Heart Disease and Coenzyme Q10

Coronary Disease

Coenzyme Q10 has the ability to protect the heart during periods of ischemia (lack of  oxygen).3 This lack of  oxygen occurs in heart disease and is usually caused by narrowing or blockage of the  coronary arteries. Ischemia can also occur during medical procedures such as open heart  surgery, coronary bypass and angioplasty, and is responsible for causing serious physical  symptoms such as angina, heart failure, and sudden death.

Recent medical studies have reported that pretreatment with Coenzyme Q10 minimizes the  myocardial injury caused by heart bypass surgery and improves heart function compared to  patients not pretreated with Coenzyme Q10.8

In one study 150 mg per day of Coenzyme Q10 reduced the frequency of anginal attacks by  up to 46% while improving the capacity for physical activity in patients with angina.3

Congestive Heart Failure

Several clinical trials have recently shown that when patients with heart failure are  treated with Coenzyme Q10 for months to years, serious complications such as pulmonary  edema and ventricular arrhythmia are reduced in frequency. The number of hospitalizations  is reduced and survival is increased.10

Another large clinical study involving 1715 patients concluded that a short period of  treatment (4 weeks) with 50 mg per day Coenzyme Q10 improves shortness of breath,  palpitations, cyanosis, edema, heart rate and blood pressure in patients with stabilized  heart failure. The study's author concluded that a daily dosage of 50-100 mg increases  contractile activity rapidly.13

Patients with heart failure generally respond to Coenzyme Q10, as their tissues and  blood have deficient levels of Coenzyme Q10 that results from inadequate cellular  biosynthesis.11

Myocardial tissue levels of Coenzyme Q10 can be significantly restored with an oral  dosage of 100 mg per day for 5 months. Deficient tissue levels can be  increased and may be  normalized with proper compliance.12

Heart Disease Hypertension and Coenzyme Q10

MEDLINE EXPRESS (R) 10/97-11/97 1 of 45

TI: Statin drugs: a double-edged sword? [letter]
AU: Levin-WM
SO: Hosp-Pract-Off-Ed. 1997 Aug 15; 32(8): 44

MEDLINE EXPRESS (R) 1/97-9/97 15 of 45

TI: Plasma ubiquinol-10 is decreased in patients with hyperlipidaemia.
AU: Kontush-A; Reich-A; Baum-K; Spranger-T; Finckh-B; Kohlschutter-A; Beisiegel-U
SO: Atherosclerosis. 1997 Feb 28; 129(1): 119-26
AB: Ubiquinol-10, the reduced form of ubiquinone-10 (coenzyme Q10), is a potent lipophilic antioxidant present in nearly all human tissues. The exceptional oxidative lability of ubiquinol-10 implies that it may represent a sensitive index of oxidative stress. The present study was undertaken to assess the hypothesis that the level of ubiquinol-10 in human plasma can discriminate between healthy subjects and patients who are expected to be subjected to an increased oxidative stress in vivo.  Using a newly developed method, we measured plasma ubiquinol-10 in 38 hyperlipidaemic patients with and without further complications, such as coronary heart disease, hypertension, or liver disease, and in 30 healthy subjects. The oxidizability of plasma samples obtained from hyperlipidaemic patients was found to be increased in comparison with control subjects, suggesting that the patients were subjected to a higher oxidative stress in vivo than the controls. Plasma ubiquinol-10, expressed as a percentage of total ubiquinol-10 + ubiquinone-10 or normalized to plasma lipids, was lower in the patients than in controls (P = 0.001 and 0.008, respectively). The proportion of ubiquinol-10 decreased in the order young controls > aged controls > hyperlipidaemic patients without complications > hyperlipidaemic patients with complications (P = 0.003). A negative correlation was found between the proportion of ubiquinol-10 and plasma triglycerides. The hyperlipidaemic patients with hypertension had a lower proportion of ubiquinol-10 than subjects without. When the study population was divided into smokers and non-smokers, plasma ubiquinol-10 was found to be reduced amongst smokers, independently of whether it was expressed as a percentage of total ubiquinol-10 + ubiquinone-10 (P = 0.006) or normalized to plasma lipids (P = 0.009). These data suggest that the level of ubiquinol-10 in human plasma may represent a sensitive index of oxidative stress in vivo especially indicative of early oxidative damage. Measuring plasma ubiquinol-10 can be proposed as a practical approach to assess oxidative stress in humans.

MEDLINE EXPRESS (R) 1/97-9/97 18 of 45
TI: Prognostic implications of elevated creatine kinase after coronary angioplasty [letter]
AU: Herschfus-JA
SO: JAMA. 1997 May 28; 277(20): 1593

MEDLINE EXPRESS (R) 1/97-9/97 22 of 45
TI: Dietary coenzyme Q10 supplementation alters platelet size and inhibits human vitronectin (CD51/CD61) receptor expression.
AU: Serebruany-VL; Ordonez-JV; Herzog-WR; Rohde-M; Mortensen-SA; Folkers-K; Gurbel-PA
SO: J-Cardiovasc-Pharmacol. 1997 Jan; 29(1): 16-22
AB: Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10, ubiquinone). Several mechanisms have been proposed to explain the effects of CoQ10, but a comprehensive explanation of its cardioprotective properties is still lacking. One attractive theory links ubiquinone with the inhibition of platelets. The effect of CoQ10 intake on platelet size and surface antigens was examined in human volunteers. Study participants received 100 mg of CoQ10 twice daily in addition to their usual diet for 20 days. Receptor expression was measured by flow cytometry  with monoclonal murine anti-human antibodies CD9 (p24), CD42B (Ib), CD41b (IIb), CD61 (IIIa), CD41a (IIb/IIIa), CD49b (VLA-2), CD62p (P selectin), CD31 (PECAM-1), and CD51/CD61 (vitronectin). An increase of total serum CoQ10 level (from 0.6 +/- 0.1 to 1.8 +/- 0.3 micrograms/ml; p  MEDLINE EXPRESS (R) 1/97-9/97 27 of 45

TI: Effect of protection and repair of injury of mitochondrial membrane-phospholipid on prognosis in patients with dilated cardiomyopathy.
 AU: Ma-A; Zhang-W; Liu-Z
SO: Blood-Press-Suppl. 1996; 3: 53-5
AB: We have already proved that the mitochondrial membrane-phospholipid (MMP) injury changes of peripheral lymphocytes in patients with heart failure can be used as an injury indicator of myocardia, and are related to the long-term prognosis. In the present study, MMP localization of the peripheral lymphocytes was performed by modified Demer's tricomplex flocculation method, and we compared the changes,  after classification, between the pre-treatment and the 12-week post-treatment, of coenzyme Q10 (Co.Q10) and captopril in 61 hospitalized patients with dilated cardiomyopathy (DCM). They were followed up for 16.1 +/- 7.8 months (mean). The results showed that compared with the placebo, Co.Q10 and captopril could significantly protect against and repair MMP injury and improve the heart function of patients with DCM after 12 weeks, and the 2-year survival rate rose significantly by 72.7% for Co.Q10, and 64.0% for captopril, vs 24.7% for placebo. As for Longrank test, X2 equals 4.660 and 6.318, respectively, with both p  MEDLINE EXPRESS (R) 1/97-9/97 32 of 45

TI: Metabolic approach to myocardial ischemia: a novel therapeutic strategy for patients with coronary artery disease?
AU: Rizzon-P; Iliceto-S; Marangelli-V
SO: Cardiologia. 1995 Oct; 40(10): 717-20

MEDLINE EXPRESS (R) 1/97-9/97 33 of 45

TI: [Coenzyme Q10 and alpha-tocopherol in patients after heart transplantation]
AU: Kucharska-J; Gvozdjakova-A; Mizera-S; Margitfalvi-P; Schreinerova-Z; Schramekova-E; Solcanska-K; Notova-P; Pechan-I; Fabian-J
SO: Bratisl-Lek-Listy. 1996 Oct; 97(10): 603-6
AB: Pathobiochemical mechanisms which participate in the rejection of transplanted heart are not fully clarified. A significant role in this process can be played by endogenous antioxidants, especially coenzyme Q10 which aside from its antioxidative properties is inevitable for cellular bioenergy. The authors investigated the concentration of Q10 alpha-tocopherol in endomyocardial biopsies in the blood in 11 patients from 1 to 9 years of age after transplantation of the heart (HTx-pat) examined in UKVCH in Bratislava who were compared with the group of 13 patients with cardiopathies of unclear origin (KPNP-pat) as possible candidates for  transplantation. They detected a decreased concentration of coenzyme Q10 in the myocardium and blood of HTx-patients. Levels of alpha-to-copherol in the myocardium were identical in both groups, in plasma they were higher in patients after HTx. The authors suppose that the levels of coenzyme Q10 in patients after HTx can be influenced by an increased production of free oxygen radicals during rejection episodes, as well as immunosuppressive therapy, and indicate to the possible consequences of this decrease. The presented results provide the first information on the levels of coenzyme Q10 and alpha-tocopherol in patients after transplantation of the heart, registered and controlled in the Slovak Republic. They can contribute to the clarification of some pathobiochemical mechanisms of rejection, respectively to their therapeutic effect. (Fig. 2, Ref. 16.).

MEDLINE EXPRESS (R) 1/97-9/97 37 of 45

TI: Lipid-lowering drugs and mitochondrial function: effects of HMG-CoA reductase inhibitors on serum ubiquinone and blood lactate/pyruvate ratio.
AU: De-Pinieux-G; Chariot-P; Ammi-Said-M; Louarn-F; Lejonc-JL; Astier-A; Jacotot-B; Gherardi-R
SO: Br-J-Clin-Pharmacol. 1996 Sep; 42(3): 333-7
AB: 1. Statins inhibit synthesis of mevalonate, a precursor of ubiquinone that is a central compound of the mitochondrial respiratory chain. The main adverse effect of  statins is a toxic myopathy possibly related to mitochondrial dysfunction. 2. This study was designed to evaluate the effect of lipid-lowering drugs on ubiquinone (coenzyme Q10) serum level and on mitochondrial function assessed by blood lactate/pyruvate ratio. 3. Eighty hypercholesterolaemic patients (40 treated by statins, 20 treated by fibrates, and 20 untreated patients, all 80 having total cholesterol levels > 6.0 mmol l-1) and 20 healthy controls were included. Ubiquinone serum level and blood lactate/pyruvate ratio used as a test for mitochondrial dysfunction were evaluated in all subjects. 4. Lactate/pyruvate ratios were significantly higher in patients treated by statins than in untreated hypercholesterolaemic patients or in healthy controls (P  MEDLINE EXPRESS (R) 1/97-2/97 1 of 40
TI: Coenzyme Q10 treatment may be protective during coronary artery bypass operations [letter]
AU: Mortensen-SA
SO: Ann-Thorac-Surg. 1996 Oct; 62(4): 1243-4

MEDLINE EXPRESS (R) 1/96-11/96 5 of 25
TI: Protection by coenzyme Q10 of tissue reperfusion injury during abdominal aortic cross-clamping.
AU: Chello-M; Mastroroberto-P; Romano-R; Castaldo-P; Bevacqua-E; Marchese-AR
SO: J-Cardiovasc-Surg-Torino. 1996 Jun; 37(3): 229-35
AB: PURPOSE: To evaluate the effect of coenzyme Q10 in reducing the skeletal muscle reperfusion injury following clamping and declamping the abdominal aorta.  METHODS: 30 patients undergoing elective vascular surgery for abdominal aortic aneurysm or obstructive aorto-iliac disease were randomly divided into two groups: patients in group I were treated with coenzyme Q10 (150 mg/day) for seven days before operation, and those in group II received a placebo. We studied the hemodynamic profile in each patient during clamping and declamping of the abdominal aorta. The plasma concentrations of thiobarbituric acid reactive substances (malondialdhehyde), conjugated dienes, creatine kinase and lactate dehydrogenase were measured in samples from both arterial and inferior vena cava sites. Serial sampling was performed after induction of anesthesia, 5 and 30 minutes after abdominal aortic cross clamping, 5 and 30 minutes after aortic cross-clamp removal. RESULTS: The concentrations of malondialdehyde, conjugated dienes, creatine kinase and lactate dehydrogenase in patients who received CoQ10 were significantly lower than in the placebo group. Decrease of plasma malondialdehyde concentrations correlated positively (p MEDLINE EXPRESS (R) 1/96-10/96 6 of 469
TI: Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations.
AU: Taggart-DP; Jenkins-M; Hooper-J; Hadjinikolas-L; Kemp-M; Hue-D; Bennett-G
SO: Ann-Thorac-Surg. 1996 Mar; 61(3): 829-33
AB: BACKGROUND: Coenzyme Q10 (CoQ10) is a naturally occurring vitamin-like substance that may have a beneficial role in ischemia-reperfusion injury. Coenzyme Q10 administered either as an additive to cardioplegia or as long-term preoperative oral supplementation has been reported to ameliorate myocardial injury after cardiac operations. METHODS: To determine whether short-term supplementation with large doses of CoQ10 (600 mg in divided doses 12 hours before operation) was effective in myocardial protection, 20 patients with well-preserved left ventricular  function (ejection fraction greater than 0.50) undergoing elective coronary revascularization were enrolled in a prospective, double-blind, placebo-controlled randomized trial. Serial concentrations of CoQ10, myoglobin, creatine kinase MD fraction, and cardiac troponin T were measured preoperatively and 1, 6, 24, 72, and 120 hours postoperatively. Efficacy of myocardial protection was also assessed by clinical outcome and serial changes in electrocardiographic indices. RESULTS: The patient groups were similar with respect to preoperative and intraoperative characteristics. There was no significant difference in the preoperative plasma levels of CoQ10. These levels fell significantly in both groups after operation, although the magnitude of the decrease was less in the CoQ10-supplemented group (43% versus 60%). In both groups, there were significant postoperative increases in myoglobin, creatine kinase MB fraction, and cardiac troponin T. The magnitude of increases in  cardiac troponin T was greater in the CoQ10-supplemented group, reaching marginal overall statistical significance (p = 0.06). CONCLUSIONS: Short-term supplementation with large doses of CoQ10 does not lead to improved myocardial protection in patients undergoing coronary revascularization with well-preserved ventricular function and relatively short ischemic times.

MEDLINE EXPRESS (R) 1/96-10/96 8 of 469
TI: Elucidation of a tripartite mechanism underlying the improvement in cardiac tolerance to ischemia by coenzyme Q10 pretreatment.
AU: Crestanello-JA; Kamelgard-J; Lingle-DM; Mortensen-SA; Rhode-M; Whitman-GJ
SO: J-Thorac-Cardiovasc-Surg. 1996 Feb; 111(2): 443-50
AB: Coenzyme Q10, which is involved in mitochondrial adenosine triphosphate production, is also a powerful antioxidant. We hypothesize that coenzyme Q10 pretreatment protects myocardium from ischemia reperfusion injury both by its ability to increase aerobic energy production and by protecting creatine kinase from oxidative inactivation during reperfusion. Isolated hearts (six per group) from rats pretreated with either coenzyme Q10, 20 mg/kg intramuscularly and 10 mg/kg intraperitoneally (treatment) or vehicle only (control) 24 and 2 hours before the experiment were subjected to 15 minutes of equilibration, 25 minutes of ischemia,  and 40 minutes of reperfusion. Developed pressure, contractility, compliance, myocardial oxygen consumption, and myocardial aerobic efficiency were measured. Phosphorus 31 nuclear magnetic resonance (31P-NMR) spectroscopy was used to determine adenosine triphosphate and phosphocreatine concentrations as a percentage of a methylene diphosphonic acid standard. Hearts were assayed for myocardial coenzyme Q10 and myocardial creatine kinase activity at end equilibration and at reperfusion. Treated hearts showed higher myocardial coenzyme Q10 levels (133 +/- 5 micrograms/gm ventricle versus 117 +/- 4 micrograms/gm ventricle, p  MEDLINE EXPRESS (R) 1/96-10/96 18 of 469
TI: Free radicals, oxidative stress, oxidized low density lipoprotein (LDL), and the heart: antioxidants and other strategies to limit cardiovascular damage.
AU: Sinatra-ST; DeMarco-J
SO: Conn-Med. 1995 Oct; 59(10): 579-88
AB: The heart is the most susceptible of all the organs to premature aging and free radical oxidative stress. Clinical research has clearly documented the role of free radical damage and the progression of numerous degenerative diseases, particularly cardiovascular disease. This may be the result of acute ischemia-reperfusion injury, endothelial damage of hyperhomocysteinemia, as well as chronic oxidative damage secondary to lipid peroxidation. Fortunately, although highly responsive, and  therefore vulnerable to the effects of oxidative stress, the heart is also receptive to the benefits of targeted phytonutrients, antioxidants, and nutritionals. The effects of antioxidant nutrients have been extensively evaluated in epidemiological, population, and clinical studies. Phytonutrients such as the natural flavonoids and carotenoids found in fresh fruits and vegetables or vitamins C, E, and beta-carotene have powerful antioxidant effects. In addition, minerals like selenium and nutrients such as coenzyme Q10 will minimize free radical risk and optimize a favorable outcome from the ubiquitous presence of oxidative stress on the cardiovascular system. The B complex, particularly folic acid, B12, and B6 are also essential in the prevention of hyperhomocysteinemia, another major risk factor for the circulatory system. Measures to minimize accumulation of heavy metals in the body, especially iron and copper, which are capable of initiating adverse free radical reactions, will also help to assuage oxidative stress. Thus, the combination of a healthy diet supplemented with antioxidants and phytonutrients may be useful in the prevention and promotion of optimum cardiovascular health.

MEDLINE EXPRESS (R) 1/96-10/96 19 of 469
TI: Human atherosclerotic plaque contains both oxidized lipids and relatively large amounts of alpha-tocopherol and ascorbate.
 AU: Suarna-C; Dean-RT; May-J; Stocker-R
SO: Arterioscler-Thromb-Vasc-Biol. 1995 Oct; 15(10): 1616-24
AB: We assessed the antioxidant status and contents of unoxidized and oxidized lipids in freshly obtained, homogenized samples of both normal human iliac arteries and carotid and femoral atherosclerotic plaque. Optimal sample preparation involved homogenization of human atherosclerotic plaque for 5 minutes, which resulted in  recovery of most of the unoxidized and oxidized lipids without substantial destruction of endogenous vitamins C and E and 87% and 43% recoveries of added standards of alpha-tocotrienol and isoascorbate, respectively. The total protein, lipid, and antioxidant levels obtained from human plaque varied among donors, although the reproducibility of replicates from a single sample was within 3%, except for ubiquinone-10 and ascorbate, which varied by 20% and 25%, respectively. Plaque samples contained significantly more ascorbate and urate than control arteries, with no discernible difference in the vitamin C redox status between plaque and control materials. The concentrations of alpha-tocopherol and ubiquinone-10 were comparable in plaque samples and control arteries. However, approximately 9 mol percent of plaque alpha-tocopherol was present as alpha-tocopherylquinone, whereas this oxidation product of vitamin E was not detectable in control arteries.  Coenzyme Q10 in plaque and control arteries was only detected in the oxidized form ubiquinone-10, although coenzyme Q10 oxidation may have occurred during processing. The most abundant of all studied lipids in plaque samples was free cholesterol, followed by cholesteryl oleate and cholesteryl linoleate (Ch18:2). Approximately 30% of plaque Ch18:2 was oxidized, with 17%, 12%, and 1% present as fatty acyl hydroxides, ketones, and hydroperoxides, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

MEDLINE EXPRESS (R) 1991-1995 21 of 469
TI: The roles of coenzyme Q10 and vitamin E on the peroxidation of human low density lipoprotein subfractions.
AU: Alleva-R; Tomasetti-M; Battino-M; Curatola-G; Littarru-GP; Folkers-K
SO: Proc-Natl-Acad-Sci-U-S-A. 1995 Sep 26; 92(20): 9388-91
AB: The aim of our study was to investigate the relationships between the levels of coenzyme Q10 (CoQ10) and vitamin E and the levels of hydroperoxide in three  subfractions of low density lipoproteins (LDL) that were isolated from healthy donors. LDL3, the densest of the three subfractions, has shown statistically significant lower levels of CoQ10 and vitamin E, which were associated with higher hydroperoxide levels when compared with the lighter counterparts. After CoQ10 supplementation, all three LDL subfractions had significantly increased CoQ10 levels. In particular, LDL3 showed the highest CoQ10 increase when compared with  LDL1 and LDL2 and was associated with a significant decrease in hydroperoxide level. These results support the hypothesis that the CoQ10 endowment in subfractions of LDL affects their oxidizability, and they have important implications for the treatment of disease.

MEDLINE EXPRESS (R) 1991-1995 23 of 469
TI: Treatment of warfarin-induced hair loss with ubidecarenone [letter]
AU: Nagao-T; Ibayashi-S; Fujii-K; Sugimori-H; Sadoshima-S; Fujishima-M
SO: Lancet. 1995 Oct 21; 346(8982): 1104-5

MEDLINE EXPRESS (R) 1991-1995 51 of 469
TI: Treatment of essential hypertension with coenzyme Q10.
AU: Langsjoen-P; Langsjoen-P; Willis-R; Folkers-K
SO: Mol-Aspects-Med. 1994; 15 Suppl: S265-72
AB: A total of 109 patients with symptomatic essential hypertension presenting to a private cardiology practice were observed after the addition of CoQ10 (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 CoQ10 (average 9.2 years). Only one patient was dropped from analysis due to noncompliance. The dosage of CoQ10 was not fixed and was adjusted according to clinical response and blood CoQ10 levels. Our aim was to attain blood levels greater than 2.0 micrograms/ml (average 3.02 micrograms/ml on CoQ10). 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  MEDLINE EXPRESS (R) 1991-1995 52 of 469
TI: Effect of dietary coenzyme Q10 as an antioxidant in human plasma.
AU: Weber-C; Jakobsen-TS; Mortensen-SA; Paulsen-G; Holmer-G
SO: Mol-Aspects-Med. 1994; 15 Suppl: s97-102
AB: A human study including 22 volunteers was conducted to investigate the antioxidative effect in blood of dietary coenzyme Q10 supplementation. The levels of alpha-tocopherol, ascorbic acid, lipid peroxidation (measured as TBARS) and the redox status of CoQ10 (reduced CoQ10/total CoQ10) were measured in plasma as markers for the antioxidative status once a week during the study period. To introduce an increased oxidative stress, a fish oil supplementation was given. The  levels of alpha-tocopherol and ascorbic acid and the redox status did not change upon CoQ10 supplementation, while the level of TBARS decreased. The decrease in TBARS might be ascribed to an antioxidative effect of the supplied CoQ10. The constant redox level of CoQ10 during the CoQ10 supplementation shows that the exogenous CoQ10 is reduced during absorption and subsequent incorporation into lipoproteins, which is a prerequisite for its antioxidative function. The fish oil  supplementation resulted in a higher TBARS level and a lower alpha-tocopherol level, but the redox level of CoQ10 was unchanged. In conclusion, the CoQ10 supplementation resulted in a higher plasma level of reduced CoQ10 and a lower TBARS level, but sparing of other plasma antioxidants (i.e. ascorbic acid and alpha-tocopherol) was not observed.

MEDLINE EXPRESS (R) 1991-1995 54 of 469
TI: Metabolic implications of coenzyme Q10 in red blood cells and plasma lipoproteins.
AU: Littarru-GP; Battino-M; Tomasetti-M; Mordente-A; Santini-S; Oradei-A; Manto-A; Ghirlanda-G
SO: Mol-Aspects-Med. 1994; 15 Suppl: s67-72
AB: Plasma coenzyme Q10 (CoQ10) is currently assayed in our laboratory for its well-known diagnostic meaning; in fact plasma CoQ10 levels are inversely related to metabolic demand. Definite levels of CoQ10 are also found in white and red blood cell components, as well as in platelets. Plasma and erythrocyte CoQ10 has a well assessed antioxidant role, which was demonstrated through a series of experiments. Erythrocytes previously enriched with exogenous CoQ10 were found more resistant to a hemolysis induced by a free radical initiator. Several enzymatic activities of erythrocyte ghosts were also protected by different side chain CoQ homologues, both when reduced and, although at a lesser extent, in the oxidized state. CoQ was not effective in preventing metal-catalyzed oxidation of erythrocyte membrane enzymes, and this effect is likely to be due to lack of interaction of CoQ with the metal target. Moreover CoQ was able to protect isolated enzymes and erythrocyte membrane bound enzymes from the inactivating effect of free radicals generated by water sonolysis or radiolysis. As far as plasma lipoproteins are concerned it is well known that LDL isolated from healthy volunteers supplemented with CoQ10 are more resistant to peroxidation induced by an azoinitiator. We  started to systematically investigate CoQ10 and vitamin E levels in isolated human LDL and HDL. Both CoQ10 and vitamin E concentrations, referred to protein, were found higher in LDL than in HDL. Susceptibility to exogenously applied peroxidation did not correlate with the endogeneous content of the two antioxidants, possibly on the basis of different lipid content of these lipoproteins.

MEDLINE EXPRESS (R) 1991-1995 56 of 469
TI: Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure. CoQ10 Drug Surveillance Investigators.
AU: Baggio-E; Gandini-R; Plancher-AC; Passeri-M; Carmosino-G
SO: Mol-Aspects-Med. 1994; 15 Suppl: s287-94
AB: Digitalis, diuretics and vasodilators are considered the standard therapy for patients with congestive heart failure, for which treatment is tailored according to the severity of the syndrome and the patient profile. Apart from the clinical seriousness, heart failure is always characterized by an energy depletion status, as indicated by low intramyocardial ATP and coenzyme Q10 levels. We investigated safety and clinical efficacy of Coenzyme Q10 (CoQ10) adjunctive treatment in congestive heart failure which had been diagnosed at least 6 months previously and treated with standard therapy. A total of 2664 patients in NYHA classes II and III were enrolled in this open noncomparative 3-month postmarketing study in 173 Italian centers. The daily dosage of CoQ10 was 50-150 mg orally, with the majority of patients (78%) receiving 100 mg/day. Clinical and laboratory parameters were evaluated at the entry into the study and on day 90; the assessment of clinical signs and symptoms was made using from two-to seven-point scales. The results show a low incidence of side effects: 38 adverse effects were reported in 36 patients (1.5%)  of which 22 events were considered as correlated to the test treatment. After three months of test treatment the proportions of patients with improvement in clinical signs and symptoms were as follows: cyanosis 78.1%, oedema 78.6%, pulmonary rales 77.8%, enlargement of liver area 49.3%, jugular reflux 71.81%, dyspnoea 52.7%, palpitations 75.4%, sweating 79.8%, subjective arrhythmia 63.4%, insomnia 662.8%, vertigo 73.1% and nocturia 53.6%. Moreover we observed a contemporary  improvement of at least three symptoms in 54% of patients; this could be interpreted as an index of improved quality of life.

MEDLINE EXPRESS (R) 1991-1995 59 of 469
TI: Coenzyme Q10 in essential hypertension.
AU: Digiesi-V; Cantini-F; Oradei-A; Bisi-G; Guarino-GC; Brocchi-A; Bellandi-F; Mancini-M; Littarru-GP
SO: Mol-Aspects-Med. 1994; 15 Suppl: s257-63
AB: This study was undertaken to clarify the mechanism of the antihypertensive effect of coenzyme Q10 (CoQ10). Twenty-six patients with essential arterial hypertension were treated with oral CoQ10, 50 mg twice daily for 10 weeks. Plasma CoQ10, serum total and high-density lipoprotein (HDL) cholesterol, and blood pressure were determined in all patients before and at the end of the 10-week period. At the end of the treatment, systolic blood pressure (SBP) decreased from 164.5 +/- 3.1 to 146.7 +/- 4.1 mmHg and diastolic blood pressure (DBP) decreased from 98.1 +/- 1.7 to 86.1 +/- 1.3 mmHg (P MEDLINE EXPRESS (R) 1991-1995 64 of 469
TI: Coenzyme Q10 levels, plasma lipids and peroxidation extent in renal failure and in hemodialytic patients.
AU: Lippa-S; Colacicco-L; Calla-C; Sagliaschi-G; Angelitti-AG
SO: Mol-Aspects-Med. 1994; 15 Suppl: s213-9
AB: Coenzyme Q10 (CoQ10), vitamin E, triglycerides and conjugated dienes were measured in a group of 48 patients on chronic hemodialysis, in 15 uremic patients  and in a control group of 10 normal subjects. CoQ10 levels were significantly lower (P  MEDLINE EXPRESS (R) 1991-1995 67 of 469
TI: Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors.
AU: Bargossi-AM; Grossi-G; Fiorella-PL; Gaddi-A; Di-Giulio-R; Battino-M
SO: Mol-Aspects-Med. 1994; 15 Suppl: s187-93
AB: The biosynthetic pathway of the CoQ polyisoprenoid side chain, starting from acetyl-CoA and proceeding through mevalonate and isopentenylpyrophosphate, is the same as that of cholesterol. We performed this study to evaluate whether vastatins (hypocholesterolemic drugs that inhibit HMG-CoA reductase) modify blood levels of ubiquinone. Thirty-four unrelated outpatients with hypercholesterolemia (IIa phenotype) were treated with 20 mg of simvastatin for a 6-month period (group S) or with 20 mg of simvastatin plus 100 mg CoQ10 (group US). The following  parameters were evaluated at time 0, 45, 90, 135 and 180 days: total plasma cholesterol (TC), HDL-cholesterol, LDL-cholesterol (LDL-C), triglycerides (TG), apo A1, apo B and CoQ10 in plasma and platelets. In the S group, there was a marked decrease in TC and LDL-C (from 290.3 mg/dl to 228.7 mg/dl for TC and from 228.7 mg/dl to 167.6 mg/dl for LDL-C) and in plasma CoQ10 levels from 1.08 mg/dl to 0.80 mg/dl. In contrast, in the US group we observed a significant increase of CoQ10 in plasma (from 1.20 to 1.48 mg/dl) while the hypocholesterolemic effect was similar to that observed in the S group. Platelet CoQ10 also decreased in the S group (from 104 to 90 ng/mg) and increased in the US group (from 95 to 145 ng/mg). This study demonstrates that simvastatin lowers both LDL-C and apo B plasma levels together with the plasma and platelet levels of CoQ10, and that CoQ10 therapy prevents both plasma and platelet CoQ10 decrease, without affecting the cholesterol lowering effect of simvastatin.

MEDLINE EXPRESS (R) 1991-1995 69 of 469
TI: Usefulness of coenzyme Q10 in clinical cardiology: a long-term study.
AU: Langsjoen-H; Langsjoen-P; Langsjoen-P; Willis-R; Folkers-K
SO: Mol-Aspects-Med. 1994; 15 Suppl: s165-75
AB: Over an eight year period (1985-1993), we treated 424 patients with various forms of cardiovascular disease by adding coenzyme Q10 (CoQ10) to their medical  regimens. Doses of CoQ10 ranged from 75 to 600 mg/day by mouth (average 242 mg). Treatment was primarily guided by the patient's clinical response. In many instances, CoQ10 levels were employed with the aim of producing a whole blood level greater than or equal to 2.10 micrograms/ml (average 2.92 micrograms/ml, n = 297). Patients were followed for an average of 17.8 months, with a total accumulation of 632 patient years. Eleven patients were omitted from this study: 10 due to non-compliance and one who experienced nausea. Eighteen deaths occurred during the study period with 10 attributable to cardiac causes. Patients were divided into six diagnostic categories: ischemic cardiomyopathy (ICM), dilated cardiomyopathy (DCM), primary diastolic dysfunction (PDD), hypertension (HTN), mitral valve prolapse (MVP) and valvular heart disease (VHD). For the entire group and for each diagnostic category, we evaluated clinical response according to the New York Heart Association (NYHA) functional scale, and found significant improvement. Of 424 patients, 58 per cent improved by one NYHA class, 28% by two classes and 1.2% by three classes. A statistically significant improvement in myocardial function was documented using the following echocardiographic parameters: left ventricular wall thickness, mitral valve inflow slope and fractional shortening. Before treatment with CoQ10, most patients were taking from one to five cardiac medications. During this study, overall medication requirements dropped considerably: 43% stopped between one and three drugs. Only 6% of the patients required the addition of one drug. No apparent side effects from CoQ10 treatment were noted other than a single case of transient nausea. In conclusion, CoQ10 is a safe and effective adjunctive treatment for a broad range of cardiovascular diseases, producing gratifying clinical responses while easing the medical and financial burden of multidrug therapy.

MEDLINE EXPRESS (R) 1991-1995 70 of 469
TI: Noninvasive evaluation of cardiac hemodynamics during exercise in patients with chronic heart failure: effects of short-term coenzyme Q10 treatment.
AU: Morisco-C; Nappi-A; Argenziano-L; Sarno-D; Fonatana-D; Imbriaco-M; Nicolai-E; Romano-M; Rosiello-G; Cuocolo-A
SO: Mol-Aspects-Med. 1994; 15 Suppl: s155-63
AB: In patients with chronic heart failure (CHF), the addition of coenzyme Q10 to  conventional therapy reduces the hospitalization rate for worsening of heart failure and the incidence of serious cardiovascular complications. The present study was planned to assess the hemodynamic mechanisms underlying this phenomenon. Cardiac hemodynamics was evaluated continuously using an ambulatory radionuclide detector (VEST) which allows a noninvasive monitoring of left ventricular function. Six patients wit CHF (mean ejection fraction (EF): 29%)  clinically documented were studied. This study was organized as a randomized double-blind, placebo controlled, cross-over trial. The enrolled patients, after a washout period, underwent the first hemodynamic evaluation with VEST. Subsequently they were randomized to receive placebo or coenzyme Q10 for 4 weeks. At the end of this period they underwent the second VEST study. The third VEST study was performed after a further 4-week period with inverted treatment. Cardiac hemodynamics were evaluated during bicycle exercise. The EF in control conditions (CC) changed from 27 +/- 11%, at rest, to 24 +/- 8%, at peak exercise. During coenzyme Q10 treatment EF showed a significant increase both at rest (33 +/- 13%, P  MEDLINE EXPRESS (R) 1991-1995 71 of 469
TI: Recovery of load-induced left ventricular diastolic dysfunction by coenzyme Q10: echocardiographic study.
AU: Oda-T
SO: Mol-Aspects-Med. 1994; 15 Suppl: s149-54
AB: Load-induced cardiac dysfunction (LCD), in which a supernormal left ventricular (LV) systolic performance at rest decreases due to an afterload challenge, usually occurs among children with mitral valve prolapse (MVP). However, diastolic performance is also important because relaxation, like contraction, is based on a process that requires energy. The aim of this study was to examine LV diastolic response patterns to stress in patients with LCD before and after coenzyme Q10 (CoQ) therapy and in controls. The D-E slope, E-F slope and maximal diastolic endocardial velocity were used as echographic diastolic indices. Thirty subjects, aged 9-16 years, were divided into four groups: group 1, 10 normals; group 2, 10 patients with LCD; group 3, the same 10 as in group 2, who recovered with CoQ, 3.0-3.4 mg/kg/day for 7 days; group 4, 10 asymptomatic children with MVP. The heart rate, both at rest and during handgrip (HG), showed little intergroup difference. Only in  group 2, were the ejection fraction and all the diastolic indices greater than in the other groups, but these became subnormal with HG. In the other groups, these indices increased with HG to a similar extent, although resting values were smaller than in group 2. In conclusion: (1) in normal hearts and in hearts with LCD, diastolic performance mimicked systolic performance both in resting and loading conditions; (2) CoQ improved not only the load-induced systolic but also the diastolic dysfunctions in a similar time-course, and (3) mechanical stiffness of the cardiac tissue may not be a cause of load-induced diastolic dysfunction, because the dysfunction was quickly resolved with CoQ therapy. CoQ may be a key substance which affects a common bioenergetic process in contraction and relaxation, to keep these functions normal.

MEDLINE EXPRESS (R) 1991-1995 72 of 469
TI: Coenzyme Q10 and antioxidants in acute myocardial infarction.
 AU: Kuklinski-B; Weissenbacher-E; Fahnrich-A
SO: Mol-Aspects-Med. 1994; 15 Suppl: s143-7
AB: Sixty-one patients admitted with acute myocardial infarction, and a symptom's duration of less than 6 hr were randomized into two groups. Immediately after hospitalisation, members of the verum group (n = 32) received 500 mcg of selenium (as sodium selenite). Thereafter they received a daily dosage of 100 mg coenzyme Q10 (Bio-Quinone) and 100 mcg selenium (Bio-Selenium in the form of  1-seleno-methionine) for a period of one year. The control group (n = 29) were given matching placebo preparations. The groups were comparable as with respect to age, sex and medical treatment. Biochemical parameters showed a reduced concentration of CPK- and ASAT-level in the verum group during the acute phase (although not statistically significant). None of the patients in the verum group (i.e. on antioxidative treatment) showed prolongation of the frequency corrected QT-interval. In the control group, 40% revealed a prolongation of the QT-interval by more than 440 msec (p  MEDLINE EXPRESS (R) 1991-1995 75 of 469
TI: [Do we kill our cardiac patients with statin therapy? Coenzyme Q10, what do we know? (letter; comment)]
AU: Hyams-DE; Roylance-PJ; Kruger-K; Bodd-E
SO: Tidsskr-Nor-Laegeforen. 1994 Feb 20; 114(5): 590

MEDLINE EXPRESS (R) 1991-1995 78 of 469
TI: Antioxidative effect of dietary coenzyme Q10 in human blood plasma.
AU: Weber-C; Sejersgard-Jakobsen-T; Mortensen-SA; Paulsen-G; Holmer-G
SO: Int-J-Vitam-Nutr-Res. 1994; 64(4): 311-5
AB: The effect of an oral dose of 90 mg/day coenzyme Q10 on the antioxidative status in 22 healthy young subjects (9 men and 13 women) was investigated before and after induction of an oxidative stress by fish oil supplementation. The levels of oxidized and reduced coenzyme Q10, alpha-tocopherol, ascorbate, TBARS and the fatty acid composition of phospholipids were determined in plasma. The total amount of plasma coenzyme Q10 increased significantly from 0.7 +/- 0.1 mumol/l before supplementation to 1.7 +/- 0.3 mumol/l after one week of supplementation while the redox status (reduced CoQ10/total CoQ10) remained constant, even during a following fish oil supplementation. The level of TBARS decreased during the first 2 weeks of CoQ10 ingestion while the content of alpha-tocopherol increased in the second week and ascorbate did not change. The decrease of TBARS and the presence of the majority of the orally supplemented CoQ10 in the reduced form in plasma seem to indicate an antioxidative role of CoQ10 in blood plasma.

MEDLINE EXPRESS (R) 1991-1995 88 of 469
TI: Protection by coenzyme Q10 from myocardial reperfusion injury during coronary artery bypass grafting.
AU: Chello-M; Mastroroberto-P; Romano-R; Bevacqua-E; Pantaleo-D; Ascione-R;  Marchese-AR; Spampinato-N
SO: Ann-Thorac-Surg. 1994 Nov; 58(5): 1427-32
AB: To evaluate the effect of coenzyme Q10 in reducing postoperative cardiac complications after ischemia and reperfusion, we randomly divided 40 patients undergoing elective coronary artery bypass into two groups: patients in group 1 received coenzyme Q10 (150 mg/day) for 7 days before operation, and those in group 2 were the control group. Concentrations of thiobarbituric acid-reactive substances  (malondialdehyde), conjugated dienes, and cardiac isoenzymes of creatine kinase were measured in samples from both arterial and coronary sinus sites. Serial sampling was performed 5 minutes after heparin administration, at 10 and 30 minutes during cardiopulmonary bypass, 15 and 30 minutes after aortic cross-clamp removal, and 5 minutes after protamine administration. The concentrations of malondialdehyde, conjugated dienes, and creatine kinase in group 1 were significantly lower than those in group 2. The decrease in plasma malondialdehyde concentrations correlated positively with the decrease in creatine kinase levels in the coronary sinus. The treatment group showed a significantly lower incidence of ventricular arrhythmias during the recovery period than did the control group (p  MEDLINE EXPRESS (R) 1991-1995 89 of 469
TI: Reduced effect of warfarin caused by ubidecarenone [letter]
AU: Spigset-O
SO: Lancet. 1994 Nov 12; 344(8933): 1372-3

MEDLINE EXPRESS (R) 1991-1995 94 of 469
TI: [Statin therapy and heart failure. There is a difference between statins (letter)]
AU: Fjelstrup-A
SO: Tidsskr-Nor-Laegeforen. 1994 May 20; 114(13): 1561-2

MEDLINE EXPRESS (R) 1991-1995 95 of 469
TI: [Statin therapy, Q10 and heart failure. Is there any difference between statins? (letter)]
AU: Carlsen-SM; Fougner-KJ
SO: Tidsskr-Nor-Laegeforen. 1994 Apr 30; 114(11): 1345

MEDLINE EXPRESS (R) 1991-1995 97 of 469
TI: [Statins and coenzyme Q10--idea or fact? (letter)]
AU: Vissinger-H; Larsen-ML
SO: Ugeskr-Laeger. 1994 May 23; 156(21): 3197-8

MEDLINE EXPRESS (R) 1991-1995 102 of 469
TI: Radical-mediated oxidation of isolated human very-low-density lipoprotein.
AU: Mohr-D; Stocker-R
SO: Arterioscler-Thromb. 1994 Jul; 14(7): 1186-92
AB: Oxidative modification of human low-density lipoprotein (LDL) has received much attention because of its suggested involvement in the early events of atherogenesis. In contrast, little data exist concerning the oxidation of human very-low-density lipoprotein (VLDL), although such modification promotes foam cell formation by these lipoproteins. We therefore investigated the radical-mediated oxidation of VLDL by using controlled oxidizing conditions and sensitive and specific methods to assess lipoprotein lipid oxidation and antioxidation. We observed that the ratio of alpha-tocopherol to coenzyme Q10 in VLDL was close to that of LDL, suggesting that these lipoproteins may transport some coenzyme Q10 to extrahepatic tissues, as they do tocopherol. Most of the coenzyme Q10 associated with VLDL was present in its reduced, antioxidant active form, ubiquinol-10. The small amounts of ubiquinol-10 in VLDL provided the lipoprotein lipids with a highly efficient antioxidant protection. Also, the kinetics of radical-mediated lipid peroxidation in VLDL resembled that in LDL and therefore also probably proceeded via the recently described tocopherol-mediated peroxidation mechanism. Oxidation competition experiments using aqueous radicals and physiological concentrations and molar ratios of LDL and VLDL indicated that in contrast to the situation with high-density lipoproteins, lipid peroxidation was initiated and detected  simultaneously in the former two lipoprotein particles. However, once initiated, peroxidation propagated at an approximately twofold higher rate in VLDL than LDL. Our studies suggest that radical-mediated lipid (per)oxidation proceeds via similar mechanisms in isolated LDL and VLDL. We conclude that efficient LDL antioxidants are also likely to be effective protective agents for VLDL.

MEDLINE EXPRESS (R) 1991-1995 104 of 469
TI: [Heart patients and uncritical cholesterol-inhibiting therapy using statins (letter)]
AU: Fjelstrup-AO
SO: Ugeskr-Laeger. 1994 Feb 28; 156(9): 1320

MEDLINE EXPRESS (R) 1991-1995 106 of 469
TI: [Coenzyme Q10 (ubiquinone) in the treatment of heart failure. Are any positive effects documented?]
AU: Spigset-O
SO: Tidsskr-Nor-Laegeforen. 1994 Mar 20; 114(8): 939-42
AB: Coenzyme Q10 is an endogenous substance which has a well established role  as electron carrier in the mitochondrial synthesis of adenosine triphosphate (ATP). In addition, coenzyme Q10 also has antioxidant and membrane stabilizing properties. Based on biopsy samples from patients undergoing cardiac surgery and blood samples from patients with congestive heart failure, the existence of a relative Q10 deficiency in patients with cardiac failure has been suggested. A total number of eight double blind, placebo controlled studies in patients with heart failure have  been published. Most of these studies include a small number of patients, and various methodological problems have been attributed to these. The results, judged as improvement in ejection fraction or work capacity, are inconsistent. In one large study, coenzyme Q10 was found to have a positive effect on morbidity, and in another on quality of life. However, although some of the results appear to be promising, more studies are needed, including studies designed with mortality as a primary end point, before the effect of the substance in patients with heart failure can be established.

MEDLINE EXPRESS (R) 1991-1995 109 of 469
TI: Serum coenzyme Q10 in uremic patients on chronic hemodialysis.
AU: Triolo-L; Lippa-S; Oradei-A; De-Sole-P; Mori-R
SO: Nephron. 1994; 66(2): 153-6
AB: In a group of 48 chronic hemodialysis patients, serum levels of coenzyme Q10 (CoQ) have been measured and appeared abnormally low in 62% of cases. Figures  were positively correlated to those of serum vitamin E (vit E), although the latter were within a normal range. The chronic hemodialysis (CHD) patients with normal serum values of CoQ exhibited higher blood triglycerides. Pathologically low levels of serum vit E were found only in uremic subjects on conservative regimen with dietary restrictions and low compliance to protein-caloric intake. The reduced CoQ levels may contribute to the defective serum antioxidant activity and the increased peroxidative damage in uremic patients on CHD.

MEDLINE EXPRESS (R) 1991-1995 110 of 469
TI: Effectiveness of coenzyme Q10 on myocardial preservation during hypothermic cardioplegic arrest.
AU: Chen-YF; Lin-YT; Wu-SC
SO: J-Thorac-Cardiovasc-Surg. 1994 Jan; 107(1): 242-7
AB: 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.

MEDLINE EXPRESS (R) 1991-1995 112 of 469
TI: Congestive heart failure. Drug therapy: central or peripheral approach?
AU: Remme-WJ
SO: Cardiologia. 1993 Dec; 38(12 Suppl 1): 51-9
AB: Although prevention of heart failure recently has become a realistic issue, management of heart failure once the syndrome has developed, is mainly supportive, based on the various cardiac and peripheral changes which occur in the course of heart failure. Of these, abnormal neurohormonal activation is of major pathophysiologic and prognostic significance. Consequently, modulation of  neuroendocrine activation is now recognized a prime target in the treatment of heart failure, besides diuretic therapy. In this respect, the value of converting enzyme inhibition is well established. Future developments in this area include dopaminergic agents, vasopressin antagonists, angiotensin II receptor antagonists, renin inhibitors, spironolactone and, possibly, ANF peptidase inhibitors. Besides diuretics, necessary when signs of fluid retention are present, the approach to heart failure management involves other pharmacologic issues. In view of abnormal vascular control with vasoconstriction prevailing during progressive heart failure, it clearly makes sense to vasodilate. However, of available vasodilators, only the combination of relatively high dose nitrates and hydralazine has proven to be of clinical significance, in terms of hemodynamics, exercise capacity and survival. It is possible, though, that novel generation dihydropyridine derivatives may prove beneficial as well. Thus far, there has been much debate concerning the usefulness and particularly the safety of positive inotrope therapy and inodilator treatment. Taken together, this concern relates to presence and predominance of cAMP-dependent mechanisms to induce these effects. Thus, sympathomimetic agents and phosphodiesterase inhibitors, such as milrinone or enoximone, are without beneficial effects, but instead shorten survival during long-term therapy.  This may be different where compounds which act through cAMP-independent mechanisms, i.e., calcium sensitization or sodium channel stimulation, are concerned, but needs to be confirmed yet.(ABSTRACT TRUNCATED AT 250 WORDS)

MEDLINE EXPRESS (R) 1991-1995 117 of 469
TI: Increased expression of the lactate dehydrogenase M subunit in myocardial regions with decreased thallium uptake.
AU: Lin-L; Kaijser-L; Liska-J; Sylven-C; Holmgren-A; Lindstrom-K; Jansson-E
SO: Cardiovasc-Res. 1993 Jul; 27(7): 1300-5
AB: OBJECTIVE: In ischaemic heart disease, the heart muscle is subjected to repeated episodes of regional ischaemia or to a constant underperfusion. The purpose of the present investigation was to study the myocardial metabolic adaptation to this stress. METHODS: Eighteen male patients with ischaemic heart disease were studied by biopsies taken from the left ventricular septum during bypass surgery. Citrate synthase, total lactate dehydrogenase and its H and M subunits, coenzyme Q10, and myoglobin were determined in all biopsies. Concentrations of ATP, ADP, and AMP were determined and energy charge calculated in the biopsies from the patients with ischaemic heart disease. Biopsies from the septal region of hearts obtained from brain dead kidney and liver donors were used as reference and preoperative myocardial thallium scintigraphy was performed in the patients with ischaemic heart disease to relate the myocardial biochemical markers to thallium uptake at the biopsy site. RESULTS: Myocardial activities of citrate synthase as well as contents of coenzyme Q10 and myoglobin in patients with ischaemic heart disease were not different from those of the reference group, and no linear relation was found between these three markers on the one hand and thallium uptake on the other. The energy charge was directly related and the M subunit of lactate dehydrogenase inversely related to the thallium uptake. CONCLUSION: The results suggest an absence of adaptation to ischaemia in terms of increased myocardial oxidative capacity and O2 transport and storage capacity. Furthermore, it is indicated that a stressed energy metabolism with increasing severity of ischaemic heart disease enhances anaerobic metabolism and induces a shift in myocardial lactate dehydrogenase subunit fractions.

MEDLINE EXPRESS (R) 1991-1995 121 of 469
TI: Heart failure is a dominant deficiency of coenzyme Q10 and challenges for future clinical research on CoQ10.
AU: Folkers-K
SO: Clin-Investig. 1993; 71(8 Suppl): S51-4

MEDLINE EXPRESS (R) 1991-1995 123 of 469
TI: Myocardial preservation by therapy with coenzyme Q10 during heart surgery.
AU: Judy-WV; Stogsdill-WW; Folkers-K
SO: Clin-Investig. 1993; 71(8 Suppl): S155-61
AB: Coenzyme Q10 (CoQ10) is a natural and essential cofactor in the heart. It is the primary redox coupler in the respiratory chain, a potent free radical scavenger, and a superoxide inhibitor. In this study the myocardial protective effects of CoQ10 were determined in high-risk (n = 10) patients during heart surgery compared to that found in placebo controls (n = 10). In both groups, there was a blood CoQ10 deficiency ( MEDLINE EXPRESS (R) 1991-1995 124 of 469
TI: Recovery of the Frank-Starling mechanism by coenzyme Q10 in patients with load-induced contractility depression.
AU: Oda-T
SO: Clin-Investig. 1993; 71(8 Suppl): S150-4
AB: Load-induced contractility depression, in which supernormal left ventricular ejection fraction and contractility at rest decrease by added afterload, is most often found in children with mitral valve prolapse who have symptoms. Patients have high ventricular end-diastolic pressure at rest, which is further increased by afterload challenge. The Frank-Starling mechanism may be maximally mobilized with high preload even at rest to compensate for the intrinsically depressed inotropic state. Therefore, preload reserve may be easily exhausted due to afterload addition. We aimed to determine left ventricular end-diastolic fiber length, stroke work, and contractility before and during handgrip by echocardiograms to obtain evidence for the Frank-Starling mechanism in patients and controls, including patients treated with coenzyme Q10. The subjects were divided into four groups, each consisting of 30 children aged 6-16 years: group 1, normals; group 2, patients; group 3, the same patients as in group 2 after coenzyme Q10 therapy; and group 4, patients with asymptomatic mitral valve prolapse. Baseline values and percentage increases in systolic blood pressure, heart rate, and left ventricular wall stress showed no  differences among the groups. Only in group 2 were the percentage increase in ejection fraction, fiber shortening velocity, contractility, and end-diastolic dimension strongly negative, despite supernormal baseline levels. In other groups, these were significantly positive, without intergroup differences. We conclude that in the heart with load-induced contractility depression, the Frank-Starling mechanism deviates from normal. The normal Frank-Starling mechanism was recovered due to coenzyme Q10, which may improve disturbed bioenergetic function at the molecular level.

MEDLINE EXPRESS (R) 1991-1995 125 of 469
TI: Italian multicenter study on the safety and efficacy of coenzyme Q10 as adjunctive therapy in heart failure (interim analysis). The CoQ10 Drug Surveillance Investigators.
AU: Baggio-E; Gandini-R; Plancher-AC; Passeri-M; Carmosino-G
SO: Clin-Investig. 1993; 71(8 Suppl): S145-9
AB: Digitalis, diuretics, and vasodilators are considered standard therapy for patients with congestive heart failure, for which treatment is tailored according to the severity of the syndrome and the patient profile. Apart from the clinical seriousness, heart failure is always characterized by an energy depletion status, as indicated by low intramyocardial ATP and coenzyme Q10 levels. We investigated safety and clinical efficacy of coenzyme Q10 (CoQ10) adjunctive treatment in congestive heart failure, which had been diagnosed at least 6 months previously and treated with standard therapy. A total of 2500 patients in NYHA classes II and III were enrolled in this open noncomparative 3-month postmarketing drug surveillance study in 173 Italian centers. The daily dose of CoQ10 was 50-150 mg orally, with the majority of patients (78%) receiving 100 mg/day. Clinical and laboratory parameters were evaluated at the entry into the study and on day 90; the assessment of clinical signs and symptoms was made using from two- to seven-point scales. Preliminary results on 1113 patients (mean age 69.5 years) show a low incidence of side effects: 10 adverse reactions were reported in 8 (0.8%) patients, of which only 5 reactions were considered as correlated to the test treatment. After 3 months of test treatment the proportions of patients with improvement in clinical signs and  symptoms were as follows: cyanosis 81%, edema 76.9%, pulmonary rales 78.4%, enlargement of the liver area 49.3%, jugular reflux 81.5%, dyspnea 54.2%, palpitations 75.7%, sweating 82.4%, arrhythmia 62%, insomnia 60.2%, vertigo 73%, and nocturia 50.7%.(ABSTRACT TRUNCATED AT 250 WORDS)

MEDLINE EXPRESS (R) 1991-1995 126 of 469
TI: Isolated diastolic dysfunction of the myocardium and its response to CoQ10 treatment.
AU: Langsjoen-PH; Langsjoen-PH; Folkers-K
SO: Clin-Investig. 1993; 71(8 Suppl): S140-4
AB: Symptoms of fatigue and activity impairment, atypical precordial pain, and cardiac arrhythmia frequently precede by years the development of congestive heart failure. Of 115 patients with these symptoms, 60 were diagnosed as having hypertensive cardiovascular disease, 27 mitral valve prolapse syndrome, and 28 chronic fatigue syndrome. These symptoms are common with diastolic dysfunction,  and diastolic function is energy dependent. All patients had blood pressure, clinical status, coenzyme Q10 (CoQ10) blood levels and echocardiographic measurement of diastolic function, systolic function, and myocardial thickness recorded before and after CoQ10 replacement. At control, 63 patients were functional class III and 54 class II; all showed diastolic dysfunction; the mean CoQ10 blood level was 0.855 micrograms/ml; 65%, 15%, and 7% showed significant myocardial hypertrophy, and 87%, 30%, and 11% had elevated blood pressure readings in hypertensive disease, mitral valve prolapse and chronic fatigue syndrome respectively. Except for higher blood pressure levels and more myocardial thickening in the hypertensive patients, there was little difference between the three groups. CoQ10 administration resulted in improvement in all; reduction in high blood pressure in 80%, and improvement in  diastolic function in all patients with follow-up echocardiograms to date; a reduction in myocardial thickness in 53% of hypertensives and 36% of the combined prolapse and fatigue syndrome groups; and a reduced fractional shortening in those high at control and an increase in those initially low.(ABSTRACT TRUNCATED AT 250 WORDS)

MEDLINE EXPRESS (R) 1991-1995 127 of 469
TI: Statistical data support prediction of death within 6 months on low levels of coenzyme Q10 and other entities.
AU: Jameson-S
SO: Clin-Investig. 1993; 71(8 Suppl): S137-9
AB: Ninety-four consecutive hospital patients aged over 50 years were included in a cross-sectional study. Serum samples were analyzed for coenzyme Q10, alpha-tocopherol, and free cholesterol levels. Patients who died within a follow-up period of 6 months or had congestive heart failure or severe myalgia, and/or received  cytostatic or lipid-lowering drug therapy showed significantly lower free cholesterol-related coenzyme Q10 values. Prospective controlled clinical trials will determine whether coenzyme Q10 has a potential to protect patients from such complications and become a useful therapy.

MEDLINE EXPRESS (R) 1991-1995 128 of 469
TI: Effect of coenzyme Q10 therapy in patients with congestive heart failure: a long-term multicenter randomized study.
 AU: Morisco-C; Trimarco-B; Condorelli-M
SO: Clin-Investig. 1993; 71(8 Suppl): S134-6
AB: The improved cardiac function in patients with congestive heart failure treated with coenzyme Q10 supports the hypothesis that this condition is characterized by mitochondrial dysfunction and energy starvation, so that it may be ameliorated by coenzyme Q10 supplementation. However, the main clinical problems in patients  with congestive heart failure are the frequent need of hospitalization and the high incidence of life-threatening arrhythmias, pulmonary edema, and other serious complications. Thus, we studied the influence of coenzyme Q10 long-term treatment on these events in patients with chronic congestive heart failure (New York Heart Association functional class III and IV) receiving conventional treatment for heart failure. They were randomly assigned to receive either placebo (n = 322, mean age 67 years, range 30-88 years) or coenzyme Q10 (n = 319, mean age 67 years, range 26-89 years) at the dosage of 2 mg/kg per day in a 1-year double-blind trial. The number of patients who required hospitalization for worsening heart failure was smaller in the coenzyme Q10 treated group (n = 73) than in the control group (n = 118, P  MEDLINE EXPRESS (R) 1991-1995 129 of 469
TI: Italian multicenter study on the efficacy and safety of coenzyme Q10 as adjuvant therapy in heart failure.
AU: Lampertico-M; Comis-S
SO: Clin-Investig. 1993; 71(8 Suppl): S129-33
AB: This multicenter study evaluated the efficacy and tolerability of coenzyme Q10 in 1715 outpatients with chronic heart failure (New York Heart Association classes II and III), stabilized with standard therapy for 3 months. The patients were treated with coenzyme Q10 at a daily dose of 50 mg for 4 weeks, in addition to receiving conventional therapy. The efficacy of coenzyme Q10 was assessed by an open study that evaluated the improvement in clinical signs and symptoms of heart failure. After the baseline evaluation the subjects were seen on days 15 and 30. The intensity of signs and symptoms was assessed by a semiquantitative 4-point scale. Our results demonstrate that the administration of coenzyme Q10 in association with standard therapy improves dyspnea at rest, exertional dyspnea, palpitations, cyanosis, hepatomegaly, pulmonary rales, ankle edema, heart rate, and systolic and diastolic blood pressure in patients with stabilized heart failure. The rate of improvement and the low number of side effects in this large group of patients demonstrate that despite some methodological limitations in the study design and the short period of treatment (4 weeks) coenzyme Q10 given at a daily dose of 50 mg led to an improvement in the signs and symptoms of heart failure and in the quality of life.

MEDLINE EXPRESS (R) 1991-1995 130 of 469
TI: Role of metabolic therapy in cardiovascular disease.
AU: Rengo-F; Abete-P; Landino-P; Leosco-D; Covelluzzi-F; Vitale-D; Fedi-V; Ferrara-N
SO: Clin-Investig. 1993; 71(8 Suppl): S124-8
AB: The pathophysiological basis for the use of metabolic therapy in the treatment of heart failure is analyzed. Bioenergetical processes related to ATP bioavailability play a central role in regulating myocardial contractility at rest and on effort. Furthermore, a significant correlation has been demonstrated in diseased heart between ATP content, revealed at endomyocardial biopsy, and systolic and diastolic left ventricular indexes evaluated with invasive and noninvasive methods. Several international investigations demonstrate the beneficial effects of ubiquinone (coenzyme Q10) in the treatment of heart failure. Here the results of a study are reported that was conducted on patients with heart failure treated with ubiquinone.  After 7 months of oral drug administration (100 mg/day), a significant improvement was observed in echocardiographic indexes of systolic function, cardiothoracic ratio, and clinical signs and symptoms of congestive heart failure. In conclusion, the introduction of metabolic drugs, such as ubiquinone, in the treatment of heart failure opens new horizons in the therapeutic approach to an ailment that entails substantial human and social costs.

MEDLINE EXPRESS (R) 1991-1995 131 of 469
TI: Perspectives on therapy of cardiovascular diseases with coenzyme Q10 (ubiquinone).
AU: Mortensen-SA
SO: Clin-Investig. 1993; 71(8 Suppl): S116-23
AB: A defective myocardial energy supply--due to lack of substrates and/or essential cofactors and a poor utilization efficiency of oxygen--may be a common final pathway in the progression of myocardial diseases of various etiologies. The vitamin-like  essential substance coenzyme Q10, or ubiquinone, is a natural antioxidant and has a key role in oxidative phosphorylation. A biochemical rationale for using coenzyme Q10 as a therapy in heart disease was established years ago by Folkers and associates; however, this has been further strengthened by investigations of viable myocardial tissue from the author's series of 45 patients with various cardiomyopathies. Myocardial tissue levels of coenzyme Q10 determined by high-performance lipid chromatography were found to be significantly lower in patients with more advanced heart failure compared with those in the milder stages of heart failure. Furthermore, the myocardial tissue coenzyme Q10 deficiency might be restored significantly by oral supplementation in selected cases. In the author's open clinical protocol study with coenzyme Q10 therapy (100 mg daily) nearly two-thirds of patients revealed clinical improvement, most pronounced in those with dilated cardiomyopathy. Double-blind placebo-controlled trials have definitely confirmed that coenzyme Q10 has a place as adjunctive treatment in heart failure with beneficial effects on the clinical outcome, the patients' physical activity, and their quality of life. The positive results have been above and beyond the clinical status obtained from treatment with traditional principles--including angiotensin-converting enzyme inhibitors.

MEDLINE EXPRESS (R) 1991-1995 132 of 469
TI: Coenzyme Q10 and coronary artery disease.
AU: Hanaki-Y; Sugiyama-S; Ozawa-T; Ohno-M
SO: Clin-Investig. 1993; 71(8 Suppl): S112-5
AB: 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.

MEDLINE EXPRESS (R) 1991-1995 140 of 469
TI: Normal levels of coenzyme Q-10 in patients awaiting cardiac transplantation.
 AU: Sehested-J; Heidt-P; Hetzer-R
SO: Transplant-Proc. 1993 Jun; 25(3): 2365-7

MEDLINE EXPRESS (R) 1991-1995 159 of 469
TI: [Coenzyme Q10: contractile dysfunction of the myocardial cell and metabolic therapy]
AU: Davini-A; Cellerini-F; Topi-PL
SO: Minerva-Cardioangiol. 1992 Nov; 40(11): 449-53
AB: Coenzyme Q10, a mitoquinone involved in mitochondrial energy synthesis and the removal of free radicals, may be lacking in a number of cardiac pathologies  leading to reduced contractile activity. The administration of exogenous coenzyme Q10 may help to improve contractile activity. In order to assess this hypothesis 63 patients suffering from altered myocardial contractile function (29 dilated cardiopathies, 15 valvular cardiopathies, 19 ischemic cardiopathies) which presented a NYHA class above 2 were selected. The study was open and patients were subdivided into two groups, one of which received conventional therapy alone whereas the other also received exogenous coenzyme Q10. After 4 months of follow-up clinical (NYHA class, effort tolerance) and echocardiographical (ventricular diameter and contraction fraction %) parameters were evaluated. In those patients treated with coenzyme Q10 and suffering from dilated cardiomyopathy a significant reduction in the NYHA class and a marked improvement in echocardiographic parameters were observed at the end of this period. The variations observed in other groups of patients treated were less conspicuous and not always statistically significant. The results of this study confirm that the association of coenzyme Q10 and conventional therapy may lad to a marked improvement in contractile function and correlated clinical conditions.

MEDLINE EXPRESS (R) 1991-1995 164 of 469
TI: Ubiquinone (coenzyme Q10) in the long-term treatment of idiopathic dilated cardiomyopathy.
 AU: Permanetter-B; Rossy-W; Klein-G; Weingartner-F; Seidl-KF; Blomer-H
SO: Eur-Heart-J. 1992 Nov; 13(11): 1528-33
AB: Using a placebo-controlled, double-blind cross-over study the potential therapeutic effect of ubiquinone (coenzyme Q10) was investigated in 25 patients suffering from idiopathic dilated cardiomyopathy (New York Heart Association functional classification I, II and III). Over an initial period of 4 months, 15 patients  were administered verum (3 x 33.3 mg coenzyme Q10 x day-1 p.o.) and subsequently given a placebo during the ensuing 4 months (V/P). The sequence of treatment was reversed within the remaining 10 patients (P/V). Therapeutic efficacy was assessed by means of echocardiogram, chest X-ray, radionuclide ventriculography in combination with exercise test and impedance cardiography. Control values for left ventricular function parameters were similar in both groups; left ventricular ejection fraction: 39.5 +/- 11.5% (P/V), 37.6 +/- 17.0% (V/P); left ventricular end-diastolic diameter: 65 +/- 9 mm (P/V), 67 +/- 8 mm (P/V); and cardiac output: 5.1 +/- 1.41 x min-1 (P/V), 5.1 +/- 1.11 x min-1 (V/P). Chronic treatment with ubiquinone had no influence on haemodynamic parameters, electrocardiogram, incidence of ventricular arrhythmias or on exercise tolerance. It was therefore impossible to demonstrate any therapeutic effect of ubiquinone in patients suffering from idiopathic dilated cardiomyopathy.

MEDLINE EXPRESS (R) 1991-1995 166 of 469
TI: Positive correlation between aortic valve pressure gradient and mitochondrial respiratory chain capacity in hypertrophied human left ventricle.
AU: Maurer-I; Zierz-S
SO: Clin-Investig. 1992 Oct; 70(10): 896-901
AB: The effect of chronic left ventricular pressure overload on the activities of mitochondrial respiratory chain enzymes was investigated in myocardial biopsies  from the left ventricular apex of 13 patients undergoing aortic valve replacement for aortic valve stenosis. Transvalvular pressure gradients measured by left-sided heart catheterization ranged from 52 to 100 mmHg. The specific activity of mitochondrial respiratory chain enzyme complexes I+III (antimycin A sensitive NADH cytochrome c oxidoreductase) and the myocardial concentrations of coenzyme Q10 (CoQ10) increased significantly (P  MEDLINE EXPRESS (R) 1991-1995 172 of 469
TI: Plasma ubiquinone, alpha-tocopherol and cholesterol in man.
AU: Karlsson-J; Diamant-B; Edlund-PO; Lund-B; Folkers-K; Theorell-H
SO: Int-J-Vitam-Nutr-Res. 1992; 62(2): 160-4
AB: Plasma ubiquinone, coenzyme Q10 or CoQ10 has been analyzed in plasma together with alpha-tocopherol and free cholesterol in healthy sedentary male subjects (SS), endurance trained male athletes (ET) and male patients with severe  ischemic heart disease (IHD). Higher means were found in SS compared to both IHD and ET. Moreover, the ratios CoQ10 and alpha-tocopherol over free cholesterol were higher. In all groups significant relationships were found between the two products of the mevalonate pathway: CoQ10 and cholesterol (r ranged 0.66-0.86, p less than 0.01). The two lipophilic antioxidants, CoQ10 and alpha-tocopherol, were interrelated only in IHD (r = 0.86, p less than 0.001), borderline in SS (r = 0.51, p less than 0.05) but not in ET. It is assumed that plasma free cholesterol reflects the capacity to transport lipids and lipophilic compounds in blood. With metabolic stress and an elevated radical formation as in IHD and ET, the lower CoQ10 and alpha-tocopherol to cholesterol ratios mirror a subsequent toll on the scavenging potential. The difference in LDL levels between IHD and ET and the different storage capacity of CoQ10 and alpha-tocopherol might explain the tight coupling in IHD but not in ET. It is possible that the toll reflects both an intra- and extracellular radical quenching activity. The joint effect of the two lipophilic, extracellular antioxidants CoQ10 and alpha-tocopherol role in protecting e.g. LDL particles from peroxidation is suggested.

MEDLINE EXPRESS (R) 1991-1995 178 of 469
TI: Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation.
AU: Mohr-D; Bowry-VW; Stocker-R
SO: Biochim-Biophys-Acta. 1992 Jun 26; 1126(3): 247-54
AB: Ubiquinol-10 (CoQH2, the reduced form of coenzyme Q10) is a potent antioxidant present in human low-density lipoprotein (LDL). Supplementation of humans with ubiquinone-10 (CoQ, the oxidized coenzyme) increased the concentrations of CoQH2 in plasma and in all of its lipoproteins. Intake of a single oral dose of 100 or 200 mg CoQ increased the total plasma coenzyme content by 80 or 150%, respectively, within 6 h. Long-term supplementation (three times 100 mg CoQ/day) resulted in 4-fold enrichment of CoQH2 in plasma and LDL with the latter containing 2.8 CoQH2 molecules per LDL particle (on day 11). Approx. 80% of the coenzyme was present as CoQH2 and the CoQH2/CoQ ratio was unaffected by supplementation, indicating that the redox state of coenzyme Q10 is tightly controlled in the blood. Oxidation of LDL containing various [CoQH2] by a mild, steady flux of aqueous peroxyl radicals resulted immediately in very slow formation of lipid hydroperoxides. However, in each case the rate of lipid oxidation increased markedly with the disappearance of 80-90% CoQH2. Moreover, the cumulative radical dose required to reach this 'break point' in lipid oxidation was proportional to the amount of CoQH2 incorporated in vivo into the LDL. Thus, oral supplementation with CoQ increases CoQH2 in the plasma and all lipoproteins thereby increasing the resistance of LDL to radical oxidation.

MEDLINE EXPRESS (R) 1991-1995 179 of 469
TI: Ischaemic heart disease, skeletal muscle fibres and exercise capacity.
AU: Karlsson-J; Diamant-B; Folkers-K; Astrom-H; Gunnes-S; Liska-J; Semb-B
SO: Eur-Heart-J. 1992 Jun; 13(6): 758-62
AB: Twenty-eight male patients with ischaemic heart disease (IHD) performed OBLA (onset of blood lactate accumulation) exercise stress tests and had muscle biopsies taken from their vastus lateralis muscle the day before coronary bypass grafting. All 28 patients showed the same exercise performance pattern as compared to healthy sedentary, age-matched, controls: a low exercise intensity eliciting a blood lactate concentration of 2.0 mmol x l-1 (WOBLA), WOBLA corresponded to a high fraction (% WOBLA) of WSL (symptom limited or 'maximal' capacity), and a low peak blood  lactate concentration. The high % WOBLA and low peak blood lactate indicated a reduced glycogenolytic capacity ('anaerobic' performance). Muscle fibre composition disclosed a high mean value of fast twitch (FT), type II or 'white' muscle fibres, as compared to sedentary healthy controls. This indicated that this patient group constituted an extreme subgroup of the age-matched population. The distorted muscle fibre composition in IHD could reflect both heredity as well as adaptation to  physical inactivity, degenerative cytosolic properties, etc. Muscle and blood contents of a mitochondrial electron translocator and nonspecific radical scavenger, ubiquinone or coenzyme Q10(CoQ10), were low, which coincided with an elevated frequency of the fibre subgroup FT(c). The presence of the FT(c) fibre type is assumed to reflect histological trauma.

MEDLINE EXPRESS (R) 1991-1995 185 of 469
TI: Usefulness of taurine in chronic congestive heart failure and its  prospective application.
AU: Azuma-J; Sawamura-A; Awata-N
SO: Jpn-Circ-J. 1992 Jan; 56(1): 95-9
AB: We compared the effect of oral administration of taurine (3 g/day) and coenzyme Q10 (CoQ10) (30 mg/day) in 17 patients with congestive heart failure secondary to ischemic or idiopathic dilated cardiomyopathy, whose ejection fraction assessed by echocardiography was less than 50%. The changes in echocardiographic parameters  produced by 6 weeks of treatment were evaluated in a double-blind fashion. In the taurine-treated group significant treatment effect was observed on systolic left ventricular function after 6 weeks. Such an effect was not observed in the CoQ10-treated group.

MEDLINE EXPRESS (R) 1991-1995 187 of 469
TI: Therapy with coenzyme Q10 of patients in heart failure who are eligible or ineligible for a transplant.
AU: Folkers-K; Langsjoen-P; Langsjoen-PH
SO: Biochem-Biophys-Res-Commun. 1992 Jan 15; 182(1): 247-53
AB: Twenty years of international open and seven double blind trials established the efficacy and safety of coenzyme Q10 (CoQ10) to treat patients in heart failure. In the U.S., ca. 20,000 patients under 65 years are eligible for transplants, but donors are less than 1/10th of those eligible, and there are many more such patients over 65, both eligible and ineligible. We treated eleven exemplary transplant candidates with CoQ10; all improved; three improved from Class IV to Class I; four improved from Classes III-IV to Class II; and two improved from Class III to Class I or II. After CoQ10, some patients required no conventional drugs and had no limitation in lifestyle. The marked improvement is based upon correcting myocardial deficiencies of CoQ10 which improve mitochondrial bioenergetics and cardiac performance. These case histories, and very substantial background proof of efficacy and safety, justify  treating with CoQ10 patients in failure awaiting transplantation.

MEDLINE EXPRESS (R) 1991-1995 199 of 469
TI: Coenzyme Q10, alpha-tocopherol and free cholesterol in HDL and LDL fractions.
AU: Johansen-K; Theorell-H; Karlsson-J; Diamant-B; Folkers-K
SO: Ann-Med. 1991 Dec; 23(6): 649-56
AB: Twenty-three randomly selected plasma samples from apparently healthy, middle aged men were analysed for coenzyme Q10 (CoQ10), alpha-tocopherol (AT) and free cholesterol (FC) in: 1) whole plasma, 2) the HDL lipoprotein fraction after LDL precipitation (VLDL + LDL). CoQ10, AT and FC in plasma averaged 0.69 +/- .11, 6.74 +/- 1.78 micrograms x ml-1 and 0.59 +/- .11 mg x ml-1 and in HDL 0.17, 3.24 micrograms x ml-1 and 0.17 mg x ml-1 or 29, 48 and 29% of plasma values. Amounts of CoQ10 and AT were correlated to that of FC in all pools. The amount of HDL-CoQ10 but not of HDL-AT fell, with the HDL-FC expressed as the fraction of plasma FC. In all pools, N-AT versus AT initially increased and then leveled off, indicating saturation like conditions in contrast to CoQ10. Thus, CoQ10 and AT are differently allocated in HDL and LDL. This might have a bearing both on the suggested lipoprotein protection against peroxidation by these two antioxidants, but also on the distribution and allocation in different organs of CoQ10 and AT by HDL and LDL transportation.

MEDLINE EXPRESS (R) 1991-1995 202 of 469
TI: Muscle fibre types, ubiquinone content and exercise capacity in hypertension and effort angina.
AU: Karlsson-J; Diamant-B; Folkers-K; Lund-B
SO: Ann-Med. 1991 Aug; 23(3): 339-44
AB: The composition of skeletal muscle fibre expressed as a percentage of slow twitch (ST), type I or "red" and fast twitch (FT), type II or "white" were determined in patients with hypertension (HT) or with severe ischaemic heart disease (IHD) and  compared to age matched controls. Similarly, exercise capacity expressed as the cycle intensity eliciting a blood lactate concentration corresponding to 2.0 mmol x 1-1 were compared with healthy controls. Both patient groups had a higher percentage of FT fibres with relatively lower exercise capacities than their controls. The exercise capacities were reduced even when the relationship of decreased capacity with the percentage of increased FT was considered. There was an increase IHD but not in HT in patients with fibre subgroup FTc, which most probably reflected fibre trauma. Both patient groups were low in the skeletal muscle mitochondrial electron carrier and unspecific antioxidant ubiquinone, coenzyme Q10 or CoQ10. Patients with IHD but not HT showed, however, a faster fall in the ratio CoQ10 over ST% the higher the percentage value of ST. The ratio reflects the antioxidant activity related to CoQ10 in the fibre hosting most of the oxidative metabolism. A low ratio indicates a risk of metabolic lesion and cell trauma. This could explain fibre plasticity and offer an alternative cause to heredity in elucidating in deviating muscle fibre composition in patients with HT and IHD.

MEDLINE EXPRESS (R) 1991-1995 210 of 469
TI: Clinical experience of coenzyme Q10 to enhance intraoperative myocardial protection in coronary artery revascularization.
 AU: Sunamori-M; Tanaka-H; Maruyama-T; Sultan-I; Sakamoto-T; Suzuki-A
SO: Cardiovasc-Drugs-Ther. 1991 Mar; 5 Suppl 2: 297-300
AB: Seventy-eight patients undergoing coronary artery bypass grafting (CABG) were compared retrospectively to evaluate whether pretreatment with coenzyme Q10 (CoQ) is effective in preventing left ventricular depression in early reperfusion following CABG. CoQ (5 mg/kg, intravenously) was given to 60 patients, 2 hours prior to the onset of cardiopulmonary bypass (CPB). CABG was performed using saphenous vein under CPB associated with cold cardioplegia in the standard fashion. Heart rate, mean arterial pressure, and cardiac index showed no significant difference between the CoQ and control groups. However, left ventricular stroke work index was significantly elevated at 6 and 10 hours of reperfusion following CABG in the CoQ-treated group compared with the controls. Serum MB-CK was  lower at 0 and 6 hours of reperfusion in the CoQ group compared with the controls. These results suggest that pretreatment with intravenous CoQ is effective in preventing left ventricular depression in early reperfusion and in minimizing myocardial cellular injury during CABG followed by reperfusion.