What is cardiology?

Science and Profession

Cardiology is the study of the heart and its various diseases: inflammation of the heart muscle, diseases of the heart valves, atherosclerosis and arteriosclerosis (athero meaning “deposits of soft material,” arterio meaning “pertaining to the arteries,” and sclerosis meaning “hardening”), and congenital defects. This field also concerns related diseases, such as hypertension (high blood pressure) and certain renal, endocrine, and lung disorders.

The heart contains four chambers, the right and left atria on top and the right and left ventricles below. The walls of the heart are three layers of tissue: the outer layer, the epicardium; the middle layer, the myocardium; and an inner layer, the endocardium, which includes the heart valves. The heart is contained in a protective sac, called the pericardium.

The pumping of the heart is a coordinated contraction. The right atrium receives blood from the veins and contracts, pumping blood through the tricuspid valve into the right ventricle. The right ventricle then contracts, pumping blood through the pulmonary valve into the lungs, where it gives up carbon dioxide and receives oxygen. Blood then enters the left atrium and travels through the mitral valve to the left ventricle. The blood then enters the venous system, first into the venules (tiny veins that lead to larger veins) and finally to one of the two branches of the vena cava: the superior vena cava from the upper part of the body, and the inferior vena cava from the lower. They connect outside the heart and bring blood back into the right atrium.

The heartbeat, the rhythmic contraction of the heart muscle, is controlled by the conduction system. Electrochemical impulses cause muscle fibers to contract, pumping blood through the chambers, and relax, letting the chambers fill again. The contractions are initiated by specialized “pacemaker” tissues in the sinoatrial (S-A) or sinus node, in the junction of the superior vena cava and the right atrium. The pacemaker signal travels to the atrioventricular (A-V) node, near the tricuspid valve. The impulse crosses the A-V node and travels to the bundle of His, specialized fibers that carry it to the ventricles.

Virtually every part of the heart is subject to disease: each layer of the heart muscle, each valve, each chamber, and the coronary arteries. The coronary arteries are quite small and are subject to the accumulation of plaque on their inner walls, a condition known as atherosclerosis. This plaque can be cholesterol, scar tissue, clotted blood, or calcium. As the plaque accumulates, the artery narrows, reducing the flow of blood into the heart muscle. The reduction in blood flow reduces the heart’s supply of oxygen, causing myocardial ischemia (lack of blood). There is usually a signal of pain called angina pectoris (angina meaning “choking pain” and pectoris meaning “of the chest”). Often, the patient feels tightening in the chest with sharp pain behind the sternum. The pain can radiate into either arm or the jaw. It is usually caused by overexertion, exposure to cold, stress, or overeating.

As a rule, an attack of angina pectoris lasts only a few minutes and is relieved by rest, but it can signal the beginning of a heart attack. In addition, coronary arteries contain muscle fibers that can go into spasm and tighten, reducing blood flow into the heart. This condition, too, can cause anginal pain, heart attack, and death. Some patients who have myocardial ischemia do not have anginal pain. This is known as silent ischemia, and it is usually discovered only with an electrocardiogram (ECG) or exercise stress test.

There are four major classes of angina pectoris: stable angina, in which pain begins when the heart’s need for oxygen exceeds the amount that it receives; unstable angina, which is significantly more serious than stable angina; variant angina, which is characterized by chest pain at rest and may be caused by spasm of the coronary arteries; and postinfarction angina, unstable angina that appears after acute myocardial infarction.

When atherosclerotic plaque builds up in the coronary arteries, the inner lining of the vessel becomes rough. As a result, a thrombus (blood clot) can form on the plaque, making the vessel even narrower or clogging it completely (coronary thrombosis). When this occurs, blood flow to parts of the heart is stopped, and heart cells die from lack of oxygen. This condition is medically known as myocardial infarction (from infarct, meaning “an area of dead cells”) and commonly known as a heart attack.

The prognosis for patients who survive a heart attack is variable. In two-thirds of patients, spontaneous thrombolysis (the dissolution of the blood clot) starts to occur within twenty-four hours. About half of heart attack patients, however, will go on to develop postinfarction angina, which usually indicates severe, multivessel coronary artery disease.

Diseases of the conduction system can result in arrhythmias, or disturbances in the regularity of the heartbeat. Arrhythmias can be relatively benign or can severely restrict the patient’s physical activity. They can also cause sudden cardiac death. The most common arrhythmias are bradycardia, slowing of the heartbeat, and tachycardia, quickening of the heartbeat.

Normally, the chambers beat in synchronization with each other. In some arrhythmias, the chambers of the heart beat out of synchronization. These arrhythmias include atrial fibrillation, paroxysmal atrial tachycardia, ventricular tachycardia, and ventricular fibrillation. In atrial fibrillation, the atria beat very rapidly (three hundred beats per minute), out of synchronization with the ventricles. When the condition is prolonged, blood clots may form in the atria and may be carried to the cerebral vessels, where they cause a stroke, or the stoppage of blood flow in a blood vessel. With paroxysmal atrial tachycardia, a disturbance in the conduction of the A-V node causes the heart to beat up to two hundred fifty times a minute. The condition is usually not serious, but if it persists, fainting or heart failure could develop. Ventricular tachycardia exists when ectopic, or irregular, beats develop in the ventricular muscle; if they go on, blood pressure falls. In ventricular fibrillation, which is the leading cause of sudden cardiac death, ventricular contractions are weak, ineffective, and uncoordinated. Blood flow stops, and the patient faints. If the condition is not corrected, the patient can die in minutes.

Heart block can be another consequence of conduction disease. If, for various reasons, all the impulses from the sinus node do not pass through the A-V node and the bundle of His, the result is one of three degrees of heart block. First-degree heart block, which is not apparent to the patient, appears on the ECG as a delay in the impulse from the atria to the ventricles. Second-degree heart block occurs when some of the impulses from the atria fail to reach the ventricles. Often, the result is an irregular pulse. This condition can be attributable to a certain heart drug and may disappear when the drug is discontinued. In third-degree heart block, impulses from the pacemaker tissues fail to reach the ventricles. A lower pacemaker assumes the function of stimulating contractions of the ventricles in an “escape rhythm.” When this occurs in third-degree heart block, the heart rate often slows down so precipitously that blood flow to the brain and other organs is severely restricted. Dizziness and loss of consciousness may follow. Heart block can also result from a congenital
defect, inflammation, myocardial infarction, or other causes.

Disorders in the valves of the heart are most often caused by congenital defects or the effects of rheumatic fever. Rheumatic fever is caused by streptococcal bacteria and usually begins with a throat infection. If strep throat is not treated, rheumatic fever may develop. Acute rheumatic fever is associated with mitral or aortic valve insufficiency (leakage). Chronic rheumatic heart disease can include mitral or aortic stenosis (narrowing). Valves are scarred with fibrous tissue and/or calcific (calcium-containing) deposits that cause the valve openings to become narrower.

Mitral stenosis usually develops slowly. Ten to twenty years after rheumatic fever, the valve narrows so much that blood flow from the atrium into the ventricle is impeded. As blood accumulates in the left atrium, pressure within the atrium increases, and the chamber becomes enlarged. Blood is forced back into the lungs, resulting in pulmonary edema (fluid in the lungs). Blood vessels in the lungs become engorged; the increased pressure forces fluid into the air sacs. Symptoms of mitral stenosis include shortness of breath, fatigue, feelings of suffocation, wheezing, agitation, and anxiety. In severe cases, fluid may also accumulate in the lower extremities. Mitral stenosis can also cause atrial fibrillation, which in turn can generate potentially lethal blood clots.

Mitral regurgitation, also known as mitral insufficiency, another mitral valve disorder, can be due to rheumatic fever or other causes. The valve fails to close completely during left ventricle contraction. Blood leaks back into the left atrium, and blood flow into the aorta is reduced. The heart has to work harder to pump blood into the body. Mitral regurgitation may lead to enlargement of the left atrium and left ventricle. Pulmonary edema, shortness of breath, fatigue, and palpitations are late symptoms of severe disease.

Still another disorder is mitral valve prolapse, which can also result in mitral regurgitation. The mitral valve consists of two leaflets of tissue that fall apart to open and come together to close. Prolapse occurs when either or both of these leaflets bulge into the left atrium, as occurs in a significant percentage of the population whose valves consist of “floppy” (myxomatous) tissue. The condition is usually of little clinical significance, but some patients experience palpitations and chest pain, and some have a heart murmur. In rare cases, significant valve leakage occurs, requiring surgery.

The aortic valve consists of three leaflets or “cusps” that can become fused, calcified, or otherwise compromised because of rheumatic fever or a congenital heart defect. The opening narrows, and blood flow into the aorta is reduced. Pressure increases inside the left ventricle, causing it to pump harder. The wall of the left ventricle thickens, a condition called ventricular hypertrophy. Aortic stenosis
may not be evident until it is quite advanced. Symptoms include heart murmur, weakness, fatigue, anginal pain, breathlessness, and fainting.

Tricuspid stenosis and regurgitation are relatively rare, as is pulmonary regurgitation. Pulmonary or pulmonic valve stenosis, however, is a common congenital heart defect. There is a characteristic heart murmur produced by turbulence of blood through the narrow pulmonary valve. Pressure increases in the right ventricle. Fainting and heart failure are possible in severe cases.

In congestive heart failure, the heart pumps inefficiently, failing to deliver blood to the body and allowing blood to back up into the veins. It may occur on the left or the right side, or both. If the left side of the heart is pumping inefficiently, blood flows back into the lungs, causing pulmonary edema. If the right side of the heart is inefficient, blood seeps back into the legs, resulting in edema of the extremities. Blood can also back up into the liver and the kidneys, resulting in engorgement and reduced arterial flow that prevent these organs from getting the nutrition and oxygen they need to function. The most common cause of heart failure is ischemic cardiomyopathy due to coronary artery disease, other cardiomyopathies, and valvular disease.

Cardiomyopathy refers to diseases of the myocardium. There are many possible causes, including “end-stage” coronary artery disease; infectious agents such as fungi, viruses, and parasites; overconsumption of alcohol; or genetic defects. The three main classes of cardiomyopathy are dilated congestive cardiomyopathy, hypertrophic cardiomyopathy, and restrictive cardiomyopathy. In dilated congestive cardiomyopathy, either all of the heart chambers are involved (diffuse) or some but not all chambers are involved (nondiffuse). The cause of this class of cardiomyopathy is usually ischemia, but viral infection (myocarditis), drugs, alcohol, and nonviral diseases may be responsible. The heart pumps inefficiently, causing fatigue, breathlessness, and edema in the lower extremities. The heart chambers may enlarge, and blood clots may form. With hypertrophic cardiomyopathy, the myocardium thickens and reduces the cavity of the left ventricle so that blood flow into the aorta is reduced. The condition is usually chronic, with fainting, fatigue, and breathlessness as symptoms. Restrictive cardiomyopathy is rare. With this condition, the heart muscle loses elasticity and cannot expand to fill with blood between contractions. Symptoms include edema, breathlessness, and atrial and ventricular arrhythmias.

The endocardium and the pericardium can become inflamed because of infection or injury, resulting in endocarditis or pericarditis. Bacterial endocarditis usually affects abnormal valves and heart structures that have been damaged by rheumatic fever or congenital defects. Fulminant (sudden and severe) infections can destroy normal heart valves, especially with intravenous drug abuse. The symptoms of bacterial endocarditis are fever, weight loss, malaise, night sweats, fatigue, and heart murmurs. The condition can be fatal if the invading organism is not eradicated. Nonbacterial thrombotic endocarditis or noninfective endocarditis arises from the formation of thrombi on cardiac valves and endocardium caused by trauma, immune complexes, or vascular disease. Pericarditis often occurs concomitantly with, or as a result of, viral respiratory infection. The inflamed pericardium rubs against the epicardium, causing acute pain. Large amounts of fluid may develop and press on the heart in cardiac tamponade. This condition can impede heart action and blood flow and can be life-threatening. In constrictive pericarditis, the pericardium becomes thicker and contracts. This action prevents the heart chambers from filling, decreasing the amount of blood drawn into the heart and pumped out to the body.

Primary cardiac tumors, those originating in the heart, are rare. While usually benign, they can have fatal complications. Malignant tumors also occur, and metastasis (movement of cancer cells throughout the body) may bring malignancies to the heart.

Congenital heart defects occur in approximately eight in every 1,000 live births. Ventricular septal defect, a hole in the wall between the ventricles, is the most common. It is detected by a loud murmur. Atrial septal defect is common but rarely leads to symptoms until the third decade of life.

Diagnostic and Treatment Techniques

The stethoscope, ECGs, and the x-ray are basic tools that the cardiologist uses for the diagnosis of heart conditions. By listening to heart sounds through the stethoscope, the physician can learn much about the status of heart function, particularly heart rhythm, congenital defects, and valve dysfunction.

ECG patterns of electrical impulses help the physician discover chamber enlargement and other cardiac abnormalities. In a stress test, the ECG is attached to a patient who is running on a treadmill or riding an apparatus similar to a bicycle. The test assesses the exercise tolerance of patients with coronary artery disease and other conditions.

The chest x-ray provides a picture of the size and configuration of the heart, the aorta, the pulmonary arteries, and related structures. It can detect enlarged chambers and vessels and other disorders. In some cases, radioactive isotopes are injected into the patient, and the patterns that they form in the heart and surrounding arteries are read by a scanner to help the physician make a diagnosis. The echocardiogram uses ultrasound to outline heart chambers and detect abnormalities within them and in the myocardium. It is also used to analyze patterns of blood flow.

More sophisticated instruments the cardiologist uses include fast-computed tomography, called cine-CT because it gives the physician a visualization of heart activity. Magnetic resonance imaging (MRI), MR spectroscopy, and positron emission tomography (PET) scanning help the cardiologist investigate heart function and anatomy.

These techniques and procedures are conducted outside the body. Sometimes it is necessary, however, to go into the body. One such technique is diagnostic catheterization with angiography. A thin flexible tube (catheter) is inserted into a blood vessel in the groin or arm and threaded into a coronary artery or the heart. Pressures and blood oxygen are measured in the heart chambers. A radiopaque dye is then injected through the catheter. The inside of the artery or the heart becomes visible to the x-ray and is recorded on film (a process sometimes called cineangiography). Angiography can also be used with radioactive isotopes. The radiation detected by a scanner can help the physician discover abnormalities in the coronary arteries and the heart.

Diagnosis of angina pectoris is usually based upon the patient’s complaint of chest pain. An ECG can help confirm the diagnosis. Yet many patients with coronary artery disease have normal ECGs at rest, so stress testing with the ECG is considered more reliable. Patients may be given pharmacologic stress tests if they are unable to do physical exercise.

Drug therapy for coronary artery disease and angina pectoris is directed at keeping the coronary arteries open and avoiding myocardial ischemia. Primary among the drugs used is nitroglycerin, taken under the tongue or in a transdermal (through-the-skin) patch—or, in emergencies, intravenously. There are many nitrate compounds that fulfill similar functions. Beta-adrenergic blocking agents, or beta-blockers, decrease heart rate and blood pressure, reducing the heart’s oxygen requirement and workload, thus reducing the incidence of angina. Some serious arrhythmias are also suppressed. Calcium-channel blockers dilate coronary arteries and maintain coronary blood flow while decreasing blood pressure, reducing heart work, and stabilizing heart rhythm. Angiotensin-converting enzyme (ACE) inhibitors help to relax the blood vessels, thereby reducing blood pressure. Cholesterol-lowering medications help to reduce the amount of cholesterol in the blood, thereby reducing plaque deposits and helping to prevent atherosclerosis, and low-dose aspirin and other blood thinners can also help to reduce to the risk of obstruction of the coronary arteries by blood clots.

If coronary artery disease progresses to the point where there is risk of myocardial infarction, various catheter and surgical procedures may be considered. Coronary angioplasty is used to open a clogged artery mechanically. The cardiologist threads a catheter with a tiny balloon into the clogged artery and inflates the balloon at the site of the blockage. This procedure is repeated until the vessel is open. A stent may be inserted into the artery to help prevent future blockages. Another procedure used when coronary arteries are blocked is coronary artery bypass surgery. The surgeon takes sections of vein or artery from another part of the body and implants them between the aorta and the heart, creating new coronary arteries and bypassing those that are clogged.

When clogged coronary arteries cause a myocardial infarction, the patient should be treated in a special medical facility, preferably in a coronary care unit (CCU). Heart attacks rarely begin in the hospital, however, so the medical team must keep the patient alive on the way to the CCU. Primary ventricular fibrillation is the greatest danger, and it must be corrected immediately by medication or electrical defibrillation. Sometimes heart block and profound bradycardia occur, which could cause a drop in blood pressure that could in turn cause cardiac arrest.

The aims of emergency myocardial infarction treatment are to ease discomfort, minimize the mass of infarcted myocardial tissue, reduce heart work, stabilize heart rhythm, and maintain oxygen perfusion throughout the body by regulating blood pressure. Treatment and medications used in the CCU include continuous ECG monitoring (both during and after the heart attack), oxygen, nitroglycerin, antiarrhythmia agents, analgesics for pain, thrombolytic agents to dissolve clots, diuretics, agents to treat shock, and sedatives. Beta-blockers, calcium-channel blockers, anticoagulants, and antianxiety drugs may also be used.

About 60 percent of patients who have suffered from myocardial infarction develop congestive heart failure. In treating congestive heart failure from heart attacks or other causes, the cardiologist uses both dietary instruction and medication. Salt restriction is recommended to reduce edema. The three most commonly prescribed drugs are diuretics to reduce edema, digitalis (digoxin or digitoxin) to increase the force of the heart’s contraction, and vasodilators to reduce the resistance of blood vessel walls, to facilitate blood flow, and to reduce heart work. Intractable congestive heart failure may be a reason for a heart transplant.

The main goals of therapy for cardiac arrhythmias are to improve heart function and to prevent sudden cardiac death. Drug therapy must be individualized to correct the particular arrhythmia. Digitalis, procainamide, tocainamide, and atropine are often used. Beta-blockers and calcium-channel blockers are also helpful in stabilizing heart rhythm. If heart block becomes severe, an artificial pacemaker is implanted in the chest to regulate the heartbeat.

Disorders of the heart valves are not usually treated with drugs. While awaiting surgery, it may be necessary to treat heart failure, or the effects of valve disease in other parts of the body. For example, diuretics may be required to reduce edema, an antiarrhythmia agent may be needed to control atrial fibrillation, or anticoagulants may be used to prevent blood clots. Some stenotic valves can be opened using a modification of the balloon catheter technique, or surgical reconstruction may be possible. Often, it is necessary to replace the valve with a new one made of human or porcine tissue, or with a mechanical valve.

Pulmonary edema is a severe form of heart failure and is life-threatening. In emergencies, oxygen is given, in severe cases by inserting a breathing tube into the patient’s trachea. Medications are given to relieve pulmonary congestion, and if the pumping action of the heart is compromised, digitalis or another medication can strengthen the contractility of the heart.

In treating dilated cardiomyopathy, the cardiologist uses appropriate medications that may include diuretics, vasodilators, antiarrhythmia agents, and digitalis. Alcohol restriction is required.

If bacteria or other microorganisms are involved, appropriate antibiotic therapy must be instituted to eradicate the cause. Patients with congenital or valvular heart disease are high risks for cardiac and valve infection. They are given preventive antibiotic therapy before undergoing surgical or dental procedures.

In acute pericarditis, if excessive fluid builds up, a procedure called pericardiocentesis may be performed to drain the fluid between the pericardium and the heart wall. In cardiac tamponade, pericardiocentesis may be life-saving. In chronic constrictive pericarditis, an operation may be necessary to remove tissue that has stiffened and strangled the heart.

Perspective and Prospects

Cardiology is a major medical specialty because heart disease is the leading cause of death worldwide. Today’s cardiologist turns increasingly to preventive medicine as a means of reducing morbidity (the relative incidence of a disease) and mortality. These measures include programs against smoking and programs advocating cholesterol reduction, stress reduction, increased exercise, and other measures that have been found useful in preventing heart disease.

Ongoing studies continue to accumulate data on increasingly large populations in more and more countries. Links between behavior, habits, nutrition, and ecology may be found that will give a clearer picture of how to prevent and treat heart disease. Increased knowledge will improve diagnosis and treatment, improving patient care and the quality of life for sufferers of heart disease.

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