trying to slow or prevent enlargement and subsequent deterioration of the myocardium.
There is abundant research demonstrating that several nutritional supplements help to significantly control ventricular arrhythmias. Magnesium therapy(3-9), sometimes combined with potassium(4-5), usually brings about the most immediate improvement. There is also research demonstrating that selenium(10-11), fish oil(12-17), L-carnitine(2,18-19), and garlic(20-21) can help reduce the occurrence of arrhythmias.
Additional research demonstrates that some nutritional supplements help to reduce cardiac enlargement and other symptoms of CHF. In addition to its antiarrhythmic potential noted above, carnitine has also been shown to reduce the ventricular dilation associated with cardiomyopathy.(18) Another supplement, Coenzyme Q10 (CoQ10)(22-26), has been shown to significantly strengthen myocardial contraction and possibly reduce the frequency of arrhythmias. It is now recommended that CoQ10 be added to the regimen of all cardiomyopathy patients.(22) Long-term survival has been shown to be more than three times as great in patients taking CoQ10.(23) Further, patients who take CoQ10 feel significantly better and important measurements of the heart often show substantial improvement within months of initiating CoQ10 therapy.(22) There is also research indicating that taurine can, in some cases, help treat cardiomyopathy as well as relieve symptoms of CHF.(27-28)
Looking at nutritional supplements in a collective fashion, Sole et al concluded that restoring adequate myocyte nutrition could be an essential therapy for CHF patients. They documented several metabolic deficiencies in the failing myocardium including unusually low levels of L-carnitine, CoQ10, creatine, thiamin, taurine and other antioxidants. They also described studies in which replenishment of these was beneficial in both people and animals. Given the numerous deficiencies associated with heart disease, they concluded that the best nutritional approach is to supplement to control a wide array of deficiencies, not just one or two.(29)
Research supporting use of the nutritional supplements introduced above, along with a few others, will now be presented.
Magnesium and Potassium
The membrane and action potential of cardiac cells, including formation of tachyarrhythmias, is affected by the fluxes of sodium, potassium, calcium and magnesium ions. Atrial and ventricular tachyarrhythmias occur by (1) repetitive automatic or triggered impulses or (2) reentrant circus movement which usually follows an ectopic automatic or triggered premature beat.(4) Reentrant tachycardia can also begin from asynchronous propagation of an automatic or a triggered impulse, whether single or multiple. Iseri et al reported that a decrease in magnesium ions can induce triggered ectopic impulses, and a decrease in potassium ions can delay conduction of these impulses to set up reentrant tachycardia. Both magnesium and potassium have, accordingly, proven useful in treating arrhythmias. Iseri et al also noted that magnesium deficiency can induce coronary spasm and create an ischemic environment for ionic balance. They cited four double-blind randomized studies that have shown infusion of magnesium during the first 24 hours after acute myocardial infarction reduced the development of VT and ventrical fibrillation (VF). They questioned the use of diuretics as the first-line treatment of hypertension and CHF since diuretics are the most common cause of magnesium and potassium depletion. In this same report, Iseri et al recommended 250 mg. or more of elemental magnesium per day in humans, along with a diet rich in magnesium.(6)
In another review article, Iseri et al noted that in some cases when magnesium was used to successfully abort the recurrence of VT and VF, serum potassium levels decreased. When potassium was added to the regimen, control of arrhythmias was made more effective.(4) In a separate report, Iseri noted several cases where serum potassium and/or sodium levels fell precipitously during magnesium treatment.(7) Potassium and magnesium supplementation should be considered even if serum levels are normal since serum magnesium and potassium levels do not necessarily reflect the levels of these elements within the myocardium.
In 1990, Iseri reported on a study where eleven of 12 patients with VF and/or VT converted to sinus or paced rhythm within 5 minutes of a 2 g infusion of magnesium. Arrhythmias in the twelfth patient were also successfully controlled, although they took longer to initially control. In one case, despite intravenous administration of lidocaine and phenytoin, the patient had 18 episodes of VF that required countershock treatment. A dose of 12 g of magnesium raised serum magnesium to 3.9 mEq/liter and controlled VF. In another patient, after controlling initial VT with intravenous magnesium, a combination of oral magnesium chloride, 2 tablets 3 times daily, along with amiodarone, controlled VT for 1 year. Iseri noted that patients with cardiopulmonary disease are highly susceptible to magnesium deficiency, some of which may not be revealed by low serum levels. In the absence of renal insufficiency, magnesium infusion is safe and can be quite effective in controlling intractable VT and VF whether or not the patient is hypomagnesemic.(8)
Ceremuzynski et al reported in 2000 that intravenous magnesium sulphate can be a safe and effective antiarrhythmic intervention which should be considered more often in medical practice before resorting to pharmacological antiarrhythmic medications. They found that intravenous administration of magnesium caused a significant decrease in the number of ventricular ectopic beats (P < 0.0001), couplets (P < 0.003) and episodes of nonsustained VT (P < 0.01).(9)
Zehender et al reported in 1997 on a randomized, double-blind study with 232 patients experiencing frequent ventricular arrhythmias. Patients were treated either with a combination of oral magnesium and potassium, or with a placebo. Treatment involved a relatively small dose of magnesium and potassium (only 50% above recommended minimum daily dietary intake) yet still produced a moderate but significant antiarrhythmic effect when compared to placebo. They concluded that in light of its simplicity, cost-effectiveness, and safety, increasing the daily intake of magnesium and potassium may provide another first-line option for treating patients with frequent but not life-threatening ventricular tachyarrhythmias.(5)
Bean et al in 1994 speculated that hypomagnesemia, like hypokalemia, may potentiate arrhythmias caused by catecholamine excess. They reported that acute administration of magnesium in normal dogs increased the arrhythmogenic threshold for epinephrine, further supporting the use of magnesium as an antiarrhythmic agent.(3)
Based upon the evidence presented above, magnesium supplementation can clearly be useful in the treatment of arrhythmias. Unfortunately, some forms of oral magnesium are associated with a high incidence of emesis, diarrhea and soft stools. This rarely occurs, however, with use of magnesium lactate, even in large doses. Magnesium lactate is manufactured by Niche Pharmaceuticals in a 12-hour time release tablet form (84 mg/tablet) known as Mag-Tab SR.
Robbins et al reported that magnesium lactate has many properties suggesting that it is a good form of magnesium to use as a dietary supplement. It is soluble at neutral pH, the anion is well absorbed and well tolerated, and it is 10% magnesium by weight. This time-release form of magnesium is easy on the stomach, and offers a much more consistent serum level of magnesium when compared to enteric-coated magnesium chloride tablets. When magnesium lactate was given to dogs, the mean level of serum magnesium was found to rise quickly, peaked at four hours, then dropped slowly over subsequent hours.(30)
In 1998, Tanguy et al reported on the use of selenium supplementation to control VT and VF. Selenium was added to the diet of rats at the rate of 50 mcg selenium per kg of food. Selenium significantly affected the incidence of reperfusion-induced VT (91% in controls vs. 36% in selenium-supplemented rats, p=0.03; Chi2 test corrected for continuity using the Yates' method.) While not statistically significant, the incidence of total VF was also reduced in the selenium group (91% in controls vs. 45% in selenium-supplemented rats, p=0.07, ns; Chi2 test corrected for continuity using the Yates' method). The reduction was much more pronounced for sustained VF, which was markedly and significantly decreased in the selenium group (45% in controls vs. 0% in selenium-supplemented rats, p=0.04; Chi2 test corrected for continuity using the Yates' method). These findings confirmed that selenium supplementation decreased the severity of reperfusion arrhythmias. Tanguy et al also noted other studies that indicated a negative relationship between plasma selenium levels and the incidence of cardiovascular disease. Some of these studies further demonstrated that plasma levels of selenium are significantly lower during the acute phase of myocardial infarction.(10)
In 1994, Lehr reported that a patient with several years of episodic occurrence of disabling ventricular bigemini returned to unbroken normal sinus rhythm one week after introduction of selenium supplementation. While selenium supplementation was among a multiplicity of possible reasons for this development, Lehr reported that it was the most obvious, though only a tentative explanation. Selenium represented the sole modification of otherwise reasonably standardized conditions of antiarrhythmic therapy, lifestyle and diet.(11)
Lehr also noted studies that indicated a high rate of cardiovascular disease in the coastal plain of Georgia might have been caused by selenium deficiency in the soil. Further, he described a study in which a group of investigators showed that selenium deficiency in soil is one of the principal factors responsible for a form of dilated cardiomyopathy known as Keshan disease. Lehr also reported that a negative selenium balance might be created if no attention is paid to selenium intake in persons on hypocaloric diets, in paranteral nutrition, and in the case of anorexia nervosa. Further, he noted that 6% of young women afflicted with anorexia nervosa, and without underlying heart disease, die suddenly, usually with intractable VT. In humans, up to 750 to 850 mcg of selenium can be ingested daily without the development of selenosis. Nutritional sources of selenium include grains, shrimp, as well as various meats and milk. In an effort to forestall sudden cardiac death from intractable cardiac arrhythmias, Lehr suggested close attention be paid to adequate selenium supplementation based upon postulated influences of selenium on cardiac function.(11)
Billman et al in 1999 reported on nine studies which demonstrated omega 3 polyunsaturated fatty acids (PUFAs) prevent fatal cardiac ventricular ischemia-induced arrhythmias in animals, and another six studies which demonstrated probable benefit in humans. In their own study, they reported that a fish oil preparation helped prevent fatal VF in dogs. They then studied independently the various constituents of fish oil to determine which may be responsible for its positive effect. They demonstrated that the three most common dietary PUFAs of the omega 3 class are all potent antiarrhythmic agents when infused intravenously just before exercise-plus-ischemia stress in dogs. While not immediately antiarrhythmic in a dietary form, in the case of ischemia, severe exertion, or major sympathetic adrenergic discharge, phospholipases and lipases quickly liberate stored fatty acids, especially omega 3 PUFAs, and these in their free form can prevent arrhythmias. If fish oil is ingested on a regular basis, the PUFAs will be present in the stored forms to be available when needed.(12)
Sellmayer et al cited in 1995 two carefully controlled dietary trials with omega 3 fatty acid enrichment that found improved survival after acute myocardial infarction due to the potential antiarrhythmic effect of omega 3 fatty acids. Also cited was a small Danish study with VT that revealed a greater, though not statistically significant, reduction in VPCs in the group treated with fish oil as compared to those treated with corn oil. Sellmayer et al also reported on their own prospective, double-blind and placebo-controlled study in which patients were advised to take 15 ml of fish oil or placebo (sunflower oil) daily for the study period of 16 weeks after which time tissue levels of omega 3 fatty acids should have reached a steady state. During the trial, VPCs decreased by 48% after 16 weeks in the fish oil group, compared to only a 25% reduction in the placebo group. Further, 44% of patients in the fish oil group had reduction of VPCs greater than 70% while only 15% in the placebo group had this same level of reduction. Fish oil exerted a moderate antiarrhythmic effect when compared with group IC drugs flecainide and encainide. The two drugs, however, adversely affected survival in highly selected patients after myocardial infarction, whereas, in two different trials, omega 3 fatty acids significantly improved survival, even in unselected patients after myocardial infarction. This benefit was credited to the antiarrhythmic effect of fish oils. Among several thousand patients in controlled trials, no side effects of omega 3 supplementation have been observed. It is thought fish oil fatty acids may regulate calcium fluxes and suppress intracellular calcium activity. Sellmayer et al cited three studies which found increased intracellular calcium activity caused ventricular electrical inhomogeneity and thus contributed to arrhythmias by phase 2 reentry or early afterdepolarizations.(13)
In 1994 Isensee et al reported on their study in rats comparing the effects of various oils, as well as a low-fat diet, on ischemia-induced arrhythmias. They found that the incidence of VT was 60% in the low fat group, 60% in the linseed oil group, 56% in the coconut oil group, 44% in the corn oil group, and 0% in the fish oil group. Further, the incidence of VF was 75% in the low fat group, 67% in the coconut oil group, 44% in the corn oil group, 40% in the linseed oil group, and only 10% in the fish oil group. They also reported that the length of time between coronary occlusion and the first occurrence of extrasystole was shortest in the coconut oil group and longest in the fish oil group. After trying the same experiment using aspirin to inhibit cyclooxygenase, they found the protective effects of PUFAs were completely abolished by cyclooxygenase inhibition. Elimination of all the favorable effects of PUFAs by cyclooxygenase inhibition indicates the prostaglandin system plays an essential role in the protection offered by PUFAs from ventricular arrhythmias. (In contrast, the antiarrhythmic effects of various forms of garlic, as described later in this report, were only partially abolished by aspirin.)(14)
Hock et al in 1990 reported on the influence of omega 3 fatty acids on myocardial ischemia and reperfusion. Rats were fed a diet in which the lipid was replaced with either corn oil or fish oil. Both the incidence and severity of ventricular tachycardia and ventricular fibrillation were significantly reduced during the ischemic and reperfusion periods with fish oil feeding. The incidence of ventricular fibrillation was only 14% in the fish oil group versus 91% in the corn oil group. When the incidence, number, and duration of the arrhythmias were taken into account using an arrhythmia scoring scale, the fish oil group had a significantly lower arrhythmia score compared to the corn oil group (1.3 ± 0.7 vs. 5.6 ± 0.8, P < 0.01). Survival after 24 hours of reperfusion was 76% in the fish oil group and 41% in the corn oil group.(15)
In 1989 McLennan et al reported on a study they did on the influence of dietary fat in sudden cardiac death of rats. The study compared diets enriched with sheep perirenal fat, sunflower oil or tuna fish oil. During coronary artery occlusion the number of animals having episodes of VT or VF was significantly diminished by the sunflower oil and fish oil diets. Moreover, in the animals in which VT or VF did occur it was less severe (shorter lasting) in the sunflower oil and fish oil groups. While 70% of sheep fat supplemented animals suffered VF and 30% died, only 12% of fish oil supplemented animals fibrillated and none died.(16)
In 1980 Culp et al reported on a study they did exploring the effect of fish oil on experimental myocardial infarction in dogs. In control animals, the frequency of ectopic beats rose from less than 10% at the beginning of the experiment to about 80% after 19 to 24 hours of stimulation of the left circumflex coronary artery. In contrast, the fish oil fed dogs maintained a more normal ECG pattern showing less than 30% ectopic beats after 19 hours, and less severe myocardial damage was found in those with elevated omega 3 fatty acids.(17)
Rizos in 2000 reported on the three-year survival of patients treated with L-carnitine at the rate of 2 g/day orally for CHF caused by dilated cardiomyopathy. The study began with 80 patients, was double-blind and placebo-controlled for the initial 3-month period, and then unblinded for the remaining 33 months. The 3-year mortality rate was found to be statistically significant in favor of the carnitine group with a mortality rate of only 3% versus 18% in the placebo group (P < 0.04). Atrial fibrillation developed in 7 patients in the placebo group. In contrast, only one patient in the carnitine group was unable to maintain sinus rhythm for the entire follow-up period. Electrical stability of the carnitine group may explain mortality risk reduction as evidenced by improved sinus rhythm scores in that group.(19)
In 2000 Helton et al conducted a multicenter retrospective study to investigate the outcome of patients treated with carnitine. They found carnitine useful in treating cardiomyopathy based upon its role of shuttling fatty acids across the mitochondrial membrane of the heart, delivering them for beta-oxidation and the production of energy. They found carnitine patients tended to have lower mortality from cardiomyopathy as the primary diagnosis than controls (6.8% vs. 17.9%), and that there was less transplantation among carnitine-treated patients than control patients (9.6% vs. 15.0%). Their analysis of the association between concomitant medications and clinical outcome unexpectedly revealed that the population of patients who received ACE inhibitors had significantly poorer survival. Significant improvement in survival was observed both for carnitine-treated patients who did not receive ACE inhibitors versus control patients (P = 0.46) as well as for control patients who did not receive ACE inhibitors compared to controls who did (P=.0001). The incidence density in the ACE inhibitor-treated group was approximately 4.4 times higher than the non-ACE inhibitor-treated group in both the carnitine-treated and control groups, indicating many more events per person per day of follow-up among ACE inhibitor-treated patients. Helton et al suggested that while there could be short to intermediate term improvements in myocardial function with ACE inhibitors, the data of their study suggested uncertainty for improvements in long-term mortality through ACE inhibitor use.(2)
In 1998 Signh et al reviewed several studies on the administration of carnitine in coronary artery disease and cardiomyopathy. They made note of a randomized, double-blind and placebo-controlled trial in which it was found that after 2 g/day of L-carnitine administration, carnitine-treated patients showed a significant reduction in mean infarct size compared to the placebo group. Further, electrocardiographic QRS-score was significantly less in the carnitine group compared to placebo while serum glutamic oxalaspartate transaminase and lactate dehydrogenase and lipid peroxides showed significant reduction in the carnitine group. In another study noted by Signh et al, of 146 acute myocardial infarction (AMI) patients (97 in the control and 49 in the treatment group) those treated with carnitine had no deaths, while those in the control group had 18 deaths. The dose of L-carnitine was 9 g/day IV for 3 days followed by 4 g/day oral for 21 days. In another study, 100 randomly selected angina pectoris patients were administered L-carnitine (2 g/day) for six months. There was a significant decrease in VPCs at rest, increased tolerance to exercise, and other positive cardiac effects. In yet another reviewed study 81 AMI patients were selected to receive 4 g/day of L-carnitine for one year, and were compared to 79 controls. Carnitine caused significant reduction in heart rate, angina pectoris, and most notably a reduction of deaths (1.2% vs. 12.5%, p < 0.05) in the intervention group compared to the control group. In a more recent study involving 472 first AMI patients, treatment with carnitine was associated with a significant attenuation of left ventricular dilation in the first year after treatment compared to placebo. The combined incidence of death and CHF after discharge was 6% in the carnitine group versus 9.6% in the placebo group (P=NS). Singh et al also reported that carnitine supplementation in patients with cardiomyopathy is usually associated with rapid beneficial effects characterized by improvement in cardiac function. In one 5.5 year old boy, left ventricular ejection fraction was increased from 39% to 75% after only one month of treatment. Clinical benefits from carnitine may be reduction in heart size and heart failure and reduction in the amplitude of T-waves recorded in precordial leads.(18)
Red meat, milk and milk products are rich sources of carnitine. Adverse reactions that have been observed in carnitine therapy consist of mild gastrointestinal complaints such as nausea, vomiting, diarrhea and abdominal cramps. These effects usually resolve with a reduction of carnitine dosage.(18)
Carnitine-Related Amino Acids and Cofactors
According to the PDR for Nutritional Supplements, only 20% of a supplement containing 2 g of L-carnitine is absorbed following ingestion.(31) As such, it may be useful to supplement with other amino acids that have been found to aid in the absorption and synthesis of carnitine. Singh et al noted that L-lysine and L-methionine are important for the biosynthesis of carnitine, and foods rich in these amino acids may help increase absorption of carnitine.(18)
In 1993 Pierrefiche et al reported that potentiation of carnitine is increased threefold when given with an equimolar dose of L-lysine. As such, they suggested that an equivalent effect can be obtained with lower doses of carnitine when combined with lysine. The potentiation of carnitine resulted from lysine increasing availability of carnitine in the target organs caused by endogenous synthesis of carnitine from lysine. Lysine also reduced plasma peaks of carnitine, diminished urinary loss of carnitine, and improved the uptake and utilization of carnitine by the target organs. Various proportions of the carnitine/lysine combination were studied, and under the experimental conditions used, the optimum ratio was found to be 1:1 to 1:2. In other experiments, no potentiation of carnitine was observed with concomitant administration of arginine, ornithine or aspartic acid; only lysine was effective. Further, the L-isomer form of carnitine was found to be much more effective than the D,L form.(32) Various reports recommend against supplementing with the D,L form of carnitine.
In 1984 Bamji reported that in adult human volunteers, plasma carnitine showed a significant increase 3 to 6 hours after administration of oral lysine. In that report, the phenomenon was found to be specific for lysine and not observed when other amino acids such as tryptophan and threonine were administered. Bamji also reported that carnitine deficiency may arise in the case of dietary deficiency of either of the precursor amino acids (lysine and methionine) or any of the cofactors (iron, ascorbic acid, vitamin B6 and niacin) required by the enzymes of the lysine-carnitine pathway. In a different study noted by Bamji, supplementation with threonine along with lysine also produced improvement in cardiac carnitine levels.(33) It may, therefore, be prudent in the case of cardiomyopathy or CHF to supplement with lysine, methionine, iron, ascorbic acid, vitamin B6, niacin and threonine, along with carnitine. Adverse effects have been noted from L-methionine supplementation, so it may be best to obtain methionine strictly from food sources.(31)
In 1996 Dodson et al reported that choline supplementation causes significantly more supplemented carnitine to be retained in muscle tissues with less being excreted in urine. They also noted a study that indicated choline may be needed to aid in the transport of carnitine into cells.(34) Accordingly, it may be beneficial to supplement with choline to help increase the efficacy of carnitine therapy.
In addition to the fact that niacin, as a cofactor, may bolster the effectiveness of carnitine supplementation, several studies have shown that niacin on its own may exhibit certain cardioprotective effects. Niacin comes in three forms, nicotinic acid, niacinamide and inositol, each with very different effects on the body. Nicotinic acid (NA) is the form most often shown to have significant effects on the myocardium. NA in very high doses lowers the serum level of low-density lipoprotein cholesterol (LDL-C), however, at these doses, it can also cause severe adverse reactions including hepatic toxicity.(31) Research indicates that NA may also offer other cardioprotective benefits, even at safe, nutritional levels.
In 2000 Trueblood et al reported that NA has been shown to decrease myocyte injury. They found NA significantly improved functional and metabolic parameters providing rationale for its use as a therapeutic agent in patients with ischemic heart disease.(35)
In 1984 Talesnik et al reported that NA may be of significance as an adjuvant in the treatment of coronary insufficiencies. They noted studies indicating NA to be one of the most active anti-lipolytic agents in adipose tissue and that it also inhibits the lipolytic effect of isoproterenol in cardiac muscle. This is of particular relevance since the increased cardiac contractility induced by tachycardia has been shown to produce endogenous triglyceride lipolysis. They also noted a study in 1947 by Calder on rabbits which demonstrated that NA restored rhythm, tension development and coronary flow in failing hearts.(36)
In 1975 Rowe et al reported that when a nicotinic-acid analogue (NAA) was given within 5 hours of the onset of myocardial infarction, the incidence of R-on-apex T ventricular premature beats and beats in which the ectopic R wave interrupted the apex of the T wave of a previous ventricular premature beat were reduced.(37)
In 1993 Isensee et al reported on a study evaluating the cardioprotective actions of garlic (Allium sativum). In their experiments using rat hearts, a marked cardioprotection during ischemia and reperfusion was found, especially with respect to the development of fatal irreversible VF. The diet of evaluated rats was enriched with 1% garlic powder. The powder was standardized to an allicin content of 1.3% with a capacity for liberation of allicin of 0.6%. When compared to controls, the hearts of the garlic group beat significantly longer in normal sinus rhythm. While 35.5% of control hearts developed VT, none of the garlic hearts developed VT. The incidence of VF was 88% in the control group, and significantly reduced in the garlic group at 50%. The ischemic areas of the hearts of the garlic group were significantly smaller (31.7 ± 2.4%) than those of the control group (40.9% ± 2.3%). In the case of reperfusion-induced arrhythmias, 90% of hearts developed VF in the control group (of which 20% were reversible) while only 30% in the garlic group developed VF (of which 80% were reversible). Further, the incidence of VT was halved by the garlic diet. The study did not confirm what component of garlic exhibited a protective effect, although allicin is the component of garlic most often thought to be cardioprotective.(20)
In another study, Rietz et al reported on the cardioprotective actions of wild garlic (Allium ursinum). In that study, rat diets were enriched with 2% pulverized dried leaves of wild garlic. The time until occurrence of extrasystole was increased significantly from 3.4 minutes in the control group to 7.1 minutes in the wild garlic group. Although the time until occurrence of VT was likewise prolonged, there was no significant difference in the incidence of VT. The most notable finding was that the incidence of VF was reduced from 88% in the control group to 20% in the wild garlic group. The ischemic zones of the hearts of the wild garlic group were significantly smaller than those of the control hearts (33.6% versus 40.9% of total cardiac tissue). In the case of reperfusion-induced arrhythmias, rats fed the diet containing wild garlic powder showed a significant reduction in both the incidence of VT (70% vs. 100%) and VF (50% vs. 90%). It was also reported that the antiarrhythmic effects of wild garlic were not related to the fatty acid composition of the heart.(21)
CoQ10 appears to be the first therapy that significantly improves the strength of myocardial contraction and maintains this improvement over months to years. No conventional cardiac drugs can biochemically substitute for CoQ10 because of their different organic structure.(24)
Langsjoen et al reported in 1997 on their treatment of patients with hypertrophic cardiomyopathy using CoQ10. Patients were treated with an average of 200 mg/day of CoQ10. All patients noted improvement in symptoms of fatigue and dyspnea with no side effects. One patient even noted complete resolution of her frequent and severe chest pain. After three months of treatment with CoQ10, the mean intraventricular septal thickness improved significantly from 1.51 ± 0.17 cm to 1.14 ± 0.13 cm, a 24% reduction (P < 0.002). The mean posterior wall thickness improved significantly from 1.37 ± 0.13 cm to 1.01 ± 0.15 cm, a 26% reduction (P < 0.005). The one patient in the study with subaortic obstruction also showed an improvement in resting pressure gradient after CoQ10 (70 mmHg to 30 mmHg). These clinical and echocardiographic improvements were sustained for up to 48 months (range 3 - 48 months with a mean of 21-months follow-up to the date the report was published). They went on to note several previous studies indicating consistent improvement in both left ventricular wall thickness and diastolic function in hypertensive heart disease treated with CoQ10.(22)
In a separate report in 1990, Langsjoen et al found a pronounced increase of survival of patients with cardiomyopathy when treated with CoQ10 along with conventional therapy. In that study, 137 patients were treated with CoQ10, of which 43 had ejection fractions (EF) below 40%. The survival rate for all 137 patients treated with CoQ10 including the 43 with EF below 40% was 75% after 46 months. This survival rate was of extraordinary significance because 182 patients with EF below 46% on conventional therapy, without CoQ10, had a survival rate of only 25% after a shorter period of 36 months. The use of CoQ10 demonstrated a three-fold increase in long term survival when compared to conventional therapy. The dose of CoQ10 used in this study was 33.3 mg three times per day, encased with soybean oil. Langsjoen et al noted several other studies that also demonstrated extraordinary clinical improvement after CoQ10 therapy and went on to state, "CoQ10 is so effective for patients with advanced cardiomyopathy who are dying that it seems unethical to extend the blind trial with placebo when an effective treatment is available."(23)
Also in 1990, Langsjoen et al reported on a six-year clinical study using CoQ10 to treat cardiomyopathy in 143 patients with chronic, stable, non-secondary, non-hypertrophic cardiomyopathy, 98% of which were in NYHA Classes III and IV. Each patient was given 100 mg/day CoQ10 orally, divided into three doses, in addition to their conventional medical program in an open-label long-term study. Mean EF of 44% measured by systolic time interval analysis rose to 60% within 6 months and stabilized at that level with 84% of patients showing statistically significant improvement. 85% of patients improved by one or two NYHA classes. The survival rate was also encouraging with only 11.1% mortality in 12 months. (Other studies show a mortality rate as high as 66% in 12 months when CoQ10 was not included in the regimen.) There was only 17.8% mortality in 24 months which also compared favorably with reports in the literature. CoQ10 treated patients lived as much as five times longer, or more, when compared to those on conventional therapy alone. There was no evidence of toxicity or intolerance in a total of 368.9 patient-years of exposure.(25)
In 1988 Langsjoen et al reported on yet another trial of CoQ10 in 88 patients. 75% to 85% of patients showed statistically significant increases in two monitored cardiac parameters. Patients with the lowest ejection fractions (approximately 10% - 30%) showed the highest increases (115% - 210%) and those with higher ejection fractions (50% - 80%) showed increases of approximately 10% - 25%. By functional classification, 17/21 in class IV, 52/62 in class III, and 4/5 in class II improved to lower classes. Clinical responses appeared maximal with blood levels of approximately 2.5 µg CoQ10/ml and higher during therapy. The dosage was 100 mg of CoQ10 in soybean oil daily for each patient.(24)
Sacher et al in 1997 reported on their study of 19 congestive cardiomyopathy patients treated with CoQ10. After four months of CoQ10 therapy, functional class improved 20% (3.0 ± 0.4 to 2.4 ± 0.6, p < 0.001) and there was a 27% improvement in mean CHF score (2.8 ± 0.4 to 2.2 ± 0.4, p < 0.001). Therapy with CoQ10 was associated with a mean 25.4% increase in exercise duration and a 14.3% increase in workload. Patients received 30 mg CoQ10 three times per day for 16 weeks. They noted other studies which reported that 75% of patients usually respond to CoQ10 within 90 days and that this is probably based on the time required for CoQ10 apoenzyme biosynthesis. They concluded that CoQ10 therapy is associated with significant functional, clinical, and hemodynamic improvements within the context of an extremely favorable benefit-to-risk ratio. CoQ10 was found to enhance cardiac output by exerting a positive inotropic effect upon the myocardium as well as mild vasodilation. They also noted that in some studies CoQ10 was also shown to exhibit an antiarrhythmic effect.(26)
Schaffer et al in 1999 reviewed various studies demonstrating that taurine supplementation may lead to improvements in patients being treated for cardiomyopathy and CHF. They described a study that found when taurine is substantially decreased in the feline myocardium through dietary changes, the animal develops cardiomyopathy. They also noted a study that found the mortality rate of rabbits with experimental heart failure was significantly reduced in animals maintained on a diet containing 100 mg/kg taurine. Another reviewed study found that a daily oral dose of 4 g taurine caused improvement in symptoms among people with CHF. Schaffer et al described three theories as to why taurine may have beneficial effects on the heart. First, taurine may help reduce salt and fluid load. Second, it may improve contractile function thereby lessening congestive symptoms. Third, it may inhibit the actions of angiotensin II, thereby mimicking the actions of ACE inhibitors.(27)
In 2003, Singh et al studied the combined use of taurine and CoQ10 in 51 patients with AMI or unstable angina. Patients were randomized to receive a combination of 6 g taurine and 120 mg CoQ10 daily (each divided into three doses), or placebo. The mean infarct size was significantly smaller in the intervention group compared to the placebo group. Also, the sum of Q or R waves, the site anterior or inferior to the necrosis, the amplitude and changes in the curves during surveillance were all significantly lower in the intervention group. Further, total complications were shown to be significantly lower in the intervention group than the control group (6 vs. 21, p < 0.05). They reported that combined treatment with taurine and CoQ10 can provide cardioprotective benefits in patients with AMI.(28)
Sole et al reported in 2002 that specific metabolic deficiencies are observed in the failing myocardium including deficiencies of carnitine, CoQ10, thiamin, creatine, taurine and antioxidant vitamins. They described how studies of supplementation with single nutrients in a pharmacological fashion have yielded mixed results and concluded that replacement of just one nutrient is unlikely to completely correct the cascade of interconnected abnormalities found in the failing myocardium. Rather, they recommended supplementation with a wide array of nutrients that could be lacking in the case of CHF. In order to test their theory, Sole et al compared a placebo diet with one enriched with taurine, CoQ10, carnitine, thiamin, creatine, vitamin E, vitamin C and selenium, and fed to cardiomyopathyic hamsters in late stages of the disease. Supplementation for 3 months markedly improved myocyte sarcomeric ultrastructure, developed pressure, +dp/dt and -dp/dt measured in a Langendorff apparatus. Further, they reported on a double-blind, placebo-controlled trial containing these same nutrients given to human patients with ischemic cardiomyopathy. The supplemented group had myocardial levels of taurine, CoQ10 and carnitine restored resulting in a significant decrease in left ventricular end-diastolic volume.(29)
Based upon the numerous studies indicating significant improvement after nutritional supplementation, it seems most treatment protocols for cardiomyopathy, CHF and/or arrhythmias in humans as well as animals would benefit from the inclusion of at least some, if not several, of the nutrients detailed in this report. A proposed nutritional protocol is presented below. While the supplements presented in this protocol have not yet been scientifically tested together for use in cardiac patients, the recommended nutrients are all common in foods and are not known to have toxic effects when given at the doses presented.
It is possible that nutritional supplementation could lessen or eliminate the need for some conventional pharmacological treatments, as has already been documented in some cases with magnesium. Since this is new ground, any reduction of conventional medications should only be done with careful and consistent monitoring by a healthcare professional.
Complex relationships exist between some of the nutrients reported on here and further study is needed to determine ideal doses and combinations of nutritional supplements, both with and without conventional medications, when used to treat diseases of the myocardium.
Proposed Nutritional Protocol Based Upon Current Research
Warning: A few supplements, particularly at higher doses, may cause adverse reactions when combined with some conventional medications. A healthcare professional should review and monitor any nutritional protocol.
Most of the nutrients outlined above are found in a wide variety of food products. It may be possible to obtain adequate amounts of some of these through proper food choices. Below are links to Web pages provided by the U.S. Department of Agriculture which can display detailed nutrient content for most common food products.
USDA Nutrient Database: www.nal.usda.gov/fnic/cgi-bin/nut_search.pl
View the nutrient content of most common food products using this online database.
Nutrient Lists: www.nal.usda.gov/fnic/foodcomp/Data/SR15/wtrank/wt_rank.html
View detailed reports listing foods rich in nutrients such as magnesium or potassium.
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