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Oxygen is carried by hemoglobin in red blood cells to the tissues. The normal level of hemoglobin in circulating blood is 11.5–15.5 g/dl (115–155 g/L) in women and 15 to 17 g/dl in men. A normal structural heart with normal function can tolerate hemoglobin of 7 g/dl for approximately one year without causing cardiac damage or heart failure. Levels of 6 g/dl or less may cause cardiac dysfunction after approximately 6 months. In patients with angina, chest pain may be precipitated, because lack of oxygen to the myocardium produces myocardial ischemia that causes pain. Patients with sickle cell anemia commonly have hemoglobin in the range of 7–8 g/dl. In these individuals cardiac, enlargement with dilation occurs early in the course of the disease. Because of the anemia and poor delivery of oxygen to tissues, cardiac output increases to compensate and deliver the supply of nutrients. This entails more work for the heart. By age 40, these individuals manifest symptoms of poor cardiac function.

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.

Well-known anti-allergy medications may occasionally cause an increase in the pulse rate because they have an atropine-like effect. In some individuals, the heart rate may become rapid. These sensations, called palpitations caused by arrhythmia, subside over time and usually cause no harm. Patients with angina, however, should be cautious with the use of antihistamines, because an increase in heart rate may trigger an attack of angina. Blood pressure is usually not increased by antihistamine use, but many remedies containing antihistamines contain the decongestant phenylpropanolamine, which elevates blood pressure. This should be avoided by patients with hypertension and angina.

Cardiovascular disease is a much more common cause of death and disability in women than all forms of cancer, pneumonia, and AIDS. Women incorrectly perceive their risk of cancer of the breast and uterus as much greater than that of heart disease or stroke. Symptoms of a genuine heart attack are not significantly different in women and men. Some women suffer with shortness of breath or nausea instead of pain during a heart attack, but so do a few men. Diagnosis of a heart attack is similar in women and men. An ECG records the same information for both. The medical treatment for heart attack is virtually the same for both women and men, and the response is the same. All blood pressure lowering medications work equally well in women and men to prevent stroke or heart failure. Bypass surgery and angioplasty in the elderly carry a greater risk, and the results of angioplasty appear to be less impressive in women.

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.

High-altitude pulmonary edema and severe shortness of breath due to accumulation of fluid in air sacs of the lungs may occur in young, healthy, susceptible adults who ascend rapidly to altitudes in excess of 2500 m. The first symptom is usually dyspnea on exertion and a reduced exercise tolerance, greater than expected for the altitude. Symptoms may become much worse when these individuals engage in strenuous exercise at such high altitudes before they become acclimatized. Cough, shortness of breath, and reduced effort tolerance may increase within hours and progress to fulminant pulmonary edema, which is heralded by extreme shortness of breath, including shortness of breath when the individual is lying in bed. Death may occur in young individuals who have no structural heart disease. The risk for pulmonary edema is related to the rapidity of ascent, the level of exertion, and individual susceptibility.

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.

C-reactive protein (CRP) is an acute phase reactant produced by the liver in response to inflammatory cytokines (1L-1, 1L-6) and tumor necrosis factor-α (TNF-α). C-reactive protein has been identified as a marker of risk for coronary events, independent of other factors. The exact source of elevated CRP levels among patients with acute coronary syndromes remains unclear. In some studies, CRP has been found to have prognostic value among patients without evidence of myocardial necrosis. In patients with acute coronary syndromes and negative troponin-T, elevated CRP appears to be predictive of future adverse events. In addition, it has been observed that CRP is a strong independent predictor of short- and long-term mortality among patients treated with early revascularization.

Caffeine is a psychoactive drug that occurs naturally in many foods and beverages including coffee, tea, chocolate, and cocoa. It has found its way into many commercial soft drinks because of its proven mild stimulant effect and relative safety when consumed in small amounts. But caffeine can produce beneficial effects in one individual and potentially harmful effects in another. Caffeine is the most widely used psychoactive substance. This chapter starts with the biochemistry of caffeine, which is a xanthine derivative—1, 3, 7-trimethylxanthine. Caffeine is a powerful central nervous stimulant, and moderate doses of 200 mg contained in two cups of coffee, activate the cerebral cortex sufficiently to slow changes in an individual's electroencephalogram (EEG). Caffeine is also a mild cardiac stimulant. This chapter also discusses the effects that caffeine can generate. Caffeine has mild and variable effects on the heart rate, the heart muscle, blood pressure, blood flow, and blood cholesterol.

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 addresses the epidemiologic studies that strongly support the hypothesis that cigarette smoking increases the incidence of fatal and nonfatal heart attacks. Low-tar cigarettes and smokeless tobacco are shown to increase the risk of cardiovascular events in comparison to nonsmokers. Passive smoke is associated with about a 30% increase in risk of cardiac events compared with an 80% increase in active smokers. A smoke free environment in several cities has reportedly resulted in a decreased incidence of cardiac events. Cigarette smoke is divided into two phases: a tar phase and a gas phase. Tobacco smoke contains more than 4000 components. Some of these are nicotine, carbon monoxide, ammonia, benzene, nitrobenzene, phenol, 2,4,dimethylphenol, acetaldehyde, hydrogen cyanide, toluene, and O-cresol. Nicotine stimulates the adrenal glands to put out excessive adrenaline and noradrenaline. The higher the nicotine concentration inhaled, the greater the outpouring of adrenaline.

This chapter explains the alternative therapies with herbal, dietary, and vitamin supplements that have considerably escalated in the Western world during the past 10 years. Alternative therapies were used in more than 40% of adults in the United States during 1997, and a consumer poll in 1998 indicated that more than 30% of respondents use herbal remedies. It appears that of patients who take prescription medications, nearly 20% use herbal remedies, high-dose dietary supplements, or both. More importantly, adverse drug interactions involving prescribed medications and herbal remedies are common. Drugs such as ephedrine, chlorpheniramine, and testosterone are also contained in so-called herbal remedies. Because most herbal products are considered dietary supplements rather than medicines, they are not required to meet standards specified in the Federal Food, Drug, and Cosmetic Act. The manufacturer of a herbal or dietary supplement can market the product as long as there is no claim of effectiveness for the prevention and treatment of a specific disease.

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.

This chapter is the clinical study related to chelation. Chelation, a method for clearing the obstruction, is analogous to using Drano to clean obstructed pipes. Chelation therapy using EDTA is an unproven, but widely used, alternative therapy for ischemic heart disease. The objective is to determine whether current EDTA protocols have a favorable impact on exercise ischemia threshold and quality of life measures in patients with stable ischemic heart disease.

This chapter focuses on diuretics, which are the water pills beneficial for the management of hypertension. A diuretic is the drug of choice for the initial treatment in individuals of African origin over age 60, because these agents have been shown to be more effective than the three other agents available for the management of hypertension. Diuretics are not as effective in the younger individuals of African origin. A diuretic is necessary for the management of hypertension in patients with heart failure or edema and in patients who have not responded adequately to one of the three antihypertensive agents, beta-blockers, Angiotensin-converting enzyme (ACE) inhibitors, or calcium antagonists. Diuretics, particularly loop diuretics such as furosemide and torsemide, are the mainstay of therapy for the millions of patients with moderate-to-severe heart failure.

Valve diseases are caused due to the damage to heart valves. This damage is caused by rheumatic fever, mitral valve prolapse, infections, such as bacterial endocarditis and syphilis, degenerative diseases, and complications of coronary artery disease and cardiomyopathy. The major symptoms of serious valve disease are increasing shortness of breath on mild exertion and on lying flat, cough, and occasional blood-tinged sputum. Damage to heart valves often occurs during an attack of rheumatic fever. Rheumatic fever is the most common between the ages of 5 and 25, and occurs in susceptible individuals after a beta-hemolytic streptococcal sore throat. The streptococcus bacterium sets up an allergic-like reaction on the valves and in the joints. There are usually fever and joint pains, and murmurs are heard over the swollen heart valves. A blood test to show a reaction to the streptococcus usually confirms the diagnosis.

Sudden cardiac death occurs most often within a few hours of wakening from sleep. Arousal from sleep causes circulatory, neural, and hormonal alterations that affect the heart and entire circulatory system. Arousal from sleep has profound influences on the cardiovascular system. Recently, sleep apnea and the arousal reaction are shown to play a role in increasing morbidity in patients with heart failure. It is explained that sleep apneas do not cause heart failure in individuals with normal hearts and normal ventricular function. Sleep apneas are not associated with the epidemic of atherothrombosis, which is the main cause for heart attack and stroke. This chapter outlines obstructive sleep apnea (OSA) and central sleep apnea (CSA), which are the two major recognized forms of sleep apnea. Obstructive sleep apneas and hypopneas are caused by complete or partial collapse of an abnormally narrowed pharynx.

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 argues that being overweight is also a major cause of heart attack. It defines the Framingham Study that shows that in the 5000 people studied, being overweight appeared to increase the risk of sudden death and angina, but it did not increase the frequency of heart attacks. When adjustments were made for the prevalence of hypertension and hypercholesterolemia, being overweight—or obesity—appeared to play a much less significant role. If a patient with coronary heart disease manifested by recurrent chest pain on exertion (angina), or a myocardial infarction is overweight, chest pains are likely to be more frequent, as the heart has to work harder. Therefore, weight reduction helps in relieving pain in patients with angina pectoris, and less medication is then required. In patients with heart failure, weight reduction is necessary because increased weight means more work for the heart.

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.

The natriuretic peptide system includes atrial (ANP) and brain, or B-type (BNP), natriuretic peptide. Brain natriuretic peptide is a 32 amino acid cardiac natriuretic peptide, which was originally isolated from porcine brain tissue. The human BNP gene is located in chromosome 1 and encodes the 108 amino acid prohormone pro-BNP, which circulates with the 32 amino acid biologically active BNP and the N terminal 76 amino acid component of the prohormone (NT-proBNP). These three components can be measured by immunoassay. BNP is released by cardiac myocytes of the ventricles in response to myocardial wall stress. This is brought on by increased transmural wall tension and elevations of end diastolic pressure, ventricular volume expansion and pressure overload. The secretion of this important peptide serves to regulate sodium and water balance by the kidneys and causes vasodilatation of arteries, which benefits the failing heart. Elevated BNP levels are detected in the blood of patients with heart failure, but BNP levels are normal in patients with shortness of breath caused by pulmonary disease. The rapid measurement of levels of BNP in the blood has proved useful in the diagnosis of heart failure. More importantly, in emergency rooms, the BNP test rapidly clarifies whether severe shortness of breath is caused by heart failure or by pulmonary disease.

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.

This chapter starts with the historical review and usage of aspirin for heart disease. It provides a historic review of aspirin, discussing the works of Von Gerhardt, Lawerence Craven, John Vane, Lewis and colleagues, and ISIS-2. As early as BC 350, Hippocrates tried to relieve the pain of his patients by asking them to chew willow bark, a natural substance which contains salicylic acid. Today pain can be relieved by aspirin, which also contains salicylic acid. Following the historical review, recognized indications for aspirin and dose are discussed. Based on the proven benefits observed in ISIS-2, taking aspirin is a life-saving measure when taken within a few hours of chest pain, or symptoms resulting from a developing heart attack. The dose should be one plain 325-mg tablet of aspirin, chewed and swallowed, or preferably, 2–4 chewable aspirins (80 mg each, a dose of 160–320 mg). It is important for the public at large to recognize that chewable aspirin taken immediately during the pain of heart attack can either prevent a heart attack or prevent death in a significant number of individuals.

This chapter discusses cardiopulmonary resuscitation (CPR), for which the fundamentals have undergone minimal changes. The main goal in applying CPR is trying to get oxygen to the individual's brain to keep it alive until expert help arrives. Mouth-to-mouth ventilation oxygenates the blood, and chest compressions cause forward flow of blood, although a small flow, that results in some cardiac output into the circulation so that oxygenated blood reaches the vital organs. The chapter summarizes the relevant points of CPR so that if one is faced with an individual who has “dropped dead” or appears to have lost consciousness in one's presence, one may be able to render assistance. Patients may lose consciousness and fall because of several reasons such as syncope, seizure, stroke, or cardiac arrest. The chapter discusses all these reasons.

This chapter discusses coenzyme Q10, a quinine, that was discovered in 1957. Since then, there has been considerable controversy regarding its use in heart failure and other forms of heart disease. This enzyme serves as a mitochondrial enzyme supplement and appears to improve defective myocyte energetics in patients with heart failure. Coenzyme Q10 plays an intermediary role in the electron transport chain during the oxidation of reduced nicotamide adenine dinucleotide (NADH) or succinate, with the conversion of oxygen to water within the mitochondria. This enzyme is involved in electron proton transfer during oxidative phosphorylation. Also, coenzyme Q10 possesses antioxidant, free radical scavenging, and membrane stabilizing properties.

Modified low-density lipoprotein (LDL) cholesterol could be responsible for the accumulation of lipid within macrophages. Only some antioxidants prevent the oxidation of LDL cholesterol, which plays an important role in the pathogenesis of the atherosclerotic process and its progression to blockage of arteries. The harmful effect of LDL cholesterol is augmented by oxidized LDL cholesterol particles. Prevention of the oxidation of LDL cholesterol particles by chemical agents and natural products is an area of intensive research. Natural substances and chemical compounds; which may protect lipids from attack by oxygen free radicals, increase resistance to lipid peroxidation, reverse endothelial dysfunction, and increase nitric oxide (NO) mediated vasodilation; will remain an interesting area of research and development, despite the negative results observed in many clinical trials.

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.

Murmurs is a sound heard on auscultation with a stethoscope placed at various locations over the chest or neck vessels and over dilated arteries. Typically, these sounds are periodic and of short duration. They coincide with the short systolic or diastolic timing of the heart's contraction and relaxation during which blood is ejected or the chambers are filled during systole and diastole, respectively. Heart murmurs result from disturbances of normal blood flow patterns in the heart. They are classified on the basis of their timing as systolic, diastolic, or continuous. The most common murmur is systolic. Systolic murmurs occur during the contraction of the ventricles. Many systolic murmurs are nonsignificant, and they may occur in individuals where no evidence of heart disease can be found and do not disturb the function of the heart.

The electric total artificial heart was designed for permanent use and was completely implantable. Pneumatic total artificial hearts have not proved successful in small group studies. A completely novel approach to the artificial heart was conceived by engineers from the Abiomed company. The AbioCor is a totally implantable artificial heart that is electric, as opposed to the failed Jarvik-7, which is a pneumatic system. AbioCor is the Abiomed (Danvers, MA) total artificial heart. This chapter discusses left ventricular assist device that are implanted only in patients who are eligible for cardiac transplantation. These devices are used as bridges to transplantation. There are three left ventricular assist devices available at present: Thoratec, the HeartMate, and Novacor.

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 focuses echocardiography, which becomes more advanced after the development of the doppler echocardiography. The chapter also discusses the echocardiographic examination, which is done through echocardiographic window, transthoracic echocardiogram, and transesophageal echocardiogram. The standard transthoracic echocardiogram provides views of the heart with the transducer position on the left chest wall. It gives an adequate visualization of the structures of the heart and abnormalities in more than 95% of patients with valvular heart disease, heart attacks, ischemic heart disease, heart failure, cardiomyopathy, hypertensive heart disease, and assessment of left ventricular hypertrophy. The chapter argues that echocardiographic evaluation of heart disease is used extensively to verify many clinical diagnoses and assist with the formulation and timing of treatment strategies.

Hypertension is commonly known as blood pressure and can lead to early death or serious physical handicaps. Blood pressure is the pressure exerted by the blood against the inner walls of the blood vessels, especially the arteries. The blood pressure changes from minute to minute and is influenced by many factors such as activity, age, health, or emotional tension. Constriction of the blood vessels causes high blood pressure and greatly increases the work of the heart. Arteries are traumatized by high blood pressure and this increases the hardening of the arteries owing to plaques of atheroma. There are generally very few symptoms associated with high blood pressure. Dizziness and headaches may occur in some patients but generally health complaints may not surface for 5–20 years, thus the term “the silent killer.” The instrument used to measure blood pressure is called a sphygmomanometer. It measures the air pressure needed to raise a column of mercury (Hg).

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.

This chapter discusses angina, which is the pain or discomfort in the chest, throat, jaw, or arms caused by severe, but temporary, lack of blood and oxygen to a part of the heart muscle. Angina is caused by coronary artery disease (CAD), but is often referred to as coronary heart disease (CHD). Since obstructive coronary artery disease causes a lack of blood to reach the heart muscle (ischemia), the condition is also called ischemic heart disease (IHD). Angina affects men more commonly than women, and the underlying disease condition is not surprisingly referred to as ‘‘the widow-maker.’’ Angina is caused by CAD. Atherosclerosis of the coronary arteries causes obstruction to blood flow and deprives the heart muscle of blood. Obstructive atherosclerotic CAD leads to stable or unstable angina, fatal or nonfatal myocardial infarction, sudden death, heart failure, arrhythmias, atrial fibrillation, and thromboembolism that may cause stroke.

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.

The development of the modern electrocardiographic instrument illustrates how medicine, a branch of the biologic sciences, took advantage of the concepts of physical science and its instrumentation. The invention of the electrocardiographic instrument would not have been possible without the notable orchestrated work of engineers, physicists, physiologists, and researchers. Despite the advent of expensive and sophisticated cardiologic tests, the electrocardiogram remains the most reliable tool for the confirmation of acute myocardial infarction. The electrocardiogram—not the cardiac enzymes, troponins, CK–MB, echocardiogram, or Sector PET scan—dictates the rapid administration of lifesaving thrombolytic therapy. There is no test to rival the electrocardiogram in the diagnosis of arrhythmia, which is a common problem, seen in clinical practice. Also, the diagnosis of acute pericarditis can only be confirmed by electrocardiographic findings. The electrocardiogram picks up the heart's electrical impulses transmitted through the skin of the chest.

This chapter discusses the Anderson-Fabry Disease, which is a rare, inborn, x-linked lysosomal storage disorder. The major substrate of the deficient alpha-galactosidase, an enzyme, globotriaosylceramide, accumulates in cells of the cardiovascular system. This leads to structural valvular abnormalities and enlargement of the heart with left ventricular hypertrophy, particularly in patients over age 40.

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.

This chapter discusses the diagnosis and management of Antiphospholipid Antibody (APLA) Syndrome. This complex syndrome is described as primary (not associated with another illness) and secondary (associated with SLE or another rheumatic disease). The APLA is detected in more than one-third of patients with lupus. This syndrome is defined as the presence of either APLA or a lupus anticoagulant accompanied by some clinical manifestations. One of those manifestations is recurrent thrombosis of veins or arteries that are unexplained, that is, the usual causes of thrombosis, such as immobilization or postsurgical, are lacking. This syndrome is rare. Individuals who have lupus and other autoimmune diseases may test positive for the antiphospholipid antibody syndrome.

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.