CoQ10
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This is a wonderful general overview of CoQ10.

Journal of Orthomolecular Medicine 2000; 15(2):63-68.

A Brief Update on Ubiquinone (Coenzyme Q10)

John T. A. Ely, Ph.D.

Radiation Studies, University of Washington, Seattle, WA 98195

And Cheryl A. Krone, Ph.D.

Applied Research Institute, Palmerston North, NZ

Abstract

Ubiquinone is one of the two most important essential nutrients (the other being ascorbic acid). These two molecules, along with other essential nutrients, have been rejected as unpatentable and unprofitable by certain "authorities" and interests, according to expose's by Pauling and others.[1,2] This has been one of the most lethal errors of modern medicine because no cell, organ, function, remedy, etc, can avoid failure unless essential nutrients, especially these two, are optimal. Supplementation of both is mandatory: for ascorbate, lifelong (since humans can't synthesize it); for ubiquinone, increasingly with

age. In this update, to facilitate study of ubiquinone, we seek to assemble in one place vital information that is not widely known.

[we have complete study to link to]

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Another article extolling the virtues of CoQ10.

[Format change 4-26]

Co-enzyme Q10: a new drug for cardiovascular disease.

Greenberg S, Frishman WH.

Department of Medicine, Mt. Sinai Hospital and Medical Center, New York, New York.

Co-enzyme Q10 (ubiquinone) is a naturally occurring substance which has properties potentially beneficial for preventing cellular damage during myocardial ischemia and reperfusion. It plays a role in oxidative phosphorylation and has membrane stabilizing activity. The substance has been used in oral form to treat various cardiovascular disorders including angina pectoris, hypertension, and congestive heart failure. Its clinical importance is now being established in clinical trails worldwide.

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This study describes how beneficial Over-The-Counter (OTC) supplements can be in heart health; especially anti-oxidants. CoQ10 is a very powerful anti-oxidant.

[need to change formatting of 4-5]

Metabolic and nutritional support in acute cardiac failure.

Berger MM, Mustafa I.

Intensive Care Unit and Burns Centre, University Hospital, Lausanne, Switzerland. mette.berger@chuv.hospvd.ch

PURPOSE OF REVIEW: Cardiovascular disease is one of the most important causes of morbidity and mortality in western countries, generating an increasing number of admissions to intensive care units. Cardiac failure has long been associated with nutritional disorders, malnutrition and cachexia being frequent during the late phases of congestive heart failure: undernutrition is also a determinant of outcome, even after cardiac transplantation. RECENT FINDINGS: It has been shown that early metabolic support can improve the recovery of the ischaemic heart. This paper reviews recent findings on substrates that can support the failing myocardium, which are mainly glucose-insulin, glutamine, taurine, selenium, thiamine, folic acid, and omega-3 fatty acids. Ischaemia-reperfusion generates tissue lesions that can be partly prevented through substrate manipulation. SUMMARY: Shifting the substrate metabolism from lipids to carbohydrates and reinforcing the antioxidant status reduces the deleterious biological and clinical consequences of acute ischaemic events. The use of the glucose-insulin-potassium infusion has become widespread with the re-discovery of its value in modulating cellular metabolism and accelerating recovery of the ischaemic myocardium. Antioxidants have gained acceptance in the perioperative phase, as well as in chronic heart failure. This constitutes another piece of evidence in favour of early metabolic and nutritional intervention. There also appears to be room for the prevention of acute deterioration of cardiac function after surgery with the preoperative administration of oral supplements containing omega-3 fatty acids.

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How CoQ10 and carnitine—both provided in CardioFuel--work together.

[ 5-8]

Protective synergic effect of coenzyme Q10 and carnitine on hyperbaric oxygen toxicity.

Bertelli A, Bertelli AA, Giovannini L, Spaggiari P.

Department of Pharmacology, University of Milan, Italy.

The comparative biochemical activities of coenzyme QIO and carnitine can explain the protective synergistic effect of combination of these two substances in preventing the hyperbaric oxygen toxicity in mice. Both convulsions and mortality percentages are more significantly reduced in treated animals with these two substances in combination rather than separately.

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CoQ10 and Vitamin E

Nature usually provides variations on a theme. "Natural" Vitamin E is actually a spread of closely resembled molecules called tocopherols. What is usually sold as "natural" Vitamin E is only alpha-tocopherol, thereby missing the other important variations, such as the beta, delta and gamma varieties. We now know that alpha tocopherol (remember, it's what most people buy as "Vitamin E") can not only act as an anti-oxidant, but also as an oxidant! That means it can oxidize LDL (bad cholesterol), which makes the LDL stick to the lining of the arteries. But this is inhibited in the presence of CoQ10 (called "ubiquinol-10" in this study).

So, his study shows how CoQ10 helps prevent the most commonly used form of Vitamin E from hurting us (which can happen). Read the label!

 [4-7]

Prevention of tocopherol-mediated peroxidation in ubiquinol-10-free human low density lipoprotein.

Bowry VW, Mohr D, Cleary J, Stocker R.

Biochemistry Group, Heart Research Institute, Sydney, New South Wales, Australia.

Oxidation of low density lipoprotein (LDL) may be involved in the development of atherosclerosis. It has recently been shown that alpha-tocopherol (alpha-TOH) can act either as an antioxidant or prooxidant for isolated low density lipoprotein (LDL). In the absence of an effective co-antioxidant, alpha-TOH is a prooxidant and this activity is evidently due to reaction of the alpha-tocopheroxyl radical (alpha-TO.) with the LDL's polyunsaturated lipids (Bowry, V. B., and Stocker, R. (1993) J. Am. Chem. Soc. 115, 6029-6045). Herein we examined the effectiveness of selected natural and synthetic radical scavengers as co-antioxidants for inhibiting peroxyl radical-induced peroxidation in LDL that is devoid of ubiquinol-10 (an effective endogenous co-antioxidant) but still contains most of its natural complement of alpha-TOH. Various quinols, catechols, and aminophenols, as well as ascorbate, 6-palmityl ascorbate, and bilirubin, were very effective co-antioxidants under our test conditions, whereas ordinary phenolic antioxidants, including short-tailed alpha-TOH homologues, were less effective. Reduced glutathione, urate, and Probucol were ineffective. These findings confirm that the prooxidant activity of alpha-TOH in LDL relies heavily on the segregation of water-insoluble radicals (particularly alpha-TO.) into individual LDL particles, since it was those compounds that are expected to either irreversibly reduce alpha-TO. or accelerate the diffusion of radicals between particles which most effectively inhibited the tocopherol-mediated phase of peroxidation. Theoretical and practical implications of these findings are discussed, as is their relevance to the "LDL oxidation" hypothesis of atherogenesis.

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An interesting discussion of the role and mechanism of CoQ10 with respect to its anti-oxidant effects, as well as a link to the aging process.

[4-15]

Ubiquinol: an endogenous antioxidant in aerobic organisms.

Ernster L, Forsmark-Andree P.

Department of Biochemistry, Arrhenius Laboratories, Stockholm University.

Ubiquinone (coenzyme Q), in addition to its function as an electron and proton carrier in mitochondrial and bacterial electron transport linked to ATP synthesis, acts in its reduced form (ubiquinol) as an antioxidant, preventing the initiation and/or propagation of lipid peroxidation in biological membranes and in serum low-density lipoprotein. The antioxidant activity of ubiquinol is independent of the effect of vitamin E, which acts as a chain-breaking antioxidant inhibiting the propagation of lipid peroxidation. In addition, ubiquinol can efficiently sustain the effect of vitamin E by regenerating the vitamin from the tocopheroxyl radical, which otherwise must rely on water-soluble agents such as ascorbate (vitamin C). Ubiquinol is the only known lipid-soluble antioxidant that animal cells can synthesize de novo, and for which there exist enzymic mechanisms that can regenerate the antioxidant from its oxidized form resulting from its inhibitory effect of lipid peroxidation. These features, together with its high degree of hydrophobicity and its widespread occurrence in biological membranes and in low-density lipoprotein, suggest an important role of ubiquinol in cellular defense against oxidative damage. Degenerative diseases and aging may be manifestations of a decreased capacity to maintain adequate ubiquinol levels.

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According to this study, it looks as though a high LDL ("bad cholesterol") to ubiquinone (another name for CoQ10) ratio is a legitimate risk factor for cardiovascular disease. Statin drugs lower CHOL, and LDL, but also CoQ10. We should keep this in mind.

[4-28}

Coenzyme Q10 and coronary artery disease.

Hanaki Y, Sugiyama S, Ozawa T, Ohno M.

Department of Cardiology, Toyohashi National Hospital.

It has been postulated that oxidatively modified low-density lipoprotein (LDL) contributes to the genesis of atherosclerosis. Ubiquinone has been suggested to be an important physiological lipid-soluble antioxidant and is found in LDL fractions in the blood. We measured plasma level of ubiquinone using high-performance liquid chromatography and plasma levels of total cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides in 245 normal subjects (186 males, 59 females) and in 104 patients (55 males, 49 females) who had coronary artery disease not receiving pravastatin and 29 patients (12 males, 17 females) receiving pravastatin. In the normal subjects, the plasma ubiquinone levels did not vary with age. In the patient groups, the plasma total cholesterol and LDL levels were higher and the plasma ubiquinone level lower than in the normal subject group. The LDL/ubiquinone ratio was higher in the patient groups. We found that ubiquinone level, either alone or when expressed in relation to LDL levels, was significantly lower in the patient groups compared with the normal subject group. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitor is thought to prevent atherosclerosis, however, it also inhibits ubiquinone production. The present study revealed that HMG CoA reductase inhibitor decreased plasma cholesterol level, and that it did not improve either the ubiquinone level or the LDL/ubiquinone ratio. From these results, the LDL/ubiquinone ratio is likely to be a risk factor for atherogenesis, and administration of ubiquinone to patients at risk might be needed

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More evidence of how statin drugs deplete all-important CoQ10.

[4-24]

Evidence of plasma CoQ10-lowering effect by HMG-CoA reductase inhibitors: a double-blind, placebo-controlled study.

Ghirlanda G, Oradei A, Manto A, Lippa S, Uccioli L, Caputo S, Greco AV, Littarru GP.

Institute of Internal Medicine, Catholic University Medical School, Rome, Italy.

Inhibitors of HMG-CoA reductase are new safe and effective cholesterol-lowering agents. Elevation of alanine-amino transferase (ALT) and aspartate-amino transferase (AST) has been described in a few cases and a myopathy with elevation of creatinine kinase (CK) has been reported rarely. The inhibition of HMG-CoA reductase affects also the biosynthesis of ubiquinone (CoQIO). We studied two groups of five healthy volunteers treated with 20 mg/day of pravastatin (Squibb, Italy) or simvastatin (MSD) for a month. Then we treated 30 hypercholesterolemic patients in a double-blind controlled study with pravastatin, simvastatin (20 mg/day), or placebo for 3 months. At the beginning, and 3 months thereafter we measured plasma total cholesterol, CoQIO, ALT, AST, CK, and other parameters (urea, creatinine, uric acid, total bilirubin, gamma GT, total protein). Significant changes in the healthy volunteer group were detected for total cholesterol and CoQIO levels, which underwent about a 40% reduction after the treatment. The same extent of reduction, compared with placebo was measured in hypercholesterolemic patients treated with pravastatin or simvastatin. Our data show that the treatment with HMG-CoA reductase inhibitors lowers both total cholesterol and CoQIO plasma levels in normal volunteers and in hypercholesterolemic patients. CoQIO is essential for the production of energy and also has antioxidative properties. A diminution of CoQIO availability may be the cause of membrane alteration with consequent cellular damage.

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This paper describes why everyone who takes a statin drug--no if's, ands or buts--MUST also then take CoQ10.

Frankly, we cannot understand why all doctors who prescribe them do not tell their patients about this.

It's also good to remember the reason WHY the patient was prescribed a statin: heart disease or diabetes. Both these disease processes produce conditions which deplete, and therefore require supplementation of, CoQ10.

[4-17]

Proc. Natl. Acad. Sci. USA

Vol. 87, pp. 8931-8934, November 1990

Medical Sciences

Lovastatin decreases coenzyme Q levels in humans

(hypercholesterolemia/3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors/ubiquinone/drug side effects)

Karl Folkers*1\ Per Langsjoen*, Richard Willis*, Phillip Richardson*, Li-Jun Xia*, Chun-Qu Ye*,

AND HlROO TAMAGAWA*

'University of Texas at Austin, Austin, TX 78712; and *The Health Center at Tyler, The University of Texas at Tyler, Tyler, TX 75710

Contributed by Karl Folkers, June 20, 1990

ABSTRACT       Lovastatin is clinically used to treat patients with hypercholesterolemia and successfully lowers cholesterol levels. The mechanism of action of lovastatin is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase, an enzyme involved in the biosynthesis of cholesterol from acetyl-CoA. Inhibition of this enzyme could also inhibit the intrinsic bio­synthesis of coenzyme Qlo (CoQ10), but there have not been definitive data on whether lovastatin reduces levels of CoQ10 as it does cholesterol. The clinical use of lovastatin is to reduce a risk of cardiac disease, and if lovastatin were to reduce levels of CoQio, this reduction would constitute a new risk of cardiac disease, since it is established that CoQio is indispensable for cardiac function. We have conducted three related protocols to determine whether lovastatin does indeed inhibit the biosyn­thesis of CoQ10. One protocol was done on rats, and is reported in the preceding paper [Willis, R. A., Folkers, K., Tucker, J. L., Ye, C.-Q., Xia, L.-J. & Tamagawa, H. (1990) Proc. Natl. Acad. Sci. USA 87, 8928-8930]. The other two protocols are reported here. One involved patients in a hospital, and the other involved a volunteer who permitted extraordinary mon­itoring of CoQio and cholesterol levels and cardiac function. All data from the three protocols revealed that lovastatin does indeed lower levels of CoQ10. The five hospitalized patients, 43-72 years old, revealed increased cardiac disease from lovastatin, which was life-threatening for patients having class IV cardiomyopathy before lovastatin or after taking lovastatin. Oral administration of CoQ10 increased blood levels of CoQ10 and was generally accompanied by an improvement in cardiac function. Although a successful drug, lovastatin does have side effects, particularly including liver dysfunction, which presum­ably can be caused by the lovastatin-induced deficiency of CoQ10.

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Here we see CoQ10's amazing ability to lower high blood pressure--without dropping it too low. Taking a safe, naturally occurring substance already found in every cell of the body, instead of expensive synthetic drugs—all of which carry negative side effects!

[4-8]

Randomized, double-blind, placebo-controlled trial of coenzyme Q10 in isolated systolic hypertension.

Burke BE, Neuenschwander R, Olson RD.

Research Service, Department of Veterans Affairs Medical Center, Boise, Idaho 83702, USA.

BACKGROUND: Increasing numbers of the adult population are using alternative or complementary health resources in the treatment of chronic medical conditions. Systemic hypertension affects more than 50 million adults and is one of the most common risk factors for cardiovascular morbidity and mortality. This study evaluates the antihypertensive effectiveness of oral coenzyme Q10 (CoQ), an over-the-counter nutritional supplement, in a cohort of 46 men and 37 women with isolated systolic hypertension. METHODS: We conducted a 12-week randomized, double-blind, placebo-controlled trial with twice daily administration of 60 mg of oral CoQ and determination of plasma CoQ levels before and after the 12 weeks of treatment. RESULTS: The mean reduction in systolic blood pressure of the CoQ-treated group was 17.8 +/- 7.3 mm Hg (mean +/- SEM). None of the patients exhibited orthostatic blood pressure changes. CONCLUSIONS: Our results suggest CoQ may be safely offered to hypertensive patients as an alternative treatment option.

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After this study, does anyone think we SHOULDN'T give CoQ10 to those with high blood pressure?

[4-45]

Treatment of essential hypertension with coenzyme Q10.

Langsjoen P, Langsjoen P, Willis R, Folkers K.

Institute for Biomedical Research, University of Texas at Austin 78712, USA.

A total of 109 patients with symptomatic essential hypertension presenting to a private cardiology practice were observed after the addition of CoQIO (average dose, 225 mg/day by mouth) to their existing antihypertensive drug regimen. In 80 per cent of patients, the diagnosis of essential hypertension was established for a year or more prior to starting CoQIO (average 9.2 years). Only one patient was dropped from analysis due to noncompliance. The dosage of CoQIO was not fixed and was adjusted according to clinical response and blood CoQIO levels. Our aim was to attain blood levels greater than 2.0 micrograms/ml (average 3.02 micrograms/ml on CoQIO). Patients were followed closely with frequent clinic visits to record blood pressure and clinical status and make necessary adjustments in drug therapy. Echocardiograms were obtained at baseline in 88% of patients and both at baseline and during treatment in 39% of patients. A definite and gradual improvement in functional status was observed with the concomitant need to gradually decrease antihypertensive drug therapy within the first one to six months. Thereafter, clinical status and cardiovascular drug requirements stabilized with a significantly improved systolic and diastolic blood pressure. Overall New York Heart Association (NYHA) functional class improved from a mean of 2.40 to 1.36 (P < 0.001) and 51% of patients came completely off of between one and three antihypertensive drugs at an average of 4.4 months after starting CoQIO. Only 3% of patients required the addition of one antihypertensive drug. In the 9.4% of patients with echocardiograms both before and during treatment, we observed a highly significant improvement in left ventricular wall thickness and diastolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

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We now know when heart tissue is starved from oxygen--either by a heart attack, or during surgery--the real damage occurs not necessarily from the original oxygen depletion, but rather through chemical changes as oxygen rushes back in. CoQ10 is shown here to help this situation; again, by its tremendous impact on mitochondrial function.

[4-13]

Effect of coenzyme Q10 supplementation on mitochondrial function after myocardial ischemia reperfusion.

Crestanello JA, Doliba NM, Doliba NM, Babsky AM, Niborii K, Osbakken MD, Whitman GJ.

Division of Cardiothoracic Surgery, University of Maryland Medical System, Baltimore, Maryland, USA. crestanello.juan@mayo.edu

BACKGROUND: Coenzyme Q10 (CoQlO) protects myocardium from ischemia-reperfusion (IR) injury as evidenced by improved recovery of mechanical function, ATP, and phosphocreatine during reperfusion. This protection may result from CoQIO's bioenergetic effects on the mitochondria, from its antioxidant properties, or both. The purpose of this study was to elucidate the effects of CoQlO supplementation on mitochondrial function during myocardial ischemia-reperfusion using an isolated mitochondrial preparation. METHODS: Isolated hearts (n = 6/group) from rats pretreated with liposomal CoQlO (10 mg/kg iv, CoQlO), vehicle (liposomal only, Vehicle), or saline (Saline) 30 min before the experiments were subjected to 15 min of equilibration (EQ), 25 min of ischemia (I), and 40 min of reperfusion (RP). Left ventricular-developed pressure (DP) was measured. Mitochondria were isolated at end-equilibration (end-EQ), at end-ischemia (end-I), and at end-reperfusion (end-RP). Mitochondrial respiratory function (State 2, 3, and 4, respiratory control index (RCI, ratio of State 3 to 4), and ADP:O ratio) was measured by polarography using NADH (alpha-ketoglutarate, alpha-KG)- or FADH (succinate, SA)-dependent substrates. RESULTS: CoQlO improved recovery of DP at end-RP (67 +/-11% in CoQlO vs 47 +/- 5% in Vehicle and 50 +/- 11% in Saline, P < 0.05 vs Vehicle and Saline). CoQlO did not change preischemic mitochondrial function. IR decreased State 3 and RCI in all groups using either substrate. CoQlO had no effect in the mitochondrial oxidation of alpha-KG at end-I. CoQlO improved State 3 at end-I when SA was used (167 +/- 21 in CoQlO vs 120 +/- 10 in Saline and 111 +/- 10 ng-atoms 0/min/mg protein in Vehicle, P < 0.05). Using alpha-KG as a substrate, CoQlO improved RCI at end-RP (4.2 +/- 0.2 in CoQlO vs 3.2 +/- 0.2 in Saline and 3.0 +/- 0.3 in Vehicle, P < 0.05). Using SA, CoQlO improved State 3 (181 +/- 10 in CoQlO vs 142 +/- 9 in Saline and 140 +/- 12 ng-atoms 0/min/mg protein in Vehicle, P < 0.05) and RCI (2.21 +/- 0.06 in CoQlO vs 1.85 +/- 0.11 in Saline and 1.72 +/- 0.08 in Vehicle, P < 0.05) at end-RP. CONCLUSIONS: The cardioprotective effects of CoQlO can be attributed to the preservation of mitochondrial function during reperfusion as evidenced by improved FADH-dependent oxidation. (c)2001 Elsevier Science.

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It is necessary to cut off the flow of blood to the heart during some types of cardiac surgery. This study shows that taking CoQ10--and at dosages much less than provided by recommended daily dose of CardioFuel--for only a few days, dramatically reduces the fall off in cardiac output which occurs following such procedures, where the heart muscle is temporarily starved for oxygen.

This study shows how CoQ10 helps the heart recover after it is starved for oxygen (which always happens for a period of time during this surgery) while replacing cardiac valves. Doing so may reduce the need for “inotropic agents—drugs which forcibly increase cardiac output—which further reduce crucial ATP levels within the heart.

[1-9]

Coenzyme Q10: the prophylactic effect on low cardiac output following cardiac valve replacement

J Tanaka, R Tominaga, M Yoshitoshi, K Matsui, M Komori, A Sese, H Yasui and K Tokunaga

A randomized, prospective study of the effectiveness of preoperative administration of coenzyme Q10 on the prophylaxis of postoperative low cardiac output state was performed in 50 patients with acquired valvular diseases necessitating valve replacement. There were 25 patients in the treatment group and 25 in the control group. Patients in the treatment group received 30 to 60 mg of coenzyme Q10 orally for six days before operation. Preoperative clinical variables, operative procedures, total cardiopulmonary bypass time, and aortic cross- clamping time were similar for the two groups. Postoperatively, mild to severe low cardiac output state developed in 28 of 50 patients (56%) and necessitated the administration of considerable amounts of inotropic agent. The treatment group showed a significantly lower incidence of low cardiac output state during the recovery period than the control group (p less than 0.05). These results suggest that preoperative administration of coenzyme Q10 will increase the tolerance of human hearts to ischemia during aortic cross-clamping.

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CoQ10 is so good for the heart, it even brings great benefit for end stage heart failure patients--those waiting for a heart transplant.

[4-6]

Coenzyme Q10 in patients with end-stage heart failure awaiting cardiac transplantation: a randomized, placebo-controlled study.

Berman M, Erman A, Ben-Gal T, Dvir D, Georghiou GP, Stamler A, Vered Y, Vidne BA, Aravot D.

Department of Cardiothoracic Surgery, Heart-Lung Transplant Unit, Rabin Medical Center, Beilinson Campus, Potah Tikva, Israel. mariusby@yahoo.com

BACKGROUND: The number of patients awaiting heart transplantation is increasing in proportion to the waiting period for a donor. Studies have shown that coenzyme Q10 (CoQlO) has a beneficial effect on patients with heart failure. HYPOTHESIS: The purpose of the present double-blind, placebo-controlled, randomized study was to assess the effect of CoQlO on patients with end-stage heart failure and to determine if CoQlO can improve the pharmacological bridge to heart transplantation. METHODS: A prospective double-blind design was used. Thirty-two patients with end-stage heart failure awaiting heart transplantation were randomly allocated to receive either 60 mg U/day of Ultrasome--CoQ10 (special preparation to increase intestinal absorption) or placebo for 3 months. All patients continued their regular medication regimen. Assessments included anamnesis with an extended questionnaire based partially on the Minnesota Living with Heart Failure Questionnaire, 6-min walk test, blood tests for atrial natriuretic factor (ANF) and tumor necrosis factor (TNF), and echocardiography. RESULTS: Twenty-seven patients completed the study. The study group showed significant improvement in the 6-min walk test and a decrease in dyspnea, New York Heart Association (NYHA) classification, nocturia, and fatigue. No significant changes were noted after 3 months of treatment in echocardiography parameters (dimensions and contractility of cardiac chambers) or ANF and TNF blood levels. CONCLUSIONS: The administration of CoQlO to heart transplant candidates led to a significant improvement in functional status, clinical symptoms, and quality of life. However, there were no objective changes in echo measurements or ANF and TNF blood levels. Coenzyme Q10 may serve as an optional addition to the pharmacologic armamentarium of patients with end-stage heart failure. The apparent discrepancy between significant clinical improvement and unchanged cardiac status requires further investigation.

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Hearts harvested for transplantation are preserved in cold solutions. Here is another example of the wonderful things CoQ10 can do for cardiac tissue, with the common link being oxygen starvation.

[4-9]

Effectiveness of coenzyme Q10 on myocardial preservation during hypothermic cardioplegic arrest

Ying-Fu Chen, MD, Young-Tso Lin, MD, Su-Chuan Wu, BS

Kaohsiung, Taiwan

From the Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical College, Kaohsiung, Taiwan.

Received for publication Oct. 22, 1992. Accepted for publication April 16, 1993. Address for reprints: Ying-Fu Chen, MD, Division of Cardiovascular Surgery, Department of Surgery, Kaohsiung Medical College, 100 Shih-Chuan 1st Rd., Kaohsiung, Taiwan.

Abstract

A prospective, randomized, double-blind trial assigned 11 patients to receive coenzyme Q10 and 11 to receive none. Patients pretreated with coenzyme Q10 had a lower left atrial pressure and a lesser

incidence of low cardiac output. They also had a wider pulse pressure. The right and left ventricular myocardial ultrastructure was better preserved in patients receiving preoperative treatment with coenzyme Q10. There was no demonstrable benefit to the atrial myocardium. (J

THORAC CARDIOVASC SURG 1994;107:242-7)

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CoQ10 can even prevent the well-known heart failure caused by a certain type of cancer chemotherapy.

[4-14]

Cardiomyopathy and other chronic toxic effects induced in rabbits by doxorubicin and possible prevention by coenzyme Q10.

Domae N, Sawada H, Matsuyama E, Konishi T, Uchino M.

Cumulative dose-dependent toxic effects, particularly cardiomyopathy, induced by doxorubicin and the possible prevention by coenzyme Q10 (CoQIO) were studied in rabbits. In rabbits given doxorubicin alone, there was considerable body weight loss, alopecia, pancytopenia, significant increase in serum creatine phosphokinase and LDH, and ECG changes characterized by tachycardia, flat and inverted T wave, the premature ventricular contractions. In rabbits given doxorubicin plus CoQIO, the only change was pancytopenia. In rabbits treated with doxorubicin alone, the most prominent histologic changes were observed in mitochondria of myocytes, and these changes were characterized by loss of outer membrane, disarrangement of cristae, and formation of numerous concentric lamellae. In addition to mitochondrial changes, there were numerous vacuolizations and extensive depositions of both electron-dense and membranous laminated bodies in the sarcoplasm and disarrangement of Z-band and filamentous changes of myofibrils. Numerous vacuolizations in the capillary endothelial cytoplasm in the myocardium were also conspicuous. On the other hand, few significant morphologic changes were seen in the nuclei of myocytes. There were few ECG and histopathologic changes in rabbits treated with both doxorubicin and CoQIO. These findings suggest that the cardiomyopathy of doxorubicin may be prevented or is at least inhibited by CoQIO. The mechanisms of both doxorubicin-induced cardiomyopathy and its prevention by CoQIO are discussed.

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