Notes

The heart is a very efficient organ that pumps blood to all the tissues and organs of the body. It is very demanding in an aerobic sense because it requires a large supply of oxygen. There is a fine balance between oxygen supply and demand. The heart’s much-needed oxygen supply is delivered to the heart muscle by means of the coronary arteries. When the heart’s supply of blood carrying oxygen and energy-rich nutrients is insufficient to meet the demands of the heart, the heart muscle (or myocardium) aches. This is called angina pectoris, or chest pain. Angina pectoris results from a reduction in the oxygen supply-to-demand ratio. To alleviate the pain associated with angina, it is necessary to improve this ratio. This can be done either by increasing blood flow (which increases oxygen delivery or supply) or by decreasing oxygen demand (i.e., by decreasing myocardial oxygen consumption).
Damaged cells/tissue that result from inadequate oxygen supply is referred to as ischemia. When the heart is involved, the condition is called ischemic heart disease. Ischemic heart disease is the number-one killer in the United States today. The primary cause is a disease of the coronary arteries known as atherosclerosis (fatty plaque deposits in the arterial walls). When atherosclerotic plaques project from the walls into the lumens of these vessels, the vessels become narrow. The supply of oxygen and energy-rich nutrients needed for the heart is then decreased. This disorder is called coronary artery disease (CAD). An acute result of CAD and of ischemic heart disease is myocardial infarction (MI), or heart attack. An MI occurs when blood flow through the coronary arteries to the myocardium is completely blocked so that part of the heart muscle cannot receive any of the blood-borne nutrients (especially oxygen). If this process is not reversed immediately, that area of the heart will die and become necrotic (dead or nonfunctioning). Damage to a large enough area of the myocardium can be disabling or fatal.
The rate at which the heart pumps and the strength of each heartbeat (contractility) influence oxygen demands on the heart. There are many substances and situations that can increase heart rate and contractility and thus increase oxygen demand. These include caffeine, exercise, and stress, among others, and result in stimulation of the sympathetic nervous system, which leads to increased heart rate and contractility. In a patient with CAD who has an already overburdened heart, this stimulation can worsen the balance between myocardial oxygen supply and demand and result in angina. Some of the drugs used to treat angina are aimed at correcting the imbalance between myocardial oxygen supply and demand by decreasing heart rate and contractility.
The pain of angina is a result of the following process. Under ischemic conditions when the myocardium is deprived of oxygen, the heart shifts to anaerobic metabolism to meet its energy needs. One of the by-products of anaerobic metabolism is lactic acid. Accumulation of lactic acid and other metabolic by-products causes the pain receptors surrounding the heart to be stimulated, which produces the heart pain known as angina. This is the same pathophysiologic mechanism responsible for causing the soreness in skeletal muscles after vigorous exercise.
There are three classic types of chest pain, or angina pectoris. Chronic stable angina has atherosclerosis as its primary cause. Classic angina and effort angina are other names for it. Chronic stable angina can be triggered by exertion or other stress (e.g., cold, emotions). The nicotine in tobacco, alcohol, coffee, and other drugs that stimulate the sympathetic nervous system also can exacerbate it. The pain of chronic stable angina is commonly intense but subsides within 15 minutes of either rest or appropriate antianginal drug therapy. Unstable angina is usually the early stage of progressive CAD. It often ends in an MI in subsequent years. For this reason, unstable angina is also called preinfarction angina. Another term for this type of angina is crescendo angina because the pain increases in severity, as does the frequency of attacks. In later stages, pain may even occur while the patient is at rest. Vasospastic angina results from spasms in the layer of smooth muscle that surrounds coronary arteries. In contrast to chronic stable angina, this type of pain often occurs at rest and without any precipitating cause. It does seem to follow a regular pattern, however, usually occurring at the same time of day. This type of angina is also called Prinzmetal angina or variant angina. Dysrhythmias and electrocardiogram (ECG) changes often accompany these different types of anginal attacks.