-IBIS-1.7.6-
tx
cardiovascular system
congestive heart failure
Nutrition
dietary guidelines
eating principles:
low sugar
low fat diet with unsaturated fats
calorie percentages: 70% complex carbohydrates, protein 12-15%, fat 15-18%
high fiber
low cholesterol
low Sodium/Sodium-restricted diet
vegetarian cleansing diet or short fasts
foods that cool the Liver and Stomach
Fasting, General Sample Diet, General Guidelines for Eating, Sample Vegetarian Diet
specific remedies:
take 15 g of mango skin and 30 g of kernel from the fruit stone. Steam in water and serve per day (Yin-fang and Cheng-jun, 35.)
eat fresh pineapple two to three times daily (Yin-fang and Cheng-jun, 79.)
crack open a fresh coconut and drink the juice three times daily (Yin-fang and Cheng-jun, 86.)
avoid:
meat, alcohol, milk, hot sauces, spicy foods, fried foods, fatty foods, rich foods, salty foods
supplements
Vitamin E: 400-1200 IU per day (Marz R. 267, 1997.)
Calcium citrate: 1gm per day, see also below regarding digoxin (Marz R. 266, 1997.)
Magnesium: 500 mg per day, see also below regarding digoxin. It has also been used IM and IV. In more advanced cases IV magnesium as part of the "Myers cocktail" once every week. "Myers cocktail" is a combination of vitamin B12, B complex, B5, B6, calcium, magnesium and vitamin C that is an IV formulation put together by a Dr. Myer, a physician whom Dr. Gaby took over for back in the early 1980s.
(Wester P, Dyckner T. Act Med Scand. 1986;707:33-36; Packer M, et al. Am J Med 1986;80 (Suppl 4A):23-29; Bashir Y, et al. Am J Cardiol 1993;72:1156-1162; Marz R. 266, 1997)
Potassium: 100 mg per day, see also below regarding digoxin.
(Wester P, Dyckner T. Act Med Scand. 1986;707:33-36; Packer M, et al. Am J Med 1986;80 (Suppl 4A):23-29; Marz R. 266, 1997.)
Coenzyme Q10: 20-100 mg, three times per day, prevents fatty acid oxidation and enhances exercise tolerance. Recent research by questions the ability of Coenzyme Q10 to affect ejection fraction, peak oxygen consumption, or exercise duration in patients with congestive heart failure receiving standard medical therapy.
(Morisco C, et al. Clin Invest 1993;71:S134-136; Mortensen S.. Drugs Exp Clin Res 1985;11(8):581-593; Khatta M, et al. Ann Intern Med. 2000 Apr 18;132(8):636-640.)
Arginine: 1 gm, three times daily. Arginine is concentrated in the muscles and may be deficient in individuals with congestive heart failure. In double blind research Rector et al reported significant beneficial effects when individuals with congestive heart failure took 5.6-12.6 grams of arginine per day.
(Rector TS, et al. Circulation 1996;93:2135-2141; Marz R. 267, 1997.)
Creatine: Researchers have found that individuals with congestive heart failure who were given 20g daily of creatine for five days experienced decreased muscle weakness and an increassed ability to exercise.
(Gordon A, et al. Cardiovasc Res 1995;30:413-418; Andrews R, et al. Eur Heart J 1998 Apr;19(4):617-622.)
L-Carnitine: 500 mg, two to three times per day. Most research has been done using propionyl-L-carnitine (PC). Mancini et al conducted a double blind trial in which subjects who took 500 mg PC per day experienced a 26% increase in exercise capacity after six months
(Bartels GL, et al. Am J Cardiol 1994;74:125-130; Suzuki Y, et al. Lancet 1982;i:116; Mancini M, et al. Arzneimittelforschung 1992;42:1101-1104; Pucciarelli G, et al. Clin Ther 1992;141:379-384; Kobayashi A, et al. Jpn Circ J 1992;56:86-94.)
Taurine: 500 mg three times daily, up to 4 gms per day. Investigators have reported that taurine levels are often three times lower in the mycocardium of CHF patients. Alan Gaby has reported that many times patients can come directly off Lasix and digitalis with the above treatment.
(Azuma J, et al. Curr Ther Res 1983;34(4):543-557; Azuma J, et al. Int J Cardiol 1982;2:303-304; Azuma J, et al. Clin Ther 1983;5(4):398-408; Azuma J, et al. Prog Clin Biol Res 1985;179:195-213; Awata N, et al. Cardiovasc Res. 1987 Apr;21(4):241-247; Mortensen S. Drugs Exp Clin Res 1985;11(8):581-593; Sawamura A, et al. Eur J Pharmacol. 1986 Jan 21;120(2):235-239; Langsjoen P. Klin Wochenschr 61988;6:583-590; Marz, p. 266, 1997; Schaffer SW, et al. Adv Exp Med Biol. 1998;442:145-152.)
Testosterone or DHEA: consider if levels are low (Marz, p. 267, 1997)
Thyroid
Note: Concerning idiopathic hypertrophic subaortic stenosis (IHSS), it has been found that IHSS may have hypothyroidism as a possible etiological factor. One study found that of 17 patients with documented hypothyroidism, 15 of them had IHSS. When they were treated with thyroid hormone the IHSS went away. (as per Marz, 1997)
» drug interaction:
Thiamine and furosemide (Lasix): causes increased urinary excretion of vitamin B1 (thiamine) (Seligman, et al., 1991; 91:151.)
Sodium, Potassium and triamterene (Dyrenium) or spironolactone (Aldactone): these Potassium-sparing diuretics increase urinary Sodium and reduce urinary Potassium; note: KCl is contraindicated; even small amounts of fruit may lead to hyperkalemia
Calcium and digoxin (Lanoxin): small increases in plasma Calcium increase digoxin toxicity. (Whang, et al., 1985;145(4):655)
Note: avoid high calcium foods for two hours before and after taking this drug.
Potassium, Magnesium and digoxin (Lanoxin): Potassium and Magnesium deficiencies may lead to arrhythmias in patients on digoxin.
footnotes
[No authors listed] I have congestive heart failure. Should I try coenzyme Q-10? Johns Hopkins Med Lett Health After 50. 1999 Aug;11(6):8.
Andrews R, Greenhaff P, Curtis S, Perry A, Cowley AJ. The effect of dietary creatine supplementation on skeletal muscle metabolism in congestive heart failure. Eur Heart J 1998 Apr;19(4):617-622.
Abstract: AIMS: To assess the effects of dietary creatine supplementation on skeletal muscle metabolism and endurance in patients with chronic heart failure. METHODS: A forearm model of muscle metabolism was used, with a cannula inserted retrogradely into an antecubital vein of the dominant forearm. Maximum voluntary contraction was measured using handgrip dynanometry. Subjects performed handgrip exercise, 5 s contraction followed by 5 s rest for 5 min at 25%, 50%, and 75% of maximum voluntary contraction or until exhaustion. Blood was taken at rest and 0 and 2 min after exercise for measurement of lactate and ammonia. After 30 min the procedure was repeated with fixed workloads of 7 kg, 14 kg and 21 kg. Patients were assigned to creatine 20 g daily or matching placebo for 5 days and returned after 6 days for repeat study. RESULTS: Contractions (median (25th, 75th interquartiles)) until exhaustion at 75% of maximum voluntary contraction increased after creatine treatment (8 (6, 14) vs 14 (8, 17), P = 0.025) with no significant placebo effect. Ammonia per contraction at 75% maximum voluntary contraction (11.6 mumol/l/contraction (8.3, 15.7) vs 8.9 mumol/l/contraction (5.9, 10.8), P = 0.037) and lactate per contraction at 75% maximum voluntary contraction (0.32 mmol/l/contraction (0.28, 0.61) vs 0.27 mmol/l/contraction (0.19, 0.49), P = 0.07) fell after creatine but not after placebo. CONCLUSIONS: Creatine supplementation in chronic heart failure augments skeletal muscle endurance and attenuates the abnormal skeletal muscle metabolic response to exercise.
Awata N, Azuma J, Hamaguchi T, Tanaka Y, Ohta H, Takihara K, Harada H, Sawamura A, Kishimoto S. Acute haemodynamic effect of taurine on hearts in vivo with normal and depressed myocardial function. Cardiovasc Res. 1987 Apr;21(4):241-247.
Azuma J. Long-term effect of taurine in congestive heart failure: preliminary report. Heart Failure Research with Taurine Group. Adv Exp Med Biol. 1994;359:425-333.
Azuma J, Hasegawa H, Sawamura A, Awata N, Ogura K, Harada H, Yamamura Y, Kishimoto S. Therapy of congestive heart failure with orally administered taurine. Clin Ther. 1983;5(4):398-408.
Abstract: The clinical efficacy of 2 gm BID of oral taurine (2-aminoethane sulfonic acid) was studied in 24 patients with congestive heart failure (CHF). We expressed the severity of CHF by a score based on clinical signs and symptoms and on roentgenographic data. The maximum possible score, corresponding to the worst CHF, was 23 points. How much the 24 patients improved after receiving taurine for four or eight weeks was estimated by the difference between their pretreatment and posttreatment scores. In 19 of the 24 patients, taurine was effective. In the group as a whole, mean (+/- SEM) scores fell significantly, from 7.3 +/- 0.6 before treatment to 4.4 +/- 0.5 after treatment. Thirteen of the 15 patients who were designated as New York Heart Association (NYHA) functional class III or IV before receiving taurine could be designated as class II after they completed the study. This pilot study should prompt further investigation into the possible use of taurine in the treatment of patients with CHF.
Azuma J, Hasegawa H, Awata N, Sawamura A, Harada H, Ogura K, Ohta H, Yamauchi K, Kishimoto S. Taurine for treatment of congestive heart failure in humans. Prog Clin Biol Res. 1983;125:61-72.
Azuma J, Sawamura A, Awata N, et al. Double-blind randomized crossover trial of taurine in congestive heart failure. Curr Ther Res 1983;34(4):543-557.
Azuma J, Sawamura A, Awata N, Ohta H, Hamaguchi T, Harada H, Takihara K, Hasegawa H, Yamagami T, Ishiyama T, et al. Therapeutic effect of taurine in congestive heart failure: a double-blind crossover trial. Clin Cardiol. 1985 May;8(5):276-282.
Abstract: In a double-blind, randomized, crossover, placebo-controlled study, we investigated the effects of adding taurine to the conventional treatment in 14 patients with congestive heart failure for a 4-week period. Compared with placebo, taurine significantly improved the New York Heart Association functional class (p less than 0.02), pulmonary crackles (p less than 0.02), and chest film abnormalities (p less than 0.01). A benefit of taurine over placebo was demonstrated when an overall treatment response for each patient was evaluated on the basis of clinical examination (p less than 0.05). No patient worsened during taurine administration, but four patients did during placebo. Pre-ejection period (corrected for heart rate) decreased from 148 +/- 14 ms before taurine treatment to 137 +/- 12 ms after taurine (p less than 0.001), and the quotient pre-ejection period/left ventricular ejection time decreased from 47 +/- 9 to 42 +/- 8% (p less than 0.001). Side effects did not occur in the patients during taurine. The results indicate that addition of taurine to conventional therapy is safe and effective for the treatment of patients with congestive heart failure.
Azuma J, Sawamura A, Awata N. Usefulness of taurine in chronic congestive heart failure and its prospective application. Jpn Circ J. 1992 Jan;56(1):95-99.
Abstract: 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.
Azuma J, Takihara K, Awata N, Sawamura A, Ohta H, Hamaguchi T, Tanaka Y, Fukuda K, Kishimoto S. Taurine and failing heart: experimental and clinical aspects. Prog Clin Biol Res. 1985;179:195-213.
Bartels GL, Remme WJ, Pillay M, et al. Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris. Am J Cardiol 1994;74:125-130.
Bashir Y, Sneddon JF, Staunton A, et al. Effects of long-term oral magnesium chloride replacement in congestive heart failure secondary to coronary artery disease. Am J Cardiol 1993;72:1156-1162.
Coto V, D'Alessandro L, Grattarola G, Imparato L, Lingetti M, Mancini M, Nolfe G, Rengo F. Evaluation of the therapeutic efficacy and tolerability of levocarnitine propionyl in the treatment of chronic obstructive arteriopathies of the lower extremities: a multicentre controlled study vs. placebo. Drugs Exp Clin Res. 1992;18(1):29-36.
Gordon A, Hultman E, Kaijser L, et al. Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance. Cardiovasc Res 1995;30:413-418.
Huertas JR, Martinez-Velasco E, Ibanez S, Lopez-Frias M, Ochoa JJ, Quiles J, Parenti Castelli G, Mataix J, Lenaz G. Virgin olive oil and coenzyme Q10 protect heart mitochondria from peroxidative damage during aging. Biofactors. 1999;9(2-4):337-343.
Khatta M, Alexander BS, Krichten CM, Fisher ML, Freudenberger R, Robinson SW, Gottlieb SS. The effect of coenzyme Q10 in patients with congestive heart failure. Ann Intern Med. 2000 Apr 18;132(8):636-640.
Abstract: BACKGROUND: Coenzyme Q10 is commonly used to treat congestive heart failure on the basis of data from several unblinded, subjective studies. Few randomized, blinded, controlled studies have evaluated objective measures of cardiac performance. OBJECTIVE: To determine the effect of coenzyme Q10 on peak oxygen consumption, exercise duration, and ejection fraction. DESIGN: Randomized, double-blind, controlled trial. SETTING: University and Veterans Affairs hospitals. PATIENTS: 55 patients who had congestive heart failure with New York Heart Association class III and IV symptoms, ejection fraction less than 40%, and peak oxygen consumption less than 17.0 mL/kg per minute (or <50% of predicted) during standard therapy were randomly assigned. Forty-six patients completed the study. INTERVENTION: Coenzyme Q10, 200 mg/d, or placebo. MEASUREMENTS: Left ventricular ejection fraction (measured by radionuclide ventriculography) and peak oxygen consumption and exercise duration (measured by a graded exercise evaluation using the Naughton protocol) with continuous metabolic monitoring. RESULTS: Although the mean (+/-SD) serum concentration of coenzyme Q10 increased from 0.95+/-0.62 microg/mL to 2.2+/-1.2 microg/mL in patients who received active treatment, ejection fraction, peak oxygen consumption, and exercise duration remained unchanged in both the coenzyme Q10 and placebo groups. CONCLUSION: Coenzyme Q10 does not affect ejection fraction, peak oxygen consumption, or exercise duration in patients with congestive heart failure receiving standard medical therapy.
Kobayashi A, Masumura Y, Yamazaki N. L-carnitine treatment for congestive heart failure - experimental and clinical study. Jpn Circ J 1992;56:86-94.
Kogan AKh, Syrkin AL, Drinitsina SV, Kokanova IV. [The antioxidant protection of the heart by coenzyme Q10 in stable stenocardia of effort]. Patol Fiziol Eksp Ter. 1999 Oct-Dec;(4):16-19. [Article in Russian]
Kubo SH, Rector TS, Bank AJ. Endothelial nitric oxide pathway function in the peripheral vasculature of patients with heart failure. J Card Fail. 1996 Dec;2(4 Suppl):S217-223. (Review)
Langsjoen P. Effective and safe therapy with Coenzyme Q10 for cardiomyopathy. Klin Wochenschr 1988;66:583-590.
Abstract: 88 patients with congestive heart failure due to cardiomyopathy received 100mg of Coenzyme Q10/day for periods ranging from 1-24 months. Responses were monitored by ejection fraction, cardiac output, and improvement in functional New York Heart Association classification. 75-85% of patients showed significant improvements in 2 monitored cardiac parameters. By functional classification, about 82% of those patients improved to lower classes. Blood levels of Coenzyme Q10 were below normal prior to treatment in a substantial % of patients.
Langsjoen PH, Langsjoen AM. Overview of the use of CoQ10 in cardiovascular disease. Biofactors. 1999;9(2-4):273-284. (Review)
Lass A, Kwong L, Sohal RS. Mitochondrial coenzyme Q content and aging. Biofactors. 1999;9(2-4):199-205.
Mancini M, Rengo F, Lingetti M, Sorrentino GP, Nolfe G. Controlled study on the therapeutic efficacy of propionyl-L-carnitine in patients with congestive heart failure. Arzneimittelforschung 1992 Sep;42(9):1101-1104.
Abstract: A double-blind phase II study of propionyl-L-carnitine (CAS 17298-37-2) versus placebo was carried out on a group of 60 patients with mild to moderate (II and III NYHA class) congestive heart failure. The group was made up of men and women aged between 48 and 73 years in chronic treatment with digitalis and diuretics for at least 3 months and who still displayed symptoms. Thirty of these patients were chosen randomly and for 180 days, 500 mg of propionyl-L-carnitine was orally administered, 3 times a day in addition to their usual treatment. At basal conditions and after 30, 90 and 180 days the maximum exercise time was evaluated using an exercise tolerance test performed on an ergometer bicycle and the left ventricular ejection fraction was tested by means of bidimensional echocardiography. After one month of treatment, the patients treated with propionyl-L-carnitine, compared to the control group, showed significant increases in the values of both tests, increases which became even more evident after 90 and 180 days. At the stated times the increases in the maximum exercise time were 16.4%, 22.9%, and 25.9%, respectively. The ventricular ejection fraction increased by 8.4%, 11.6% and 13.6%, respectively. On the basis of these results, having studied the particular mechanism of action of propionyl-L-carnitine the authors conclude that it represents a drug of undoubted therapeutic interest in patients with congestive heart failure, in whom it could be efficaciously administered along with a standard pharmacological therapy.
Maulik N, Yoshida T, Engelman RM, Bagchi D, Otani H, Das DK. Dietary coenzyme Q(10) supplement renders swine hearts resistant to ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol. 2000 Apr;278(4):H1084-1090.
Morisco C, Trimarco B, Condorelli M. Effect of coenzyme Q10 in patients with congestive heart failure: a long-term multicenter randomized study. Clin Invest 1993;71:S134136.
Abstract: 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 < 0.001). Similarly, the episodes of pulmonary edema or cardiac asthma were reduced in the control group (20 versus 51 and 97 versus 198, respectively; both P < 0.001) as compared to the placebo group. Our results demonstrate that the addition of coenzyme Q10 to conventional therapy significantly reduces hospitalization for worsening of heart failure and the incidence of serious complications in patients with chronic congestive heart failure.
Mortensen S. Long-term Coenzyme Q10 therapy: A major advance in the management of resistant myocardial failure. Drugs Exp Clin Res 1985;11(8):581-593.
Abstract: 12 patients with advanced congestive heart failure and an insufficient response to diuretics and digitalis received Coenzyme Q10 100mg daily and were followed for a mean period of 7 months. In 30 days 8/12 showed definite improvement, feeling less tired. Their general activity tolerance increased and dyspnea at rest disappeared. Heart rate fell; there was a significant decrease in atrial size and overall improved myocardial performance. Withdrawal of the supplement caused severe clinical relapse with improvement upon resumption.
Munkholm H, Hansen HH, Rasmussen K. Coenzyme Q10 treatment in serious heart failure. Biofactors. 1999;9(2-4):285-289.
Niibori K, Wroblewski KP, Yokoyama H, Crestanello JA, Whitman GJ. Bioenergetic effect of liposomal coenzyme Q10 on myocardial ischemia reperfusion injury. Biofactors. 1999;9(2-4):307-313.
Overvad K, Diamant B, Holm L, Holmer G, Mortensen SA, Stender S. Coenzyme Q10 in health and disease. Eur J Clin Nutr. 1999 Oct;53(10):764-770. (Review)
Packer M, Gottlieb SS, Kessler PD. Hormone-electrolyte interactions in the pathogenesis of lethal cardiac arrhythmias in patients with congestive heart failure. Am J Med 1986;80 (Suppl 4A):23-29.
Pedersen HS, Mortensen SA, Rohde M, Deguchi Y, Mulvad G, Bjerregaard P, Hansen JC. High serum coenzyme Q10, positively correlated with age, selenium and cholesterol, in Inuit of Greenland. A pilot study. Biofactors. 1999;9(2-4):319-323.
Pucciarelli G, Mastursi M, Latte S, et al. The clinical and hemodynamic effects of propionyl-L-carnitine in the treatment of congestive heart failure. Clin Ther 1992;141:379-384.
Rector TS, Bank AJ, Mullen KA, Tschumperlin LK, Sih R, Pillai K, Kubo SH. Randomized, double-blind, placebo-controlled study of supplemental oral L-arginine in patients with heart failure. Circulation. 1996 Jun 15;93(12):2135-2141.
Abstract: BACKGROUND. Patients with heart failure have reduced peripheral blood flow at rest, during exercise, and in response to endothelium-dependent vasodilators. Nitric oxide formed from L-arginine metabolism in endothelial cells contributes to regulation of blood flow under these conditions. A randomized, double-blind crossover study design was used to determine whether supplemental oral L-arginine can augment peripheral blood flow and improve functional status in patients with moderate to severe heart failure. METHODS AND RESULTS. Fifteen subjects were given 6 weeks of oral L-arginine hydrochloride (5.6 to 12.6 g/d) and 6 weeks of matched placebo capsules in random sequence. Compared with placebo, supplemental oral L-arginine significantly increased forearm blood flow during forearm exercise, on average from 5.1 +/- 2.8 to 6.6 +/- 3.4 mL. min-1. dL-1 (P < .05). Furthermore, functional status was significantly better on L-arginine compared with placebo, as indicated by increased distances during a 6-minute walk test (390 +/- 91 versus 422 +/- 86 m, P < .05) and lower scores on the Living With Heart Failure questionnaire (55 +/- 28 versus 42 +/- 26, P < .05). Oral L-arginine also improved arterial compliance from 1.99 +/- 0.38 to 2.36 +/- 0.30 mL/mm Hg (P < .001) and reduced circulating levels of endothelin from 1.9 +/- 1.1 to 1.5 +/- 1.1 pmol/L (P < .05). CONCLUSIONS. Supplemental oral L-arginine had beneficial effects in patients with heart failure. Further studies are needed to confirm the therapeutic potential of supplemental oral L-arginine and to identify mechanisms of action in patients with heart failure.
Rosenfeldt FL, Pepe S, Ou R, Mariani JA, Rowland MA, Nagley P, Linnane AW. Coenzyme Q10 improves the tolerance of the senescent myocardium to aerobic and ischemic stress: studies in rats and in human atrial tissue. Biofactors. 1999;9(2-4):291-299.
Sacher HL, Sacher ML, Landau SW, Kersten R, Dooley F, Sacher A, Sacher M, Dietrick K, Ichkhan K. The clinical and hemodynamic effects of Coenzyme Q10 in congestive cardiomyopathy. Am J Ther. 1997 Feb 1;4(2/3):66-72.
Sawamura A, Sperelakis N, Azuma J. Protective effect of taurine against decline of cardiac slow action potentials during hypoxia. Eur J Pharmacol. 1986 Jan 21;120(2):235-239.
Sawamura A, Sada H, Azuma J, Kishimoto S, Sperelakis N. Taurine modulates ion influx through cardiac Ca2+ channels. Cell Calcium. 1990 Apr;11(4):251-259.
Schaffer SW, Ballard-Croft C, Takahashi K, Azuma J. Effect of taurine depletion on angiotensin II-mediated modulation of myocardial function. Adv Exp Med Biol. 1998;442:145-152.
Schaffer SW, Punna S, Duan J, Harada H, Hamaguchi T, Azuma J. Mechanism underlying physiological modulation of myocardial contraction by taurine. Adv Exp Med Biol. 1992;315:193-8.
Suzuki Y, Masumura Y, Kobayashi A, et al. Myocardial carnitine deficiency in chronic heart failure. Lancet 1982;i:116 (Letter)
Wester PO, Dyckner T. Intracellular electrolytes in cardiac failure. Acta Med Scand Suppl. 1986;707:33-36.
Abstract: In congestive heart failure (CHF) there are several compensatory mechanisms operating which may influence electrolyte metabolism. The activation of the renin-angiotensin-aldosterone system causes retention of sodium (Na) and losses of potassium (K) and magnesium (Mg). The secondary hyperaldosteronism may give rise to high intracellular Na and low intracellular K through a direct permeability effect on the cell membrane. The Mg deficiency may lead to a further increase of intracellular Na and decrease of intracellular K since Mg is a necessary ion for the function of the Na-K pump. In 297 patients with diuretic treated CHF we found that 42% had hypokalemia, 37% hypomagnesemia and 12% hyponatremia. We also found that 57% had excess muscle Na, 52% had depletion of muscle K and 43% had low muscle Mg. We have also shown that the low muscle K cannot be corrected by K supplementation when there is a concomitant Mg deficiency and that Mg infusions may change the disturbed relation between extra- and intracellular electrolytes towards normal.
Zhou M, Zhi Q, Tang Y, Yu D, Han J. Effects of coenzyme Q10 on myocardial protection during cardiac valve replacement and scavenging free radical activity in vitro. J Cardiovasc Surg (Torino). 1999 Jun;40(3):355-361.