Cardiac Imaging E-Book

• Herausgeber: Thieme
• Kategorie: Fachliteratur
• Sprache: Englisch

Seitenzahl: 824

Veröffentlichungsjahr: 2008

Beschreibung

An excellent atlas on modern diagnostic imaging of the heart

Written by an interdisciplinary team of experts, Cardiac Imaging: A Multimodality Approach features an in-depth introduction to all current imaging modalities for the diagnostic assessment of the heart as well as a clinical overview of cardiac diseases and main indications for cardiac imaging. With a particular emphasis on CT and MRI, the first part of the atlas also covers conventional radiography, echocardiography, angiography and nuclear medicine imaging. Leading specialists demonstrate the latest advances in the field, and compare the strengths and weaknesses of each modality. The book's second part features clinical chapters on heart defects, endocarditis, coronary heart disease, cardiomyopathies, myocarditis, cardiac tumors, pericardial diseases, pulmonary vascular diseases, and diseases of the thoracic aorta. The authors address anatomy, pathophysiology, and clinical features, and evaluate the various diagnostic options.

Key features:

• Highly regarded experts in cardiology and radiology offer image-based teaching of the latest techniques
• Readers learn how to decide which modality to use for which indication
• Visually highlighted tables and essential points allow for easy navigation through the text
• More than 600 outstanding images show up-to-date technology and current imaging protocols

Cardiac Imaging: A Multimodality Approach is a must-have desk reference for cardiologists and radiologists in practice, as well as a study guide for residents in both fields. It will also appeal to cardiac surgeons, general practitioners, and medical physicists with a special interest in imaging of the heart.

Leseprobe

Library of Congress Cataloging-in-Publication Data

Bildgebende Kardiodiagnostik. English

Cardiac imaging: a multimodality approach/edited by Manfred Thelen…

[et al.]; with contributions by N. Abegundewardene…[et al.].

XXp.; XXcm.

Includes bibliographical references and index.

ISBN 978-3-13-147781-1 (alk. paper)

1. Heart--Imaging. 2. Heart--Diseases--Diagnosis. I. Thelen, Manfred. II. Title.

[DNLM: 1. Heart Diseases--diagnosis. 2. Diagnostic Imaging--methods. WG

141 B585c2009a]

RC683.5.I42B5513 2009

616.1'20754–dc22

2008038221

This book is an authorized and revised translation of the German edition published and copyrighted 2007 by Georg Thieme Verlag, Stuttgart, Germany. Title of the German edition: Bildgebende Kardiodiagnostik mit MRT, CT, Echokardiographie und anderen Verfahren.

Translator: Terry Telger, Fort Worth, Texas, USA

Illustrator: Otto Nehren, Achern, Germany

© 2009 Georg Thieme Verlag,Rüdigerstrasse 14,70469 Stuttgart, Germanyhttp://www.thieme.deThieme New York, 333 Seventh Avenue,New York, NY 10001, USAhttp://http://www.thieme.com

Cover design: Thieme Publishing GroupTypesetting by F3 Media, Weil im Schönbuch, GermanyPrinted in Germany by Grammlich, PliezhausenISBN 978-3-13-147781-1        123456

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Contributors

Nico Abegunewardene, MDSecond Medical Clinic and PolyclinicJohannes Gutenberg University HospitalMainz, Germany

Joerg Barkhausen, MDProfessor of RadiologyDepartment of Radiology and Nuclear MedicineUniversity Hospital Schleswig-Holstein, Campus LübeckLübeck, Germany

Andreas Bockisch, MD, PhDProfessor of Nuclear MedicineDepartment of Nuclear MedicineUniversity Hospital EssenEssen, Germany

Frank Breuckmann, MDDepartment of CardiologyWest Germany Heart Center EssenUniversity Hospital EssenEssen, Germany

Christian Bruch, MDMedical Clinic and PolyclinicMuenster University HospitalMuenster, Germany

Oliver Bruder, MDSupervising PhysicianDepartment of CardiologyElisabeth Hospital EssenEssen, Germany

Thomas Buck, MD, FACC, FESCAssociate Professor and Supervising PhysicianDepartment of CardiologyWest Germany Heart Center EssenEssen University HospitalEssen, Germany

Holger Eggebrecht, MD, FESCSupervising PhysicianDepartment of CardiologyWest Germany Heart Center EssenUniversity Hospital of EssenEssen, Germany

Raimund Erbel, MDProfessor of CardiologyDepartment of CardiologyWest German Heart Center EssenUniversity Hospital EssenEssen, Germany

Christoph U. Herborn, MD, MBAAssociate Professor of RadiologyUniversity Medical Center Hamburg-EppendorfHamburg, Germany

Georg Horstick, MDAssociate Professor of CardiologyHead of PharmacologySanofi-Aventis Deutschland GmbHTD Cardiovascular DiseasesFrankfurt, Germany

Peter Hunold, MDSupervising PhysicianDepartment of Diagnostic and Interventional Radiologyand NeuroradiologyUniversity Hospital EssenEssen, Germany

Katja Koch, MDSpecialistClinic and Polyclinic for Diagnostic and InterventionalRadiologyJohannes Gutenberg University HospitalMainz, Germany

Karl-Friedrich Kreitner, MDProfessor of RadiologyClinic and Polyclinic for Diagnostic and InterventionalRadiologyJohannes Gutenberg University HospitalMainz, Germany

Sebastian Ley, MD, SpecialistClinic and Polyclinic for Diagnosticand Interventional RadiologyRuprecht Karl University HospitalHeidelberg, Germany

Annett Magedanz, MD, SpecialistBethany Cardiovascular CenterFrankfurt, Germany

Kai Nassenstein, MDSpecialistDepartment of Diagnostic and InterventionalRadiology and NeuroradiologyUniversity Hospital EssenEssen, Germany

Bjoern Plicht, MDDepartment of CardiologyWest Germany Heart Center EssenUniversity Hospital EssenEssen, Germany

Sandra Julia Rosenbaum-Krumme, MDSupervising PhysicianDepartment of Nuclear MedicineUniversity Hospital EssenEssen, Germany

Katherine Sattler, MDDepartment of CardiologyWest Germany Heart Center EssenUniversity Hospital EssenEssen, Germany

Thomas Schlosser, MDSupervising PhysicianDepartment of Diagnostic and InterventionalRadiology and NeuroradiologyUniversity Hospital EssenEssen, Germany

Axel Schmermund, MD, FESCAssociate Professor of CardiologyBethany Cardiovascular CenterFrankfurt, Germany

Wolfgang Schreiber, MDProfessor and Head of Medical Physics SectionClinic and Polyclinic for Diagnostic andInterventional RadiologyJohannes Gutenberg University HospitalMainz, Germany

Manfred Thelen, MDProfessor Emeritus of RadiologyJohannes Gutenberg University HospitalMainz, Germany

Thomas Voigtlaender, MDAssociate Professor of CardiologyBethany Cardiovascular CenterFrankfurt, Germany

Markus Vosseler, MDSecond Medical Clinic and PolyclinicJohannes Gutenberg University HospitalMainz, Germany

Kai-Uwe Waltering, MDSupervising PhysicianClinic for Diagnostic and Interventional RadiologyHospital Essen-MitteEssen, Germany

Preface

Diagnostic imaging of the heart has a long tradition in Germany, starting over a century ago with the discovery of Wilhelm Conrad Röntgen, which forms the basis for all radio-graphic techniques of cardiac imaging. Another milestone was the development of cardiac ultrasonography, which began in Germany during the 1940s and was perfected by Edler and Hertz, who recorded the first tracings of the heart based on ultrasound reflection. Professor Sven Effert introduced the method in Germany and was instrumental in gaining national and international recognition. Other key milestones were the development of computed tomography and magnetic resonance imaging.

The creation of this book was motivated by a desire to combine expert knowledge from the two medical specialties of cardiology and radiology, which have been responsible for tremendous advances in the diagnosis of heart diseases.

A third essential field in developing cardiac imaging is medical physics, which has fostered fascinating developments based on work that gained several Nobel Prize awards to physicists. Equally essential is the sectional imaging triad of echocardiography, computed tomography, and magnetic resonance imaging, whose basic physical principles have contributed to the current worldwide high level of development through systematic advances in medical technology.

Against this background of innovations and advances, it has been a genuine pleasure for the editors and authors to compile a synopsis of modern cardiac imaging and summarize the advances in this field, which are most clearly reflected in sectional imaging modalities. The new role of nuclear medicine imaging(PET-CT) is also considered in this context. Despite the profound insights that modern techniques have provided into the pathological anatomy of the heart and especially its function, conventional radiographs are far from obsolete and are available for almost every patient. Radiographs should not be ordered indiscriminately, however; this relatively low-cost and well-tolerated study should be applied critically and selectively. Recognizing that decades of experience in the analysis of chest radiographs should be fully exploited, we open this book by reviewing the basic aspects of conventional radiography.

It takes more than a detailed knowledge of sectional imaging studies to maintain high medical standards and obtain certification. It is also necessary to have well-planned organizational and communication structures within and among the different specialties as well as a command of current and traditional knowledge in order to achieve a true “state of the art status.”

Manfred ThelenRaimund ErbelKarl-Friedrich KreitnerJoerg Barkhausen

Acknowledgments

Even in the age of internet-based media, the printed page still has an undisputed role in medical education. Information technology is less a competitor of books than a tool to enhance the visual impact of a book and make its zcontents more accessible to the reader.

Cardiac Imaging takes full advantage of these modern capabilities, particularly in its illustrations, which were processed with the aid of digital image processing techniques.

This has all been made possible by the ambitious and dedicated support of Thieme Medical Publishers under the direction of Dr. Abert Hauff and his colleagues. The editors and authors express special thanks to the project manager of this book, Ms. Susanne Huiss, and to Ms. Martina Dörsam, who was responsible for production of the book. We are also grateful to Dr. Christian Urbanowicz, who outlined the cost parameters for the book so that it could be presented in its current form.

The editors and authors thank all of our colleagues at hospitals and other institutions who helped compile the superb illustrations for this book. We are grateful to the entire staff at the Echocardiography Laboratory of the Department of Cardiology, University of Essen, and especially to Ms. Christiane Plato, the medical technologist at that institution. We extend special thanks to our colleagues Björn Plicht, Alexander Lind, Philip Kahlert, and Dirk Böse for their help in compiling the illustrations.

Dr. Peter Hunold Dr. Thomas Schlosser, Ms. Lena Schäfter, and Mr. Kai Reiter of the Department of Diagnostic and Interventional Radiology, Essen University Hospital, were instrumental in the preparation of this book, and their help is gratefully acknowledged.

We express thanks to Ms. Ine Mayer and Ms. Josefine Kestel, radiology technologists at the Department of Diagnostic and Interventional Radiology university hospital Mainz, and we thank our photographer, Ms. Anne Marie Keuchel, for her conscientious and dedicated work.

Manfred ThelenRaimund ErbelKarl-Friedrich KreitnerJoerg Barkhausen

Abbreviations

Note: Abbreviations used in the illustrations are explained in this list of abbreviations. Abbreviations used in the text and tables are also listed. Any abbreviation used without explanation may be identified in this list. For clarity and as an aide-memoire, some abbreviations are expanded at their use within the text.

ABI

Ankle-brachial index

ACB

Aorto coronary bypass

ACE

Angiotensin-converting enzyme

ACVB

Aortocoronary venous bypass

AHA

American Heart Association

AI

Aortic insufficiency

AIDS

Acquired immuno deficiency syndrome

AMI

Acute myocardiac infarction

AML

Anterior mitral valve leaflet

Ao

Aorta

Ao asc.

Ascending aorta

Ao desc.

Descending aorta

A-P

Anteroposterior

ARDS

Acute respiratory distress syndrome

ARVC

Arrhythmogenic right ventricular cardiomyopathy

ARVD

Arrhythmogenic right ventricular dysplasia

AS

Aortic stenosis

ASD

Atrial septal defect

A. subc.

Subclavian artery

AoV

Aortic valve

A.U.

Arbitrary units

AV

Arteriovenous/aortic valve

AV fistula

Arterio venous fistula

AVM

Arterio venous malformation

AVOA

Aortic valve orifice area

BCT

Brachiocephalic trunk

BMI

Body mass index

bpm

Beats per minute

BSA

Body surface area

bw

Body weight

CA

Cardiac apex

CAD

Coronary artery disease

CEMRA

Contrast-enhanced MR angiography

CEMRI

Contrast-enhanced MR imaging

CFR

Coronary flow reserve

CHD

Coronary heart disease

CNR

Contrast-to-noise ratio

CO

Cardiac output

CoA

Coarctation of the aorta

COPD

Chronic obstructive pulmonary disease

CRP

C-reactive protein

CSA

Cross-sectional area

CT ratio

Cardiothoraci cratio

CT

Computed tomography, computed tomogram

CTA

CT angiography

CTCA

CT coronary angiography

CTEPH

Chronic thrombo embolic pulmonary hypertension

CVP

Central venous pressure

CW Doppler

Continuous-wave Doppler

DA

Direct angiography

DCM

Dilated cardiomyopathy

DD

Differential diagnosis

DSA

Digital subtraction angiography

DSCT

Dual-source computed tomography

EBCT

Electron-beam computed tomography

ECG

Electrocardiogram

EDD

End-diastolic diameter

EDV

End-diastolic volume

EF

Ejection fraction

EPSS

E-point septal separation (in echocardiography)

EROA

Effective regurgitant orifice area

ESD

End-systolic diameter

ESV

End-systolic volume

Fr

French [gauge]

FA

Flip angle

FDG

Fluorodeoxyglucose

FFR

Fractional flow reserve

FFRmyo

Fractional myocardial flow reserve

FFT

Fast Fourier transform

FL

False lumen

FLASH

Fast low-angle shot

FOV

Field of view

FS

Fat saturation, fractional shortening

GEA

Gastroepiploic artery

Gd

Gadolinium

Gd-BOPTA

Gadolinium benzyloxy propionic tetraacetate

Gd-DOTA

Gadolinium tetraazacy clodode canete traacetic acid

Gd-DTPA

Gadolinium diethylenetriamine pentaacetic acid

GE

Gradient echo

GRAPPA

Generalized autocalibrating partially parallel acquisition

HASTE

Half-Fourier acquisition single-turbo spin echo

HCM

Hypertrophic cardiomyopathy

HIV

Human immunodeficiency virus

HNCM

Hypertrophic nonobstructive cardiomyopathy

HOCM

Hypertrophic obstructive cardiomyopathy

HR

Heart rate

HU

Hounsfield unit

IAS

Interatrial septum, atrial septum

ICD

Intracoronary Doppler ultrasound

ICU

Intensive care unit

IMA

Internal mammary artery

IMH

Intramural hematoma

IRGRE

Inversion recovery-gradient echo

IR

Inversion recovery

IRAD

International Registry of Aortic Dissection

IRP

Isovolumic relaxation period

ISFC

International Society and Federation of Cardiology

IV

Intravenous

IVS

Interventricular septum

IVUS

Intravascular ultrasound

LA

Left atrium

LAO

left anterior oblique

LA pressure

Left atrial pressure

LAD

Left anterior descending coronary artery

LBBB

left bundle branch block

LCA

Left coronary artery

LCC

left coronary cusp

LCX

Left circumfle xartery

LE

Late enhancement

LIMA

Left internal mammary artery

LV

Left ventricle, left ventricular

LVEDP

Left ventricular end-diastolic pressure

LVEDV

Left ventricular end-diastolic volume

LVEF

Left ventricular ejection fraction

LVESD

Left ventricular end-systolic diameter

LVESV

Left ventricular end-systolic volume

LVNC

Left ventricular non compaction

LVOT

Left ventricular outflow tract

LVSV

Left ventricular stroke volume

MaxPG

Maximum pressure gradient

MBF

Myocardial blood flow

MCE

Myocardial contrast echocardiography

MI

Mitral insufficiency; myocardial infarction

MIBG

Metaiodobenzylguanidine

MIBI

Methoxyisobuty lisonitrile

MIP

Maximum intensity projection

MM

Myocardial mass

MO

Microvascular obstruction

MPG

Mean pressure gradient

PI

Myocardial performance index

PR

Multiplanar reformatting

PRI

Myocardial perfusion reserve index

RA

MR angiography

RCA

MR coronary angiography

R

Magnetic resonance

RI

Magnetic resonance imaging

S

Mitral stenosis

S-CT

Multislice CT

Sv

Millisievert

V

Mitral valve

VA/MVOA

Mitral valve orifice area

NCC

Noncoronary cusp

OCT

Optical coherence tomography

OSAS

Obstructive sleep apnea syndrome

PA

Pulmonary artery

P-A

Posteroanterior

PAI

Plasminogen activator inhibitor

PAOD

Peripheral arterial occlusive disease

PAP

Pulmonary arterial pressure

PAPVC

Partial anomalous pulmonary venous connection

PAS

Pulmonary arterial sarcoma

PAU

Penetrating aortic ulcer

PAVM

Pulmonary arteriovenous malformation

PCH

Pulmonary capillary hemangioma

PE

Pericardial effusion

PEA

Pulmonary endarterectomy

PET

Positron emission tomography

PFO

Patent foramen ovale

PH

Pulmonary hypertension

PHT

Pressure half-time

PI

Pulmonary valve insufficiency, pulmonary insufficiency

PISA

Proximal isovelocity surface area

PIVB

Posterior interventricular branch of right coronary artery

PLVED

Pressure in left ventricle at end diastole (left ventricular end-diastolic pressure)

PL

Pleural effusion

PLB

Posterolateral branch

PML

Posterior mitral valve leaflet

PPG

Peak pressure gradient

P(RA)

Right atrial pressure

PROCAM

Prospective Cardiovascular Münster Study

PRVED

Pressure in right ventricle at end diastole (right ventricular end-diastolic pressure)

PSIR

Phase-sensitive inversion-recovery

PTCA

Percutaneous transluminal coronary angioplasty

PTE

Pulmonary thromboendarterectomy

PV

Pulmonary vein, pulmonary valve

PVS

Pulmonary venous sarcoma

PW

Posterior wall

PW Doppler

Pulsed-wave Doppler

QP

Pulmonary circulation

QS

Systemic circulation

RA

Right atrium

RA pressure

Right atrial pressure

RAO projection

Right anterior oblique projection

RAP

Right atrial filling pressure

RCA

Right coronary artery

RCC

Right coronary cusp

RCM

Restrictive cardiomyopathy

RCX

Circumflex coronary artery

RF

Radiofrequency

RIMA

Right internal mammary artery

rMBF

Regional myocardial blood flow

rMBV

Regional myocardial blood volume

ROI

Region of interest

RstAC

Rest attenuation corrected

RV

Right ventricle

RVEDV

Right ventricular end-diastolic volume

RVEF

Right ventricular ejection fraction

RVESV

Right ventricular end-systolic volume

RVOT

Right ventricular outflow tract

SAM

Systolic anterior motion

SAR

Specific absorption rate (W/kg)

SE

Spin echo

SENSE

Sensitivity encoding

SNR

Signal-to-noise ratio

SPAMM

Spatial modulation of magnetization

SPAP

Systolic pulmonary arterial pressure

SPECT

Single-photon emission computed tomography

SPGR

Fast spoiled gradient-echo acquisition

Spiral CT

Spiral computed tomography

SR

Saturation recovery

SSFP

Steady-state free precession

STIR

Short-tau inversion recovery

StrAC

Stress attenuation corrected

SV

Stroke volume

SVC

Superior vena cava

T

Tesla

T2 prep

T2 preparation pulse

TA

Acquisition time

TAA

Thoracic aortic aneurysm

TAPVC

Total anomalous pulmonary venous connection

TASH

Transcoronary ablation of septal hypertrophy

Tc

Technetium

TDE

Tissue Doppler echocardiography

TDI

Tissue Doppler imaging

TE

Echo time

TEE

Transesophageal echocardiography

TEI

Time ejection index

TI

Inversion time, tricuspid insufficiency

TL

True lumen

TlCl

Thallium chloride

TP

Pulmonary trunk

TR

Repetition time

TS

Tricuspid stenosis

TSE

Turbo spin echo

TTE

Transthoracic echocardiography

TV

Tricuspid valve

TVI

Tricuspid valve insufficiency

VCATS

Volume coronary angiography with targeted scans

VCi

Inferior vena cava

VCs, Vcs

Superior vena cava

Venc

Encoding velocity

Vm

Mean velocity

Vmax

Maximum velocity

VOA

Valve orifice area

VR

Volume rendering

VRT

Volume rendering technique

VSD

Ventricular septal defect

VTI

Velocity-time integral

WHO

World Health Organization

WMSI

Wall motion score index

Contents

I Imaging Modalities

1 Conventional Radiography

M. Thelen

Clinical Manifestations of Heart Diseases

Radiographic Anatomy

Radiographic Technique

Enlargement of the Cardiac Chambers

Radiographic Determination of Cardiac Size

Cardiac Hypertrophy and Dilatation

Importance of Pulmonary Vasculature in Cardiac Diagnosis

Lymphatic System

Pleural Effusion

Cardiac Malposition

Heart Failure

Coronary Heart Disease

Cardiomyopathies

Systemic Hypertension

Pulmonary Arterial Hypertension (Cor pulmonale)

Pericardium

Aorta

2 Echocardiography

R. Erbel

Basic Principles of Echocardiography

Basic Principles of Ultrasound Imaging

Types of Echocardiography

Specific Applications of Echocardiography

Contrast Echocardiography

Stress Echocardiography

Transesophageal Echocardiography

Intraoperative Echocardiography

Intracardiac Echocardiography

Examination Techniques

Transthoracic Echocardiography

Transesophageal Echocardiography

Quantification Using M-Mode and 2D Echocardiography

M-Mode Echocardiography

Two-Dimensional Echocardiography

Principles of Doppler Echocardiography

Pulsed Doppler

Continuous-Wave Doppler

Color Doppler

Color Doppler M-Mode Echocardiography

Tissue Doppler Echocardiography

Reference Values for Doppler Echocardiography

Strain Rate Imaging

Echocardiographic Assessment of Hemodynamics

Stroke Volume

Regurgitant Volume

Shunt Flow

Pressure Gradients

Valve Orifice Area

Intracardiac Pressures

Assessment of Left Ventricular Function

Global Left Ventricular Function

Assessment of Regional Ventricular Function

Diastolic Ventricular Function

Grade I Diastolic Dysfunction

Grade II Diastolic Dysfunction

Grade III Diastolic Dysfunction

Grade IV Diastolic Dysfunction

3 Angiography

H. Eggebrecht

Cardiac Catheterization Technique for Pressure and Oxygen Measurements and for Angiocardiography

Cardiac Catheterization Measurements

Pressure Measurements

Oxygen Saturation Measurements

Cardiac Output and Derivative Parameters

Detection of Shunt Lesions

Selective Angiocardiography

Coronary Angiography

Special Invasive Imaging Techniques

Intravascular Ultrasound

Intracoronary Doppler

Intracoronary Pressure Wire

4 Nuclear Medicine Imaging

A. Bockisch, K. Sattler, and S. J. Rosenbaum-Krumme

Basic Principles

Myocardial Scintigraphy

Examination Technique

Tracers

Interpretation of Scintiscans

Clinical Significance of Myocardial Scintigraphy

Positron Emission Tomography

Examination Technique

Tracers

Interpretation of PET

Clinical Significance of PET

Special Nuclear Medicine Studies

MIBG Scintigraphy

Plaque Imaging

5 Computed Tomography

Coronary Calcium Determination

A. Schmermund, Th. Schlosser, A. Magedanz, and Th. Voigtländer

Examination Techniques

Interpretation

Scanning Protocol

Reporting of Coronary Calcium Findings

Outlook

CT Coronary Angiography

Th. Schlosser

Principle of Computed Tomography

Patient Preparation

Planning the Examination

Contrast Media

Examination Technique

Interpretation

Clinical Applications

CT Angiography of the Great Vessels

K. Koch

Basic Physical Principles

Methodological Requirements

Examination and Analysis Techniques

Clinical Applications

6 Magnetic Resonance Imaging

K. Nassenstein

Planning the Examination

System Requirements

Patient Preparation

Pulse Sequences

Planning the Examination

Basic Protocol for Cardiac MRI

Extended Scan Protocol

Morphology

K.-U. Waltering

Pulse Sequences

Steady-State Free-Precession Sequences

Normal Anatomy

Variants and Anomalies

Function

S. Ley and K.-F. Kreitner

Analysis of Cardiac Function

Flow Measurement

Myocardial Perfusion

W. G. Schreiber

Physiology

Principle of Perfusion MRI

Applications

Comments on Methodology

Delayed Enhancement

P. Hunold

Pathophysiology of Delayed Enhancement

Pulse Sequences

Protocol for Delayed-Enhancement Imaging

Delayed Enhancement—From Image to Differential Diagnosis

Magnetic Resonance Angiography of the Coronary Arteries

C. U. Herborn

Planning the Examination

Compensation for Cardiac Motion

Compensation for Respiratory Motion

Contrast Mechanisms in Coronary Magnetic Resonance Angiography

Contrast Agents for Coronary Magnetic Resonance Angiography

Clinical Applications

Magnetic Resonance Angiography of the Great Vessels

K.-F. Kreitner

Basic Technical Principles

Techniques of Examination and Interpretation

Clinical Applications

II Imaging of Specific Cardiac Diseases

7 Heart Defects and Endocarditis

T. Buck, B. Plicht, T. Schlosser, and R. Erbel

Congenital Heart Disease in Adults

Atrial Septal Defect

Patent Foramen Ovale

Ventricular Septal Defect

Acquired Valvular Heart Disease

Mitral Stenosis

Mitral Insufficiency

Aortic Stenosis

Aortic Insufficiency

Combined Mitral and Aortic Valve Disease

Tricuspid Stenosis

Tricuspid Insufficiency

Pulmonary Valve Stenosis

Pulmonary Insufficiency

Prosthetic Heart Valves

8 Coronary Heart Disease

Subclinical Signs of Coronary Atherosclerosis (Prevention, Screening, and Risk Stratification)

R. Erbel

Early Detection of Coronary Heart Disease

Pathogenesis of Atherosclerosis

Detection of Subclinical Atherosclerosis

Detection of Complicated Plaques

Preventive Cardiology

Acute Ischemia

G. Horstick, N. Abegunewardene, M. Vosseler, and K.-F. Kreitner

Pathophysiology of Myocardial Ischemia in Relation to Cardiac MRI

Viability Assessment in Cardiac MRI

Chronic Coronary Artery Disease

P. Hunold and F. Breuckmann

Pathophysiology of Chronic Coronary Artery Disease

Clinical Features

Diagnosis of Chronic Coronary Artery Disease

Differential Diagnosis of Stenotic Coronary Heart Disease

Postoperative and Postinterventional Imaging

K.-F. Kreitner and G. Horstick

Postoperative Imaging

Postinterventional Imaging

9 Cardiomyopathies and Myocarditis

O. Bruder, R. Erbel, and K.-F. Kreitner

Cardiomyopathies

Hypertrophic Cardiomyopathy

Restrictive Cardiomyopathy

Arrhythmogenic Right Ventricular Cardiomyopathy

Unclassified Cardiomyopathies

Myocarditis

10 Cardiac Tumors

J. Barkhausen and H. Eggebrecht

Diagnostic Techniques

Benign Primary Cardiac Tumors

Myxoma

Cardiac Lipoma

Papillary Fibroelastoma

Cardiac Hemangioma

Pheochromocytoma

Rhabdomyoma

Fibroma

Lymphangioma

Teratoma

Malignant Primary Cardiac Tumors

Angiosarcoma

Other Primary Cardiac Sarcomas

Primary Cardiac Lymphoma

Pericardial Mesothelioma

Rhabdomyosarcoma

Secondary Cardiac Tumors

Metastases

Direct Extension

Nonneoplastic Cardiac Masses

Intracardiac Thrombi

Aneurysms

Anatomical Variants

11 Diseases of the Pericardium

C. U. Herborn, C. Bruch, and R. Erbel

Anatomy

Imaging Modalities

Chest Radiographs

Echocardiography

Computed Tomography

Magnetic Resonance Imaging

Specific Diseases

Pericardial Cysts and Diverticula

Pericarditis

Constrictive Pericarditis

Malignant Pericardial Diseases

Pericardial Aplasia

12 Diseases of the Great Pulmonary Vessels

S. Ley, K.-F. Kreitner, and G. Horstick

Pulmonary Arterial Disorders

Acute Pulmonary Embolism

Chronic Recurrent Pulmonary Embolism

Other Forms of Pulmonary Arterial Hypertension

Tumors of the Pulmonary Vessels

Pulmonary Capillary Hemangioma

Arteriovenous Malformations

Pulmonary Venous Disorders

Congenital Anomalies

Acquired Pulmonary Venous Disorders

Extravascular Disorders

13 Diseases of the Thoracic Aorta

H. Eggebrecht, J. Barkhausen, and K.-F. Kreitner

Congenital Anomalies

Right Descending Aorta

Double Aortic Arch

Aortic Arch Anomalies

Coarctation of the Aorta

Acquired Aortic Diseases

Degenerative Aortic Diseases

Acute Aortic Syndrome

Inflammatory Aortic Diseases

Index

I Imaging Modalities

1 Conventional Radiography

Clinical Manifestations of Heart Diseases

Radiographic Anatomy

2 Echocardiography

Basic Principles of Echocardiography

Basic Principles of Ultrasound Imaging

Specific Applications of Echocardiography

Examination Techniques

Quantification Using M-Mode and 2D Echocardiography

Principles of Doppler Echocardiography

Echocardiographic Assessment of Hemodynamics

Assessment of Left Ventricular Function

Diastolic Ventricular Function

3 Angiography

Cardiac Catheterization Technique for Pressure and Oxygen Measurements and for Angiocardiography

Cardiac Catheterization Measurements

Selective Angiocardiography

Coronary Angiography

Special Invasive Imaging Techniques

4 Nuclear Medicine Imaging

Basic Principles

Myocardial Scintigraphy

Positron Emission Tomography

Special Nuclear Medicine Studies

5 Computed Tomography

Coronary Calcium Determination

CT Coronary Angiography

CT Angiography of the Great Vessels

6 Magnetic Resonance Imaging

Planning the Examination

Morphology

Function

Myocardial Perfusion

Delayed Enhancement

Magnetic Resonance Angiography of the Coronary Arteries

Magnetic Resonance Angiography of the Great Vessels

1 Conventional Radiography

M. Thelen

Clinical Manifestations of Heart Diseases

In cardiology as in other specialties, the indication for examining the heart is based on patient complaints.1–8 In this section the main clinical manifestations of heart diseases are briefly reviewed from a differential diagnostic standpoint. Conventional X-ray films of the chest, or projection radiographs, are a basic tool in the differential diagnostic investigation of these symptom complexes.8

Chest Pain

This complaint is almost always related to heart disease. It typically induces fear of an imminent life-threatening heart attack. If the pain is of brief duration, it is referred to as a typical episode of angina pectoris.

Essential Point

Approximately one-third of patients with myocardial ischemia, especially diabetics, do not experience chest pain.

If the pain lasts longer than 15 minutes, extracardiac causes should also be considered. The differential diagnosis of chest pain is thus highly complex:

• Angina pectoris (myocardial ischemia), myocardial infarction

• Hypertrophic cardiomyopathy

• Dilated cardiomyopathy

• Arrhythmias

• Acute pericarditis (pericarditis sicca)

• Mitral valve prolapse

• Aortic aneurysm

• Aortic dissection

• Massive pulmonary embolism

• Small or moderate pulmonary embolism combined with pulmonary infarction

• Pneumothorax

• Pleuritis sicca

• Pneumonia

• Broad range of esophageal disorders

• Broad range of musculoskeletal disorders

• Broad range of abdominal diseases in which pain is projected to the chest

• Neurogenic diseases (neuralgia, radicular syndromes, herpes zoster)

• Functional cardiac complaints

The differential diagnosis of chest pain is extremely challenging. The establishment of a chest pain unit in the emergency room, chiefly in university hospitals, is an initiative aimed at addressing this problem.

Edema

Edema results from an imbalance between the quantity of fluids, salts, and proteins which leave and re-enter the capillary system. It may be a manifestation of heart disease. A classic example is biventricular heart failure, which may develop as a result of myocardial, pericardial, or valvular heart disease, as well as of other cardiac lesions.

Dyspnea

Dyspnea, or respiratory distress, is characterized by very different degrees of severity; it may occur during rest or exercise, and may be position-dependent (orthopnea) or may present as an abnormal respiratory pattern. The underlying cause may be a disturbance of ventilation, gas exchange, or lung perfusion.

In addition to pulmonary causes, various cardiac abnormalities may be the underlying symptoms of respiratory distress. Possible causes include pulmonary outflow obstruction or left-sided heart failure as a result of myocardial, valvular, or coronary heart disease.

Cyanosis

Cyanosis is a reflection of insufficient pulmonary oxygen uptake or peripheral oxygen depletion. Pulmonary cyanosis may be caused by:

• Ventilatory impairment

• Diffusion impairment

• Increased intrapulmonary venous admixture of blood in unventilated but perfused lung areas, or the arteriovenous shunting of blood.

Cardiac central cyanosis may be caused by:

• Congenital heart defects with a right-to-left shunt

• Congenital defects with decreased pulmonary blood flow

These heart defects lead to central cyanosis. This condition is to be distinguished from peripheral cardiac cyanosis, in which cardiac output is reduced by myocardial insufficiency or caused by congestion, e. g., mitral stenosis).

Arrhythmias

Tachycardiac arrhythmias are present when the rate of ventricular contractions increases to 100 bpm or more. They may occur in association with:

• Primary defects of the impulse conduction system (e. g., congenital anomalies)

• Coronary heart disease

• Myocardial diseases

• Valvular heart diseases

• Severe left ventricular dysfunction

• Pericardial diseases

• Right ventricular dysplasia (cardiomyopathy)

Hypertension

The potential causes of hypertension are extremely diverse. The most important causes are listed below:

• Decreased elasticity of the aorta and great vessels due to atherosclerosis

• Coarctation of the aorta

• Conditions causing an increase in stroke volume and cardiac output

• Heart failure

• Renal causes

Over time, all of these conditions lead to cardiac symptoms which may be reflected in a change in the cardiac silhouette.

Hypotension

Primary forms of cardiac hypotension result from a decrease in cardiac output due to

• Impaired myocardial contractility (heart failure)

• Cardiac arrhythmias (bradycardiac and tachycardiac)

• Impaired diastolic filling of the heart

• Valvular heart disease

The most common form of acute cardiac hypotension is cardiogenic shock due to myocardial infarction or severe heart failure. Chronic cardiovascular forms of hypotension are associated with the following conditions:

• Aortic valve disease

• Mitral valve disease

• Aortic arch syndrome

• Constrictive pericarditis

Syncope

Brief syncopal episodes lasting 1 minute or less may have a cardiac cause. The cause may be mechanical, relating to abnormalities of left ventricular emptying or filling. Syncope may also result from septal defects (including atrial septal defects), as well as thrombus formation in the left atrium associated with mitral stenosis.

The following mechanical causes of syncope can be differentiated by imaging studies:

• Abnormalities of left ventricular emptying

• Abnormalities of left atrial emptying

• Aortic stenosis

• Hypertrophic obstructive cardiomyopathy

• Heart failure

• Myocardial infarction

Conventional radiography continues to have an established place even with the availability of modern electrophysiology, echocardiography, invasive cardiac testing, and sectional imaging modalities such as CT and MRI, although its role needs to be redefined.9–18 Thus, sophisticated cardiological tests are not state of the art unless standard biplane chest films are also obtained. Radiographs are also widely used in the follow-up of cardiac status. This applies to the follow-up of conservative and interventional therapies and, in particular, to preoperative treatment planning or perioperative monitoring and follow-up after surgical intervention.6,19–21

The information necessary for understanding and interpreting a normal chest radiograph is derived from specific pathophysiological parameters that are based on changes in hemodynamics.

Radiographic Anatomy

The standard projections for cardiac radiography are the frontal (posteroanterior, P-A) projection and the left lateral projection (with an esophagogram). A plain radiograph of the heart is a summation image of the individual cardiac chambers. The cardiac borders and their shape changes are therefore the sole indicators in determining the location of the individual cardiac chambers and assessing their size in radiographs. The structures that form the borders of the heart cannot always be conclusively identified, even when all standard views are obtained (Fig. 1.1).22

Frontal (P-A) Radiograph

The following structures normally form the cardiac borders in the frontal radiograph:

• Left side of mediastinum (from above downward):

– Distal portion of the aortic arch

– Main pulmonary artery trunk

– Left atrial appendage (part of the left atrium)

– Left ventricle

• Right side of mediastinum (from above downward):

– Superior vena cava

– Right atrium

The protrusion located below the aortic arch on the P-A radiograph is termed the pulmonary segment. This is an arch-shaped structure formed by the pulmonary trunk and not by the conus pulmonalis, which is located below the pulmonary valves. The pulmonary segment may be very prominent owing to dilatation of the pulmonary artery.

Lateral Radiograph

The lateral radiograph shows the following topography:

• Anterior structures (from above downward):

– Ascending aorta

– Pulmonary trunk

– Right ventricle

Fig. 1.1a, b Diagrammatic representation of the radiographic anatomy of the heart.

a P-A radiograph.

b Lateral radiograph.

The retrosternal space normally appears as a narrow space between the anterosuperior border of the heart and the anterior chest wall.

• Posterior structures (from above downward):

– Descending aorta and pulmonary vessels

– Left atrium

– Left ventricle

– Inferior vena cava

The space between the posterior cardiac border and vertebral column represents the retrocardiac space. The space bounded by the left atrium, vertebral column, and aortic arch (superior vascular pedicle) is called the aortic window. If the aortic window is notably devoid of structures, this indicates the presence of small main pulmonary arteries. The close relationship between the esophagus and left atrium explains why an enlarged left atrium causes circumscribed posterior displacement of the esophagus in the lateral chest radiograph.

Given the typical location and arrangement of the cardiac chambers, the enlargement of specific chambers may produce characteristic changes in the size and shape of the cardiac silhouette that can be identified in the various projections.23–25

Radiographic Technique

P-A View

Conventional radiographic examination of the heart begins with a P-A projection, which is obtained when the patient is first admitted. A left lateral radiograph at full inspiration shows an overview of the anterior and posterior cardiac borders and may yield important information on the relative sizes of the cardiac chambers.26

Oblique Views24

Today, the traditional right anterior oblique (RAO) and left anterior oblique (LAO) views of the chest are important only in angiocardiography. They are no longer included in a standard radiographic series.

Contrast Radiography of the Esophagus

Oral contrast radiography of the esophagus, especially in the lateral projection, is useful for evaluating the position of the aortic arch, the course of the descending aorta, and anomalies of the aortic arch vessels. It is also useful in the assessment of the size of the left atrium on the posterior border of the heart.

Preliminary Fluoroscopy27,28

Cardiac fluoroscopy, in which different projections are obtained by rotating the patient, is used to screen for cardiac calcifications and to evaluate the motion of the cardiac borders. Despite its demonstrable value, fluoroscopy is rarely included in routine cardiac imaging. It can supply information on:

• Severely calcified coronary vessels

• Calcified cardiac valves

• Calcifications of the myocardium, pericardium, or fibrous ring

• Movement and location of implanted pacemaker leads

• Wobbling or other instability of implanted valves or valve rings (Fig. 1.2)

Enlargement of the Cardiac Chambers

Right Ventricle

P-A View When the right ventricle is enlarged, it expands upward in the direction of its outflow tract and from right (posterior) to left (anterior), and to the side (Fig. 1.3). This displaces the pulmonary artery upward, causing it to occupy most of the concavity of the cardiac waist in the P-A view. This type of cardiac silhouette is referred to as a right ventricular configuration. It is a common normal finding in children and is very infrequently found in healthy adolescents and adults. At the same time, the associated rotation of the heart toward the left side shifts the left ventricle more or even completely toward the posterior side of the heart. The right ventricle may expand on the anterior side of the heart and, in rare cases, forms the left border of the cardiac silhouette (Fig. 1.4).

Fig. 1.2a–f Sites of occurrence of intracardiac calcifications (diagrammatic representation).

a Calcified mitral valve annulus; P-A and lateral views.

b Calcification of the aortic and mitral valve; lateral view.

c Calcification of the LAD and left coronary artery; RAO view.

d Calcification of the left atrial wall; P-A and lateral views.

e Calcification of the pericardium, calcifying pericarditis; P-A and RAO views.

f Calcified myocardial aneurysm; P-A view.

Essential Point

Dilatation of the right ventricle rotates the heart to the left, shifting the left ventricle posteriorly about the cardiac axis.

Lateral View In the left lateral view, dilatation of the right ventricle leads to narrowing and obliteration of the retrosternal space. This is considered a reliable sign of right ventricular enlargement. When enlargement is extreme, the left ventricle is shifted so far posteriorly that it may cause narrowing of the retrocardiac space near the diaphragm (Fig. 1.5).

Left Ventricle29–31

P-A View Enlargement of the left ventricle expands the heart downward, backward, and toward the left side. The cardiac silhouette in the P-A view appears broadened, and the cardiac waist is accentuated. This pattern is generally described as an aortic or left ventricular configuration. With few exceptions (congenital heart defects, e. g., Fallot-type cardiac anomalies), it is typical of left ventricular enlargement (Figs. 1.6, 1.7).

Fig. 1.3a, b Change in cardiac shape caused by pronounced enlargement of the right ventricle.

a P-A radiograph.

b Lateral radiograph.

Fig. 1.4 Diagrammatic representation of the change in cardiac shape caused by significant rotation to the right (left ventricular dilatation) and to the left (right ventricular dilatation) compared with the normal position.

Fig. 1.5a–c Pronounced right ventricular configuration in stage III cor pulmonale. With the heart rotated to the left, the dilated right ventricle forms the anterior cardiac border. It also extends to the left cardiac border, displacing the left ventricle posteriorly (c). Typical signs of pulmonary hypertension are:

• Prominence of the pulmonary segment

• Large central pulmonary arteries

• Cardiac rotation due to right ventricular dilatation.

a P-A radiograph.

b Left lateral radiograph with esophagogram.

c Cardiac CT scan at the level of the ventricular plane demonstrates the dilated right ventricle, the nearly horizontal orientation of the septum, and posterior displacement of the left ventricle.

Essential Point

The P-A view is useful in distinguishing between dilatation of the right and left ventricles, as it enables one to differentiate between a right ventricular configuration of the cardiac silhouette and an aortic or left ventricular configuration.

Lateral View Narrowing of the retrocardiac space is an indicator of left ventricular enlargement in the left lateral radiograph. The left ventricle is definitely enlarged if it extends more than 18 mm past the inferior vena cava. The enlarged left ventricle may displace the lower portion of the barium-filled esophagus, forming a posterior convexity, or it may slide back past the esophagus without altering its course.

Right Atrium32

P-A View Normally the right atrium forms almost the entire right border of the cardiac silhouette in the P-A view. An enlarged right atrium forms a convex protrusion toward the right, which may be most conspicuous at the upper right cardiac border (Fig. 1.8). The enlarged right atrium also expands toward the left side, however, and broadening of the heart on the right side is thus not directly proportional to the degree of atrial dilatation.

Fig. 1.6a, b Change in cardiac shape caused by left ventricular enlargement in the P-A radiograph (a) and lateral radiograph (b).

Fig. 1.7 Typical aortic or left ventricular configuration in a patient with combined aortic valve disease with left ventricular dilatation. The ascending aorta is expanded because of a jet effect resulting from aortic stenosis.

Fig. 1.8 Change in cardiac shape caused by dilatation of the right atrium.

Lateral View In the left lateral view an enlarged right atrium causes no apparent cardiac abnormalities and no esophageal displacement.

Left Atrium33–38

When the left atrium is enlarged, it expands posteriorly in accordance with its location on the posterior heart wall. It may also project toward the right side, and less commonly it may broaden the left side of the cardiac silhouette. Because the left atrium is located in close proximity to the esophagus, dilatation of the left atrium always leads to circumscribed displacement of the barium-filled esophagus. The size of the left atrium can be determined on an upright contrast radiograph of the esophagus in the left lateral projection taken at full inspiration.

When the dilated left atrium is viewed in the frontal chest radiograph, the superimposed positions of the left and right atria often create a double contour along the upper right cardiac border, especially taken with harder x-rays or digitally postprocessed images. A markedly enlarged left atrium may even project past the right cardiac border. On the left side, the enlarged left atrium may fill out the cardiac waist or create a lateral protrusion. The esophagus below the tracheal bifurcation is displaced by a markedly dilated left atrium to the right and only infrequently to the left. Extreme dilatation of the left atrium may displace the left main bronchus upward or even narrow it, causing an increase in the tracheal bifurcation angle (normally ~70°). Enlargement of the left atrium is most easily detected in radiographs following routine opacification of the esophagus (Figs. 1.9, 1.10).

Fig. 1.9a, b Change in cardiac shape due to enlargement of the left atrium, which displaces the opacified esophagus posteriorly and toward the right side.

a PA radiograph.

b Lateral radiograph.

Fig. 1.10a, b Combined mitral valve defect with predominant stenosis. PA chest radiograph (a) and left lateral radiograph with an esophagogram (b). Enlargement of the left atrium is manifested by a double contour along the right cardiac border, a prominent atrial appendage, and deep indentation and posterior curving of the opacified esophagus.

It should be noted that barium opacification of the esophagus may prove troublesome in subsequent tests such as angiocardiography (contrast material in the transverse colon superimposed over the heart), and therefore a barium swallow is frequently omitted.

Combined Change39–48

Enlarged cardiac chambers may displace other normal-sized cardiac segments in ways that are difficult to interpret. For example, a significantly dilated right ventricle may displace the left ventricle posteriorly, making it difficult to assess the size of the left ventricle in the presence of a markedly enlarged right ventricle (e. g., combined mitral valve disease). Similarly, a severely dilated left atrium may displace the right ventricle forward. Even when the left atrium is definitely enlarged, this does not necessarily signify mitral valve disease. Impairment of blood flow through the mitral valve may have other causes, such as a fixed or floating atrial tumor or a large thrombus in the left atrium, resulting in obstruction of the mitral valve. In some cases this can lead to marked enlargement of the left atrium.22,49 The degree of dilatation depends on its duration and the hemodynamic effects of the lesion. Thus, echocardiography has replaced radiography for routine clinical measurements of the cardiac chambers, although chest films still provide important initial information on the nature of the underlying heart disease (Figs. 1.11, 1.12).

Radiographic Determination of Cardiac Size50–59

Radiographically visible enlargement of the heart is an important indicator of heart disease. Although there is no established correlation between cardiac size and the severity of heart disease, the presence of an abnormally enlarged heart and especially its progression over time can still provide important information. Cardiac size is determined on a standard chest radiograph with a 2-m film-focus distance, which will display the heart in its approximate actual size.

Cardiac size is determined by measuring the transverse diameter of the heart, i. e., the horizontal distance between the outermost right and left cardiac borders on the P-A chest radiograph measured from the midline. The ratio of the transverse cardiac diameter to the transverse thoracic diameter (measured between the inner rib margins at the level of the right hemidiaphragm at normal inspiration) is termed the cardiothoracic (CT) ratio. The CT ratio for a normal-sized heart should not exceed 1:2.

When the heart is viewed in supine radiographs (e. g., taken under ICU conditions), it appears enlarged owing to the decreased film–focus distance (1 m) and greater object–film distance (posterior cassette). The elevated position of the diaphragm also causes apparent transverse broadening of the heart. Thus, in evaluating the size of the heart (e. g., after cardiac surgery) it is helpful, though not strictly necessary, to have a preoperative bedside radiograph available to enable a meticulous comparison of the pre- and postoperative chest radiographs.60

Essential Point

The CT ratio in supine radiographs is of limited value in determining cardiac size, but can be useful in follow-up examinations.

Since the advent of sonographic, angiographic, computed tomographic, and magnetic resonance methods for determining cardiac volume and the size of the individual cardiac chambers, chest radiographs have become obsolete for cardiac volumetry.

Fig. 1.11a–f Schematic representation of the change in cardiac configuration associated with acquired valvular diseases (from Bücheler E, Lackner K-J, Thelen M. Einführung in die Radiologie. Thieme, Stuttgart, 2006. Fig. 6.23, p. 350).

a Mitral stenosis.

b Mitral insufficiency.

c Aortic valve disease.

d Tricuspid stenosis.

e Tricuspid insufficiency.

f Pulmonary valve disease.

Fig. 1.12a, b Multivalvular disease (combined aortic, mitral, and tricuspid valve disease).

a PA radiograph b Lateral radiograph with esophagogram.

• Prominent right cardiac border due to enlargement of the right atrium (RA).

• Significantly enlarged left atrium (LA) causes convexity of the cardiac waist and is viewed as a faint double contour on the right cardiac border.

• Massive cardiac dilatation is also present at the ventricular level.

• Lateral radiograph shows right ventricular outflow tract dilatation and displacement toward the retrocardiac space.

• The left ventricle occupies the retrocardiac space completely.

• The esophagus is curved posteriorly by the enlarged left atrium.

• Calcification of the aortic (AV) and mitral (MV) valves.

Cardiac Hypertrophy and Dilatation

Ventricular hypertrophy is the basic mechanism through which the heart compensates for an increased load.61–63

Pressure Overload

Pressure overload on the heart is characterized by an increase in systolic wall tension. The initial cardiac manifestation is wall thickening, followed by concentric myocardial hypertrophy with an associated reduction of inner volume. Some dilatation may also occur as an adaptive response to chronic pressure overload, although it does not yet constitute myogenic dilatation. Hypertrophy is always the dominant initial response of the heart to an isolated pressure overload.

Volume Overload

Volume overload, characterized by increased diastolic wall tension of the dilated ventricles, leads to elongation of the myocardial fibers followed by eccentric hypertrophy with an expanded inner volume. Volume overload causes less wall thickening than pressure overload. The dominant feature of volume overload is therefore dilatation, while hypertrophy is secondary.64

Underlying Diseases

Tables 1.1 and 1.2 list the most common underlying diseases leading to left- and right-sided cardiac enlargement, illustrated here for diseases causing a pressure or volume overload.

Importance of Pulmonary Vasculature in Cardiac Diagnosis18,65

Because of the low intravascular pressures in the pulmonary circulation, gravity has a much greater effect on blood flow in the lung than in the systemic circulation. Hydrostatic pressures are added to the intravascular pressures in the lower lung zones. Because of these effects, blood flow in the lower lung zones is three times greater than in the upper zones. Accordingly, pulmonary vascular markings appear larger in the basal than in the apical lung in the P-A radiograph. A reduction in the caliber of the basal vessels indicates a redistribution of blood flow that may signify the presence of pulmonary or cardiac disease. This phenomenon, described as upper lobe blood diversion is, however, appreciated only in upright P-A radiographs (Table 1.3, Fig. 1.13).

Table 1.1

Examples of diseases causing pressure and volume overload of the left heart

Pressure overload

• Aortic stenosis

• Coarctation of aorta

• Systemic arterial hypertension

Volume overload

• Aortic insufficiency

• Mitral insufficiency

• Ventricular septal defect

• Patent ductus arteriosus

• Aortopulmonary window

• AV fistula

Table 1.2

Causes of pressure and volume overload of the right ventricle

Pressure overload of the right ventricle

Frequent causes—pulmonary arterial hypertension due to:

• Primary parenchymal lung disease

• Primary or secondary pulmonary vascular obstruction

• Shunt lesions

• Severe mitral valve disease

• Severe aortic valve disease

• Pulmonary congestion due to left-sided heart failure

Rare causes:

• Pulmonary stenosis

Volume overload of the right ventricle

Frequent causes:

• Atrial septal defect

• Anomalous pulmonary venous return

Rare causes:

• Tricuspid insufficiency

• Pulmonary insufficiency

• Ventricular septal defect

Pulmonary Congestion

When normal venous return from the lungs to the heart is impaired, this leads to congestion of blood flow in the pulmonary veins. The earliest sign of this process is a visible increase in the caliber of the upper lobe veins. The increase in left ventricular filling pressure leads to a rise of pulmonary venous and pulmonary capillary pressure, altering the balance between capillary fluid extravasation and reabsorption in favor of extravasation. The resulting increase in tissue pressure eventually leads to a reduction of blood flow in the basal lung zones. This redistribution of blood flow is manifested by enlarged arteries and veins in the upper lung zones and by small vessels in the lower zones. This consequence of decreased left ventricular inflow can be appreciated in the plain chest radiograph, which also shows enlargement of the left atrium.

In patients with severe mitral valve stenosis or chronic heart failure (Table 1.4), there is an additional active arterial vasoconstriction with intimal proliferation, leading to a rise in pulmonary arterial pressure.66–68 Radiographs show signs of pulmonary arterial hypertension with large central pulmonary arteries and narrow peripheral arteries. As this state continues to progress, marked by a growing imbalance between fluid extravasation and reabsorption, fluid begins to accumulate in the pulmonary interstitium. This is followed by the entry of fluid into the alveoli and finally into the bronchioles. As this occurs, the clinical picture progresses from acute dyspnea to manifest pulmonary edema (Table 1.5, Fig. 1.14).69

Table 1.3

Radiographic appearance of pulmonary vasculature because of changes in pulmonary pressure as a result of congenital or acquired heart disease

Large apical veins and arteries (upper lobe blood diversion)

Pulmonary venous hypertension due to early mitral stenosis, heart failure, or atrial tumor

Narrow basal veins, large apical veins, small peripheral arteries, large central arteries

Pulmonary arterial hypertension due to late mitral stenosis, chronic heart failure

Large arteries and veins in all lung zones

Hyperemia due to ASD, VSD, ductus arteriosus, etc.

Narrow peripheral arteries and veins, large central pulmonary arteries

Severe pulmonary arterial hypertension with vascular proliferation due to ASD, VSD, or ductus arteriosus

Small central and peripheral arteries and veins

Hypemia due, for example to pulmonary stenosis, Ebstein anomaly, pericardial effusion, heart defects with a right-to-left shunt (Fallot group), relative tricuspid insufficiency based on right-sided heart failure

Narrow peripheral arteries, large central pulmonary arteries

Pulmonary arterial hypertension due to pulmonary sarcoidosis, pneumoconiosis, panarteritis nodosa, primary pulmonary hypertension

Table 1.4

Principal causes of chronic heart failure

• Loss of contractile muscle mass (myocardial infarction, coronary heart disease)

• Persistent pressure overload (hypertension, aortic stenosis, coarctation of the aorta, pulmonary hypertension, pulmonary stenosis, congenital heart disease with elevated right ventricular pressure)

• Persistent volume overload (valvular insufficiency, congenital heart disease, vascular malformations with right-to-left shunt, arteriovenous fistulas, Paget disease)

• Abnormal heart rate (hypercritical tachycardia, abnormal bradycardia, arrhythmias)

• Noncoronary cardiomyopathy (myocarditis, dilated cardiomyopathy, toxic and metabolic cardiomyopathies, endocrine myocardial alteration)

• Impaired ventricular filling (restrictive cardiomyopathies, constrictive pericarditis, storage diseases, cardiac tumors, cardiac thrombi)

a Normal vascular pattern.

b Pulmonary venous congestion with large upper lobe veins and reduced calibers of lower lobe vessels.

c Pulmonary arterial hypertension due to chronic pulmonary congestion, with large central pulmonary arteries, slightly enlarged upper lobe veins, and narrow peripheral arteries and veins.

d Pulmonary hyperemia with enlargement of pulmonary arteries and peripheral arteries and veins due to increased blood flow.

e Pulmonary arterial hypertension as a result of persistent hyperemia.

f Small peripheral and central vessels due to decreased pulmonary blood flow.

g Pulmonary arterial hypertension (parenchymal cor pulmonale) with small peripheral vessels and large central pulmonary arteries.

Table 1.5

Principal causes of acute heart failure and cardiogenic shock, which may be accompanied by pulmonary edema

Myocardium

• Myocardial infarction

• Septal rupture

• Advanced cardiomyopathy

• Myocarditis

Valve apparatus

• Decompensated valvular heart disease

• Papillary muscle rupture

• Chordae tendineae rupture

Pericardium

• Ventricular tamponade due to hemopericardium

• Ventricular wall rupture

• Effusion

Cardiac rhythm

• Severe tachycardia

• Bradycardia

Outflow tract

• Hypertensive crisis

• Massive pulmonary artery embolism

• Dissecting aortic aneurysm

Fig. 1.14a–ea Radiographic changes in the pulmonary vasculature and interstitium resulting from increased pulmonary venous pressure (diagrammatic representation).

b Normal pulmonary blood flow.

c Pulmonary hyperemia. Ventricular septal defect due to postinfarction rupture of the septum.

d Pulmonary congestion with Kerley B lines (arrow).

e Decreased pulmonary vascular markings with small, indistinct peripheral pulmonary vessels (hyperlucent lung) in a patient with hemodynamically significant pericardial effusion.

Decreased Pulmonary Blood Flow

The lung may show signs of diminished blood flow with small central and peripheral vessels in the frontal chest radiograph, indicating a decrease in the blood supply to the lung. Possible causes include hemodynamically significant pulmonary stenosis, congenital heart defects with a primary right-to-left shunt (e. g., Fallot group), Ebstein anomaly, rare primary tricuspid insufficiency, hemodynamically significant pleural effusion, and relative tricuspid insufficiency resulting from global heart failure (Table 1.6).

Pulmonary Hyperemia

A general increase in pulmonary blood flow (active pulmonary hyperemia, not to be confused with pulmonary congestion) due to intracardiac or extracardiac shunting of blood leads to volume overload, causing dilatation of all the pulmonary arteries and veins. Over time, this increased pulmonary blood flow induces endothelial hyperplasia at the arteriolar level with intimal fibrosis in the small vessels. The subsequent rise in vascular resistance eventually leads to pulmonary arterial hypertension, with large central pulmonary arteries, narrow peripheral arteries, and a reversal of the cardiac shunt (Table 1.7).

Pulmonary Arterial Hypertension (Cor Pulmonale)70,71

The cardiac causes of pulmonary arterial hypertension are to be distinguished from pulmonary hypertension resulting from a primary lung disease (Table 1.8; see Other Forms of Pulmonary Arterial Hypertension, Chapter 12, p. 256). The signs of pulmonary arterial hypertension in these cases (large central pulmonary arteries with peripheral pruning of vessels) are accompanied by signs of the underlying disease. The central pulmonary arteries are considered to be enlarged if the width of the right descending pulmonary artery is greater than 16 mm. In a chronic obstructive syndrome with emphysema, the lung shows a generalized increase in radiolucency (Table 1.9). This state is characterized by a destruction of interalveolar septa and loss of the capillary bed, leading to precapillary pulmonary arterial hypertension. The pulmonary hypertension that develops in interstitial lung disease (e. g., sarcoidosis, pneumoconiosis) or panarteritis nodosa of the lung is based on a decrease in pulmonary vasculature. The peripheral arterial branches appear narrowed, and the veins are also reduced in caliber as a result of diminished venous return. The pulmonary hypertension imposes an increased pressure load on the right ventricle, leading by definition to a state of cor pulmonale.

Table 1.6

Principal causes of decreased pulmonary blood flow

• Heart defects with a right-to-left shunt (Fallot symptom complex)

• Hemodynamically significant pulmonary stenosis

• Ebstein anomaly

• Organic tricuspid insufficiency

• Relative tricuspid insufficiency developing as a result of global heart failure

• Hemodynamically significant pericardial effusion

Table 1.7

Principal causes of pulmonary hyperemia

Intracardiac

• Ventricular septal defect (including septal rupture after myocardial infarction)

• Atrial septal defect

• Anomalous pulmonary venous return

Extracardiac

• Patent ductus arteriosus

• Aortopulmonary window

• Coronary fistula to pulmonary circulation

• Large peripheral AV shunts (including large hemodialysis fistulas)

Table 1.8

2004 Venice Classification of Pulmonary Arterial Hypertension

Pulmonary arterial hypertension (PAH)

• Sporadic, familial

• Associated with collagen diseases, toxins, HIV, or PHT

• Significant venous or capillary involvement

PAH associated with diseases of the left heart

• LV dysfunction, mitral or aortic valve disease

PAH associated with hypoxia and/or respiratory diseases

• COPD, interstitial lung disease, SAS, alveolar hypoventilation, alveolocapillary dysplasia, congenital heart disease

PAH associated with chronic thromboembolism or emboli

• Proximal and distal thromboembolic or embolic obstruction of PAH

Miscellaneous

• Sarcoidosis, histiocytosis X, lymphangiomatosis, extrinsic compression

Table 1.9

Causes of cor pulmonale

Pulmonary vascular diseases

Large or multiple emboli

Decrease in cardiac output due to acute obstruction

Small emboli, vasculitis, extensive lung destruction (ARDS)

Pulmonary hypertension due to extensive hypoxia and microvascular obstruction

Moderately large or recurrent emboli, primary pulmonary hypertension, dietary or drug-induced vasculopathy

Pulmonary hypertension due to vascular obstruction, with low or normal cardiac output

Respiratory diseases

Obstructive:

• Chronic bronchitis and emphysema

• Chronic bronchial asthma

Pulmonary hypertension due to hypoxia, straightening and loss of vessels, external impairment of cardiac filling after pulmonary hyperinflation, with normal or increased cardiac output

Restrictive:

• Intrinsic interstitial fibrosis, lung resection

• Extrinsic: obesity, myoedema, muscle weakness, kyphoscoliosis, lower airway obstruction, decreased respiratory drive at high altitudes

• Hypertension due to hypoxia, torsion, and loss of vessels; normal or diminished cardiac output

• Hypertension due to alveolar hypoxia, normal or increased cardiac output

The radiographic hallmarks of pulmonary arterial hypertension are as follows:

• Dilatation of the main pulmonary artery trunk (prominent pulmonary segment)

• Enlargement of the central pulmonary arteries. This sign is particularly important in follow-up examinations which show a increasing diameter of the right descending pulmonary artery not previously present.

• Pruning of vessels, i. e., rapid tapering of vascular calibers from the enlarged lobar arteries (second-order vessels) to the narrowed segmental arteries (third-order vessels).

• Narrowing of the peripheral arteries and veins. The frontal chest film shows almost no vascularity in the peripheral subcostal lung, which appears abnormally lucent. This decrease in peripheral vascularity is among the most common signs of pulmonary artery hypertension.

Lymphatic System

Interstitial lung edema is associated with an increased removal of excess tissue fluid via lymphatic channels. As a result, these lymphatics are distended and become radiographically visible owing to the summation effect of overlapping projections. There are several disorders in which lymphatic structures may become visible in the P-A chest radiograph:

• Pulmonary venous hypertension relating to mitral valve disease, chronic or acute left heart failure, or pulmonary edema

• Primary lymphatic diseases

• Neoplasias (e. g., carcinomatous lymphangiitis)

Kerley A and B lines in the chest radiograph (Fig. 1.15) represent the summation images of many thickened lymphatic channels and septa. Kerley A lines are linear opacities ~1 mm thick and several centimeters long which radiate from the hila into the central portion of the lung. Kerley B lines are located in the periphery of the lung. They appear as thin, horizontal lines ~1 cm long and are commonly found near the costophrenic angle. They represent thickened interlobar septa and distended lymphatics. Confluent Kerley B lines (severe forms of pulmonary venous hypertension in mitral stenosis) lead to a reticular pattern of interstitial lung markings.27,72

In cases of severe chronic pulmonary venous congestion (especially with severe mitral stenosis), pigment deposition may occur in basal portions of the pulmonary interstitium (hemosiderin due to erythrocyte migration), giving rise to ossified foci of hemosiderin fibrosis. These basal foci are differentiated from calcified tuberculous lesions in that the latter are located primarily in apical lung zones.

Pleural Effusion

Pleural effusion may develop as a result of pulmonary edema or stasis-related intra-abdominal fluid collections (ascites), due partly to a rise in pulmonary venous pressure and partly to venous hypoxia, leading to increased capillary permeability. The earliest radiographic sign of pleural effusion is a thickening of the pleura between the pulmonary lobes (pleural edema). Increasing fluid transudation subsequently leads to pleural effusion of varying extent. The location of the effusion is position dependent: it may overlie the diaphragm or may appear as a crescent-shaped accumulation along the lateral chest wall in the upright patient. Pleural effusions may also be subpulmonary without separation of the lateral pleural layers. This type of effusion, especially when small, is not detectable in the P-A chest radiograph. A subpulmonary effusion is best documented by positioning the patient on the affected side. Pleural effusions are more common on the right than the left side, as a larger pleural surface area is available for fluid transudation on the right side. Moreover, intra-abdominal fluid (ascites in right-sided heart failure) can drain directly into the right pleura from the abdominal cavity via lymphatic connections.

Fig. 1.15 Diagrammatic representation of Kerley lines associated with fluid accumulation in the pulmonary interstitium.

Cardiac Malposition

The most common type of cardiac malposition is dextrocardia, in which the major portion of the heart is located to the right of the vertebral column. Three forms are distinguished:

• Inversion (mirror-image dextrocardia)

• Dextroversion

• Dextroposition

Inversion Mirror-image dextrocardia occurs relatively often as an isolated anomaly in the absence of associated heart defects. A mirror image of normal cardiac anatomy, it is usually accompanied by inversion of the abdominal organs so that the stomach bubble is visualized below the right hemidiaphragm (complete transposition of the viscera).

Dextroversion Dextroversion is usually accompanied by congenital heart disease and is characterized by rotation of the heart toward the right side. The right ventricle is shifted upward and to the right, while the left ventricle is shifted downward and forward, creating a prominent bulge in the upper right portion of the cardiac silhouette. A cardiac apex cannot be identified in the P-A radiograph. The aortic arch occupies a typical location on the left side. This finding differentiates dextroversion from inversion, in which the aortic arch is on the right side.

Dextroposition In dextroposition, the heart is displaced or deviated to the right owing to an extracardiac abnormality, such as a left diaphragmatic hernia or right-sided pleural thickening.

Heart Failure

Acute Heart Failure73–75

In heart failure of acute onset, clinical manifestations are characterized by an abrupt decline in cardiac output. The dominant features include acute pulmonary congestion or edema and arterial hypotension.