-IBIS-1.7.6-
tx
cardiovascular system
angina pectoris
Nutrition
dietary guidelines
eating principles:
low sugar
low fat diet with unsaturated fats
calorie percentages: 70% complex carbohydrates, protein 12-15%, fat 15-18%
low cholesterol
low Sodium/Sodium-restricted diet
vegetarian cleansing diet or short fasts
Fasting, General Sample Diet, General Guidelines for Eating, Sample Vegetarian Diet
therapeutic foods:
apples, lentils, okra, potato broth
foods rich in Potassium
Vitamin B15 (Airola, 39.)
Vitamin E (Airola, 39.)
» if due to atherosclerosis :
garlic, wheat germ, liquid chlorophyll, alfalfa sprouts, buckwheat, watercress, rice polishings, apple, celery, cherries (Ni, 120.)
foods high in water-soluble fiber: psyllium seed, flax seed, pectin, guar gum, oat bran
onions, beans, legumes, soy, ginger, alfalfa, yogurt (Marz)
increase omega-3 and omega-6 fatty acids: vegetable, nut, seed oils, salmon, herring, mackerel, sardines, walnuts, flaxseed oil, evening primrose oil, black currant oil
fresh juices:
carrot and pineapple
liquid chlorophyll or alfalfa (Jensen)
parsley, alfalfa, and pineapple (Jensen)
apple
carrot, beet, and cucumber (Walker, 122.)
carrot (Walker, 122.)
carrot, celery, parsley, and spinach (Walker, 122.)
carrot (Walker, 122.)
spinach (Walker, 122.)
carrot, beet, and celery (Walker, 123.)
celery, lettuce, and spinach (Walker, 123.)
asparagus and honey (Ni, 120.)
avoid:
trans-fatty acids, hydrogenated oils (margarine, vegetable shortenings, imitation butter spreads, most commercial peanut butters), oxidized fats (deep fried foods, fast food, ghee, barbequed meats)
meat, animal products, refined carbohydrates, coffee, alcohol, hot sauces, spicy foods, fatty foods, rich foods, salty foods
grapefruit juice and drug interaction: grapefruit juice increases the bioavailability of nifedipine (Procardia, Adalat) by 8-69%, possibly through bioflavonoid interfernece with cytochrome P450 (Cantoni, et al., 1982; 307; 1079.)
drug interactions:
Grapefruit juice and nifepidine (Procardia, Adalat): Grapefruit juice has been shown to increase the bioavailability of the drug
supplements
Pantethine 300 mg three times daily. Pantethine is the stable form of pantetheine, the active form of pantothenic acid and the key component of coenzyme A (CoA). Patethine is the preferred therapeutic form because the synthetic pathway from pantethine to CoA is much shorter than that of pantothenic acid. Pantethine also exerts significant lipid-lowering effects.
(Gaddi A, et al. Atherosclerosis 1984 Jan;50(1):73-83; Arsenio L, et al. Clin Ther 1986;8(5):537-545; Borets VM, et al. Vopr Pitan 1987 Mar-Apr;(2):15-17; Miccoli R, et al. Curr Ther Res 36:5450549, 1984; Hayashi H, et al. Jpn Heart J 1985 Mar;26(2):289-296.)
Vitamin E 200-400 IU, three times daily, inhibits platelet aggregation
Magnesium 200-400 mg three times daily, preferably bound to aspartate, citrate or other Krebs cycle intermediates, will help normalize cardiac muscle contractility; check WBC Mg levels,
(Hampton EM, et al. Ann Pharmacother 1994 Feb;28(2):212-219; Teo KK, Yusuf S. Drugs 1993 Sep;46(3):347-359.)
L-carnitine 300-500 mg two to three times daily. Carnitine is essential in the transport of fatty acids into the mitochondria. Carnitine plays a critical role in normal heart function, especially contractility of cardiac muscle. A deficiency of carnitine results in a decrease in fatty acid concentrations in mitochondria, reduced energy production, and increased risk for angina. Further, since angina patients suffer from a reduced supply of oxygen to the heart they usually demonstrate lowered levels of carnitine. Supplememental carnitine raises heart carnitine levels and thereby can prevent the production of toxic fatty acid metabolites which contribute to damage of heart tissue.
(Bartels GL, et al. Eur Heart J 1996 Mar;17(3):414-20; Bartels GL, et al. Am J Cardiol 1994 Jul 15;74(2):125-130; Lagioia R, et al. Int J Cardiol 1992 Feb;34(2):167-172; Davini P, et al. Drugs Exp Clin Res 1992;18(8):355-365; Fernandez C, et al. Clin Ter 1992 Apr;140(4):353-377; Cacciatore L, et al. Drugs Exp Clin Res 1991;17(4):225-235.)
L-Taurine 100 mg to 2 g twice daily, normalizes contractility of cardiac muscle; watch for stomach ulcers at higher doses
Coenzyme Q10 150-300 mg daily facilitates oxygenation of tissues and strength of cardiac muscle (Kamikawa, 1985, 247.)
Essential Fatty Acids 1,000-1,500 mg once or twice daily can lower cholesterol and reduce inflammation
Bromelain 200-500 mg, three times daily, on an empty stomach, reduces platelet aggregation; can help relieve symptoms
» if underlying atherosclerosis:
Folic acid 5 mg per day
Vitamin B3 100 mg three times daily working up to 6 g per day (POSSIBLE LIVER PROBLEMS with some forms)
- best form for treating hypercholesterolemia is inositol hexoniacinate: 500 mg three times daily for two weeks, then increase to 1,000 mg three times daily (Murray and Pizzorno, 1998, p. 354) Or if you use niacin, 1-6 g per day start out with 100 mg three times daily with meals. Niacinamide is not effective for lowering cholesterol.
(Grundy. J. Lipid research 22:24-36,1981; Carlson and Oro. Atherosclerosis 18:9,1973; Canner J. Am. Coll. Cardiol. 5:442,1985)
Vitamin B6 40 mg per day
Vitamin B-complex
Vitamin C 1 g three times daily
Vitamin E 600 IU three times daily (POSSIBLE PROBLEMS WITH HYPERTENSION) (Steiner, 1976)
Calcium 1.5 mg per day; if patient is taking verapamil, Calcium supplementation in small doses only to reduce hypotensive effect (see below)
Magnesium 500 mg per day
Chromium picolinate, 200-400 mcg per day
Copper 2-4 mg per day, avoid taking > 15 mg Zinc if no Copper being taken
Selenium 200 mcg per day (Stead, 1984)
bromelain 400-1000 mg per day
L-carnitine 1500 mg twice daily
Coenzyme Q10 30 mg per day in divided doses
omega-3 fatty acids 5 g per day (Saynor, et al. Lancet. 1:1335,1983)
omega-6 fatty acids
phosphatidyl choline
pantothenic acid 600-1200 mg per day
rice bran oil 3.5 g per day
» drug interactions:
Calcium and verapamil (Calan, Isoptin, Verelan): Calcium interferes with the hypotensive effect of this drug which is intended to act as a Calcium channel blocker; if patient is taking verapamil, Calcium supplementation in small doses only to reduce hypotensive effect
footnotes
Arsenian MA. Carnitine and its derivatives in cardiovascular disease. Prog Cardiovasc Dis 1997 Nov-Dec;40(3):265-286. (Review)
Abstract: Carnitine and its derivative propionyl-L-carnitine are endogenous cofactors which enhance carbohydrate metabolism and reduce the intracellular buildup of toxic metabolites in ischemic conditions. The carnitines have been, and are being used in a spectrum of diseases including multiple cardiovascular conditions. These include angina, acute myocardial infarction, postmyocardial infarction, congestive heart failure, peripheral vascular disease, dyslipidemia, and diabetes. Most published data on carnitine, propionyl-L-carnitine, and other carnitine congeners are favorable but the clinical trials have been relatively small. In currently used doses, these substances are virtually devoid of significant side effects.
Arsenio L, Bodria P, Magnati G, Strata A, Trovato R. Effectiveness of long-term treatment with pantethine in patients with dyslipidemia. Clin Ther 1986;8(5):537-545.
Abstract: A one-year clinical trial with pantethine was conducted in 24 patients with established dyslipidemia of Fredrickson's types II A, II B, and IV, alone or associated with diabetes mellitus. The treatment was well tolerated by all patients with no subjective complaints or detectable side effects. Blood lipid assays repeated after 1, 3, 6, 9, and 12 months of treatment revealed consistent and statistically significant reductions of all atherogenic lipid fractions (total cholesterol, low-density lipoprotein cholesterol, and apolipoprotein B) with parallel increases of high-density lipoprotein cholesterol and apolipoprotein A. The results were equally good in patients with uncomplicated dyslipidemia and in those with associated diabetes mellitus. The authors conclude that pantethine (a drug entity related to the natural compound, pantetheine) represents a valid therapeutic support for patients with dyslipidemia not amenable to satisfactory correction of blood lipids by diet alone.
Bartels GL, Remme WJ, Holwerda KJ, Kruijssen DA. Anti-ischaemic efficacy of L-propionylcarnitine--a promising novel metabolic approach to ischaemia? Eur Heart J 1996 Mar;17(3):414-20.
Abstract: L-propionylcarnitine, a naturally occurring derivative of L-carnitine, essential for mitochondrial fatty acid transport and high-energy phosphate exchange, acutely reduces myocardial ischaemia and improves ischaemia-induced cardiac dysfunction following intravenous administration. This randomized, crossover study was designed to compare the long-term anti-ischaemic effects of oral L-propionylcarnitine with diltiazem in patients with stable, exercise-induced angina. After a 2-week washout phase of anti-anginal medication and a 2-week single-blind placebo period, 46 patients were included in the study, 23 of whom received 1500 mg L-propionylcarnitine daily for 6 weeks, and 23 diltiazem (180 mg daily for 3 weeks, followed by 360 mg daily for 3 weeks), crossing over to the other treatment after a 1-week washout period. Three patients on L-propionylcarnitine and two on diltiazem discontinued. Both treatments resulted in comparable exercise duration (582 +/- 35 s and 588 +/- 33 s, mean +/- SEM), time to 0.1 mV ST depression (436 +/- 38 s and 465 +/- 36 s), and increase in time to 0.1 mV ST depression from baseline (20% and 28%), L-propionylcarnitine and diltiazem, respectively. Diltiazem decreased the rate-pressure product at rest and exercise, L-propionylcarnitine did not. Both compounds significantly reduced ST depression at maximal exercise [23% (L-propionylcarnitine) vs 35% (diltiazem), P < 0.05 diltiazem vs L-propionylcarnitine]. Diltiazem increased the time to onset of angina by 22%. In contrast, no significant changes occurred with L-propionylcarnitine. During the study, anginal attacks were reduced by 70% and 57%, and nitroglycerin consumption decreased by 57% and 70%, L-propionylcarnitine and diltiazem, respectively. Thus, both L-propionylcarnitine and (high-dose) diltiazem result in anti-ischaemic effects and decrease anginal attacks in daily life. Although the effect of diltiazem on exercise-induced ischaemia appears more pronounced than that of L-propionylcarnitine, this novel metabolic approach to ischaemia warrants further development.
Bartels GL, Remme WJ, Pillay M, Schonfeld DH, Kruijssen DA. Effects of L-propionylcarnitine on ischemia-induced myocardial dysfunction in men with angina pectoris. Am J Cardiol 1994 Jul 15;74(2):125-130 .
Abstract: To identify the effect of L-propionylcarnitine (LPC) on ischemia, 31 fasting, untreated male patients with left coronary artery disease were studied during 2 identical pacing stress tests 45 minutes before (atrial pacing test I [APST I]) and 15 minutes after (APST II) administration of 15 mg/kg of LPC or placebo. Hemodynamic, metabolic, and nuclear angiographic variables were studied before, during, and for 10 minutes after pacing. After LPC administration, arterial total carnitine levels increased from 47 +/- 1.7 mumol/liter (control) to 730 +/- 30 mumol/liter. Hemodynamic and metabolic variables were comparable in LPC and placebo during APSI I, and reproducible in placebo during both tests. Although LPC did not affect myocardial oxygen demand and supply, it diminished myocardial ischemia, indicated by a significant 12% and 50% reduction in ST-segment depression and left ventricular end-diastolic pressure, respectively, during APST II. Moreover, during APST II, left ventricular ejection fraction increased by 18% (p < 0.05 vs APST I). Furthermore, LPC improved recovery of myocardial function after pacing, with a reduction in the time to peak filling and a 21% increase in both peak ejection and filling rates 10 minutes after pacing (all p < 0.05). Thus, LPC prevents ischemia-induced ventricular dysfunction, not by affecting the myocardial oxygen supply-demand ratio but as a result of its intrinsic metabolic actions, increasing pyruvate dehydrogenase activity and flux through the citric acid cycle. Because it is well tolerated, it may be a valuable alternative or addition to available antiischemic therapy.
Borets VM, Lis MA, Pyrochkin VM, Kishkovich VP, Butkevich ND. [Therapeutic efficacy of pantothenic acid preparations in ischemic heart disease patients]. Vopr Pitan 1987 Mar-Apr;(2):15-7. [Article in Russian]
Abstract: The therapeutic effectiveness of the pantothenic acid drugs: calciipantothenas and pantethine, was studied in 182 patients with coronary heart disease and stable angina of effort. It is shown that both the drugs produce favourable effects on certain parameters of hemodynamics, on the metabolism of lipids, riboflavin and ascorbic acid. It is recommended that the administration of calciipantothenas in a dose of 300 mg/day, during 3 weeks, be included into the combined treatment of coronary patients with no manifest disorders of lipid metabolism. Patients with manifest hyperlipidemia should be administered pantethine in a dose of 500 mg/day.
Cacciatore L, Cerio R, Ciarimboli M, Cocozza M, Coto V, D'Alessandro A, D'Alessandro L, Grattarola G, Imparato L, Lingetti M, et al. The therapeutic effect of L-carnitine in patients with exercise-induced stable angina: a controlled study. Drugs Exp Clin Res 1991;17(4):225-35
Abstract: An investigation on the therapeutic effect of L-carnitine was performed at three different centres and included two hundred patients, 40 to 65 years of age, with exercise-induced stable angina. In one hundred randomly selected patients the drug was administered orally in daily doses of 2 g in addition to the already instituted therapy, and the effect studied over a 6-month period. Compared with the control group, these patients showed a significant reduction in the number of premature ventricular contractions (PVC) at rest, as well as an increased tolerance during ergometric cycle exercise as demonstrated by an increased maximal cardiac frequency, increased maximal systolic arterial blood pressure and therefore also increased double cardiac product and reduced ST-segment depression during maximal effort. This was accompanied by improvement in cardiac function and resultant performance, as shown by an increase in the number of patients belonging to class I of the NYHA classification and a reduction in the consumption of cardioactive drugs. Laboratory analysis showed an improvement in plasma lipid levels. The authors conclude, after having discussed the particular metabolic mechanisms, that L-carnitine undoubtedly represents an interesting therapeutic drug for patients with exercise-induced stable angina.
Canner J. Am. Coll. Cardiol. 5:442,1985; The coronary drug project research group. JAMA 213:360,1975. Abstract: Men with 1 or more MIs who took 3 g Vitamin B3 per dayhad a lower incidence of nonfatal MIs and, for several years after the study ended, a lower mortality rate.
Carlson and Oro. Effect of treatment of nicotinic acid for one month on serum lipids in patients with different types of hyperlipidemia. Atherosclerosis 18:9,1973. Abstract: 188 patients with various types of hyperlipoproteinemia were given 3 gms nicotinic acid daily. Most responsive were patients with Type V. Their cholesterols decreased 70% and triglycerides decreased 90%, followed by Type lll: decreases of 50% and 60% respectively. Both lipids were also reduced in the other types, and even patients with normal lipid levels showed a 10-20% reduction in serum lipids.
Davini P, Bigalli A, Lamanna F, Boem A. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Exp Clin Res 1992;18(8):355-65
Abstract: A controlled study was carried out on 160 patients of both sexes (age between 39 and 86 years) discharged from the Cardiology Department of the Santa Chiara Hospital, Pisa, with a diagnosis of recent myocardial infarction. L-carnitine was randomly administered to 81 patients at an oral dose of g 4/die for 12 months, in addition to the pharmacological treatment generally used. For the whole period of 12 months, these patients showed, in comparison with the controls, an improvement in heart rate (p < 0.005), systolic arterial pressure (p < 0.005) and diastolic arterial pressure (NS); a decrease of anginal attacks (p < 0.005), of rhythm disorders (NS) and of clinical signs of impaired myocardial contractility (NS), and a clear improvement in the lipid pattern (p < 0.005). The above changes were accompanied by a lower mortality in the treated group (1.2%, p < 0.005), while in the control group there was a mortality of 12.5%. Furthermore, in the control group there was a definite prevalence of deaths caused by reinfarction and sudden death. On the basis of these results, it is concluded that L-carnitine represents an effective treatment in post-infarction ischaemic cardiopathy, since it can improve the clinical evolution of this pathological condition as well as the patient's quality of life and life expectancy.
Fernandez C, Proto C. [L-carnitine in the treatment of chronic myocardial ischemia. An analysis of 3 multicenter studies and a bibliographic review]. Clin Ter 1992 Apr;140(4):353-77. [Article in Italian]
Abstract: The authors selected, from a general sample of 3525 cardiopathic patients treated with 2 g daily of L-carnitine during 1 year, 220 stable effort angina TNT-responder patients, presenting more than 15 anginal episodes per month; moreover, other 59 anginal patients in congestive heart failure have been taken into account. The evaluation of the results obtained in these samples has been done in parallel with the ones of cardiopathic patients studied in 2 multicentric trials carried out, according to a very similar protocol, in Switzerland (148 patients treated at the same posology for 6 months) and Germany (143 patients, 3 months of treatment). The analysis of the three trials showed net reduction of both rate of anginal episodes and therapeutic use of nitrates, substantiated by improvement of physical performance (demonstrated by ergometric test in the German trial) as well as of the quality of life (the Swiss trial). Furthermore, from the general sample of 3525 patients the authors selected 737 subjects with clearly pathological levels of plasma cholesterol, in order to evaluate the effect of L-carnitine treatment on lipidemic parameters; after 12 months of administration only 282 patients showed abnormal levels of cholesterolemia. Analysis of the results of the three trials and a review of the literature on carnitine identify the compound as a fundamental drug for the treatment of patients with myocardial ischemia.
Gaddi A, Descovich GC, Noseda G, Fragiacomo C, Colombo L, Craveri A, Montanari G, Sirtori CR. Controlled evaluation of pantethine, a natural hypolipidemic compound, in patients with different forms of hyperlipoproteinemia. Atherosclerosis 1984 Jan;50(1):73-83
Abstract: Pantethine (P), the stable disulphate form of pantetheine, major component and precursor of coenzyme A, was evaluated within a double-blind protocol (8 weeks for P or for a corresponding placebo) in 29 patients, 11 with type IIB hyperlipoproteinemia, 15 with type IV, and 3 with an isolated reduction of high density lipoprotein cholesterol (HDL-C) levels. In type IIB patients, P (300 mg three times daily) determined a highly significant lowering of plasma total and low density lipoprotein (LDL) associated cholesterol (-13.5% for both parameters). In the same patients, HDL-C levels increased about 10% at the end of treatment. Switching from P to placebo was associated with a rapid return to the baseline cholesterolemia. Both in type IIB and type IV patients, plasma triglyceride levels were reduced around 30%, when P was given as the first treatment; when it was preceded by placebo, reductions were less striking (respectively, -17.8% for type IIB and -13.0% for type IV, at the end of P treatment). HDL-C levels were not increased by P, either in type IV, and in the patients with low HDL cholesterolemia. In type IV, LDL cholesterol levels showed a variable response to P: they tended to increase when below 132 mg/dl, prior to treatment, and to be reduced when above this level. This study provides evidence for a significant hypocholesterolemic effect of P, a natural compound free of overt side effects. It also indicates that P may raise HDL-C levels in type IIB patients, while moderately reducing triglyceridemia.
Grundy. Influence of nicotinic acid on metabolism of cholesterol and triglycerides in man. J. Lipid research 22:24-36,1981. Abstract: 12 hyperlipidemic patients were placed on nicotinic acid for 1 month. During treatment, triglycerides decreased 52%, VLDL decreased 36%, and total cholesterol decreased 22%.
Hampton EM, Whang DD, Whang R. Intravenous magnesium therapy in acute myocardial infarction. Ann Pharmacother 1994 Feb;28(2):212-219.
Abstract: OBJECTIVE: To review the methods and summarize the findings of clinical trials evaluating the use of intravenous magnesium (Mg2+) in acute myocardial infarction (AMI); to discuss serum Mg2+ in AMI and the potential mechanisms by which intravenous Mg2+ may be effective. Tables are used extensively to provide detailed information about the various trials. DATA SOURCES: A MEDLINE search was used to identify pertinent literature. Additional references were obtained from the articles retrieved from that search. STUDY SELECTION: Studies randomized and/or placebo-controlled were selected for review. Additional relevant citations were used in the introductory material and discussion. DATA EXTRACTION: There were surprisingly few large, placebo-controlled trials. All clinical trials available at the time of publication were reviewed. Only eight trials enrolled sufficient numbers of patients and/or were of adequate design to make meaningful interpretations. The description of the methods and results of these articles are the basis of this review. Although additional controlled studies with more subjects are needed, the results to date form a foundation from which to make inferences regarding the utility of this therapeutic modality. DATA SYNTHESIS: Intravenous Mg2+ has been demonstrated, albeit inconclusively, to reduce immediate and long-term morbidity and mortality when given in the immediate postinfarction period. Six of the eight controlled trials discussed report a decrease in the overall incidence of arrhythmia or in the frequency of arrhythmia requiring treatment. Four of the eight reported statistical significance. Five of the six trials evaluating mortality reported a decrease in the mortality rate from intravenous Mg2+ administered post-MI. Four of the five reported statistical significance. The favorable effect of intravenous Mg2+ on the mortality rate appears to occur in the first 30 days post-MI and is maintained through at least one year. The effects appear to be independent of concurrent therapy and do not appear to relate to baseline serum Mg2+ concentrations. Intravenous Mg2+ appears to be safe and well tolerated. Flushing, hypotension, and atrioventricular (AV) node conduction abnormalities occur on occasion and seem related to the rate of administration. The exact dosage in this setting remains to be determined. CONCLUSIONS: Additional, well-designed, multicenter, controlled trials evaluating intravenous Mg2+ in AMI are needed. The pending Fourth International Study of Infarct Survival, with an anticipated 400,000 subjects, should clarify a number of unresolved issues regarding this therapy. Based on the information available to date, however, intravenous Mg2+ as a significant therapeutic modality for AMI shows promise. Pending further investigation, however, it should be avoided in patients with significant sinoatrial or AV conduction disturbances.
Hayashi H, Kobayashi A, Terada H, Nagao B, Nishiyama T, Kamikawa T, Yamazaki N. Effects of pantethine on action potential of canine papillary muscle during hypoxic perfusion. Jpn Heart J 1985 Mar;26(2):289-296.
Abstract: Pantethine, which is known to be converted to coenzyme A, has been reported to have antiarrhythmic action on experimental cardiac arrhythmias. Using standard microelectrode techniques, the electrophysiological effects of pantethine under hypoxic (95% N2 + 5% CO2) perfusion were studied. Hypoxia decreased resting membrane potential, action potential amplitude and maximum velocity of phase 0 and shortened action potential duration and effective refractory period. Application of pantethine 5 X 10(-3) Gm/ml under hypoxic perfusion prolonged action potential duration and effective refractory period significantly. Prolongation of action potential duration by pantethine might be caused by an increase in intracellular ATP. The findings in this study could be an explanation of the possible antiarrhythmic effects of pantethine.
Kamikawa, T. Effects of coenzyme Q10 on exercise tolerance in chronic stable angina. Am J Cardiol. 56:247, 1985.
Abstract: Ten men and women with stable angina received random order 150mg CoQ10 daily or placebo. After 4 weeks, subjects on CoQ10 expoerienced a 53% reduction in the frequency of anginal episodes. Treadmill tolerance time increased by about 20% and ST depression was delayed by 50%.
Lagioia R, Scrutinio D, Mangini SG, Ricci A, Mastropasqua F, Valentini G, Ramunni G, Totaro Fila G, Rizzon P. Propionyl-L-carnitine: a new compound in the metabolic approach to the treatment of effort angina. Int J Cardiol 1992 Feb;34(2):167-172.
Abstract: The effects of propionyl-L-carnitine on exercise tolerance of 12 patients with stable exertional angina were assessed in a double-blind, placebo-controlled, cross-over protocol using serial exercise tests. Compared to placebo, propionyl-L-carnitine significantly increased total work from 514 +/- 199 to 600 +/- 209 W (P less than 0.05) (17%) and prolonged exercise time and time to ischemic threshold from 515 +/- 115 to 565 +/- 109 sec (P less than 0.05) (10%) and from 375 +/- 102 to 427 +/- 93 sec (P less than 0.01) (14%), respectively. ST segment depression at the highest common work level was significantly reduced from 0.19 +/- 0.08 to 0.15 +/- 0.08 mV (P less than 0.05) (21%). No significant changes in heart rate, systolic blood pressure, and rate-pressure product at rest, at the highest common work level, on appearance of the ischemic threshold, or at peak exercise were observed after propionyl-L-carnitine treatment. No side effects were observed under propionyl-L-carnitine treatment. This study shows that propionyl-L-carnitine can significantly improve exercise tolerance in patients with stable angina. Our data seem to confirm that propionyl-L-carnitine most likely exerts its protective action via the metabolic pathway.
Miccoli R, Marchetti P, Sampietro T, et al. Effects of pantethine on lipids and apolipoproteins in hypercholesterolemic diabetic and non-diabetic pateients. Curr Ther Res 36:5450549, 1984.
Murray, M and Pizzorno, J, Encyclopedia of Natural Medicine. Revised Second Edition. Prima Publishing: Rocklin, CA: 1998, p. 354
Saynor, R, Verel, D. Eskimos and Their Diet. Lancet. 1:1335,1983. (Letter)
Abstract: 150 patients with angina pectoris and normal volunteers were supplemented with fish oils (MaxEPA) for up to three years. Long term patients were able to reduce nitate therapy and exhibited increased exercise tolerance while taking the supplements. Triclycerides which fell sharply during the first weeks remained low. Total cholesterol was significantly lower and HDL cholesterol was significantly higher. Bleeding time remained increased when the daily dose was3.6gms of EPA per day but not when it was 1.8g perday.
Singh RB, Niaz MA, Agarwal P, Beegum R, Rastogi SS, Sachan DS. A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. Postgrad Med J 1996 Jan;72(843):45-50.
Abstract: In a randomised, double-blind placebo-controlled trial, the effects of the administration of oral L-carnitine (2 g/day) for 28 days were compared in the management of 51 (carnitine group) and 50 (placebo group) patients with suspected acute myocardial infarction. At study entry, the extent of cardiac disease, cardiac enzymes and lipid peroxides were comparable between the groups, although both groups showed an increase in cardiac enzymes and lipid peroxides. At the end of the 28-day treatment period, the mean infarct size assessed by cardiac enzymes showed a significant reduction in the carnitine group compared to placebo. Electrocardiographic assessment of infarct size revealed that the QRS-score was significantly less in the carnitine group compared to placebo (7.4 +/- 1.2 vs 10.7 +/- 2.0), while serum aspartate transaminase and lipid peroxides showed significant reduction in the carnitine group. Lactate dehydrogenase measured on the sixth or seventh day following infarction showed a smaller rise in the carnitine group compared to placebo. Angina pectoris (17.6 vs 36.0%), New York Heart Association class III and IV heart failure plus left ventricular enlargement (23.4 vs 36.0%) and total arrhythmias (13.7 vs 28.0%) were significantly less in the carnitine group compared to placebo. Total cardiac events including cardiac deaths and nonfatal infarction were 15.6% in the carnitine group vs 26.0% in the placebo group. It is possible that L-carnitine supplementation in patients with suspected acute myocardial infarction may be protective against cardiac necrosis and complications during the first 28 days.
Teo KK, Yusuf S. Role of magnesium in reducing mortality in acute myocardial infarction. A review of the evidence. Drugs 1993 Sep;46(3):347-59
Abstract: A number of small, randomised clinical trials and one large trial of intravenous magnesium have been conducted on patients with acute myocardial infarction (AMI). Most of these trials indicate that treatment with magnesium has a beneficial effect on short term mortality, although in most of the small trials the results are inconclusive. A systematic overview of mortality and serious morbidity data from all the available randomised controlled trials of magnesium conducted in a total of nearly 4000 patients with AMI indicates that there were 123 deaths in 1974 patients allocated magnesium, and 193 deaths in 1949 controls (odds ratio 0.61, 95% confidence interval 0.48 to 0.76, p < 0.0001). Data on the effects of magnesium on serious ventricular arrhythmias and heart failure are incomplete, and definitions for these serious complications of AMI vary greatly among the trials. Nevertheless, the available data suggest that magnesium also significantly reduces these 2 serious forms of morbidity. These data suggest that magnesium given to patients during AMI can produce significant reductions in mortality and serious morbidity. Although the mechanism of action of magnesium is likely to be independent of other currently used agents, its value when added to thrombolytic therapy, beta-blockers, angiotensin converting enzyme (ACE) inhibitors and nitrates is not clear, and is presently being studied in the very large Fourth International Studies of Infarct Survival (ISIS-4) trial.