The World Market for Cardiovascular Diagnostics

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Cardiovascular Diagnostics

5th


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Copyright 2013 Kalorama InformationReproduction without written permission, in any media now in existence or hereafter developed,

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CARDIOVASCULARDIAGNOSTICS

A KALORAMA INFORMATION MARKET INTELLIGENCE REPORT

The Cardiovascular Diagnostics Market has been prepared by KaloramaInformation. We serve business and industrial clients in the United States and abroadwith a complete line of information services and research publications.

Kalorama Information Market Intelligence Reports are specifically designed to aidthe action-oriented executive by providing a thorough presentation of essential dataand concise analysis.

Author: Mountaintop Medical

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Table of Contentsii



C O N T E N T S

CHAPTER ONE: EXECUTIVE SUMMARY ..........................................................1

Industry at a Glance ........................................................................................................... 1

Scope and Methodology ...................................................................................................... 3

Size and Growth of the Market ......................................................................................... 4

Key Issues and Trends Affecting the Market ................................................................... 6

Leading Market Participants ............................................................................................. 6

CHAPTER TWO: INDUSTRY OVERVIEW ..........................................................9

Introduction ......................................................................................................................... 9

Cardiovascular Anatomy .................................................................................................. 9Heart ............................................................................................................................. 9

Circulatory System ..................................................................................................... 11

Cardiac Cycle .................................................................................................................. 12Coronary Circulation ...................................................................................................... 13Cardiac Myocytes ........................................................................................................... 16Molecular Contraction .................................................................................................... 16

Diseases of the Heart ......................................................................................................... 17

Ischemic Heart Disease ................................................................................................... 17Etiology ...................................................................................................................... 17

Pathophysiology ......................................................................................................... 17

Atherosclerosis ........................................................................................................... 18

Angina Pectoris .......................................................................................................... 21

Acute Ischemia and Myocardial Infarction Chronic .................................................. 22

Chronic Ischemic Cardiomyopathy ............................................................................ 23

Sudden Cardiac Death ............................................................................................... 23

Diagnostic Tests ......................................................................................................... 23

Valvular and Endocardial Diseases ................................................................................ 24Mitral Valve Disorders ............................................................................................... 25

Aortic Valve Disorders ............................................................................................... 25

Rheumatic Heart Disease ........................................................................................... 26

Endocarditis ............................................................................................................... 26


Pericardial Diseases ........................................................................................................ 27Pericardial Effusion ................................................................................................... 27

Pericarditis ................................................................................................................. 27

Myocardial Diseases ....................................................................................................... 27

Myocarditis ................................................................................................................. 28

Cardiomyopathy ......................................................................................................... 28


Congenital Heart Diseases .............................................................................................. 28Atrial Septal Defect .................................................................................................... 29

Ventral Septal Defect .................................................................................................. 29


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Table of Contentsiii



Pulmonary Stenosis ..................................................................................................... 30

Aortic Stenosis ............................................................................................................ 30

Coarctation of the Aorta ............................................................................................. 30

Patent Ductus Arteriosus ............................................................................................ 30

Truncus Arteriosus ...................................................................................................... 31

Transposition of the Great Arteries ............................................................................ 31

Tricuspid Atresia ......................................................................................................... 31

Congestive Heart Failure ................................................................................................. 32Etiology ....................................................................................................................... 32Diagnostic Tests .......................................................................................................... 32

Cardiac Dysrhythmias ..................................................................................................... 33Diagnostic Tests .......................................................................................................... 33

Hypertension ................................................................................................................... 33Risk Factors ................................................................................................................ 34Effects of High Blood Pressure ................................................................................... 35

CHAPTER THREE: ELECTROCARDIOGRAPHY ...........................................37

Introduction ....................................................................................................................... 37

Market Size and Growth ................................................................................................... 40

CHAPTER FOUR: CARDIAC DIAGNOSTIC IMAGING ..................................43

Non-Invasive Cardiac Imaging ........................................................................................ 43

X-Ray .............................................................................................................................. 43MRI ................................................................................................................................. 45

Ultrasound ....................................................................................................................... 47Computed Tomography................................................................................................... 47

Electron Beam Computed Tomography ...................................................................... 48Dual Source Computed Tomography .......................................................................... 49

Nuclear Cardiography ..................................................................................................... 49

Invasive Transcatheter Cardiac Imaging ........................................................................ 52

Cardiac Catheterization/Angiography Products .............................................................. 52Intravascular Ultrasound ................................................................................................. 55Optical Coherence Tomography ..................................................................................... 56Electrophysiology ........................................................................................................... 57

Market Size and Growth ................................................................................................... 58

Noninvasive Imaging ...................................................................................................... 58

Invasive Transcatheter Imaging ...................................................................................... 59

CHAPTER FIVE: CARDIAC DIAGNOSTIC POINT OF CARE TESTING ....63Coagulation Testing ........................................................................................................ 64Cholesterol Testing ......................................................................................................... 65

Total Cardiac Diagnostic Point-of- Care Market Size and Growth ............................. 68


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Table of Contentsiv



CHAPTER SIX: CARDIAC MARKERS ................................................................71

Total Cardiac Markers Market Size and Growth ........................................................ 73

CHAPTER SEVEN: CARDIAC DIAGNOSTIC CONTRASTAGENTS AND RADIOPHARMACEUTICALS ...................................................77Contrast Agents .............................................................................................................. 77Radiopharmaceuticals ..................................................................................................... 80

Total Cardiac Diagnostic Contrast Agents and Radiopharmaceuticals Market Size

and Growth ........................................................................................................................ 81

CHAPTER EIGHT: MARKET PARTICIPANTS.................................................87

Summary ............................................................................................................................ 87

Abbott Diagnostics ............................................................................................................ 90

Company Overview .................................................................................................... 90

Products ..................................................................................................................... 90

Acusphere .......................................................................................................................... 92

Alere, Inc ............................................................................................................................ 94

Company Overview ................................................................................................... 94

Products ..................................................................................................................... 94

Locations .................................................................................................................... 96

Analogic Corp .................................................................................................................... 97

Bayer Healthcare .............................................................................................................. 99

Company Overview .................................................................................................... 99

Products ..................................................................................................................... 99

Bracco SpA ...................................................................................................................... 101

Cardinal Health ............................................................................................................... 102

CardioDX, Inc ................................................................................................................. 103

Company Overview .................................................................................................. 103

Products ................................................................................................................... 103

C.R. Bard ......................................................................................................................... 104

Danaher Corporation ..................................................................................................... 105


Products ................................................................................................................... 105

dpiX, LLC ........................................................................................................................ 107

FluoroPharma Medical................................................................................................... 109

GE Healthcare ................................................................................................................. 111


Products and Services .............................................................................................. 112

Locations .................................................................................................................. 112


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Table of Contentsv



Hitachi Medical Systems America, Inc. ......................................................................... 113

Johnson & Johnson ......................................................................................................... 114

Company Overview ................................................................................................... 114Products .................................................................................................................... 115

King Pharmaceuticals ..................................................................................................... 116

Lantheus Medical Imaging ............................................................................................. 117

LipoScience, Inc ............................................................................................................... 119


Products .................................................................................................................... 119

Medison America, Inc. .................................................................................................... 120

Molecular Insight Pharmaceuticals, Inc. ....................................................................... 122

Nanosphere, Inc. .............................................................................................................. 124


Products .................................................................................................................... 124

PerkinElmer ..................................................................................................................... 125

Philips Healthcare ........................................................................................................... 126


Products and Services ............................................................................................... 127

Locations ................................................................................................................... 128

Roche Diagnostics US (Div of Roche) ............................................................................ 129


Products .................................................................................................................... 129

Locations ................................................................................................................... 130

Shimadzu Corp ................................................................................................................ 131

Siemens Medical Solutions .............................................................................................. 132


Products and Services ............................................................................................... 132

St. Jude Medical .............................................................................................................. 134


Products .................................................................................................................... 135

Terumo Medical Corporation ........................................................................................ 136

TomTec Imaging Systems GmbH .................................................................................. 137

Toshiba America Medical Systems, Inc ......................................................................... 139

Company Overview ................................................................................................... 139Products and Services ............................................................................................... 139

Trixell ............................................................................................................................... 142

Vascular Solutions ........................................................................................................... 144

Vermillion, Inc ................................................................................................................. 146



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Products ................................................................................................................... 146

Volcano Corp ................................................................................................................... 147

Company Overview .................................................................................................. 147Products ................................................................................................................... 147

Locations .................................................................................................................. 148

CHAPTER NINE: MARKET TRENDS AND SUMMARY ...............................149

Market Overview ............................................................................................................ 149

Market Revenues by Product Type ............................................................................... 152

Global Cardiac Diagnostic Market Analysis by Region ............................................... 155United States ............................................................................................................ 155

Europe ...................................................................................................................... 156

Japan ........................................................................................................................ 156

Rest of World ............................................................................................................ 156

Competitive Analysis .................................................................................................... 161

CHAPTER TEN: INDUSTRY DEVELOPMENTS

AND TECHNOLOGIES ........................................................................................165

Demographics .................................................................................................................. 165

Cardiovascular Disease Worldwide .............................................................................. 167European Cardiovascular Disease Statistics ................................................................. 168US-Specific Population Demographics ........................................................................ 169

Population Over Age 65 ........................................................................................... 170

Life Expectancy ........................................................................................................ 172

Increasing Incidence of Disease ............................................................................... 174

New Cardiac CT Device ................................................................................................. 175

CT Spots Seeds of Heart Disease in Healthy Patients .................................................. 176

Contrast Agent Toxicity ................................................................................................. 177

Contrast Agents Generic Competition .......................................................................... 177

MRI Catheter Guidance ................................................................................................. 178

Healthcare Reform .......................................................................................................... 179

CHAPTER ELEVEN: CONCLUSIONS ...............................................................183

LIST OF COMPANIES ..........................................................................................185


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L I S T O F E X H I B I T S

CHAPTER ONE:EXECUTIVE SUMMARY

Summary Table ................................................................................................................... 4

Global Cardiac Diagnostics Market Analysis, 2010-2017 ............................................... 4

Summary Figure ................................................................................................................. 5

Global Cardiac Diagnostics Market Analysis: 2010-2017 ............................................... 5

CHAPTER THREE: ELECTROCARDIOGRAPHY

Table 3-1 ............................................................................................................................ 40

Total Electrocardiography Testing Market Analysis, 2010-2017 ................................... 40

Figure 3-1 ........................................................................................................................... 41

Total Electrocardiography Testing Market Analysis, 2010-2017 ................................... 41

CHAPTER FOUR: IMAGING MARKET

Table 4-1 ............................................................................................................................ 62

Non-Invasive Cardiac Imaging Market Analysis, 2010-2017 ........................................ 62

Table 4-2 ............................................................................................................................ 68

Invasive Transcatheter Cardiac Imaging Market Analysis, 2010-2017 ......................... 68

Table 4-3 ............................................................................................................................ 70

Total Cardiac Diagnostic Imaging Market Analysis, 2010-2017 ................................... 70

Figure 4-1 ........................................................................................................................... 71

Total Cardiac Diagnostic Imaging Market Analysis, 2010-2017 ................................... 71

CHAPTER FIVE: CARDIAC POINT OF CARE TESTING

Table 5-1 ............................................................................................................................ 75

Cardiac Coagulation Testing Market Analysis, 2010-2017 ............................................ 75

Table 5-2 ............................................................................................................................ 77

Cardiac Cholesterol Testing Market Analysis, 2010-2017 ............................................. 77

Table 5-3 ............................................................................................................................ 78

Total Cardiac Diagnostic POC Testing Market Analysis, 2010-2017 ........................... 78

Figure 5-1 ........................................................................................................................... 79

Total Cardiac Diagnostic POC Testing Market Analysis, 2010-2017 ........................... 79


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List of Exhibitsx



Figure 9-6 ......................................................................................................................... 160

Global Cardiac Diagnostics Market Revenues by Region 2017 ($millions) ................ 160

Figure 9-7 ......................................................................................................................... 161

Global Cardiac Diagnostics by Region Percent 2017 (%) ............................................ 161

Table 9-6 .......................................................................................................................... 162

Estimated Global Cardiac Diagnostics Manufacturer Market Share 2012 .................. 162

Figure 9-8 ......................................................................................................................... 163

Estimated Global Cardiac Diagnostics Revenues and Market Share 2012 .................. 163

CHAPTER TEN: INDUSTRY DEVELOPMENTS AND TECHNOLOGIES ..165

Table 10-1 ........................................................................................................................ 166

Total Global Population by Selected Geographical Region, 2000 - 2050 .................... 166

Table 10-2 ........................................................................................................................ 168

Cardiovascular Deaths by World Region 2008 ............................................................ 168

Table 10-3 ........................................................................................................................ 169

The U.S. Population, 1980-2020 .................................................................................. 169

Figure 10-1 ....................................................................................................................... 170

The US Population, 1980-2020 (in millions) ................................................................ 170

Table 10-4 ........................................................................................................................ 171

Percent U.S. Population Over Age 65 by Year ............................................................. 171

Figure 10-2 ....................................................................................................................... 172

Estimated Population by Age Group, 2000 and 2050 ................................................... 172

Table 10-5 ........................................................................................................................ 173

Average U.S. Life Expectancy in Years 1980, 2004, 2006, 2010, 2011 (years) .......... 173

Figure 10-3 ....................................................................................................................... 174

Average U.S. Life Expectancy in Years 1980, 2004, 2006, 2010, 2011 ...................... 174

APPENDIX ...............................................................................................................185


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C H A P T E R O N E

Executive Summary

INDUSTRY AT A GLANCE

Economic conditions in several markets within the global cardiac

diagnostics market remained challenging in 2012. Demand for cardiovascular

diagnostics slowed during the historical period due to a weakened global economy,

cost cutting measures and healthcare reform issues. However, demographics

worldwide and an aging world society remain primary factors in growth. By 2020,

16 percent of the US population will be over the age of 65, up from 13% in 2010.

People are also living longer, needing more health care, further fueling the market.In 1980, the US life expectancy at birth was 74 years, today the average American

lives to be 78 years old.

Advancing technologies have also led to increased use of less invasive and

more sophisticated cardiac diagnostics. A trend toward preventive care involving

risk factor knowledge and earlier treatment of cardiovascular disease has been a

driving factor.

There are five categories of cardiac diagnostics that Kalorama assessed in

this market. These include:

ECG

Cardiac Diagnostic Imaging

Cardiac Diagnostic Point-of-Care


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One: Executive Summary2



Cardiac Markers

Cardiac Diagnostic Contrast Agents and Radiopharmaceuticals

Cardiac diagnostic imaging is the largest category within the global cardiacdiagnostic market with 50.5% of the total revenues.

Cardiac contrast agents and radiopharmaceuticals accounted for 20.8% of

revenues in 2012 and cardiac markers accounted for 14.3% of revenues. Growth in

these two areas has been growing.

ECG equipment accounted for 8.4% of revenues in 2012 and is expected to

continue to increase as the elderly population grows and the incidence of heart

disease continues to increase.

Overall, increasing incidence of heart disease and an aging population,

which typically require more diagnostic procedures, will continue to fuel growth for

cardiac diagnostics throughout the forecast period.

The economic recession had a significant impact on the cardiac diagnostics

market, which experienced falling sales in key geographies. The difficulties were

mostly felt on the high-end imaging equipment segment after many health care

institutions delayed or outright cancelled equipment purchases. There also was a

concurrent decline in patient numbers as people skipped or deferred scans because

they lost jobs and health insurance coverage, or because of the high out-of-pocket

costs associated with cardiac imaging. Some growth in the market is attributed to

the continuous improvements in image quality, and to newer techniques for imaging

specific portions of the heart.

Growth rates in the United States, Europe and Japan have moderated due to

budgetary constraints, changes in reimbursement and a global economic slowdown.

However, in Rest of World markets spending on healthcare is increasing and there

is an increasing demand for medical technologies. This is especially apparent for

China, India, Latin America, the Middle East, and Brazil.


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SCOPE AND METHODOLOGY

SCOPE AND METHODOLOGY

This report provides the reader with an overview of the global cardiac

diagnostics industry and the trends driving growth. Segments within the cardiac

diagnostic market include:

Electrocardiography including ECG testing, stress testing, Holter

monitoring, event monitoring and implantable loop.

Cardiac imaging including non-invasive X-Ray, MRI, CT,

ultrasound, and nuclear cardiography; and invasive /cardiac

catheterization/angiography, intravascular ultrasound, optical

coherence technology and electrophysiology.

Cardiac point-of-care including cholesterol testing and coagulationtesting

Cardiac markers

Cardiac contrast agents and radiopharmaceuticals

Included in the report are statistics influencing the industry, incidence of

cardiac and related diseases worldwide, demographics, life expectancy, and

company strategies. Information is presented as a global market. A market summary

includes a total market analysis. Also included is a competitive analysis of leading

cardiac diagnostic providers.

The information for this report was gathered using both primary and

secondary research including comprehensive research of secondary sources such as

company literature, databases, investment reports, and medical and business

journals. Telephone interviews and email correspondence were the primary method

of gathering information. For the purpose of this study, Kalorama Information

conducted interviews with more than 21 key industry officials, consultants, health

care providers, and government personnel. These sources were the primary basis in

gathering information specifically relating to revenue and market share data

presented in this report. Additional interviews were completed with relevant

company representatives including marketing directors, division managers, and

product representatives.


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All market data pertains to the world market at the manufacturers level.

Revenues represent sales of diagnostics that pertain to the cardiovascular arena.

The base year for data was 2012. Historical data was provided for the years 2010

and 2011, with forecast data provided for 2012 through 2017. Compound annual

growth rates (CAGRs) are provided for the 2010-2012 and 2012-2017 periods for

each region and/or segment covered. Competitive analysis is provided for the year

2012. The forecasted market analysis for 2012-2017 was largely based on

demographic trends, new developments, company performance trends, merger and

acquisitions, and national expansion.

SIZE AND GROWTH OF THE MARKET

The global cardiac diagnostics market totaled approximately $13.2 billion

in 2012, increasing at a rate of 3.1% from $12.4 billion in 2010. There are several

trends which continue to influence growth in this market. The market is expected to

increase to approximately $16.6 billion in 2017, growing at a rate of 4.8%

throughout the forecast period. New technologies in testing will likely continue to

fuel growth in combination with an aging population, increasing cardiovascular

disease incidence and prevalence, and increasing life expectancy.

Summary Table

Global Cardiac Diagnostics Market Analysis, 2010-2017

Year Revenues (millions$) Percent Change

2010 12,392.0 -

2011 12,736.0 2.8%

2012 13,176.0 335%

2013 13,701.0 4.0%

2014 14,298.5 4.4%

2015 14,987.3 4.8%2016 15,762.0 5.2%

2017 16,632.0 5.5%


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Compound Annual Growth Rate

Source: Kalorama Information

Summary Figure

Global Cardiac Diagnostics Market Analysis: 2010-2017

$0

$2,000

$4,000

$6,000

$8,000

$10,000

$12,000

$14,000

$16,000

$18,000

2010 2011 2012 2013 2014 2015 2016

Source: Kalorama Information

2010-2012 3.1%

2010-2017 4.8%

2010-2017 4.3%


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KEY ISSUES AND TRENDS AFFECTING THE MARKET

There are several primary issues and trends affecting the global cardiacdiagnostics market. Demographics, disease prevalence, and increasing life

expectancy will continue to fuel growth in the future. New developments will also

positively influence growth. Some of these issues are discussed in this study.

Issues and trends explored in this study include:

World Demographics

Aging Population

Increasing Life Expectancy

Increasing Incidence of Disease

New Cardiac CT Device

CT Spots Seeds of Heart Disease in Healthy Patients

Contrast Agent Toxicity

Contrast Agent Generic Competition

LEADING MARKET PARTICIPANTS

The global cardiac diagnostics market is competitive with a number of

providers. Companies remain competitive by offering a good selection of cardiac

diagnostic devices. Four companies, GE Healthcare, Siemens, Philips and Toshiba

dominate the industry with combined revenues of approximately $ 10.5 billion in

2012.

Several leading and unique market participants are discussed in this report

including:

Abbott Diagnostics

Acusphere

Analogic Corp

Bayer Healthcare


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Bracco SpA

Cardinal Health

CardioDX

C.R. Bard

Danaher Corporation

dpiX

FluoroPharma Medical

GE Healthcare

Hitachi Medical Systems

Johnson & Johnson

King PharmaceuticalsLantheus Medical Imaging

LipoScience

Medison America

Molecular Insight Pharmaceuticals

Nanosphere

PerkinElmer

Philips Healthcare

Roche Diagnostics

Shimadzu

Siemens

St Jude Medical

Terumo Medical

TomTec Imaging Systems

Toshiba

Trixell

Vascular Solutions

Vermillion

Volcano


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C H A P T E R T W O

Industry Overview

INTRODUCTION

The primary function of the heart is to propel blood through the vessels of

the circulatory system. Along with the lungs, the heart works to distribute

oxygenated blood and nutrients to tissues and organs of the body.

Cardiovascular Anatomy

Heart

The heart is located in the mediastinum, suspended between the lungs,behind the sternum, and in front of the vertebral column, thoracic aorta, and

esophagus. When seen from the front, the heart appears to be rotated to the left, so

that the right atrium and right ventricle are most anterior. The base of the heart

protrudes somewhat into the right side of the chest and is relatively fixed in place

by its attachments to the great vessels. The apex of the heart lies primarily in the left

anterior chest wall. With each heartbeat, a characteristic thrust, or point of maximal

impulse (PMI), is generated and can be palpated where the apex strikes against the

chest. The PMI is normally located on the left side of the chest where the fifth

intercostal space and midclavicular line intersect. Variations in heart size and

position within the chest may be related to age, body size, shape, weight, or

pathologic conditions of the heart and other nearby structures.


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Two: Industry Overview10



Functionally important cardiac tissues include connective tissues, which

form the fibrous skeleton and valves; cardiac muscle, which produces the

contractile force; and epithelial tissue, which lines the cardiac chambers and covers

the outer surfaces of the heart. The fibrous skeleton consists of four rings that

provide a firm scaffold for attachment of cardiac muscle and the cardiac valves.

Four cardiac valves control the direction of blood flow through the heart. The

mitral valve (bicuspid) directs blood flow from the left atrium to the left ventricle,

while the tricuspid valve directs blood from the right atrium to the right ventricle.

The edges of these atrioventricular (AV) valves are attached to rings formed by the

fibrous skeleton. Valve leaflets are tethered to papillary muscles of the ventricular

chambers by connective tissues called chordae tendineae. Papillary muscles attach

to ventricular walls and help prevent the valves leaflets from bending backward intothe atria during ventricular contraction. The AV valves open passively during

diastole when pressure of blood in the atria exceeds that in the ventricles.

Ventricular contraction reverses the pressure gradient and causes AV valves to snap

shut, preventing blood from flowing backward into the atria.

Two semilunar valves are located in the ventricular outflow tracts. The

pulmonic valve lies between the right ventricle and pulmonary artery and the aortic

valve lies between the left ventricle and aortic artery. Compared to the AV valves,

the semilunar valves are thicker and are not supported by fibrous cords. They open

and close passively according to pressure gradients, just as the AV valves do. When

intraventricular pressures exceed pulmonary and aortic artery pressures, the

semilunar valves remain open and then close when ventricular pressures fall below

aortic and pulmonary artery pressures.

The cardiac muscle layer (myocardium) produces the contractile force that

pushes blood through the circulatory system. Heart muscle is organized into four

separate chambers of varying muscular wall thickness, reflecting the degree of

pressure each chamber must generate to pump blood. Atria serve primarily as

conduits and have a thinner layer of muscle than the ventricles. The left ventricular

muscle is 2 to 3 times thicker than that of the right ventricle because higher

pressures are required to eject blood into the systemic circulation then into the

pulmonic system. Alterations in chamber pressures may reflect pathologic


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cardiovascular changes such as valvular disorders, blood volume abnormalities, and

heart failure.

Cardiac chambers and valves are lined by a layer of squamous epithelial

cells called endocardium. The endocardial layer provides a smooth surface on

which blood can slide, which prevents clotting and minimizes trauma to read cells.

The endocardium is continuous with endothelium of the vascular system. Outer

surfaces of the heart are also covered by a layer of epithelial cells, called

epicardium, which is part of a protective covering called the pericardium. The

pericardium is actually composed of two layers that enveloped the heart like a sack.

The inner layer (visceral pericardium) is attached directly to the hearts outer

surface, while an outer layer (parietal pericardium) forms a sack around the heart.

Visceral and parietal layers are separated by a thin, fluid-filled pericardial

space that usually contains 10 to 30 mL of serous fluid. This fluid lubricates

pericardial surfaces and reduces friction as the layers slide against one another

during cardiac contraction. Accumulations of fluid in the pericardial space or

inflammation of the pericardial sac can restrict cardiac billing and impair cardiac

output.

Circulatory System

The left-sided heart chambers produce the force to propel blood through the

vessels of the body. The left atrium receives oxygenated blood from the lungs by

way of the pulmonary veins and delivers it to the left ventricle. This oxygenated

blood is pumped by the left ventricle into the aorta, which supplies the arteries of

the systemic circulation. Venous blood is collected from capillary networks of the

body and return to the right atrium by way of the vena cava. Blood from the head

returns to the right atrium through the superior vena cava, and blood from the body

returns by the interior vena cava.

The right side of the heart receives deoxygenated blood from the systemic

circulation and pumps it through the lungs by way of the pulmonary artery. The

pulmonary artery divides into left and right branches, which subdivide to supply

blood to pulmonary capillary beds. Exchange of respiratory gases occurs at the

pulmonary capillaries so that blood delivered to the left atrium by the pulmonary

veins is well oxygenated.


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Left and right circulations are connected in series such that the output of one

becomes the input of the other. Thus, the functions of the right and left sides of the

heart are interdependent. Failure of one side of the heart pump efficiently will soon

lead to dysfunction of the other side.

Characteristic changes in the anatomy and physiology of the heart and

circulatory systems occur with aging. In general, these changes result in a decreased

cardiac reserve and it greater predisposition to cardiac muscle ischemia.

Cardiac Cycle

Each heartbeat is composed of a period of ventricular contraction (systole)

followed by a period of relaxation (diastole). The interval from one heartbeat to the

next is called the cardiac cycle and includes ventricular, atrial, and aortic events.

Each of these events is associated with characteristic pressure changes within the

cardiac chambers. Pressure changes result in valvular opening and closing and

unidirectional movement of blood through the heart. Abnormalities in these

waveforms may occur with valvular disease, changes in blood volume, or pumping

capacity of the heart. These waveforms are commonly monitored with specialized

cardiac catheters in patients with cardiac or hemodynamic disorders.

The cardiac cycle can be described sequentially, beginning with the

ventricular filling. During diastole the ventricles are relaxed and blood flows infrom the atria through open AV valves. Initially, ventricular filling occurs passively

because of a pressure gradient between the atria and ventricles. Toward the end of

ventricular diastole, the atria contract squeezing more blood through the AV valves

into the ventricles. Atrial contraction increases the ventricular blood volume by

20% to 30%. This atrial kick is particularly important during fast heart rates, when

the time for ventricular filling is shortened. Ventricular events include isovolumic

contraction, ejection, and isovolumic relaxation.

Atrial pressure waves have three characteristic curves, the a, c, and vwaves. The a wave corresponds to atrial contraction, which immediately precedes

AV valve closure. The c wave occurs early in ventricular systole and is thought to

represent bulging of AV valves into the atrial chambers. The v waves have a

gradual incline, which represents filling of the atrium as blood returns from the


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circulation. The V wave drops rapidly as atrial pressure is relieved by AV valve

opening. A large V wave is often associated with an adequate closure of the AV

valve, resulting in regurgitation of ventricular blood back into the atrium during

ventricular systole.

Aortic and pulmonary artery pressures rise and fall in relation to the cardiac

cycle. Arterial pressures fall to their lowest value just prior to semi lunar valve

opening. This lowest pressure is called diastolic blood pressure. Arterial pressure

ejection and is called systolic blood pressure.

The difference in aortic pressure between systole and diastolic is partially

dependent on the aortas elastic characteristics. During systole, the aorta stretches to

accommodate blood ejected by the ventricle. The stretched aorta has stored or

potential energy that is released during diastole to maintain driving pressure and to

keep blood flowing continuously through the circulation. Aortic stiffening, as

occurs with aging or arteriosclerosis, may result in higher systolic and lower

diastolic blood pressure due to loss of aortic elastic properties.

Coronary Circulation

The blood supply to heart muscle is provided by the coronary arteries. Right

and left coronary artery openings are located within the sinuses of Valsalva, in the

aortic root, just beyond the aortic valve. The right coronary artery (RCA) originatesnear the aortic valves anterior cusp and passes diagonally toward the right ventricle

in the AV groove. In approximately 80% of the population, the RCA gives rise to a

posterior descending vessel that supplies blood to the hearts posterior aspect. The

left main coronary artery arises near the aortic posterior cost and travels to a short

distance anteriorly before dividing into the left anterior descending and circumflex

branches. The anterior descending branch supplies septal, anterior, and apical areas

of the left ventricle, whereas the circumflex artery supplies the lateral and posterior

left ventricle. The three major coronary arteries give rise to a number of smaller

branches that penetrate the myocardium and branch into small arterials and

capillaries. Regular exercise and stable atherosclerotic plaques in the coronary

arteries are thought to stimulate the development of more extensive collateral

circulation in the heart. Collateral vessels may help limit infarct size in patients


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suffering acute coronary occlusions. Most of the hearts capillary beds drain into the

coronary veins, which then empty into the right atrium through the coronary sinus.

Blood flow through coronary vessels is determined by the same physical

principles that govern flow to other vessels of the body, namely, driving pressure

and vascular resistance to flow. Driving pressure through the coronary arteries is

determined by aortic blood pressure and right atrial pressure.

Coronary vascular resistance has two major determinants: (1) coronary

artery diameter and (2) the degree of extra compression due to myocardial

contraction. Coronary artery diameter is continuously adjusted to maintain blood

flow at a level adequate for myocardial demands. Autoregulation is the term used to

describe the intrinsic ability of the arteries to adjust blood flow according to tissue

needs. Vasodilation occurs in response to increased tissue metabolism, whereas

decreased metabolic activity results in a decreased vessel diameter.

The mechanism of autoregulation can be explained by the metabolic

hypothesis, which proposes that increase metabolism results in a buildup of

vasodilatory chemicals in the vessel. Smooth muscle circling the vessel relaxes in

response to the presence of the chemicals increasing vessel diameter. Several

vasodilation substances have been proposed, including potassium ions, hydrogen

ions, carbon dioxide, nitric oxide, prostaglandins, and adenosine. The endothelial

cells that line vessels are known to secrete a variety of relaxing and constricting

factors, many of which have not yet been identified. An increase in the level of

adenosine is currently believed to be the chief vasodilatory chemicals. Low level of

oxygen in the blood also may cause vasodilation. Whatever their identity the

vasodilatory substances are washed away as blood flow increases in response to

increased vessel diameter. A declining level of vasodilatory chemicals results in

vasoconstriction. Thus, vessel diameter is continuously adjusted according to

concentrations of vasodilatory chemicals, which are directly related to the tissues

metabolic activity.

An ATP-sensitive potassium channel has been implicated in the regulation

of coronary blood flow. Concentration of ATP in vascular smooth muscle regulates

a specific K+ channel. As ATP levels rise in response to increase coronary flow, the

channel closes, making it easier to depolarize the cell and contract vascular smooth


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muscle. Contraction of vascular smooth muscle reduces the diameter of the

coronary arteries and reduces blood flow. The opposite also occurs: a reduction in

ATP, due to low flow or increase metabolism, opens the K+ channels. Potassium

than leaks out of the vascular smooth muscle and short-circuits that the polarizing

influences. This inhibits vascular contraction, leading to vasodilation and increased

coronary blood flow. Substances other than ATP are believed to open and close

these channels and may contribute to coronary regulation during periods of

ischemia or increased metabolic demand.

Vessel diameter also is regulated by the autonomic nervous system. The

coronary arteries are primarily innervated by sympathetic nerves, but they also

receive a small amount of parasympathetic innervation. Sympathetic nervous

activity results in vasoconstriction; parasympathetic activity results in vasodilation.

Vessel diameter is, therefore, the result of an interplay between nervous system and

auto regulatory influences.

In addition to vessel diameter, coronary resistance is affected by myocardial

contraction. During systole, cardiac muscle compression creates a marked rise in

coronary resistance that reduces coronary blood flow. Blood flow to the left

ventricle is greatly decreased during systole because of the pressure generated by

the thick muscular layer. Blood vessels that penetrate the myocardium to supply the

innermost endocardial areas are more compressed during contraction than our outerepicardial vessels. Even though coronary artery driving pressure is greatest during

ventricular systole, little blood flow reaches the ventricles because of the high

external pressure applied to the coronary vessels as the myocardium contracts.

Therefore, most myocardial blood flow occurs during the diastolic interval between

ventricular contractions. The time the heart spends in diastolic is directly related to

heart rate. Faster heart rates reduce diastolic time and decrease coronary artery

blood flow.

Cardiac muscle needs a continuous supply of oxygen and nutrients toperform its pumping functions. A disruption in cardiac blood flow (ischemia)

generally results in some degree of pump failure and damaged cardiac tissues.

Myocardial ischemia may be caused by conditions that reduce coronary blood flow

or increase myocardial demands for oxygen.


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Cardiac Myocytes

Cardiac muscle cells are divided into two general types: working cells,

which have primarily mechanical pumping functions, and electrical cells, which

primarily transmit electrical impulses. Both types are excitable: they are able to

produce and transmit action potentials. Working myocardial cells are packed with

contractile filaments and make up the bulk of the arterial and ventricle muscle.

Electrical cells function to initiate and coordinate contraction of the working cells.

Microscopic inspection of the cardiac myocytes reveals a typical pattern of

banding called striation. This striated appearance is due to an organized structure of

the proteins of the contractile apparatus. The contractile proteins, actin and myosin,

are called filaments because they are long and narrow. Myosin filaments are larger

and referred to as thick filaments. Thin filaments are actually composed of three

different types of protein bundled together. Actin is the primary constituent of thin

filaments, with smaller amounts of the proteins tropomyosin and troponin bound to

it.

The thick and thin filaments are specifically arranged in contractile units

called sarcomeres. Sarcomeres are defined by dark bands called Z disks, which lie

perpendicular to actin and myosin filaments.

Molecular Contraction

The hearts pumping action is accomplished by the contractions of the many

myocytes that form the cardiac chambers. Because each myocyte contributes only a

small amount to overall muscle shortening, all cells of the chamber must shorten

simultaneously to produce a forceful contraction. The specialized cells of the

conduction system function to stimulate myocardial contraction in a coordinated

way. An action potential traveling down the conduction system is the usual trigger

for contraction. Cardiac myocyte depolarization causes ion channels in the plasma

membrane and T tubules to open, permitting sodium and calcium entry and release

of calcium from the sarcoplasmic reticulum. The presence of free calcium in the

sarcoplasmic reticulum results in contraction. These events describe the process of

excitation-contraction coupling.


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DISEASES OF THE HEART

Ischemic Heart Disease

Ischemic heart disease is characterized by insufficient delivery of

oxygenated blood to the myocardium. When metabolic demand for oxygen exceeds

supply, the myocardium becomes ischemic, which leads to a dysfunction in cardiac

pumping and predisposes to abnormal heart rhythms. If the ischemic episode is

severe or prolonged, irreversible damage to myocardial cells may result in

myocardial infarction.

Etiology

The most common cause of ischemic heart disease is coronary artery

atherosclerosis-sometimes called coronary artery disease or coronary heart disease.

Atherosclerosis causes progressive narrowing of the atrial lumen and predisposes to

a number of processes that can precipitate myocardial ischemia, including thrombus

formation, coronary vasospasm, and endothelial cell dysfunction. Less common

causes of ischemic heart disease include abnormalities of blood oxygen content and

poor perfusion pressure through the coronary arteries. Sometimes, patients

experience the signs and symptoms of cardiac ischemia but show no evidence of

coronary artery atherosclerosis when evaluated by an angiogram. These patients are

thought to have abnormalities of the microcirculation. Abnormal vascular regulationby endothelial cells in small vessels of the heart has been suggested as a probable

mechanism. Endothelial cells secrete variable quantities of vascular relaxing and

contracting factors and play a key role in controlling myocardial blood flow.

Abnormalities of the microcirculation are more difficult to detect than coronary

artery plaque, which is evident on coronary angiography. As evaluation methods

improve, disorders of the microcirculation are likely to be more frequently

recognized as factors contributing to ischemic heart disease.

PathophysiologyIschemia of cardiac cells occurs when oxygen supply is insufficient to meet

metabolic demands. Myocardial cells are able to store much energy in the form of

adenosine triphosphate (ATP) and must therefore continuously receive a supply of

oxygen for aerobics synthesis of ATP. ATP is essential for powering myocardial

contraction, as well as for cell maintenance. Because the heart is unable to stop and


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rest when ATP supplies dwindle, it is essential that a steady flow of oxygen be

provided.

Factors that decreased myocardial oxygen supply or increased myocardial

oxygen demand can upset the balance and result in cellular ischemia. Thats the

critical factors in meeting cellular demands for oxygen are (1) the rate of coronary

perfusion and (2) myocardial workload. Coronary perfusion can be impaired in

several ways, including (1) large, stable atherosclerotic plaque, (2) acute platelet

aggregation and thrombosis, (3) vasospasm, (4) failure of autoregulation by the

microcirculation, and (5) poor perfusion pressure.

Myocardial workload depends on heart rate, preload, after load, and an

increase in any of these variables increases myocardial oxygen requirements and

may precipitate ischemia. However, even conditions resulting in very high

myocardial oxygen consumption will seldom lead to ischemia unless some

underlying impairment in coronary perfusion is present.

One or more of the aforementioned mechanisms are operative in producing

clinically significant myocardial ischemia resulting in the syndromes of MI,

ischemic cardiomyopathy, and sudden cardiac death.

therosclerosis

Knowledge about mechanisms of plaque formation in the coronary arterieshas rapidly accumulated in recent years. Epidemiologic studies reported in the

1960s suggested associations among certain traits and habits and the development

of coronary heart disease. More recent studies have confirmed and expanded upon

these risk factors which now include age, family history, hyperlipidemia, cigarette

smoking, hypertension, diabetes, and obesity. Although males and females succumb

to heart disease in equal numbers, male gender is a risk factor for earlier

development of heart disease (on average about 10 years earlier). The risk factors

for coronary heart disease are the same as those for atherosclerosis in other arteries.

The observation that atherosclerotic plaque is composed primarily of lipid

prompted the idea that abnormal lipid metabolism was a probable culprit in the

development of coronary heart disease. Lipids may accumulate in the arterial wall

for many reasons, including vessel trauma, inflammation, and infection. A great

deal of evidence supports the idea that hyperlipidemia is a major factor promoting


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the development of coronary atherosclerosis. The risk of coronary heart disease

increases proportionately as the serum lipid level increases.

Lipids are transported through the bloodstream in combination with specific

proteins (apoproteins). Certain liquid-protein molecules (lipoproteins) are

associated with a greater risk of atherosclerosis. High levels of low-density

lipoproteins (LDLs), which are high in cholesterol, have been associated with the

highest risk. Very-low-density lipoproteins, have been correlated with a decreased

risk of atherosclerosis.

High-density lipoproteins are thought to transport cholesterol from the

vessel back to the liver for excretion, thus clearing away atheromatous plaque. The

role of low-density and indirectly very-low-density lipoproteins is to bring

cholesterol to the peripheral tissues. Cholesterol uptake by peripheral cells is

mediated by receptors (LDL receptors) on cell surfaces that bind and promote

endocytosis of cholesterol. The liver normally binds and internalizes about 75% of

the circulating LDL cholesterol.

Extreme cases of hyperlipidemia occur in individuals who have genetic

derangements in lipid metabolism. These disorders run in families and are

associated with the development of severe coronary atherosclerosis at a young age

unless aggressively treated. The most common form of genetic hyperlipidemia is

due to a defect in the LDL receptor on liver cells. It is associated with the inability

of the liver to effectively remove cholesterol from the bloodstream, which results in

hyperlipidemia. Even when lipid metabolism is normal, a high-fat diet can

overwhelm the livers ability to clear LDL cholesterol from the circulation and

result in hyperlipidemia. Dietary fat restriction may be beneficial in reducing

cholesterol in this case.

Atherosclerotic lesions generally increase in size over many years and

progressively occlude the lumen of the vessels. A significant reduction in blood

flow can result when plaque occupies 75% or more of the arterial lumen. Clinically

significant atherosclerotic plaque may be located anywhere within the three major

coronary arteries or major secondary branches. All three coronary arteries are often

simultaneously affected, although some individuals have only one or two diseased


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vessels. Surprisingly, the extent and severity of atherosclerotic lesions are not good

predictors of the severity of ischemia.

The American Heart Association system for classification of coronary

lesions is helpful in understanding the types of coronary lesions that have been

characterized and attempts made to correlate the anatomic descriptions with plaque

development and behavior. In general, plaque is thought to progress sequentially

from type I through type VI, although the more advanced stages may not develop in

some individuals. Types IV, V, and VI are considered to be advanced lesions and

may cause the clinical syndromes of ischemia, including angina, infarction,

ischemic cardiomyopathy and sudden cardiac death.

Type I, II, and III lesions are silent precursors to the deadly processes of

advanced plaque formation. Type I and II lesions are present in childhood. Type I

lesions are characterized by the accumulation of lipids within macrophages located

in the intimal layer of the coronary artery. These lipid-laden macrophages are called

foam cells. In childhood, foam cells tend to reside in the areas of adaptive arterial

thickening-such as occurs at arterial branch points. In persons with hyperlipidemia,

foam cells may accumulate in other arterial regions. Type I lesions are present in

about 50% of infants at eight months of age. Foam cells are few and scattered in

type I lesions and are not visible to the unaided eye.

Type II lesions are also composed primarily of macrophage foam cells, but

they are more numerous and begin to coalesce. In addition, intimal smooth muscle

cells also begin to accumulate intracellular lipids. Nearly all the lipid in the arterial

wall at this stage is still confined to the intracellular compartment. Type II lesions

are visible on gross inspection and appear as yellowish fatty streaks or spots. In the

early 1900s when early childhood mentality was high, autopsy studies revealed that

type II lesions were initiated at early stages. Type II lesions were not seen before

age 9 years and became prevalent at puberty. The incidence of type II lesions was

noted to increase with age, being present in 30% of nine-year-olds, 60% of 10-to14-year-olds and 75% of 15-to 19-year-olds.

Type III lesions are considered to be links between the nearly universal and

asymptomatic type I and II lesions and the pathologic forms of advanced lesions.

The main histologic difference between type II and III lesions is that extracellular


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lipid droplets begin to accumulate in the matrix. However, the lipids have not yet

formed a pocket as occurs in type IV lesions. Type III lesions, like types I and II,

are asymptomatic.

Advanced lesions include types IV, V, and VI and carry a significant risk of

producing disruptions in coronary blood flow. Type IV lesions contain a large

amount of free lipid that forms a pocket in the intima just under the layer of

macrophage foam cells. Lipids forming the core are derived primarily from plasma,

and elevated serum cholesterol is a major factor in lesion progression from type III

to Type IV. Lesions do not protrude into the arterial lumen, but they are prone to

rupture and precipitate thrombus formation at the site. Acute thrombus formation

can suddenly occlude the artery resulting in cardiac ischemia. If the thrombus is

small, it may not occlude the artery lumen but may instead become incorporated

into the lesion and cause it to enlarge into a more advanced type. Type IV lesions

are of special interest because they may be more responsive to lipid-lowering

strategies than are the more dense lesions.

Type V lesions are characterized by the inclusion of fibrous connective

tissue within the plaque. The fibrous tissue forms a cap on the plaque that may

make it more stable and less prone to rupture than type for lesions the appearance of

type V morphology heralds the onset of progressive narrowing of the arterial lumen.

Over time, smooth muscle cells in the intima proliferate and fibrous connectivetissue expands into the lumen. Type V lesions are also prone to disruptions in the

plaque surface leading to intraplaque hemorrhage and thrombus formation.

When a type IV or type V lesion is complicated by plaque disruption and

thrombus formation, it is then classified as a type VI lesion. Type IV, V, and VI

lesions are responsible for the clinical syndromes of ischemia associated with

coronary heart disease.

ngina Pectoris

Angina pectoris is characterized by chest pain associated with intermittent

myocardial ischemia. The link in the severity of the myocardial ischemia is

insufficient to result in the death of cells. Bouts of chest pain and associated

symptoms are generally recurrent and may be precipitated by conditions that

increase myocardial oxygen demand such as exercise, stress, sympathetic nervous


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system activation, and increase preload, after load, heart rate, or muscle mass.

Ischemic pain receptors from the myocardium travel to the central nervous system

with the eighth cervical and the first through fourth thoracic dorsal root ganglia.

Sensory neurons from the jaw, neck, and arm also travel in these nerve trunks, so

heart pain may be perceived as emanating from these body parts. This phenomenon

is called referred pain. Anginal pain may be described as burning, crushing,

squeezing, or choking. Pain is sometimes represented by expressions such as an

elephant is sitting on my chest or by the patient placing a tight fist on the chest.

Anginal pain may be mistakenly attributed to indigestion or dental pain.

Anginal ischemia, although temporary, may result in insufficient cardiac

pumping with resultant pulmonary congestion and shortness of breath. Three

patterns of angina pectoris have been described: stable or typical angina, Prinsmetal

or variant angina, and unstable or crescendo angina. All these patterns are

associated with underlying coronary vessel disease and may be exhibited in a

particular individual at different times and under different conditions.

cute Ischemia and Myocardial Infarction Chronic

Unstable angina and MI are difficult to distinguish on the basis of clinical

manifestations. Both are characterized by chest pain that may be more severe and

last longer than the patients typical angina. In both cases, plaque rupture with

subsequent acute thrombus development is thought to occur. In unstable angina, theocclusion is partial when the clot is broken down before the death of the myocardial

tissue. In MI, the occlusion is complete and the thrombus persists long enough for

development of irreversible damage to myocardial cells. In the past, differentiation

of unstable angina and MI was based on laboratory evaluation of serum enzyme

levels such as MB band of creatine kinase (CK-MB), lactate dehydrogenase (LDH).

If cardiac enzymes were elevated which is indicative of necrosis, a diagnosis of MI

was made; if not a diagnosis of unstable angina was appropriate.

Two types of MI have been described, each having different morphologyand clinical significance. A transmural infarct involves the entire thickness of the

ventricular wall and is the more serious of the two types. It is also more common. A

nonQ wave infarct affects only the inner third to half of the ventricular wall and

is generally associated with less severe symptoms. These lesions are not exclusive:


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a non--Q wave MI can extend across the ventricular wall to become a transmural

MI under certain circumstances.

Chronic Ischemic CardiomyopathyChronic ischemic cardiomyopathy refers to a disorder in which heart failure

develops insidiously as a consequence of progressive ischemic myocardial damage.

In most cases, individuals affected have a history of angina or MI, often many years

before the onset of heart failure. Heart failure appears to be a consequence of slow,

progressive atrophy or death of myocytes from chronic ischemia. The disease is

usually found in elderly individuals. Atrophic and dead cells are scattered

throughout the myocardium rather than being localized, as occurs with MI. The

prognosis for patients with chronic ischemic cardiomyopathy is quite poor, with

death from congestive heart failure the common outcome.

Sudden Cardiac Death

Sudden cardiac death is usually defined as unexpected death from cardiac

causes within one hour of the onset of symptoms. Ischemic heart disease is at the

root of the vast majority of cases of sudden cardiac death. Rarely, sudden cardiac

death may be a complication of hereditary or required structural or electrical

abnormalities. It is estimated that 300,000 to 400,000 individuals die each year in

the United States of sudden cardiac death. It is most often associated with coronary

atherosclerosis and may be the initial manifestation of the disease. MI occurs in

only a small subset of cases of sudden cardiac death. A lethal dysrhythmia such as

asystole or ventricular fibrillation is usually the primary cause of death. Ischemia

from multi-vessel atherosclerosis, diffuse myocardial atrophy, scarring and fibrous

of old MI tissue, and electrolyte imbalances are factors that may predispose the

heart to the electrical abnormalities that lead to sudden cardiac death

Diagnostic Tests

The diagnosis of ischemic heart disease is frequently made on the basis of

the patients history. Diagnosis of angina may also be facilitated by ECG, Holtermonitor, coronary angiography, and stress testing.


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Valvular and Endocardial Diseases

Endocardial and valvular structures may be damaged by inflammation and

scarring, calcification, or congenital malformations. These processes interfere with

the normal valvular property of unimpeded, unidirectional flow. Although

congenital bowel formations may affect any valve, acquired valvular disorders

generally involve the mitral or aortic valves. Abnormalities in valvular function

cause altered hemodynamics in the heart and generally result in increased

myocardial workload. Ultimately, heart failure may result from significant valvular

dysfunction.

Normally heart valves open completely, so blood flows through with little or

no pressure difference across the valve. Failure of the valve to open completely is

termed stenosis. Significant hemodynamic consequences generally begin to occur

when the valve opening is reduced to half normal. The severity of stenosis can be

estimated by the degree of pressure gradient across the valve. Stenosis results in

extra pressure work for the heart because blood must be forced through the high

resistance of a narrow valve opening. Stenosis generally progresses slowly over

years to decades, which allows time for affected heart chambers to compensate

through myocardial cell hypertrophy.

Regurgitation or insufficiency refers to the inability of a valve to close

completely thereby allowing blood to flow in the reverse direction. Regurgitationmay develop suddenly from valvular infection or rupture of a supporting papillary

muscle. Sudden regurgitation is poorly tolerated inasmuch as little compensation is

possible. Regurgitation results in increased work for the heart because more blood

must be pumped to maintain adequate workflow.

Diseased valves may exhibit elements of both stenosis and regurgitation,

although one problem usually predominates. Post inflammatory scarring from

rheumatic heart disease and valvular calcification with aging of the primary causes

of stenosis. A wide variety of diseases of the endocardium may lead to valvularregurgitation. Damaged cells are susceptible to infection, and antibiotic prophylaxis

is therefore indicated for dental, surgical, and diagnostic procedures.


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itral Valve Disorders

Three important disorders of the mitral valve are stenosis, regurgitation, and

mitral valve prolapse. In mitral stenosis the flow of blood from the left atrium into

the left ventricle is impaired. Mitral stenosis is, therefore, characterized by anabnormal left atrial-left ventricle pressure gradient during ventricular diastole.

Normally the pressure in the atrium and ventricle are nearly equal during ventricular

diastole when the mitral valve is opened. As stenosis worsens, the pressure gradient

often increases. Increased pressure work of the left atrium leads to atrial chamber

enlargement and hypertrophy. Progressive narrowing of the mitral valve may lead

to markedly elevated left atrial pressures and subsequent increased pulmonary

vascul

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