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Manual of
Cardiac Diagnosis
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Manual of
Cardiac Diagnosis
Editors
Kanu Chatterjee
MBBS
Clinical Professor of Medicine
The Carver College of Medicine
University of Iowa
United States of America
Emeritus Professor of Medicine
University of California, San Francisco
Jaypee-Highlights Medical Publishers Inc
City of Knowledge, Bld. 237, Clayton
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Phone: +977-9741283608
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© 2014, Jaypee Brothers Medical Publishers
The views and opinions expressed in this book are solely those of the original
contributor(s)/author(s) and do not necessarily represent those of editor(s) of the book.
Contributors
Abhimanyu (Manu)
Uberoi MD
Department of Cardiology
The Stanford School of Medicine
Palo Alto, California, USA
Amardeep K Singh MD
Department of Cardiology
University of California
San Francisco, USA
Andrew Boyle MD
Assistant Professor of Medicine
University of California
San Francisco, USA
Brad H Thompson MD
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Ellen El Gordon MD
Associate Professor of Medicine
The Carver College of Medicine
Byron F Vandenberg MD
Cardiology Division
The Carver College of Medicine
University of Iowa, USA
Donald Brown MD
Associate Professor of Medicine
The Carver College of Medicine
University of California
San Francisco, USA
Professor of Medicine
The Carver College of Medicine
University of Iowa, USA
Isidore C Okere MBBS
Edwin JR van Beek MD
Jagat Narula MD PhD
Professor of Medicine
Chair of Clinical Radiology
Clinical Research Imaging Centre
Queen’s Medical Research Institute
University of Edinburgh, United
Kingdom
University of Iowa, USA
Department of Cardiology
The Carver College of Medicine
University of Iowa, USA
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Manual of Cardiac Diagnosis
Mohan Brar MD
Assistant Clinical Professor of
Medicine
The Carver College of Medicine
University of Iowa, USA
Nelson B Schiller MD
Professor of Medicine
University of California
San Francisco, USA
Paul Lindower MD
Professor of Medicine
The Carver College of Medicine
Teresa De Marco MD
Professor of Medicine
University of California
San Francisco, USA
Teruyoshi Kume MD
Stanford School of Medicine
Palo Alto, California, USA
Victor F Froelicher MD
Professor of Medicine
The Stanford University School of
Medicine
Pala Alto, California, USA
Vijay U Rao MD PhD
Department of Cardiology
University of California
San Francisco, USA
Wassef Karrowni MD
Division of Cardiology
The Carver College of Medicine
University of Iowa, USA
of cardiovascular pathology. Molecular imaging, threedimensional echocardiography, and intravascular ultrasound
imaging have been introduced. Advances have occurred
in cardiovascular nuclear, computerized tomographic, and
magnetic resonance imaging.
In this book, the advancements in these diagnostic
techniques and their clinical applications in the practice of
cardiology have been extensively discussed. The role of resting
and stress electrocardiography and echocardiography has also
been elaborated upon.
The success of cardiac angiography stimulated the
continued development of selective catheter coronary
arteriography, which is the driving force in the progress and
increased effectiveness of coronary artery bypass surgery,
prosthetic valve replacement, and valve repair.
With contributions from nationally and internationally
recognized experts, an effort has been made to bring forth a
book that will serve as a useful diagnostic manual for students
and practitioners, whole-heartedly involved in the field of
cardiology.
Kanu Chatterjee
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137
Introduction 137
Before the Test 138
Methodology of Exercise Testing 142
During the Test 147
After the Test 160
Screening 166
6. Left Ventricle
Rakesh K Mishra, Nelson B Schiller
96
18
General Appearance 18
Measurement of Arterial Pressure 23
Auscultation 40
References 68
3.Plain Film Imaging of Adult Cardiovascular Disease
Brad H Thompson, Edwin JR van Beek
1
177
Introduction 177
Systolic Function 178
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Manual of Cardiac Diagnosis
Introduction 233
Determinants of Left Ventricular Performance 233
Left Ventricular Pump Function 240
Heart Rate 247
Diastolic Function 249
Right Ventricular Function 251
8.Transthoracic Echocardiography
Byron F Vandenberg, Richard E Kerber
233
357
Introduction 357
History 357
Guidelines 358
Performance 358
Safety 359
Views 359
Major Clinical Applications 360
Structural Valve Assessment 366
Acute Aortic Dissection 371
Procedural Adjunct or Intraoperative Transesophageal
Echocardiography (TEE) 372
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Contents
11. Real-time Three-dimensional Echocardiography
Manjula V Burri, Richard E Kerber
Elias H Botvinick
Introduction 497
Pathophysiologic Considerations 498
Myocardial Perfusion Imaging 505
Risk Assessment of General and Specific Patient Populations 521
Positron Emission Tomography Perfusion and Metabolism 524
Imaging Myocardial Viability 526
Imaging Perfusion 530
Quantitation of Regional Coronary Flow and Flow Reserve 532
Blood Pool Imaging—Equilibrium Radionuclide Angiography
and First Pass Radionuclide Angiography 533
First Pass Curve Analysis 535
Equilibrium Gated Imaging—Erna 538
The Value of Functional Imaging 540
15.Cardiovascular Magnetic Resonance
Robert M Weiss
557
602
Introduction 602
Diagnosis of Epicardial Coronary Artery Stenosis 603
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709
Introduction 709
History and Devices 709
Techniques 711
Introduction 750
Historical Perspective and Evolution of Catheter Designs 750
Placement of Balloon Flotation Catheters 751
Normal Pressures and Waveforms 754
Abnormal Pressures and Waveforms 758
Clinical Applications 759
Indications for Pulmonary Artery Catheterization 768
Complications 769
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Contents
xiii
20.Coronary Angiography and Catheter-based Coronary
Intervention776
Elaine M Demetroulis, Mohan Brar
Indications for Coronary Angiography 778
Contraindications for Coronary Angiography 780
Patient Preparation 781
Sites and Techniques of Vascular Access 782
Catheters for Coronary Angiography 786
Catheters for Bypass Grafts 788
Arterial Nomenclature and Extent Of Disease 790
Angiographic Projections 792
Normal Coronary Anatomy 793
Congenital Anomalies of the Coronary Circulation 801
General Principles for Coronary and/or Graft Cannulation 806
The Fluoroscopic Imaging System 814
Characteristics of Contrast Media 816
Contrast-Induced Renal Failure 817
Access Site Hemostasis 819
Complications of Cardiac Catheterization 821
Lesion Quantification 824
Degenerated Saphenous Vein Grafts 828
Lesion Calcification 828
Physiologic Assessment of Angiographically Indeterminate
Coronary Lesions 829
Clinical Use of Translesional Physiologic Measurements 830
Non-Atherosclerotic Coronary Artery Disease and Transplant
Vasculopathy 831
Potential Errors In Interpretation of the Coronary
Angiogram 834
Percutaneous Coronary Intervention 838
Pharmacotherapy for PCI 839
Parenteral Anticoagulant Therapy 846
Equipment for Coronary Interventions 848
–– Analysis of Symptoms
The history and physical examination are essential, not only
for the diagnosis of cardiovascular disorders but also to assess
its severity to establish a plan of its management and to assess
the prognosis. Appropriate history and physical examination are
also essential to decide what tests are necessary for a patient as
presently a plethora of tests is available for the diagnosis and
management of the same cardiac disorder. For example, for the
diagnosis of the etiology of chest pain due to coronary artery
disease, one can perform many noninvasive, semiinvasive and
invasive tests to establish or exclude the presence of obstructive
coronary artery disease. It should also be appreciated that “history
and physical examination” are cost-effective. Many tests that
are frequently performed today are unnecessary and are much
more expensive. During examination of the patient, the physician
can gain the confidence of the patient and of the family and can
establish a good rapport that is necessary for the appropriate
management of the problem of the patient. During examination,
the physician has the opportunity to demonstrate sincerity, which
facilitates to gain trust of the patient and the family.
In today’s electronic age, the patients and their relatives
are often more familiar than the physicians about the recent
developments in the diagnostic techniques and therapies. It
is thus preferable (but sometimes impossible) to have this
knowledge before examining the patient. In today’s health care
environment, there are severe constraints on time available
for taking appropriate history and to do adequate physical
examination.1 Frequently, the physicians have to order the
“tests” because of time constraints even before examining
palpitations, dizziness, and syncope.
Analysis of Symptoms
Chest Pain or Discomfort
Chest pain is one of the very common presenting symptoms that
patients present to the cardiologists for their expert views for
the diagnosis of its etiology and management. The chest pain
or discomfort can be caused by various cardiac and noncardiac
causes that are summarized in Tables 1 to 4.
“Cardiac pain” may be due to myocardial ischemia or it
can be nonischemic in origin. The cardiac pain resulting from
myocardial ischemia is called “Angina pectoris”. The precise
mechanism of cardiac pain due to myocardial ischemia has not
been elucidated. It has been postulated that small nonmedullated
sympathetic nerve fibers, which are present in the epicardium
along the coronary arteries, serve as the afferent pathways for
angina pectoris. The afferent impulses enter the spinal cord in C8
TABLE 1
Cardiac chest pain
•
•
•
•
•
•
•
Coronary artery disease
cute coronary syndromes
A
3
TABLE 3
Cardiac causes of chest discomfort
•
•
•
•
•
ortic stenosis
A
Aortic regurgitations
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Pulmonary hypertension
TABLE 4
Noncardiac chest pain
Musculoskeletal
• Costochondritis
• Intercostal muscle cramps
• Cervical disk disease
Other causes
• Herpes zoster
• Emotional
• Chest wall tumor
• Disorders of breast
to T4 segments and are transmitted to the sympathetic ganglia of
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Manual of Cardiac Diagnosis
likelihood ratio is 0.2:0.3.2 When chest pain is much localized
and can be indicated by one or two finger tips, it is unlikely
to be angina pectoris.
The radiation of angina pain may be to one or both shoulders,
one or both arms and hands, one or both sides of the neck,
lower jaw and interscapular area. The radiation can also occur
to armpits, epigastrium, and subcostal areas. The radiation is
usually from the center to the periphery (centripetal) and rarely
from the periphery to center (centrifugal). The radiation to one
or both shoulders is associated with the likelihood ratios of
2.3:4.7.2
Patient’s gestures during describing the chest discomfort
have been thought to be useful in the diagnosis of its etiology.
The prevalences, specificities, and positive predictive values of
the Levine sign, the palm sign, the arm sign and the pointing
sign (Figs 1A to D) have been assessed in a prospective obser
vational study.3 The prevalence of the Levine, palm, arm and
pointing signs was 11%, 35%, 16% and 4%, respectively. The
specificities of Levine sign and arm sign were 78% and 86%,
respectively, but the positive predictive values were only 50%
and 55%, respectively. The pointing sign had a specificity of
98% for nonischemic chest discomfort.
The intensity of angina increases slowly and reaches its
peak in minutes, not instantaneously. Similarly, it is relieved
gradually, not abruptly. Analysis of the duration of chest
The effort angina is also relieved by sublingual nitroglycerin.
The time for relief after using nitroglycerin sublingually is
not instantaneous. It takes a few seconds (usually 30 seconds
or longer). It should be appreciated that chest pain due to
esophageal spasm is also relieved by nitroglycerin.
Exposure to cold weather precipitates angina more easily in
patients with classic angina. Similarly, carrying heavy objects
and heavy meals are also frequent precipitating factors. The
character, location and radiation of chest discomfort are similar
in the different clinical subsets of angina. However, some
distinctive features can be recognized in various subsets.
In patients with vasospastic angina, angina occurs at rest
and usually not during exercise. The duration is variable. It
tends to have cyclic phenomenon, and in the individual patient,
it tends to occur more or less at the same time.
In patients with acute coronary syndromes, the duration is
usually longer. In patients with ST segment elevation myocardial
infarction (STEMI), the relief of chest pain may not occur until
reperfusion therapy is established.
The atypical presentations frequently called “anginal
equivalents” are dyspnea, indigestion and belching, and
dizziness and syncope without chest pain. The atypical
presentations are more common in diabetics, women, and the
elderly. A few clinical features of angina are summarized in
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• Usually retrosternal, can be epigastric, interscapular
Localization
• Usually diffuse, difficult to localize
• When is very localized (point sign)—unlikely to be angina
Quality
• Pressure, heaviness, squeezing, indigestion
Radiation
• One or both arms, upper back, neck, epigastrium, shoulder
• Lower jaw (upper jaw, head, lower back, lower abdomen or lower
extremities radiation is not feature of angina )
Duration
• Usually 1–10 minutes (not a few seconds or hours)
Precipitating factors
• Physical activity, emotional stress, sexual intercourse
Aggravating factors
• Cold weather, heavy meals
Relieving factors
• Cessation of activity, nitroglycerin (if relief is instantaneous, it is
unlikely to be angina)
Associated symptoms
• Usually none, occasionally dyspnea
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History
7
• Deep, may be similar to acute coronary syndromes
Associated symptoms
• Tachypnea and dyspnea
Acute aortic dissection
Location
• Chest, back
Quality
• Shearing, tearing
Onset
• Instantaneous
Radiation
• Downwards along the spine
or Specific Activity Scale6 (Table 9). The CCS functional
classification is most frequently used to assess the severity of
angina and has been proven to be useful to assess its prognosis.7
The Specific Activity Scale, which is a more quantitative assess
ment of the severity of angina, is not used in the clinical trials.
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TABLE 8
Canadian Cardiovascular Society (CCS) functional classification
Class I
• Patients can perform to completion any activity requiring 7 metabolic equivalents
Class III
• Patients can perform to completion any activity requiring >2 metabolic equivalents (e.g. shower without stopping, strip and make
bed, clean windows, walk 2.5 mph, bowl, play golf, dress without
stopping), but cannot and do not perform to completion any activities
requiring >5 metabolic equivalents
Class IV
• Patients cannot or do not perform to completion activities requiring
>2 metabolic equivalents. Cannot carry out activities listed above
(Specific Activity Scale Class III)
In patients with suspected or documented coronary artery
disease, inquiries should be made about the risk factors.
The modifiable and nonmodifiable risk factors for atherosclerotic
coronary artery diseases are summarized in Table 10.
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History
9
TABLE 10
Cardiac and pulmonary causes of dyspnea: Differential diagnosis
defined as “labored” breathing. The precise mechanism of dyspnea
has not been established. It has been suggested that activation of
the mechanoreceptors in the lungs, pulmonary artery and heart
and activation of the chemoreceptors are involved in inducing
dyspnea. Dyspnea can occur during exertion (exertional), during
recumbency (orthopnea), or even with standing (platypnea).
There are both cardiac and noncardiac (Table 10) causes of
dyspnea. Pulmonary disease, such as chronic obstructive lung
disease, is one of the common noncardiac causes of dyspnea.
Many patients have both cardiac and pulmonary disease. It
is not uncommon in clinical practice to encounter patients
who have coronary artery disease and chronic obstructive
pulmonary disease. In such patients, to determine the cause
of dyspnea, appropriate history and physical examination
are essential. To distinguish between cardiac and noncardiac
dyspnea, the measurements of serum B-type Natriuretic
Peptide (BNP) or N-Terminal ProBNP (NTBNP) is helpful. In
noncardiac dyspnea, the natriuretic peptide levels are normal,
and in patients with heart failure, they are substantially
elevated.
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Manual of Cardiac Diagnosis
alternating periods of apnea and hyperpnea. During hyperpneic
phases, there is a progressive decrease in PCO2 with increased
pH, which inhibits the respiratory drive; during apneic phase,
CO2 accumulates with an increase in respiratory acidosis, and
the respiratory center is stimulated and breathing is initiated.
It appears that chemoreceptors-mediated stimulation of the
respiratory centers is blunted in patients with Cheyne–Stokes
respiration. Patients feel shortness of breath during the hyperpneic
phase. Central, obstructive, and mixed types of sleep apnea are
observed in patients with heart failure. The hemodynamic causes
of sleep-disordered breathing in heart failure have not been
clearly elucidated. Initially, the Cheyne–Stokes respiration was
thought to be due to low cardiac output;8 however, there does
not appear to be a good correlation between any hemodynamic
changes of systolic heart failure and Cheyne–Stokes respiration.
History of sleep-disordered breathing should be inquired, as it is
associated with worsening heart failure, pulmonary hypertension,
and increased risks of arrhythmias, and sudden cardiac death.
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History
11
Wheezing due to constriction of the bronchial smooth
muscles associated with dyspnea does not always imply
present in both conditions. A plain chest X-ray may be useful
to establish the diagnosis. In patients with pulmonary embolism,
the chest X-ray is clear and does not demonstrate radiologic
evidences of pulmonary venous hypertension. In patients with
hemodynamic pulmonary edema, prominent upper lobe vessels,
perihilar haziness, and Kerley lines and frank pulmonary edema
may be present (Fig. 3).
A careful cardiovascular examination may also reveal the
etiology of dyspnea. For example, evidence of valvular and
myocardial heart diseases suggests cardiac cause of dyspnea
(Table 11). The presence of S3 gallop usually indicates increased
left ventricular diastolic pressures except in young people and
patients with chronic primary mitral regurgitation. In patients
with heart failure, presence of S3 is also associated with the
increased levels of B-type natriuretic peptides. The presence
of characteristic physical findings of significant valvular heart
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FIGURE 3: A plain chest X-ray of a patient with acute severe mitral
regurgitation showing florid hemodynamic pulmonary edema
TABLE 11
Diagnosis of causes of cardiac dyspnea
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