Chapter 10 Heart Disorders

I. Cardiac Physical Diagnosis (Box 10-1)

• Compensatory change related to changes in pressure in the wall of the ventricle

A. Pathogenesis of left and right ventricular hypertrophy

1. Sustained pressure in the ventricles increases wall stress.

2. Changes in wall stress produce changes in gene expression.

Valve Locations for Auscultation

Locations where heart sounds are best heard do not always correlate with their anatomic location. The mitral valve (MV) is best heard at the apex; the tricuspid valve (TV) at the left parasternal border; the pulmonary valve (PV) at the left second and third intercostal spaces (ICS); and the aortic valve (AV) at the left sternal border for regurgitation murmurs and right second ICS for ejection murmurs.

Cardiac Cycle Relationships with Heart Sounds

The P wave represents atrial depolarization; the PR interval atrioventricular conduction time; the QRS ventricular depolarization; and the T wave ventricular repolarization, or recovery. The S₁ heart sound occurs at the same time as the QRS complex and marks the beginning of systole, while the S₂ heart sound occurs after the T wave and marks the beginning of diastole.

Heart Sounds

The S₁ heart sound corresponds with closure of the MV and TV during systole. The MV closes before the TV. It is best heard at the apex and corresponds with the carotid/radial pulse. The S₂ heart sound is caused by closure of the AV and PV and marks the beginning of diastole. It is best heard at the left second or third ICS. The aortic component (A₂) normally precedes the pulmonary component (P₂). Unlike the S₁ heart sound, the S₂ splits on inspiration. As the diaphragm descends, it causes a further decrease in negative intrathoracic pressure, which increases the flow of blood out of the vena cava into the right side of the heart. This causes flattening of the jugular neck veins. The excess amount of blood in the right side of the heart delays closure of the PV causing P₂ to separate away from A₂ (see schematic). This physiologic split is best heard over the PV area. A₂ and P₂ become a single sound on expiration as intrathoracic pressure becomes less negative. An accentuated A₂ is heard in essential hypertension (increased pressure causes it to snap shut), while an accentuated P₂ is heard in pulmonary hypertension.

An S₃ heart sound (see schematic) is the most clinically significant extra heart sound. It is a normal finding in children and young adults, where it reflects a more energetic expansion and filling of the left ventricle. However, it is considered a pathologic finding after 40 years of age. It is thought to be due to a sudden rush of blood entering a volume overloaded left or right ventricle. It is best heard at the apex with the patient in the left lateral decubitus position. It commonly occurs with regurgitant types of murmurs involving any of the valves. It is the first cardiac sign of congestive heart failure, where increased ventricular volume stretches the MV or TV ring causing volume overload from mitral/tricuspid regurgitation. An S₃ heart sound produces a ventricular gallop. An S₄ heart sound (see schematic) coincides with atrial contraction in late diastole and the a wave in the jugular venous pulse (JVP; see below). It is never a normal finding and is due to increased resistance to filling (decreased compliance) in the left or the right heart following a vigorous atrial contraction. It is heard best at the apex. Causes of decreased ventricular compliance include concentric ventricular hypertrophy (left/right) and a volume overloaded ventricle (no more room to expand). In a volume overloaded left or right ventricle, it is commonly present along with an S₃ heart sound. An S₄ heart sound and the a wave of a JVP are absent in atrial fibrillation. Presence of an S₄ heart sound produces an atrial gallop. Presence of an S₃ and S₄ heart sound is called a summation gallop (see schematic) and sounds like a galloping horse.

Heart Murmurs

Heart murmurs may occur in systole and diastole. They may be caused by structural valve disease (e.g., damage due to rheumatic fever) or stretching of the valve ring (e.g., volume overload in left- or right-sided heart failure). Murmurs due to stretching of valve rings are often called functional murmurs. Murmurs often radiate. For example, AV stenosis radiates into the neck and MV regurgitation radiates into the axilla. They are graded 1 to 6 in terms of their intensity. Grade 1 and 2 murmurs are very hard to hear, while grade 3 murmurs are easy to hear. Grade 4 to 6 murmurs are often accompanied by a palpable precordial thrill. Grade 6 murmurs are audible without a stethoscope. Murmurs and abnormal heart sounds (e.g., S₃ and S₄ heart sounds) change their intensity with respirations. Right-sided murmurs and abnormal heart sounds have increased intensity when the patient takes a deep inspiration and holds the breath for 3 to 5 seconds. This is due to the increase in negative intrathoracic pressure drawing blood out of the venous system into the right side of the heart, hence accentuating the murmur and abnormal heart sound. In contradistinction, left-sided heart murmurs and abnormal heart sounds do not change their intensity with deep inspiration. Continuous murmurs occur through systole and diastole. The most common cause of a continuous murmur in children is a cervical venous hum. A patent ductus arteriosus also produces a continuous murmur. Innocent murmurs occur in children from 3 to 7 years old. They are usually grade 2 systolic murmurs that are caused by increased blood flow through the PV. They are best heard in the PV area, and as expected, their intensity increases with deep, held inspiration. Stenosis murmurs occur when there is a problem in opening the valves. Because the AV and PV normally open in systole, AV and PV stenosis occur in systole. They produce an ejection type murmur (schematic A), which has a diamond-shaped configuration. The MV and TV normally open in diastole; hence, the murmurs of MV and TV stenosis are heard in diastole. MV stenosis is accompanied by an opening snap (schematic B), which occurs when the thickened valve is forced open by a forceful atrial contraction. An opening snap is usually absent in TV stenosis. Regurgitant (insufficiency) murmurs occur when there is a problem in closing a valve. Because the MV and TV normally close in systole, these murmurs occur in systole. They are even-intensity pansystolic murmurs (schematic C) that often obliterate the S₁ and S₂ heart sounds. AV and PV regurgitant murmurs occur in diastole immediately after the S₂ heart sound (schematic D).

Jugular Venous Pulses (JVPs)

Normal JVPs (see schematic) have three positive waves (a, c, v) and two negative waves (x, y). The a wave is a positive wave due to atrial contraction in late diastole. It occurs after the P wave in an electrocardiogram. It disappears in atrial fibrillation. A giant a wave occurs when there is restricted filling of the right side of the heart (e.g., TV stenosis, pulmonary hypertension, right ventricular hypertrophy). The c wave is a positive wave due to right ventricular contraction in systole causing bulging of the TV into the right atrium producing increased pressure in the atrium and jugular vein. It correlates with the S₁ heart sound and the upstroke of the carotid pulse. The x wave is a large negative wave occupying most of systole. It is due to downward displacement of the TV when blood is ejected out of the RV into the pulmonary artery. The v wave is a positive wave that correlates with right atrial filling in systole when the TV is closed. The peak of the v wave marks the end of systole and beginning of diastole. A giant c-v wave occurs in TV regurgitation as blood refluxes back into the right atrium during systole. The y wave is a negative wave occupying most of diastole. It is due to opening of the TV with rapid flow of blood into the right ventricle in diastole.

Wall stress increases gene-controlled sarcomere duplication.

3. Changes in gene expression lead to duplication of sarcomeres.

• Sarcomeres are the contractile element of muscle.

4. Changes in wall stress related to an increase in afterload

a. Afterload is the resistance the ventricle contracts against to eject blood in systole.

Afterload: resistance ventricle contracts against to eject blood in systole

b. Increased afterload produces concentric thickening of the ventricular wall (Fig. 10-1A).

• Sarcomeres duplicate parallel to the long axes of the cells; muscles are thicker.

c. Causes of concentric left ventricular hypertrophy (LVH)

(1) Essential hypertension (most common)

(2) Aortic stenosis

(3) Hypertrophic cardiomyopathy

10-1: Left ventricular hypertrophy. The heart in the middle has a normal thickness of the left ventricle (LV). The heart on the left (A) has concentric hypertrophy of the LV, while the heart on the right (B) has eccentric hypertrophy of the LV.

(Reproduced with permission from Edwards WD: Cardiac anatomy and examination of cardiac specimens. In Emmanouilides GC, Riemenschneider TA, Allen HD, Gutgesell HP [eds]: Moss and Adams Heart Disease in Infants, Children, and Adolescents: Including the Fetus and Young Adults, 5th ed. Philadelphia, Williams & Wilkins, 1995, p 86.)

Ventricular hypertrophy: increased afterload causes concentric hypertrophy

d. Causes of concentric right ventricular hypertrophy (RVH)

(1) Pulmonary hypertension

(2) Pulmonary artery stenosis

5. Changes in wall stress related to increased preload

Preload: equivalent to LVEDV and/or RVEDV

a. Preload correlates with left/right ventricle end-diastolic volume (LVEDV, RVEDV).

b. Increased preload increases stroke volume (volume of blood ejected;) via Frank-Starling pressure relationship.

c. Increased preload causes dilation and hypertrophy (eccentric hypertrophy) of ventricular wall (Fig. 10-1B).

Ventricular hypertrophy: increased preload causes eccentric hypertrophy

• Sarcomeres duplicate in series; muscle length and width are increased.

d. Causes of eccentric hypertrophy of the left ventricle

(1) Mitral valve or aortic valve regurgitation

(2) Left-to-right shunting of blood (e.g., ventricular septal defect)

• More blood returns to the left side of the heart.

e. Causes of eccentric hypertrophy of the right ventricle

• Tricuspid valve or pulmonary valve regurgitation

c. Examples

(1) Concentric LVH in essential hypertension or aortic stenosis

(2) Concentric RVH in pulmonary hypertension or pulmonary stenosis

(3) Volume overload in mitral regurgitation or tricuspid regurgitation

(4) Volume overload in aortic regurgitation or pulmonary regurgitation

III. Congestive Heart Failure (CHF)

• The heart fails when it is unable to eject blood delivered to it by the venous system.

A. Epidemiology

1. Most common hospital admission diagnosis in elderly patients

2. Types of CHF

a. Left-sided heart failure (most common type)

b. Right-sided heart failure

c. Biventricular heart failure (left- and right-sided heart failure)

d. High-output heart failure (least common type)

B. Left-sided heart failure (LHF)

1. Forward failure

Left-sided heart failure = forward failure → pulmonary edema

a. Left ventricle cannot efficiently eject blood into the aorta.

b. Causes an increase in left ventricular end-diastolic volume (LVEDV) and pressure (LVEDP).

c. Increased volume and pressure causes backup of blood into the lungs producing pulmonary edema.

• In LHF blood builds up behind the failed heart.

2. Pathogenesis

a. Decreased ventricular contraction (systolic dysfunction)

Systolic dysfunction: most common type of LHF

(1) Most common type of LHF

(2) Causes of systolic dysfunction

(a) Ischemia due to coronary artery atherosclerosis (most common cause)

(b) Post-myocardial infarction, myocardial fibrosis, myocarditis, dilated cardiomyopathy

b. Noncompliant ventricle (diastolic dysfunction)

(1) Restricted filling of the left ventricle in diastole

(2) Causes of diastolic dysfunction

Diastolic dysfunction: most common cause is hypertension

(a) Concentric LVH due to essential hypertension is the most common cause.

• Other causes include aortic stenosis, hypertrophic cardiomyopathy.

(b) Infiltration of muscle with amyloid, glycogen (restrictive cardiomyopathies)

• Ventricular distention restricts filling in diastole.

Systolic dysfunction is characterized by a low ejection fraction (EF) (>40%). The EF equals the stroke volume divided by the left ventricular end-diastolic volume. The normal value ranges from 55% to 80%.

Diastolic dysfunction is characterized by normal EF (stiff ventricle) and an S₄ atrial gallop due to increased resistance to filling in late diastole. There is an increase in left atrial pressure and pulmonary congestion. If left ventricular filling is significantly impaired, cardiac output is decreased as well as the EF.

Diastolic dysfunction: ↑ resistance to filling the ventricle; normal EF

Systolic dysfunction: ↓ ventricular contraction; ↓ EF

3. Gross and microscopic findings

a. Lungs are heavy, congested, and exude a frothy pink transudate (edema).

b. Alveolar macrophages contain hemosiderin (“heart failure” cells).

4. Clinical and laboratory findings

a. Difficulty with breathing (dyspnea)

(1) Patient cannot take a full inspiration.

Dyspnea: cannot take full inspiration

(2) Caused by interstitial fluid stimulating juxtacapillary J receptors innervated by the vagus nerve

b. Pulmonary edema

(1) Increase in LVEDV increases hydrostatic pressure in the left ventricle, left atrium, pulmonary vein, and pulmonary capillaries which overrides the pulmonary capillary oncotic pressure (refer to Chapter 4).

Pulmonary edema: hydrostatic pressure > oncotic pressure

(a) A transudate initially leaks into the interstitial space producing dyspnea and then moves into the alveoli producing pulmonary edema.

(b) Septal edema produces Kerley’s lines in a chest radiograph.

Kerley’s lines: septal edema

(2) Bibasilar inspiratory crackles

• Crackles are due to air expanding alveoli filled with fluid.

(3) Rupture of pulmonary capillaries may occur from increased hydrostatic pressure.

(a) Blood is phagocytosed by alveolar macrophages.

Heart failure cells: alveolar macrophages with hemosiderin

(b) Hemosiderin accumulates in alveolar macrophages (called heart failure cells).

• Sputum has a rusty color.

(4) Chest radiograph findings in pulmonary edema

(a) Congestion in upper lobes (early finding)

(b) Perihilar congestion (“bat wing configuration”)

c. Left-sided S₃ (first cardiac sign LHF) and S₄ heart sounds (see Box 10-1)

10-2: Chest frontal radiograph showing pulmonary edema. Note the fluffy alveolar infiltrates throughout both lung fields.

(From Goldman L, Ausiello D: Cecil’s Textbook of Medicine, 23rd ed. Philadelphia, Saunders Elsevier, 2008, p 596, Fig. 84-2.)

S₃ heart sound: first cardiac sign of LHF

d. Functional mitral valve (MV) regurgitation

• Caused by stretching of the MV ring

e. Paroxysmal nocturnal dyspnea (PND)

(1) PND refers to a choking sensation that occurs at night when the patient is supine.

(2) Without the effect of gravity, fluid from the interstitial space moves into the vascular compartment.

(3) This increases venous return to the right side of the heart and then to the failed left side of the heart.

PND/orthopnea: ↑ venous return to right side of the heart at night

(4) The failed left side of the heart cannot handle the excess load and blood backs up into the lungs, producing pulmonary edema.

(5) Dyspnea is relieved by standing or placing pillows under the head (pillow orthopnea).

• Raising the head on pillows increases the effect of gravity on reducing venous return to the heart.

f. Increased serum brain natriuretic peptide (BNP)

BNP: useful in confirming/excluding LHF

(1) Cardiac neurohormone secreted from the ventricles (refer to Chapter 4)

(2) Secreted in response to volume expansion and pressure overload in the ventricle

(3) Clinical usefulness

(a) Diagnosing LHF (increased)

(b) Excluding LHF (normal)

C. Right-sided heart failure (RHF)

1. Backward failure

RHF = backward failure → increase in venous hydrostatic pressure

a. Right side of the heart cannot pump blood from the venous system into the lungs.

b. Blood accumulates under pressure in the venous system.

• In RHF, blood builds up behind the failed heart.

2. Pathogenesis

a. Decreased contraction

• Example—right ventricular infarction

b. Noncompliant right ventricle

• Example—right ventricular hypertrophy

c. Increased afterload

• Examples—LHF (most common cause), pulmonary hypertension

d. Increased preload

• Examples—tricuspid valve regurgitation, left-to-right shunt

LHF: most common cause RHF

3. Clinical findings

a. Prominence of the jugular veins (Fig. 10-3)

• Due to increased venous hydrostatic pressure

10-3: Distention of internal jugular vein: The patient has right-sided heart failure.

(From http://courses.cvcc.vccs.edu/WisemanDljugular_vein_distention.htm)

RHF: ↑ venous hydrostatic pressure

b. Functional tricuspid valve (TV) regurgitation

• Caused by stretching of the TV ring from volume overload

c. Right-sided S₃ and S₄ heart sounds

• Both are due to volume overload in the ventricle.

d. Painful hepatomegaly

(1) Due to passive liver congestion

• Backup of venous blood into the hepatic veins and then into the central veins (see Fig. 18-5)

(2) Increase in portal vein pressure may lead to ascites.

(3) Compression of the congested liver produces jugular neck vein distention (hepatojugular reflux).

e. Dependent pitting edema (see Fig. 4-4)

• Due to an increase in venous hydrostatic pressure

RHF: neck vein distention, hepatomegaly, dependent pitting edema, ascites

f. Cyanosis of mucous membranes

(1) More likely to occur in RHF than LHF

(2) Increased time for peripheral tissue to extract O₂; hence, decreasing O₂ saturation (refer to Chapter 1)

Nonpharmacologic therapy in congestive heart failure involves restricting sodium (<2 g/day) and water (<2 L/day), both of which are increased due to the decreased cardiac output and renal retention of sodium and water (refer to Chapter 4). Systolic dysfunction is treated with drugs that reduce the workload of the left ventricle. This is accomplished by decreasing afterload and preload. A mainstay of treatment for systolic dysfunction are the angiotensin-converting enzyme (ACE) inhibitors or receptor inhibitors if patients develop chronic cough. ACE inhibitors decrease afterload by decreasing angiotensin II and decrease preload by decreasing aldosterone. Diuretics (e.g., loop diuretics, aldosterone blockers) complement ACE inhibitors by decreasing preload. β-Blockers decrease sympathetic tone, which reduces myocardial O₂ consumption. Digitalis may be useful because of its inotropic and vagotonic effects particularly in severe heart failure or those with atrial arrhythmias. Direct vasodilating drugs (e.g., hydralazine) reduce systemic vascular resistance and pulmonary venous pressure. Therapeutic options for treating diastolic dysfunction are based on the cause of diastolic dysfunction. If hypertension is the primary cause, calcium channel blockers, ACE inhibitors, and β-blockers are used, the latter decreasing heart rate, which prolongs diastolic filling. Diuretics must be used with caution, because excessive diuresis may produce volume depletion and decrease the cardiac output.

ACE inhibitors: ↓ afterload, ↓ preload

β-Blockers: ↓ myocardial O₂ consumption; ↓ heart rate

D. High-output heart failure

1. Definition

• Form of heart failure in which cardiac output is increased compared with values for the normal resting state

TPR = viscosity/radius of vessel⁴

2. Pathogenesis

a. Increase in stroke volume (SV)

• Example—hyperthyroidism

b. Decrease in blood viscosity

(1) Decreases total peripheral resistance (TPR)

(2) Increases venous return to the heart.

(3) Example—severe anemia

c. Vasodilation of peripheral resistance arterioles

(1) Increases venous return to the heart

(2) Examples—thiamine deficiency (refer to Chapter 7), early phase of endotoxic shock (refer to Chapter 4)

d. Arteriovenous fistula

(1) Arteriovenous communications bypass the microcirculation.

(2) Increases venous return to the heart

(3) Causes of arteriovenous fistulas

(a) Trauma from a knife wound (most common cause)

(b) Surgical shunt for hemodialysis

Causes high output failure: ↑ SV, ↓ TPR, arteriovenous fistula

IV. Ischemic Heart Disease

• Imbalance between myocardial O₂ demand and supply from the coronary arteries

A. Coronary artery blood flow

1. Provides oxygen to cardiac muscle

a. Coronary vessels fill in diastole.

Tachycardia: decreases diastole and filling of coronary arteries

b. Tachycardia (>180 bpm) decreases filling time, leading to ischemia.

2. Left anterior descending (LAD) coronary artery

a. Distribution

(1) Anterior portion of the left ventricle

(2) Anterior two thirds of the interventricular septum

b. Site for 40% to 50% of coronary artery thromboses

LAD: most common site of coronary artery thrombosis

3. Right coronary artery (RCA)

a. Distribution

(1) Posteroinferior part of the left ventricle

(2) Posterior one third of the interventricular septum

(3) Right ventricle

(4) Posteromedial papillary muscle in left ventricle

(5) Primary supply for atrioventricular and sinoatrial nodes

b. Site for 30% to 40% of coronary artery thromboses

4. Left circumflex coronary artery

a. Supplies the lateral wall of the left ventricle

b. Site for 15% to 20% of coronary artery thromboses

B. Epidemiology

1. Ischemic heart disease is the major cause of death in the United States.

a. It is more common in men.

b. Incidence peaks in men after age 60 and in women after age 70.

2. Types of ischemic heart disease

Angina pectoris: most common manifestation of coronary artery disease

a. Angina pectoris (most common type)

b. Chronic ischemic heart disease

c. Sudden cardiac death

d. Myocardial infarction

3. Risk factors

a. Age

Angina pectoris: age most important risk factor

• Men ≥ 45 years old, women ≥ 55 years old

b. Family history of premature coronary artery disease or stroke

c. Lipid abnormalities

(1) Low-density lipoprotein > 160 mg/dL

(2) High-density lipoprotein (HDL) < 40 mg/dL

d. Smoking tobacco, hypertension, diabetes mellitus

e. Subtract 1 from the total number of risk factors if HDL > 60 mg/dL.

C. Angina pectoris

1. Epidemiology

Angina pectoris: males > females

a. Most common in middle-aged males and elderly males

b. Females usually affected after menopause

c. Within 1 year of a diagnosis of stable angina, 10% to 20% will develop an acute myocardial infarction or unstable angina.

2. Chronic (stable) angina

Stable angina: most common type of angina

a. Most common variant

b. Causes of stable angina

(1) Fixed, atherosclerotic coronary artery disease (most common)

(a) One or more vessel obstructions is likely.

(b) Severity of stenosis is usually >70%.

(2) Aortic stenosis or hypertension with concentric LVH

• O₂ supply is not adequate for the thickened muscle wall.

(3) Hypertrophic cardiomyopathy

(4) Cocaine-induced coronary artery vasoconstriction

c. Pathogenesis

• Subendocardial ischemia due to decreased coronary artery blood flow or thick muscle wall

d. Clinical findings

(1) Exercise-induced substernal chest pain lasting 30 seconds to 30 minutes

(2) Often accompanied by shortness of breath, diaphoresis, numbness and pain in left arm, shoulder, or jaw

Stable angina: exercise-induced substernal chest pain

(3) Relieved by resting or nitroglycerin

(4) Stress test shows ST-segment depression > 1 mm (Fig. 10-4).

10-4: Electrocardiogram with ST segment depression. Tracing A is the patient at rest with 1 representing the PQ junction (baseline reference); 2, the J point, where the QRS complex joins the ST segment; and 3, the ST segment 80 msec from the PQ point. Tracing B shows the amount of ST segment depression measured 80 msec past the J point is 4 mm.

(From Goldman L, Ausiello D: Cecil’s Textbook of Medicine, 23rd ed. Philadelphia, Saunders Elsevier, 2008, p 481, Fig. 70-2.)

Stable angina: subendocardial ischemia with ST-segment depression

3. Prinzmetal’s angina

a. Pathogenesis

(1) Intermittent coronary artery vasospasm at rest with or without superimposed coronary artery atherosclerotic disease

(2) Vasoconstriction is due to platelet thromboxane A₂ or an increase in endothelin.

Prinzmetal’s angina: vasospasm with transmural ischemia and ST-segment elevation

b. Clinical findings

• Stress test shows ST-segment elevation (transmural ischemia).

4. Unstable angina

a. Pathogenesis

Unstable angina: angina at rest; multivessel disease; disrupted plaques

(1) Severe, fixed, multivessel atherosclerotic disease

(2) Disrupted plaques with or without platelet nonocclusive thrombi (refer to Chapters 4 and 9)

b. Clinical findings

(1) Frequent bouts of chest pain at rest or with minimal exertion

(2) May progress to acute myocardial infarction (MI)

Nonpharmacologic therapy of angina includes losing weight, cessation of smoking, placing the patient on a low cholesterol diet, and encouraging daily aerobic exercise. Pharmacologic therapy for angina involves the use of anti-ischemic agents. Nitrates (release nitric oxide) cause venodilation (reduces preload and wall tension in the ventricles), vasodilation of the coronary arteries, and vasodilation of peripheral resistance arterioles (reduces afterload). β-Blockers decrease myocardial O₂ consumption by reducing heart rate and systolic blood pressure. Calcium channel blockers cause vasodilation of the coronary arteries and peripheral resistance arteries. They are the drug of choice for treating Prinzmetal’s angina. Aspirin inhibits platelet aggregation, which decreases the risk for developing a platelet thrombus (refer to Chapters 4 and 14). Heparin plus aspirin is used for patients with unstable angina and reduces the risk for developing a myocardial infarction and refractory angina. If homocysteine levels are increased, the patient should be placed on pharmacologic doses of folate. If C-reactive protein is increased, the patient should be placed on “statin” drugs to lower the LDL levels to 70 mg/dL or less. This stabilizes disrupted plaques and reduces the risk for thrombosis. Revascularization procedures include percutaneous transluminal coronary angioplasty (PTCA) and stenting. Balloon angioplasty dilates and ruptures the atheromatous plaque to improve blood flow (restenosis commonly occurs) and intracoronary stents (the most common procedure) bypass the obstruction (restenosis less common). Complications are associated with either procedure (e.g., thrombosis, localized dissection). In order to prevent platelet thrombosis in these revascularization procedures, abciximab (inhibits the GpIIb-IIIa fibrinogen receptor in platelets; refer to Chapter 14) is used. Coronary artery bypass graft (CABG) is reserved for patients with left main coronary artery disease and for those patients with symptomatic three-vessel disease. Internal mammary artery grafts have the best graft patency after 10 years, while saphenous vein grafts commonly show “arterialization” of the vessels with fibrosis after 10 years.

Prinzmetal’s angina: calcium channel blockers vasodilate coronary arteries

D. Chronic ischemic heart disease

1. Progressive CHF resulting from long-term ischemic damage to myocardial tissue

Chronic ischemic heart disease: replacement of muscle by fibrous tissue

2. Replacement of myocardial tissue with noncontractile scar tissue

3. Clinical findings

a. Biventricular CHF

b. Angina pectoris

c. May develop dilated cardiomyopathy

E. Sudden cardiac death (SCD)

1. Unexpected death within 1 hour after the onset of symptoms

Sudden cardiac death: unexpected death within 1 hour after symptoms