Chapter 145 Angina
• Squeezing or pressure-like pain in the chest appearing immediately after exertion. Other precipitating factors include emotional tension, cold weather, or a large meal. Pain may radiate to the left shoulder blade, left arm, or jaw. The pain typically lasts for only 1 to 20 minutes.
Angina pectoris results when the supply of oxygen, and occasionally other nutrients, is inadequate to meet the metabolic needs of the heart muscle. The primary cause is atherosclerosis, although platelet aggregation, coronary artery spasm, nonvascular mechanisms such as hypoglycemia, and increased metabolic need (such as in hyperthyroidism) can also be important.
The primary lesion of atherosclerosis is the atheromatous plaque, which progressively narrows and ultimately blocks the coronary artery, resulting in a decreased supply of blood and oxygen to the heart tissue. Symptoms typically begin to appear after a major coronary artery is blocked by more than 50%.
Blood flow to the heart may also be compromised by transient platelet aggregation (discussed in more detail in Chapter 148) and coronary artery spasm. Prinzmetal’s variant angina, the most commonly recognized form of coronary artery spasm, is not due to plaque in the coronary arteries and is more apt to occur at rest or at odd times during the day or night. It is more common in women younger than age 50. Magnesium insufficiency–induced coronary artery spasm, more common in men than women, is now recognized as an important cause of myocardial infarction (MI) and may be of significance in angina pectoris.
The diagnosis of angina is frequently made by history alone. Clinical evaluation of all patients with angina should include an electrocardiogram (ECG) at rest and a chest radiograph. Because more than one half of patients with typical angina and confirmed coronary atherosclerosis have normal 12-lead ECG readings at rest, diagnosis must often be confirmed using ECG stress testing or 24-hour Holter monitoring (ambulatory ECG).
The most common diagnostic ECG changes associated with angina are evidence of previous MI and ST-segment and T-wave changes that occur during attacks of pain. The most characteristic change is displacement of the ST segment with or without T-wave inversion. Complicating diagnosis, however, is the observation that hypoglycemia-induced angina does not manifest with rate or ST-segment abnormalities.1
Angina is a serious condition that requires careful treatment and monitoring. In the severe case as well as in the initial stages of mild to moderate angina, prescription medications may be necessary. Eventually the condition should be controlled with the help of natural measures. If there is significant blockage of the coronary artery, intravenous ethylenediaminetetraacetic acid (EDTA) chelation therapy, angioplasty, or coronary artery bypass may be appropriate.
From the perspective of natural medicine, there are two primary therapeutic goals in the treatment of angina: improving energy metabolism within the heart and improving blood supply to the heart. These goals are interrelated, as an increased blood flow means improved energy metabolism and vice versa.
The heart uses fats as its major metabolic fuel. It converts free fatty acids to energy in much the same way as an automobile uses gasoline. Defects in the utilization of fats by the heart greatly increase the risk of atherosclerosis, heart attacks, and anginal pains. Specifically, impaired utilization of fatty acids by the heart results in the accumulation of high concentrations of fatty acids within the heart muscle. This makes the heart extremely susceptible to cellular damage, which ultimately leads to a heart attack.
Carnitine, pantethine, and coenzyme Q10 (CoQ10) are essential compounds in normal fat and energy metabolism and are of extreme benefit to sufferers of angina. These nutrients prevent the accumulation of fatty acids within the heart muscle by improving the conversion of fatty acids and other compounds into energy.
The use of antioxidant supplementation in patients with angina is important. In an analysis of normal controls and patients with either stable or unstable angina, the plasma level of antioxidants has been shown to be a more sensitive predictor of unstable angina than the severity of atherosclerosis.2,3 One group of researchers concluded: “These data are consistent with the hypothesis that the beneficial effects of antioxidants in coronary artery disease (CAD) may result, in part, by an influence on lesion activity rather than a reduction in the overall extent of fixed disease.”2
Antioxidant nutrients are also important in preventing nitrate tolerance. Oral nitrates are widely used in the conventional treatment of angina, but their continuous administration can result in the rapid development of tolerance. Experimental findings indicate that nitrate tolerance is associated with increased vascular production of superoxide. The superoxide anions generated quickly degrade the nitric oxide formed from the administration of nitroglycerin and result in lower levels of cyclic guanosine monophosphate (an important intracellular regulator that promotes vasorelaxation). Because vitamin C is the main aqueous-phase antioxidant and free radical scavenger of superoxide and vitamin E is the main lipid-phase antioxidant, their importance in preventing nitrate tolerance is obvious. Clinical trials have upheld this connection, showing that high-dose vitamins C and E supplementation can prevent nitrate tolerance.4,5
Carnitine, a vitamin-like compound, stimulates the breakdown of long-chain fatty acids by the energy-producing units in cells—the mitochondria. Carnitine is essential in the transport of fatty acids into the mitochondria. A deficiency in carnitine results in a decrease in fatty acid concentrations in the mitochondria and reduced energy production.
Normal heart function is critically dependent on adequate concentrations of carnitine. Although the normal heart stores more carnitine than it needs, if the heart does not have a good supply of oxygen, carnitine levels quickly decrease. This leads to decreased energy production in the heart and increased risk for angina and heart disease. Because angina patients have a decreased supply of oxygen, carnitine supplementation makes good sense.
Several clinical trials have demonstrated that carnitine improves angina and heart disease.6–10 Supplementation with carnitine normalizes heart carnitine levels and allows the heart muscle to use its limited oxygen supply more efficiently. This translates to an improvement in cases of angina. Improvements have been noted in exercise tolerance and heart function. The results indicate that carnitine is an effective alternative to drugs in cases of angina.
In one study of patients with stable angina, oral administration of 900 mg of L-carnitine increased mean exercise time and the time necessary for abnormalities to occur on a stress test (6.4 minutes in the placebo group compared with 8.8 minutes in the carnitine-treated group).10
These results indicate that carnitine may be an effective alternative to other antianginal agents such as beta blockers, calcium channel antagonists, and nitrates, especially in patients with chronic stable angina pectoris.
Carnitine, by improving fatty acid utilization and energy production in the heart muscle, may also prevent the production of toxic fatty acid metabolites. These compounds are extremely deleterious as they activate various phospholipases and disrupt cellular membrane structures. The changes in the properties of cardiac cell membranes induced by fatty acid metabolites are thought to contribute to impaired heart muscle contractility and compliance, increased susceptibility to irregular beats, and the eventual death of heart tissue. Supplemental carnitine increases heart carnitine levels and prevents the production of toxic fatty acid metabolites. This has been demonstrated clinically, where the early administration of L-carnitine (40 mg/kg per day) in patients having heart attacks was found to considerably reduce heart damage.11
Pantethine is the stable form of pantetheine, the active form of pantothenic acid, which is the fundamental component of coenzyme A (CoA). CoA is involved in the transport of fatty acids to and from cells as well as to the mitochondria. The synthetic pathway from pantethine to CoA is much shorter than that of pantothenic acid, making pantetheine the preferred therapeutic substance. In addition, pantetheine has significant lipid-lowering activity, whereas pantothenic acid has very little if any effect in lowering cholesterol and triglyceride levels.
The standard dose for pantethine is 900 mg/day. Like carnitine, pantethine has been shown in clinical trials to significantly reduce serum triglyceride and cholesterol levels while also increasing high-density-lipoprotein cholesterol levels.12–14 Its lipid-lowering effects are most impressive when its toxicity (virtually none) is compared with that of conventional lipid-lowering drugs. Its mechanism of action is due to the inhibition of cholesterol synthesis and acceleration of fatty acid breakdown in the mitochondria.
Pantethine is well indicated in angina. Like carnitine, heart pantethine levels decrease during times of reduced oxygen supply. Demonstrated effects in animals indicate that it would greatly benefit individuals with angina.15
CoQ10, also known as ubiquinone, is an essential component of the mitochondria, where it plays a major role in energy production. Like carnitine and pantethine, CoQ10 can be synthesized within the body. Nonetheless, deficiency states have been reported. Deficiency can be a result of impaired CoQ10 synthesis due to nutritional deficiencies, a genetic or acquired defect in CoQ10 synthesis, or increased tissue needs.16
Cardiovascular diseases—including angina, hypertension, mitral valve prolapse, and congestive heart failure—are examples of diseases that require increased tissue levels of CoQ10.16 In addition, many of the elderly may have increased CoQ10 requirements: the decline of CoQ10 levels that occurs with age may be partly responsible for the age-related deterioration of the immune system.
CoQ10 deficiency is common in individuals with heart disease. Heart tissue biopsies in patients with various heart diseases show a CoQ10 deficiency in 50% to 75% of cases.16 One of the most metabolically active tissues in the body, the heart may be unusually susceptible to the effects of CoQ10 deficiency. Accordingly, CoQ10 has shown great promise in the treatment of heart disease.
In one study, 12 patients with stable angina pectoris were treated with CoQ10 (150 mg/day for 4 weeks) in a double-blind crossover trial.17 Compared with placebo, CoQ10 reduced the frequency of anginal attacks by 53%. In addition, there was a significant increase in treadmill exercise tolerance (time to onset of chest pain and time to development of ECG abnormalities) during CoQ10 treatment. The results of this study and others suggest that CoQ10 is a safe and effective treatment for angina pectoris.