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Most cardiovascular agents (like all other drugs) must be avoided in the first trimester of pregnancy because they may produce congenital malformations, especially from the 3rd to the 12th week of pregnancy. When used during the second and third trimesters, several cardiac drugs may affect growth and functional development of the fetus or cause toxic effects on fetal tissues. Also, some agents must be avoided just before parturition as they may have adverse effects on labor or in the newborn.

Calcium antagonists without doubt cause an increased incidence of heart failure (HF) as observed in several well-run randomized controlled trials (RCTs)

During a heart attack, large quantities of noradrenaline are released into the heart muscle, which can precipitate abnormal heart rhythms, particularly, ventricular fibrillation. Adrenaline causes an increase in heart rate and an increase in blood pressure, thus causing the heart to work harder. Because a coronary artery is blocked during a heart attack, the increased work with less available oxygen causes further damage to the heart muscle and increases the size of the muscle damage, causing a larger heart attack. Beta-blocking drugs were originally discovered by Sir James Black of Imperial Chemical Industries. Since the introduction of the prototype, propranolol, for the management of hypertension in 1964, more than 12 beta-blocking drugs have become available. Beta-adrenergic blocking drugs have become the cornerstone of cardiac drug therapy. Beta-blockers block beta-receptors. Structurally, they resemble the catecholamines (adrenaline and noradrenaline) and block the action of these catecholamines at their receptor sites. The beta receptors are situated on the cell membrane and are believed to be a part of the adenyl cyclase system. An agonist acting on its receptor site activates adenyl cyclase to produce cyclic adenosine-5-monophosphate, which is believed to be the intracellular messenger of beta stimulation.

This chapter focuses on pulmonary arterial hypertension (PAH), which is primarily caused by primary pulmonary hypertension (PPH). The chapter also defines several disorders that cause PAH: pathophysiologic causes of severe chronic hypoxemia including alveolar hypoventilation disorders, such as chronic obstructive pulmonary disease (COPD); numerous restrictive lung diseases; chronic exposure to high altitude; sleep apnea drugs, such as appetite suppressants, pulmonary venous hypertension in which the pulmonary capillary wedge pressure is increased. The most publicized risk factor for PAH is appetite suppressant drugs. Aminorex fumarate was linked to an epidemic of PAH in Switzerland, Germany, and Austria in the sixties, and withdrawal of this agent was followed by a fall in incidence of the disorder.

Pericarditis can be caused by cancer chemotherapeutic agents, such as dantrolene, hydralazine, isoniazid, minoxidil, procainamide, phenytoin, and anticoagulants. Pericardium is defined as a double membrane that covers the heart and can be involved in infective and non-infective disorders. Pericarditis may cause severe chest pain in the retrosternal or left precordial area. Radiation to the chest may rarely cause pericarditis. Occasionally, the pain radiates to the trapezius ridge, a radiation that does not occur with angina, but it may also radiate to the neck or left arm and may stimulate angina or myocardial infarction. At times, the pain is localized to the upper epigastrium and left upper quadrant. Typical features of pain include a sharp, pleuritic pain that increases with deep inspiration, coughing, sneezing, or worsening of pain when lying down. The sharp pain that occurs in bed typically is relieved immediately by sitting and leaning forward or on standing; pain recurs with recumbency.

There has been much confusion in the use of the terms arteriosclerosis and atherosclerosis. Arteriosclerosis is a diffuse lesion, which often affects long segments of the arterial tree in which there is usually a combination of hypertrophic and fibrous changes in the entire thickness of all layers of the arterial wall. The media and adventitia are commonly affected by this disease process. Atherosclerosis is the term used for atheroma of arteries. It is typically patchy, with a focal lesion of the intima with degeneration. There are also plaques of atheroma jutting into the lumen of the vessel obstructing the flow of blood. This chapter discusses diseases that cause arteriosclerosis, such as hypertensive arteriosclerosis; monckeberg's sclerosis, which is calcification of the media; and endarteritis obliterans.

This chapter highlights erectile dysfunction (ED), which is a disorder of the blood supply to the penis. It is observed often in men with cardiovascular disease. Some investigators have suggested that ED may serve as a predictor for cardiovascular disease, because in both conditions, endothelial dysfunction is deranged. Endothelial dysfunction is a well-defined entity and is a major player in the pathogenesis of atherosclerosis, its complications, and symptomatology. Endothelial dysfunction shares many common risk factors with both atherosclerotic vascular disease and ED. The chapter claims that nitric oxide (NO) bioavailability is at the core of normal and abnormal erectile function. Nitric acid is synthesized from the amino acid L-arginine in response to sexual stimulation. Physical or emotional stimulation causes brain or neuronal NO synthase (bNOS) located in nonadrenergic, noncholinergic cavernous nerves of the penis to release NO.

A cardiac pacemaker is an electronic device that senses cardiac electrical activity and delivers electrical stimuli to the heart when needed. If the natural pacemaker is no longer working well or the electric current is blocked by disease of the conducting bundles, a pacemaker can be implanted. A cardiac pacemaker is inserted just under the skin and the pacemaker lead (electrode) is inserted into the right ventricle. The lead is then attached to the pacemaker. A small electrical current is passed through the lead at the rate set by the cardiologist. When the impulse reaches the heart muscle the muscle contracts in the same way it would as if the electrical impulse occurred naturally. The pacemaker generator can be visualized as an eye that stands guard over ventricular, and in some cases, atrial activity. If the eye sees ventricular activity, it inhibits its own output electrical pulse, but if it sees no activity, then it delivers an electrical stimulus to the ventricle to keep it beating at a programmed rate. This chapter explains the various types of pacemakers.

This chapter discusses deep vein thrombosis that occurs in the veins of the legs, thigh, and pelvis. It can lead to a life-threatening condition called pulmonary embolism, and is a common problem worldwide. Thrombosis of veins that lie deep in the calf or thigh muscle is more dangerous than clots occurring in superficial veins just under the skin, because deep veins are much larger and communicate more directly with the lungs and the heart. A thrombus that is lodged in the femoral or iliac veins may break off and travel into the bloodstream, be carried to the right heart, and pumped into the lungs. This traveling clot is called an embolus, hence the term pulmonary embolism. Thrombi form in veins of the lower limbs and pelvis because of certain factors that increase the tendency of free-flowing blood to clot. A sudden increase in the tendency of the blood to clot commonly occurs soon after surgical operations or fractures that immobilize the lower limbs. Deep vein thrombosis occurring in the lower limbs is often difficult to diagnose from the history and physical examination. Some individuals present with pain and swelling of the calf muscle, whereas others are asymptomatic.

Aorta, the largest artery, takes blood from the heart and runs from the chest into the abdomen, lying against the spine until it reaches the pelvis. It divides at that point into iliac arteries that supply blood to the pelvis, buttocks, and legs. The abdominal aorta is commonly affected by atheroma and the process of atherosclerosis. Atherosclerotic disease causes thickening of the intima. This thickening appears to reduce the diffusion of oxygen and nutrients from the aortic lumen to the strong middle wall of aorta. This causes degeneration of the elastic elements and weakening of the walls of the aorta. The elastic wall of the aorta may be stretched causing the vessel to dilate. Tension on the dilated aortic wall increases, thus, causing further expansion of the artery with aneurysmal formation. Most aneurysms occur in the abdomen at the point just after the aorta branches to the kidney and before the aorta ends in its division into iliac arteries to the pelvis. Aneurysms of the aorta in the chest are much less common than abdominal aneurysms. They are classified as the ascending, arch, or descending aortic aneurysms. Because of the etiology and natural history, treatment differs for each of these aortic segments.

This chapter focuses on the epidemic of heart failure, which is usually the result of a diseased heart. Heart failure occurs when the heart is unable to eject enough blood from its chambers into the circulation to satisfy the needs of the body. The most common cause of heart failure is a very weak heart muscle. The heart muscle is the strongest muscle in the body. During an average life span, the heart beats about 2.5 billion times, pumping more than 227 million liters of blood. If the heart muscle is severely weakened and unable to adequately expel the blood brought to the left or right ventricle, blood backs up in the veins that drain into the left or right side of the heart. In heart failure, blood and fluid overdistend or congest the veins that bring blood into the failing muscular chambers.

Patent foramen ovale (PFO) is a failure of fusion of the two flaps that cause a less than 5-mm, slit-like valvular opening in the interatrial septum. With echocardiographic visualization of the left atrium and the septum, it became apparent that PFO is present in approximately 25% percent of a randomly selected population. During fetal development, PFO allows the necessary shunting of oxygenated blood from the right atrium to the left atrium; thus, oxygenated blood flows into the systemic circulation to organs and tissues. This right-to-left shunting of blood is crucial for fetal development, but it is also vital that no shunt should occur after birth, because the right side of the heart is no longer filled with oxygenated blood. A right-to-left shunt in individuals with congenital heart disease (CHD) causes cyanotic congenital heart disease, which is life-threatening.

This chapter deals with the endocrine disorders and the heart related problems, which include acromegaly, thyroid diseases, and adernal disorders. In acromegaly, the anterior pituitary gland secretes at least seven polypeptide hormones. Two of these hormones are released by the hypothalamus: somatostatin-releasing hormone, which stimulates growth hormone secretion, and somatostatin, which regulates the release of growth hormone from the anterior pituitary. Growth hormone regulates an individual's growth. It also increases the heart rate and myocardial contractility. Its features include enlargement of the heart, premature coronary artery disease, congestive heart failure, hypertension, intraventricular conduction defects, and cardiac arrhythmias. Mild hypertension occurs in more than 50% of patients. Other manifestations include headache, visual field defects (bitemporal hemianopsia), the growth of the hands, feet, and head, coarsening facial features with elongation of the jaw giving a typical lantern jaw appearance, enlargement of the liver, and glucose intolerance.

This chapter discusses the causes, pathophysiology, and management of cardiogenic shock. Cardiogenic shock is caused by a decreased pumping ability of the heart that results in a shock-like state with insufficient blood perfusion to organs and tissues. During cardiogenic shock, systolic blood pressure is less than 90 mmHg for greater than one hour and not responsive to IV fluids. The cardiac index is less than 2.2 L/minute/m 2 , and the pulmonary capillary wedge pressure is greater than 18 mmHg. Patients usually have clouded consciousness and cold extremities. Acute myocardial infarction is the most common cause of cardiogenic shock. The complete occlusion of a coronary artery by a clot causes death of an area of heart muscle that is supplied by that blood vessel and its branches.

Coronary artery bypass grafting is a simple procedure: A vein from the patient's leg is removed and inserted into the aorta as it leaves the heart and the other end of the vein is joined to the coronary artery below the blockage. Blood then flows from the aorta through the vein graft beyond the blockage to the coronary artery and to the heart muscle. Surgeons prefer to use the internal mammary artery instead of using a vein graft to bypass the blockage in the important left anterior descending (LAD) artery. The saphenous vein is ideal for bypass of occlusions of the right coronary and circumflex coronary arteries and for their diagonal branches. A saphenous vein graft is easily harvested and is used in emergency situations. These include bypass of the LAD because the internal mammary artery is more difficult to mobilize in emergency situations. The radial artery is readily accessible in the forearm, and it is used frequently by some surgeons. Spasm and thrombosis of the artery have been minimized by careful manipulation of the vessel and the use of long-term calcium antagonists.

Stress is the main factor of heart disease. Stress produces well-known reactions in the body, such as an increase in blood pressure, which causes small blood particles to become sticky. The platelet particles stick together to form clumps or sludge that can lead to formation of a blood clot in the coronary artery. Stress causes adrenaline and noradrenaline release. These stress hormones cause the heart rate and blood pressure to increase, giving the heart more work to do. A stressful situation causes the “emotional center” in the brain to trigger certain reactions. The hypothalamus sends signals to the pituitary gland and sympathetic nervous system, which leads to secretion of the “stress hormones” cortisone, adrenaline, and noradrenaline. Cortisone causes an increase in blood glucose and an increase in blood pressure. As a result of a stressful situation, the inner compartment of the adrenal glands pours out adrenaline and noradrenaline, and these compounds are involved in the “fight or flight” reaction.

This chapter starts by giving a historical review of blood pressure. The amount of blood expelled by the heart into the arteries in one minute is called the cardiac output, which is about 5 L/minute. Blood pressure is equal to the total vascular resistance multiplied by the cardiac output. Hypertension is the medical term for high blood pressure and has nothing to do with excessive nervous tension. High blood pressure in individuals older than age 18 is defined as a systolic blood pressure of greater than 140 mmHg and/or a diastolic blood pressure of greater than 90 mmHg based on the average of two or more readings taken at each of two or more visits after an initial screening (average of at least four readings taken days or weeks apart). The chapter also discusses the classification and normal fluctuation of the blood pressure. Marked variability in blood pressure is normal. It varies from minute to minute and from day to day, like the waves of a sea, fluctuating with the force of the prevailing winds. Ambulatory blood pressure recordings may be needed in some individuals to verify the correct levels of hypertension. The blood pressure readings in a doctor's office or clinics are often higher than they are in a home setting.

This chapter discusses atrial septal defect, a hole in the septum dividing the right and left atrium, which is the most common congenital heart defect observed after age 12 and in adults, because the lesion is usually so small that it causes little disturbance in infants. Atrial septal defect accounts for approximately 10% of all congenital cardiac defects. With this defect, oxygenated blood is shunted from the left atrium into the right atrium and traverses the pulmonary arteries and lungs and returns to the left side of the heart. This circulatory disturbance is called a left to right shunt. The shunt is usually small, but if the hole is large enough, then the right ventricle works harder to pump the extra blood delivered to it from the left side into the pulmonary arteries, and through the pulmonary circulation back to the left side of the heart. The right ventricle, over time, is subjected to more strenuous work than normal. The muscle of the right ventricle becomes weaker and fails to expel sufficient blood from the chamber, and a condition referred to as right heart failure occurs. The atrial septal defect most often involves the fossa ovalis in the mid septal region; this is called an ostium secundum type of defect.

This chapter discusses Arrhythmias, which is a term used for an irregularity or rapidity of the heartbeat, or an abnormal heart rhythm. The patient experiences the sensation as stronger heartbeats, more forceful or rapid heartbeats, or skipping of beats. This sensation is commonly called palpitations. The sinus node, a very small group of specialized cells, is located in the upper right corner of the heart. The node is about 303 mm thick. Through its genetic code, and the influx and efflux of sodium and potassium into its cells, this natural pacemaker spontaneously fires infinitesimal electrical discharges that are conducted through electric cable-like bundles to the atria and ventricles causing the heart muscle to contract about 70 times a minute. Cells outside the sinus node pacemaker, for example, ventricular muscle cells, possess a pacemaker activity so weak, that the normal electrical discharge from the sinus node suppresses them. The chapter also discusses palpitation, premature beats, and irregular beats with their definition, causes, and diagnosis.

The incidence of moderate and severe forms of congenital heart disease (CHD) is about 6 per 1000 live births, but it is 19 per 1000 live births if the potentially serious bicuspid aortic valve is included. If very small muscular ventricular septal defects (VSDs) are included, the incidence of all forms of CHD increase to 75 per 1000 live births. Although several classifications are used, the oldest and the most meaningful classification is the division into cyanotic and noncyanotic CHD. Cyanotic CHD involves right-to-left shunts. The arterial circulatory system receives an overflow of deoxygenated blood from the right side of the heart resulting in a discoloration of the tongue, lips, and mucous membranes. Organs and tissues receive blood low in oxygen. Noncyanotic CHD mainly involves left-to-right shunts and valvular defects. In individuals with left-to-right shunts, oxygenated blood flows from the left side of the heart into the right atrium or ventricle, and is returned to the lungs. Usually, there is no significant hypoxemia, except in children with severe defects.

The major structural parts of the heart include the muscular wall (myocardium), the inner lining (endothelium), the outer lining (pericardium), and the blood vessels supplying the heart with blood. The muscle wall of the heart is surrounded by a thin but double membrane, the pericardium. The coronary arteries and veins run along the surface of the heart through the pericardium and traverse the muscular wall. The function of the heart is to pump blood containing oxygen, glucose, protein, fat, and salts to every organ, tissue, and living cell of the body. The heart is divided into four chambers. The upper chambers are called the right and left atrium, and the lower chambers are called the right and left ventricles. Blood from all parts of the body drains into veins, and empties into the right atrium. The systemic circulation is the part of the vascular system that carries blood from the left ventricle to organs and tissues of the body.

This chapter argues that a heart attack, medically called a myocardial infarction or coronary thrombosis, is a common occurrence, particularly, in young men aged 35–55. When a heart attack begins, the individual is suddenly stricken by pain in the center of the chest. This pain is often unbearable and may be a pressure-like discomfort accompanied by difficult breathing, profuse sweating, and a strange frightened feeling. The cause of a heart attack in the majority of cases is a blockage of a coronary artery that feeds the heart muscle with blood containing oxygen, glucose, sodium, potassium, calcium, and other nutrients. In more than 90% of patients, the blockage is shown conclusively to be due to a blood clot. This blood clot is often present on the surface of a partially obstructing plaque of atheroma that shows fissuring.

This chapter starts with the discussion of oral contraceptives. The risk of cardiovascular disease attributed to the use of oral contraceptives became immediately apparent following the use of these agents more than 40 years ago. The use of third generation oral contraceptives is purported to have a lower risk of myocardial infarction compared with second generation oral contraceptives. However, the risk of heart attack has not been minimized by the use of third generation oral contraceptives. Cigarette smoking continues to be the major factor for increased risk of heart attacks in older, childbearing women aged 33–45, and second or third generation contraceptives increase that risk. Most importantly, the increased risk for deep vein thrombosis (DVT) and thromboembolism has not been removed.

Sinoatrial (SA) node provides individuals with an automatic, infinitesimal current that sets the electrical activity and contractions of the heart. The electrical discharge from the SA node passes across the atrium and reaches the atrioventricular (AV) node. From the AV node the current is conducted to the ventricle through two bundles, a large left bundle and a thinner right bundle. Many myocardial diseases are associated with bundle branch block. The prognosis of bundle branch block reflects the underlying myocardial disease and is, therefore, variable. Mass electrocardiographic surveys indicate that many apparently healthy individuals have bundle branch block. The right bundle branch is the continuation of the penetrating AV bundle and runs as a single discrete bundle beneath the endocardium of the ventricular septum to the base of the anterior papillary muscle. The bundle then runs in the moderator band to form a rich anastomosing network of conducting fibers throughout the right ventricle. Left bundle branch block (LBBB) is common after age 60, and is due to a block of the conduction in the bundle that receives impulses from the atrium and conducts the electrical current through the left ventricle.

In thyroid heart disease, the thyroid gland in the neck may suddenly become overactive and secrete excessive amounts of the hormone thyroxine. This situation is common between age 20 and 50; it can also occur later in life. Excessive thyroxine causes increased metabolism of all tissues; therefore, weight loss can occur despite a good appetite and food intake. Shortness of breath, palpitations, tachycardia, and systolic hypertension are often observed. Other symptoms include the heart beating faster and contracting more vigorously, and the pulse rate may be 110–130 beats per minute at rest. This chapter discusses the physical signs of thyroid heart disease. The thyroid gland may become slightly enlarged and a bruit may be heard when the stethoscope is placed over the gland. Protrusion of the eyeballs (exophthalmos) may be pronounced and lid lag may be observed. The hands become warm and sweaty. Sinus tachycardia, a hyperkinetic cardiac apex, and a loud first heart sound may be accompanied by soft flow murmurs.

Blood clots are believed to occur in the coronary arteries because of platelets that become sticky when they come in contact with the damaged lining of blood vessels, where atheroma formation has commenced. Platelets interact with the damaged surfaces, and chemicals that are produced at the site cause the platelets to clump (platelet aggregation), and form a clot. Platelets are small particles present in the blood, which circulate as elliptical flat disks. They are the body's first defense against excessive bleeding. At the site of bleeding, platelets accumulate and stick together to form a clump to plug the seepage of blood. Platelets are the most sticky when they are newly released from the bone marrow. Mild cooling and chilling of the body without hypothermia can lead to an increase in the total number and stickiness of platelets and may increase clotting. This may influence the incidence of coronary thrombosis in winter.

This chapter discusses carcinoid heart disease, which may occur in patients with carcinoid syndrome. The main symptoms of flushing, diarrhea, and occasional wheezing are caused mainly by 5-hydroxytryptamine or serotonin, which is liberated from carcinoid tumors that originate from chromaffin cells (neuroendocrine cells) of the terminal ileum. These tumors of the small intestine contain neurosecretory granules that release a variety of biogenic amines: serotonin, histamine, bradykinins, tachykinins, and prostaglandins. Involvement of the heart occurs in about half of carcinoid syndrome cases. It is seen mainly in patients with malignant tumors that have metastasized to the liver. The noncardiac symptoms may be controlled with somatostatin, but the action of this drug is only minutes.

Angiotensin-converting enzyme (ACE) inhibitors, because of their unique pharmacologic properties, have proven superior to other vasodilators in the management of heart failure, and have come to play a key role in the therapy of hypertension. They are particularly useful in hypertensive patients with diabetes and proteinuria. This chapter begins with the description of the mechanism of action. The sodium concentration in the distal kidney tubules, sensed by the macula densa, controls the release of renin from the specialized juxtaglomerular cells located in the media of the afferent kidney arterioles. Renin is an enzyme that profoundly affects the cardiovascular system. Stimuli to the release of renin include: a decrease in renal blood flow, hypotension, and reduction of intravascular volume; sodium depletion or sodium diuresis; beta-adrenergic receptor activation. ACE inhibitors are used in combination with diuretics, beta-blockers, and digoxin in the majority of patients. Although these agents have provided much relief for suffering patients and have significantly decreased mortality, the effect is still modest, and newer agents must be sought.

This chapter defines the cardiovascular embryology, which is crucial to the understanding of different cardiac anomalies and the development of therapeutic and preventive strategies. The chapter argues that the commitment to the cardiogenic cell lineage occurs early in development, soon after gastrulation and approximately 48 hours following fertilization. The molecular basis for the formation of cardiac myocytes from the presumptive mesoderm requires further elucidation. The mesoderm consists of three germ layers, which are incorporated in the building of the tissues and organs of the embryo. Cells committed to the cardiac lineage are first seen to possess characteristics of cardiac myocytes prior to the formation of the tubular heart. Within 10–14 days of gestation, a pair of mainstem vessels is first differentiated; they are the primitive aortae. This pair of tubes comes to lie parallel and close to each other in the cephalic region of developing body cavity.

This chapter discusses the clinical study of arginine. It examines the argument that the many risk factors for coronary artery disease are associated with reduced production of nitric oxide (NO) by the endothelium. L-arginine supplementation appears to have modest clinical benefits in patients with angina. The effect of a medical food bar containing L-arginine, vitamin B6, B12, vitamin C, folic acid, and niacin has also been evaluated.

The aim of this chapter is to review heart disease that occurs in approximately 5% of people with AIDS. It argues that pericardial disease is the most common cardiac complication of HIV infection and it causes approximately 60% of all cardiac pathology. Approximately 5% of individuals infected with HIV show echocardiographic evidence of pericardial effusions. In more than 75% of cases, pericardial effusions are small and usually asymptomatic, but they indicate advanced disease and poor prognosis. Pericardial effusions may compress the heart, cause cardiac tamponade, and prevent adequate filling, which results in a marked fall in blood pressure, cardiogenic shock, and death. In approximately 30% of patients, the effusion resolves spontaneously. The disease of the pericardium may be caused by the following types of infections: viruses, bacterial, fungi, and neoplastic involvement.

This chapter studies cardiomyopathy, which is a rare form of heart disease that affects only the heart muscle. The term cardiomyopathy is derived from the word cardio, the heart, and myopathy, which indicates a weakness or disturbance of the muscle. Heart muscle diseases of unknown cause are classified under the term cardiomyopathy. In one form of heart muscle disease, the muscle of the ventricle becomes considerably thickened to the point that the cavity of the left ventricle becomes nearly filled with muscle mass; thus, less blood enters the chamber and less blood is expelled into the circulation. Since the muscle is enlarged, or hypertrophied, the disease is called hypertrophic cardiomyopathy. This is a disease of young adults. The muscle enlargement may be so severe that it obstructs the flow of blood into the aorta, and death may occur suddenly, particularly in individuals from age 12 to 36 years. In another form of heart muscle disease, the heart dilates without increasing the size of the muscle. The chambers are swollen, and the muscle becomes weak. This condition often results in failure of the heart to pump blood, which results in heart failure. Heart transplants are required in some of these patients.

Percutaneous transluminal coronary angioplasty (PTCA) is so named because the instrument is passed through the skin (percutaneously), and then through the lumen of the artery (transluminal) into the coronary artery, which is molded into shape (angioplasty). The balloon-tipped catheter is positioned next to the plaque of atheroma in the artery. The balloon is inflated for 30–60 seconds and then widened by pressure. The narrowed artery becomes dilated due to splitting (dissection) of the plaque and overstretching of the middle wall (media) of the artery. Transient chest pain may occur during the inflation but is quickly relieved. Several inflations may be necessary to accomplish dilation of the artery. The balloon is then deflated, and dye is injected so that the cardiologist can see if adequate dilation and flow of blood have been achieved. An optimal angiographic result (less than 20% residual stenosis) is obtained in less than 25% of patients after PTCA is associated with a favorable late clinical outcome. PTCA expands the coronary lumen by stretching and tearing the atherosclerotic plaque and vessel wall and to a lesser extent, by redistributing atherosclerotic plaque along its longitudinal axis. There is no evidence that the balloon compresses atheromatous plaques. PTCA has been transformed in the past decade with the development of angioplasty to assist with lesions exhibiting complex characteristics.

This chapter discusses mechanism of action, indications, and availability of antiplatelet agents. Today, there are more than five antiplatelet agents available. These cardioactive drugs are useful in the prevention of thrombi in coronary arteries and arteries that supply the brain, but they are much less effective in preventing thrombi that occur in veins. Antiplatelet agents are used in virtually all patients with coronary artery disease to manage the acute and chronic phases of the disease as well as its complications. Coronary thrombosis is known to be the major cause of coronary artery occlusion, resulting in fatal or nonfatal acute myocardial infarction. Antiplatelet agents are named so because they inhibit platelet aggregation, which plays a major role in coronary thrombosis, myocardial infarction, and cardiac death.

This chapter discusses chagas disease, which is caused by the protozoan Trypanosoma cruzi. Chagas affects more than 30 million individuals, with approximately 100 million at risk in Latin America. Chagas disease is transmitted to children and young adults younger than 20 years of age through the bite of a bug (reduviid, subfamily Triatominae). The bug becomes infected by feeding on infected animals such as the armadillo, opossum, raccoon, and skunks. Domestic dogs and cats also provide an extensive reduviid reservoir for infecting entire families. The bite of the bug around the eyes allows the trypanosomes to gain entry through the conjunctiva. This often results in one-sided swelling around the eye (periorbital edema) and swelling of the eyelid (Romana sign). If the entry is through the skin, a lesion called a chagoma appears. Cardiac involvement is mainly due to a cardiomyopathy that manifests about 20 years after the trypanosomal infection. At this point, the heart muscle is uniformly destroyed and replaced by fibrous tissue. The weakened heart muscle is stretched, the left ventricular chamber dilates, the pumping function is severely deranged, and heart failure supervenes. Heart failure produces changes in the heart, circulation, and veins that can be detected on examination by the physician.

This chapter focuses on the Kawasaki heart disease, which is rare in children over the age of 8 with more than 85% being younger than 5 years. In Japan and the Western world, Kawasaki disease is now a more common cause of acquired heart disease in young children than acute rheumatic fever. This disorder is virtually always accompanied by fever for more than 5 days. The fever has no identifiable cause and occurs without the common manifestation of an upper respiratory tract viral infection or flu-like illness. The cause of Kawasaki syndrome remains unknown. An infectious agent is suspected because of the following: seasonal peak in the winter and spring months in most geographic areas, and geographic focal epidemics occurred in the 1970s and 1980s.

Hypertrophy is an increase of the essential tissue of an organ. Hypertrophy of the heart affects the left ventricle of the heart; left ventricular hypertrophy is a feature of many forms of heart disease. The left atrium may, however, cause hypertrophy to assist a left ventricle that is under stress and strain imposed by pressure or volume overload. The right ventricle may hypertrophy in patients with pulmonary artery hypertension or pulmonary valve stenosis. The right atrium may hypertrophy to assist the right ventricle and also be hypertrophied in patients with chronic obstructive pulmonary disease. This chapter argues that in hypertrophy of the heart, the muscular wall becomes greatly thickened, and the weight of the heart may be twice the normal or even more. The muscle fibers are increased in thickness and length, and enlargement of the individual fibers causes an increase in muscle mass.