(Ebook) Practical Cardiovascular Pathology by Mary

N. Sheppard ISBN 9781498787550, 149878755X Pdf

Download

https://ebooknice.com/product/practical-cardiovascular-
pathology-47173326

★★★★★
4.7 out of 5.0 (57 reviews )

Instant PDF Download

ebooknice.com
 (Ebook) Practical Cardiovascular Pathology by Mary N.
Sheppard ISBN 9781498787550, 149878755X Pdf Download

EBOOK

Available Formats

■ PDF eBook Study Guide Ebook

EXCLUSIVE 2025 EDUCATIONAL COLLECTION - LIMITED TIME

INSTANT DOWNLOAD VIEW LIBRARY

Here are some recommended products that we believe you will be
interested in. You can click the link to download.

(Ebook) Practical Cardiovascular Pathology, 3rd Edition by Mary N.

Sheppard ISBN 9781498787567, 9781498787550, 149878755X, 1498787568

https://ebooknice.com/product/practical-cardiovascular-pathology-3rd-
edition-42598206

(Ebook) Practical Cardiovascular Pathology, 2nd edition by Mary

Sheppard ISBN 9780340981931, 0340981938

https://ebooknice.com/product/practical-cardiovascular-pathology-2nd-
edition-4398930

(Ebook) Practical Cardiovascular Pathology, 2nd edition by Sheppard,

Mary, Dr ISBN 9781283406642, 1283406640

https://ebooknice.com/product/practical-cardiovascular-pathology-2nd-
edition-4393882

(Ebook) Cardiovascular Pathology by L. Maximilian Buja, Jagdish Butany

ISBN 9780128222249, 0128222247

https://ebooknice.com/product/cardiovascular-pathology-43174092
(Ebook) Cardiovascular Prevention and Rehabilitation in Practice by
Jennifer Jones, John Buckley, Gill Furze, Gail Sheppard ISBN
9781118458686, 1118458680

https://ebooknice.com/product/cardiovascular-prevention-and-
rehabilitation-in-practice-10989232

(Ebook) Cardiovascular Pathology by L. Maximilian Buja, Jagdish Butany

ISBN 9780323912587, 9780128222249, 0323912583, 0128222247

https://ebooknice.com/product/cardiovascular-pathology-43180202

(Ebook) Biota Grow 2C gather 2C cook by Loucas, Jason; Viles, James

ISBN 9781459699816, 9781743365571, 9781925268492, 1459699815,
1743365578, 1925268497

https://ebooknice.com/product/biota-grow-2c-gather-2c-cook-6661374

(Ebook) Cardiovascular Pathology, Fourth Edition by L. Maximilian Buja

MD, Jagdish Butany ISBN 9780124202191, 9780128004593, 0124202195,
0128004592

https://ebooknice.com/product/cardiovascular-pathology-fourth-
edition-5432238

(Ebook) Practical Cardiovascular Medicine by Elias B. Hanna ISBN

9781119832706, 1119832705

https://ebooknice.com/product/practical-cardiovascular-
medicine-43076092
PRACTICAL
CARDIOVASCULAR
PATHOLOGY
PRACTICAL
CARDIOVASCULAR
PATHOLOGY
THIRD EDITION

Professor Mary N. Sheppard, MD,

FRCPath, FRCPI
Department of Cardiovascular Pathology
St. George’s Medical School, University of London, UK
Third edition published 2022
by CRC Press
6000 Broken Sound Parkway NW, Suite 300, Boca Raton, FL 33487-2742

and by CRC Press

2 Park Square, Milton Park, Abingdon, Oxon, OX14 4RN

© 2022 Taylor & Francis Group, LLC

First edition published 1998 by Arnold

Second edition published by Hodder Arnold 2011

CRC Press is an imprint of Taylor & Francis Group, LLC

This book contains information obtained from authentic and highly regarded sources. While
all reasonable efforts have been made to publish reliable data and information, neither the
author[s] nor the publisher can accept any legal responsibility or liability for any errors or
omissions that may be made. The publishers wish to make clear that any views or opinions
expressed in this book by individual editors, authors or contributors are personal to them and
do not necessarily reflect the views/opinions of the publishers. The information or guidance
contained in this book is intended for use by medical, scientific or health-care professionals
and is provided strictly as a supplement to the medical or other professional’s own judgement,
their knowledge of the patient’s medical history, relevant manufacturer’s instructions and the
appropriate best practice guidelines. Because of the rapid advances in medical science, any
information or advice on dosages, procedures or diagnoses should be independently verified.
The reader is strongly urged to consult the relevant national drug formulary and the drug
companies’ and device or material manufacturers’ printed instructions, and their websites,
before administering or utilizing any of the drugs, devices or materials mentioned in this book.
This book does not indicate whether a particular treatment is appropriate or suitable for a
particular individual. Ultimately it is the sole responsibility of the medical professional to
make his or her own professional judgements, so as to advise and treat patients appropriately.
The authors and publishers have also attempted to trace the copyright holders of all material
reproduced in this publication and apologize to copyright holders if permission to publish in
this form has not been obtained. If any copyright material has not been acknowledged please
write and let us know so we may rectify in any future reprint.

Except as permitted under U.S. Copyright Law, no part of this book may be reprinted, repro-
duced, transmitted, or utilized in any form by any electronic, mechanical, or other means, now
known or hereafter invented, including photocopying, microfilming, and recording, or in any
information storage or retrieval system, without written permission from the publishers.

For permission to photocopy or use material electronically from this work, access www.
copyright.com or contact the Copyright Clearance Center, Inc. (CCC), 222 Rosewood Drive,
Danvers, MA 01923, 978-750-8400. For works that are not available on CCC please contact
[email protected]

Trademark notice: Product or corporate names may be trademarks or registered trademarks

and are used only for identification and explanation without intent to infringe.

Library of Congress Cataloging-in-Publication Data

Names: Sheppard, Mary N., author.
Title: Practical cardiovascular pathology / Mary N. Sheppard.
Description: Third edition. | Boca Raton : CRC Press, 2022. | Includes bibliographical
references and index. | Summary: “In the last decade cardiac pathology has undergone a
revolution, particularly in the fields of genetics and imaging. Practical Cardiac Pathology
3e is a combined atlas and text that is designed to assist pathologists in identifying the
range of cardiovascular conditions that are found in both diagnostic and autopsy
work”-- Provided by publisher.
Identifiers: LCCN 2021012284 (print) | LCCN 2021012285 (ebook) | ISBN 9781498787550
(hardback) | ISBN 9781032018072 (paperback) | ISBN 9780429186530 (ebook)
Subjects: MESH: Cardiovascular Diseases--pathology | Autopsy--methods
Classification: LCC RC670 (print) | LCC RC670 (ebook) | NLM WG 142 | DDC 616.1075--dc23
LC record available at https://lccn.loc.gov/2021012284
LC ebook record available at https://lccn.loc.gov/2021012285

ISBN: 9781498787550 (hbk)

ISBN: 9781032018072- PB (pbk)
ISBN: 9780429186530 (ebk)

Typeset in CenturySTD-Book
by Nova Techset Private Limited, Bengaluru & Chennai, India
 DEDICATION

I dedicate this book to the Sheppard family, and to my own four children, Mary Louise, James, Francesca and
Jonathan, whose good, strong hearts will beat beyond mine into eternity, and to my first grandchild, Leo, born in
this pandemic year of lockdown, whose good, strong heart will beat beyond one hundred years into the twenty-
second century, given the revolution we have now in the treatment and prevention of cardiovascular disease. We
pathologists have and will continue to play a pivotal role in making this prolongation of the human lifespan with a
heathy heart a coming reality.
CONTENTS

Preface vii

Useful Abbreviations viii

Chapter 1 Autopsy cardiac examination 1

Chapter 2 The coronary arteries: Atherosclerosis and ischaemic heart disease 33

Chapter 3 Valve disease 75

Chapter 4 Infective endocarditis 125

Chapter 5 Cardiac hypertrophy, heart failure and cardiomyopathy 147

Chapter 6 Myocarditis 207

Chapter 7 Cardiac tumours 241

Chapter 8 Diseases of the aorta 269

Chapter 9 Deaths following cardiac surgery and invasive interventions 295

Chapter 10 Investigation of sudden cardiac death 325

Chapter 11 Arteropathies, microcirculation and vasculitis 351

Chapter 12 Pericardium 369

Index 381
 PREFACE

It is 10 years since we published the second edition of where the application of whole genome analysis is
this book, and subsequent to its success, I have been becoming a reality. We pathologists will play a vital
asked to write a third edition. This has been written role in helping with the interpretation of what these
during a global pandemic where all our lives, both per- genetic profiles mean in many cardiac and vascular
sonally and professionally, have been altered. This has pathological conditions. Also, with the application of
given me time to reflect on the vast changes in the field new therapies, we have a major contribution to make
of cardiovascular pathology and cardiology. There is an in the effectiveness of these therapies and delineating
ongoing revolution in prevention, imaging diagnosis their complications.
and cardiac genetics. The fields of cardiomyopathy, The specialist cardiac pathologist is a vital member
cardiac genetics and sudden cardiac death have moved of inherited cardiac conditions groups as part of a mul-
forward rapidly with the establishment of inherited tidisciplinary team, including interventionists, electro-
cardiac centres within the UK and other countries. The physiologists, radiologists, cardiologists, clinical
general pathologist and forensic pathologists have vital geneticists, genetic nurses, and genetic counsellors. To
roles when it comes to the investigation of sudden car- be an excellent cardiac pathologist, one needs to have
diac death in the community. an extensive knowledge of cardiology and be able to
This book is a practical guide for these pathologists carry on meaningful discussions with our clinical col-
and hopefully will help them come to a specific diagno- leagues leading to good clinicopathological correla-
sis using practical hands-on diagnostic tools. It is tion. This expertise is essential in order to come to a
essential that all pathologists examine the heart prop- specific diagnosis and do phenotype-genotype correla-
erly, take sufficient material for diagnostic purposes tion, particularly in the field of cardiomyopathies, aor-
and also take a sample that is suitable for DNA extrac- topathies and vasculopathies, which may be of the
tion when they suspect that a cardiac condition is utmost importance for other family members. Cardiac
genetic. The good news is that now, in 2021 in the UK, disease still remains the most common cause of death
this so-called molecular autopsy with genetic testing in developed countries and is increasing in other parts
will be available on the National Health Service. This, I of the world. Hopefully, this picture will alter in the
believe, will lead to a revolution in risk stratification coming decades, with the application of advances in
for cardiac conditions as well as the application of prevention, diagnosis and new therapies.
individually tailored therapies including genetic
manipulation. We stand at a pivotal point in cardiology, Mary N. Sheppard

vii
 USEFUL ABBREVIATIONS

AL anterolateral MV mitral valve

AV atrioventricular NCS noncoronary sinus
CS coronary sinus OM obtuse marginals
Cx circumflex PAs pulmonary artery (-ies)
EV eustachian valve PDAs posterior descending coronary arteries
FO fossa ovalis PM posteromedial
IVC inferior vena cava PV pulmonary valve
LA left atrium RA right atrium
LAA left atrial appendage RAA right atrial appendage
LAD left anterior descending RAVG right atrioventricular groove
LAVG left atrioventricular groove RCA right coronary artery
LCA left coronary artery RV right ventricle
LMS left main stem RVOT right ventricular outflow tract
LV left ventricle SA sinoatrial
LVOT left ventricular outflow tract SMT septomarginal trabeculation
MB moderator band SVC superior vena cava
MCV middle cardiac vein TT tendon of Todaro
MS membranous septum TV tricuspid valve

viii
 CHAPTER ONE

AUTOPSY CARDIAC
EXAMINATION

a­ natomical knowledge with variations of the normal

Inspect heart in situ in the chest organs is becoming limited. Vascular diseases of the
Note fibrous outer pericardium and any fluid within brain and heart account for the majority of deaths in
Normal – 30 ml clear serous fluid developed countries and in-depth knowledge of both
these organs is essential.
Acute accumulation – 300 ml
The excised heart displayed grossly, recorded pho-
Chronic – 1000 ml plus tographically, measured carefully and studied histolog-
Remove heart by cutting across great vessels and ically remains the gold standard against which
veins. Leave proximal 30 mm of aorta and pulmonary antemortem clinical findings are measured. Exact
artery. Also, leave 10 mm of superior vena cava and
measurements are needed to confirm cardiac atrial
cut inferior vena cava close to diaphragm
dilatation, ventricular hypertrophy or dilatation, criti-
Inspect epicardial external surface of heart
cal valve stenosis, valve regurgitation and aortic dilata-
Measure heart diameter at AV junction posteriorly tion, as well as coronary artery narrowing.
Measure longitudinal length of ventricles from When carrying out a cardiac autopsy, particularly in
crux, where right coronary artery (RCA) bends someone who has died suddenly with no previous dis-
down into posterior interventricular groove down ease and the most likely cause of death is in the heart,
to the apex. If circumflex is dominant, use this
one has to look at the heart very carefully. One must
Cut coronary arteries and branches transversely at take well-chosen histological sections and collect
2 mm intervals down to the apex on right and left
material for microbiology and particularly genetic stud-
sides
ies. Forethought and preparation on the part of the
Cut ventricles transversely up to tips of papillary
pathologist is essential in the approach to the cardiac
muscles and describe any changes. Remove
post-mortem blood clot before weighing the heart autopsy.
In the UK and the US, most autopsies are performed
Measure thickness of anterior, lateral and posterior
RV, interventricular septum, anterior, lateral and
at the request of the coroner or medical examiner, with
posterior left ventricle at midventricular level few in-hospital autopsies being carried out. Most autop-
sies ordered by the medical examiner/coroner are in
Cut into both atria and inspect both AV valves from
above patients where no death certificate can be issued. The
majority are those who had not been to a doctor
Make lateral cuts between atria and ventricles,
including AV valves recently and did not have a life-threatening disease or
were not expected to die. Of 500 000 deaths in England,
Inspect ventricles and valves. Measure
atrioventricular valve circumferences 23% result in an autopsy, the majority being coroners’
cases, amounting to 94 000 per year.1 Most are carried
Open up into right and left ventricular outflow
tracts and inspect valves and origin of the coronary
out by a pathologist working in a general hospital or a
arteries. Measure ventriculoarterial valve forensic pathologist. Retention of tissues and organs
circumference from a coronial autopsy without relatives’ consent is
Inspect aorta and pulmonary arteries. Measure permissible under Coroner’s Rule 9, to confirm the
circumference 10 mm above valves cause of death. If tissue is retained beyond the coro-
ner’s investigation, the family must consent to this
under the Human Tissue Act of 2004. 2 I believe that
Autopsy practice is changing in the modern world. pathologists must prepare in advance, especially with
There has been a marked reduction in the number of young, sudden deaths, and must be proactive in making
autopsies performed in the UK and elsewhere. a case to retain heart tissue in order to provide as accu-
Expertise is thus being reduced and detailed rate a cause of death as possible. They must

1
Autopsy Cardiac Examination

communicate via a specifically trained coroner’s that the bulk (usually more than 90% of the cardiac tis-
officer, who talks with the family before undertaking sues) can be reunited with the body in such circum-
the post mortem to prepare them for the possibility of stances, once the examination is complete.
retention of the heart and other tissues. The help of a
well-trained coroner’s officer who links with the family
directly is essential in these situations for obtaining Approach to the Heart
appropriate consent.
There are well established and published guidelines
in the Chest
for pathologists investigating sudden death in both the The heart lies in the middle of the inferior mediastinum,
UK and Europe.3,4 mainly to the left of the midline behind the second to the
All autopsy practitioners should be able to per- sixth costal cartilage, with the left edge extending to
form a basic examination of the heart and its connect- the midclavicular line (Fig. 1.1). On each side, the heart
ing vasculature – akin to the minimum dataset for a abuts the lungs and the pleural cavity overlies the right
cancer report. Minimal information, with limited for- side of the heart as far as the midline. On the left side,
mulaic descriptions of the heart with no measure- the lung and pleura are pushed to the left and in the area
ments, is unacceptable. There is a balance to be of the cardiac notch; the surface of the heart comes to
derived between the majority of autopsy cardiac lie directly against the rib cage, separated from it only
cases recognized to be routine and those requiring by the pericardium. Anatomically, because of its rotated
greater consideration. position within the chest, the right border of the heart is
The pathologist must approach the heart armed occupied by the right atrium (RA) while the inferior and
with information about the patient’s background and anterior surface is formed by the right ventricle (RV),
the circumstances of death. Information from the gen- lying on the diaphragm. The left ventricle (LV) only
eral practitioner, family and witnesses is usually comes to the anterior surface as a thin strip between the
obtained from the coroner’s office or the medical exam- anterior interventricular groove and the obtuse margin
iner’s office, particularly in cases of unexplained sud- of the heart. The left atrium (LA) is a completely poste-
den death. Communication with relevant cardiac
centres and access to clinical records are also essential
when the patient has previous cardiac interventions or
surgery, which will be dealt with in Chapter 9.
Consideration of family consent is essential before
the autopsy and critical if considering retaining the
heart and other tissues. Specialist investigation, includ- LAA
RAA
ing culture⁄transport media for toxicology, microbiol-
ogy and DNA extraction, should be taken into account
prior to the commencement of the dissection in order to
optimize sampling. I believe a pathologist approaching
a post mortem in circumstances where the dead person
has had no medical history, is failing in their duty if
they do not approach the case as paediatric patholo- P
gists approach a sudden infant death, where there are
established protocols to be followed.5
Digital photography is a quick, useful adjunct to
autopsy diagnosis and camera facilities should be avail-
able in every mortuary. Digital images of mid–low ven-
Fig. 1.1
tricular transverse sections and other views of the Opened thorax with sternum removed. Right atrial appendage
heart are helpful as a permanent record and for referral (RAA) is at the upper right margin abutting the parietal
when the heart cannot be retained. In sudden cardiac pericardium. Right ventricle (RV) occupies the right and inferior
death, organ retention and referral should be regarded margin of the heart lying on the diaphragm (D). Left ventricle
(LV) margin lies on the left lung while tip of the left atrial
as the ‘gold standard’, with cardiac examination, tissue
appendage (LAA) can be seen just to the left of the pulmonary
block and sectioning with staining being done immedi- artery (PA). Aorta (A) lies behind and to the right of the main
ately and turnaround of cases being complete within 2 pulmonary artery. Note opened fibrous pericardium (P) to the
weeks also with toxicology. Families can be reassured right.

2
 Removal of the Heart

rior structure lying close to the oesophagus. That is why and nonspecific chronic inflammation. Very rarely,
transoesophageal echocardiography gives such excel- necrotizing granulomas indicating tuberculosis or
lent views of the left side of the heart. The tips of the rheumatoid nodules may be noted.
right and left atrial appendages can be seen at the upper A short longitudinal incision 2 cm above the pulmo-
right and left margins of the heart (Fig. 1.1). Pathologists nary valve (PV) will enable a check for thromboemboli
must relate the features of the excised heart and natural in the main pulmonary trunk and two main branches in
cardiac anatomy. Thus, the under surface, mainly with situ. Needle the RA after searing at its junction with the
the RV resting on the diaphragm, is now universally inferior vena cava to obtain a sample of heart blood for
referred to as the inferior/basal surface. In the past, culture, if required. Congenital heart disease can go
pathologists called this the posterior surface. undetected clinically well into old age. Check for patent
The pericardium forms a tough, fibrous sac with an ductus arteriosus and coarctation of the aorta at the
outer thick parietal layer and an inner transparent sero- isthmus distal to the left subclavian, particularly when
sal layer firmly adherent to the heart forming the vis- there is left ventricular hypertrophy. Check the azygous
ceral layer. A thin film of fluid lies between the two and hemiazygous veins, as well as the superior and infe-
surfaces and allows movement of the heart within; rior vena cava in situ, in order to check for anomalous
20–50 ml of pale-yellow fluid is normal. The vagus and pulmonary venous drainage. Always keep the heart and
phrenic nerves run anteriorly and posteriorly respec- lungs intact if any congenital abnormalities are
tively to the pulmonary hilum on either side and are in detected in order to check the arterial and venous con-
close proximity to the pericardium. nections between the heart and lungs as well as any
aorto-pulmonary collaterals which may develop, espe-
cially in Tetralogy of Fallot, when pulmonary valve
Techniques for Examining the obstruction is severe. Dissect the superior vena cava
into the right brachiocephalic and right azygous veins
Heart in situ to check for thrombus or stenosis or to follow the path
After removal of the sternum, it is extremely important of a pacemaker from the right atrium and ventricle
to examine the pericardium in the intact state to assess Also, check the ascending aorta for evidence of exter-
for tamponade. The pericardium will be distended and nal haemorrhage, dilatation, thinning of the wall, or
full to the touch if tamponade is present as illustrated rupture. There will be a thickened wall in aortitis with
in Chapter 12. In these cases, great care must be exer- cobblestone appearance of the intima. Look for an
cised in removal of the intact pericardium. A longitudi- entry tear in acute aortic dissection, especially in the
nal cut is made through the anterior aspect of the first 3 cm above the aortic valve, as well as for dilata-
pericardial sac and the amount of blood, either fresh or tion/aneurysm formation and intramural haematoma
collected by suction into a container, should be in the within the media.
region of 500–1000 ml. If the blood has clotted, it should
be weighed. The mere presence of blood in the pericar-
dium does not indicate tamponade; the blood must dis-
tend the sac. If the blood accumulates rapidly, it will
Removal of the Heart
usually be 300–500 ml, while if the accumulation is The heart is removed by first cutting both great vessels,
slower, as with serous effusions, it can amount to the aorta and the pulmonary trunk, transversely 2 cm
1000 ml. above the semilunar valves by inserting the index and
In purulent pericarditis, the amount of pericardial middle finger into the transverse sinus of the pericar-
fluid is measured and its character noted. If indicated, dial cavity and cutting both vessels across (Fig. 1.2).
a pericardial fluid sample is taken by needling through Always be mindful of antemortem thrombi within the
an area of pericardium which has been seared for steri- main pulmonary artery where they will lie curled up
lization. The surface of the visceral as well as parietal obstructing the vessel or branches. If there is a rupture
pericardium is examined for exudates, adhesions, with or without dilation of the aorta, and a dissecting
tumour nodules or dense fibrosis associated with con- aneurysm is suspected, leave the aorta intact and dis-
strictive pericarditis, which can follow infections such sect it out, complete with abdominal aorta down to the
as tuberculosis or previous cardiac operations or may iliofemoral junction.
be idiopathic. Samples of the thickened pericardium Cut the inferior vena cava just above the diaphragm
from cases of constrictive pericarditis are often sent and lift the heart by the apex, reflecting it anteriorly
for analysis. Usually, the samples show dense fibrosis and upwards to facilitate exposure of the pulmonary

3
Autopsy Cardiac Examination

Right ventricular hypertrophy usually points to pulmo-

nary disease; look carefully in the pulmonary arteries
for atheroma which indicates pulmonary hypertension.
Left ventricular hypertrophy may be obvious exter-
A nally. Aneurysm formation in the left ventricle is usu-
ally associated with a previous infarct. Flexibility is
PA called for when dissecting the heart since each disease
process requires a different approach. When one notes
left ventricular hypertrophy, check for a history of
hypertension, check for coarctation of the aorta and
check the aortic valve carefully. Look for an impact
lesion in the left ventricular outflow tract in cases of
hypertrophic cardiomyopathy.
The epicardial surface of the heart normally con-
tains fat. The amount varies with the person’s nutrition
Fig. 1.2
and increases with age and BMI. Normally, it fills the
The aorta (A) and pulmonary artery (PA) are cut across by
inserting finger behind them into the transverse sinus and
atrioventricular (AV) groove surrounding the coronary
cutting through 30 mm above where both great vessels arise arteries and extends along the anterior and posterior
from the heart. interventricular sulci towards the apex (Figs. 1.1–1.3).
When a patient is older and obese it may completely
veins at their pericardial reflection. After confirming envelop the epicardial surface of the entire heart. Fat
that the left and right pulmonary veins enter normally also spreads into the myocardium along the intramyo-
into the left atrium, the pulmonary veins are cut (Fig. cardial vessels, particularly in the RV and into the
1.3). Then, the superior vena cava is opened to check for interatrial septum. The right ventricular wall is thin-
thrombosis or occlusion and opened up into the left and nest and contains most fat where it meets the interven-
right brachiocephalic veins before being cut across. tricular septum, particularly in elderly patients. It is
Following removal of the heart from the pericardial this area which is most likely to be ruptured during
cavity, and before weighing the specimen, post-mortem catheterization procedures. Epicardial fat is prominent
blood clots should be removed by doing a midventricu- in the anterior and lateral wall of the right ventricle in
lar slice through the ventricles and incising the atria. If normal individuals while the basal/posterior wall is
one sees aneurysmal dilatation of the right ventricular usually free of fat (Fig. 1.4). This fat can merge with the
wall, be aware of the possibility of right ventricular car- muscle layer so that it is impossible to distinguish each
diomyopathy, Ebstein’s abnormality of the tricuspid and can replace the full thickness RV wall in obese,
valve, pulmonary thrombi and pulmonary disease. middle-aged and elderly individuals. The wall needs to
be completely replaced by fat, dilated and thin-walled
with scarring to consider right ventricular involvement
in arrhythmogenic cardiomyopathy, particularly in
young people with normal BMI and normal coronary
arteries. In the left ventricle, the fat follows the epicar-
dial vessels and their branches but never infiltrates or
PV PV replaces the left ventricular myocardium. Fat never
infiltrates unless it is around penetrating vessel
branches. Epicardial fat will only be seen around the
P epicardial coronary vessels in the left ventricle
(Fig. 1.4). Fat seen partly replacing the left ventricular
wall, particularly on the epicardial surface, points to
arrhythmogenic cardiomyopathy or an old regional
Fig. 1.3 healed myocardial infarct. The external surface of the
The heart has been moved up towards the head to expose the
heart is examined visually and by palpation. The loca-
diaphragmatic surface and the posterior aspect of the left
atrium with attached pulmonary veins (PV), which have been cut
tion and size of the four heart chambers are assessed,
across with release of blood. Note inner smooth lining (parietal as are abnormalities of chamber size. Any focal or dif-
layer) of the fibrous pericardium (P). fuse disease process that has affected the epicardium

4
 Removal of the Heart

arteries. At this stage in the fresh heart, a detailed

examination of the coronary arteries is undertaken in
* routine autopsies.

MB Examination of coronary vessels

To obtain the best analysis of the coronary vessels as
regards the lumen and degree of stenosis, it is best to
perfuse the heart from the aorta with a pump which will
(via a tube placed in the aorta), under pressure of
100 mmHg, force open the coronary vessels and fix the
heart over a period of 24 hours. The coronary vessels
will maintain their lumen as in life and there will not be
the overestimation of narrowing which can be seen
when hearts are simply fixed in formalin, where the cor-
Fig. 1.4
onaries often contract down after death. Always check
This shows a short axis view of the right and left ventricle which
highlights the fat in the anterior and lateral wall of the right the origin of each artery within the respective sinus.
ventricle. There is usually no fat in the basal RV. Note that the fat While the majority arise within the right or left sinus,
merges with the underlying myocardium in the RV. Note also the there is great variation in the exact location, as we have
moderator band (MB) which extends from the anterior papillary shown in normal individuals with the ostia being at,
muscle of the tricuspid valve to the septum on the right side. The
above and below the sinotubular junction. The majority
fat on the epicardial surface of the left ventricle follows the
epicardial coronary arteries but does not infiltrate the wall
are below the junction, but do not exceed 2 mm below
except where the coronary arteries penetrate through into the it.6 Usually, there is only one ostium on the left (Fig. 1.5),
underlying muscle(*). In the RV one can visualize the papillary but in 1% of hearts an additional ostium for the circum-
muscles, chords and leaflets of the tricuspid valve viewed from flex can be identified. In the right coronary sinus, multi-
below. The trabeculae of the right ventricle are more prominent ple ostia are common (74% of cases in our study) and
and thicker than the finer trabeculae of the left ventricle. Note
give rise to branches supplying the RV, with a branch to
also the presence of the anterolateral (AL) and posteromedial
(PM) papillary muscles occupying the chamber of the LV. This is a the conus or infundibulum being particularly frequent
midventricular view from which all measurements are taken of (Fig. 1.5). The shape of the ostium can be round, ellipti-
both right and left ventricular walls to determine the thickness cal or crescentric (Fig. 1.5). A probe 1 mm in diameter
of both ventricles and septum. will easily pass into both vessels in an average adult.
With a crescentric shape, especially at the origin of the
should be apparent. Discolouration and haemorrhage
on the surface will point to acute infarction or possible
rupture. Evidence of rupture may be subtle, with a
small area of haemorrhage into fat on the surface and
not a gaping hole. Careful probing in this area is
required. White irregular flat white patches on the epi-
cardium are common, especially over the anterior sur-
face of the RV, and have been attributed to mechanical
trauma or to healed pericarditis, but there is no definite
histological evidence for either of these processes.
Histologically, there is nonspecific fibrosis with a few
lymphocytes noted (see Chapter 12). Swelling around Fig. 1.5
Aorta has been opened to show the outflow tract from the left
the root of the aorta may point to a sinus of Valsalva
ventricle. An incision has been made through the anterior wall
aneurysm, a root abscess in aortic valve endocarditis, of the left ventricle and cutting open at the commissure
or an aneurysm of the proximal coronary arteries. A between the right and left coronary sinuses. Note the rounded
careful methodical approach is needed to dissect out orifice of the left coronary artery (LCA) at the sinotubular
these structures in order to determine the origin of any junction, while the right coronary artery (RCA) shows an
elliptical opening below the sinotubular junction with an
haemorrhage or swelling in this area. A cut across the
additional orifice for a conal artery branch (arrow). Note also the
aorta above the cusps of the aortic valve will usually fatty streaks in the aortic wall above the sinuses. Note
expose the valve architecture in order to look for abnor- prominent nodule (N) in centre of leaflet close to lines of
malities and also to show the ostia of the coronary opposition – Nodule of Arantius.

5
Autopsy Cardiac Examination

right coronary artery, there is a small intramural course

of the vessel usually only 1 mm in length. It is essential A
to look at the ostia and probe the origins of both coro-
nary arteries in the coronary sinuses. Thus, anomalous
PA
origin of the coronary arteries will not be missed. Do
not probe beyond the first 1–2 mm into vessels in order
not to dislodge thrombi in the proximal vessels or miss
coronary artery dissection. RAVG
In specialist centres, the coronary arterial system is
injected with a barium–gelatin mixture and studied in
radiographs. Polyethylene tubing, the tips of which may
be flared in a flame, is used to cannulate each coronary
LAD
ostium. The tubes are secured by a ligature at the origin
of the coronary arteries, as close to the aorta as possi-
ble. The free end of each tube is attached to a hypoder-
mic needle (size 16) on the barrel of a disposable
syringe (30 ml). The pressure of injection may be gradu-
ally increased to 100–120 mmHg and maintained for
10–15 minutes. Following injection, the cannulae are
pulled out and the ligatures tightened and knotted
quickly. The heart is then fixed in formalin for 24 hours.
After washing the fixed specimen in water, radiographs
are made in anteroposterior as well as left and right Fig. 1.6
anterior oblique positions. A superior view can also be External surface of the heart showing scalpel cuts across the left
done after the ventricles have been transversely sliced anterior descending (LAD) artery at 2 mm intervals. Note
in a ‘bread-loaf’ manner. pulmonary artery (PA) lying in front of and curving to the left
The heart has large conduit vessels on the surface around the aorta (A). Also note the right atrioventricular groove
(RAVG) filled with fat in which the right coronary artery is
providing tissue perfusion through an intricate net-
embedded and hidden from surface view.
work of penetrating small vessels. In routine autopsies,
the pathologist will simply cut across the main vessels
at 2 mm intervals in the fresh heart and assess the pres-
ence of dilatation, atherosclerotic plaque formation,
thrombosis, stenosis or dissection. The coronary arter-
ies are cut transversely with a sharp scalpel blade using RAA
a gentle sawing motion – not firm pressure – to confirm
any sites of narrowing and to evaluate the pathology
directly (Fig. 1.6). Cutting the vessels longitudinally
can destroy thrombi/emboli and make the estimation of **
*
stenosis impossible (Fig. 1.7). The vessels that are usu-
ally examined in all hearts include the four major epi-
cardial coronary arteries, the left main stem (LMS), the
left anterior descending (LAD), the left circumflex (Cx)
and the right coronary arteries (RCA) and posterior
descending coronary artery (PDA). However, attention
must also be directed to smaller branches, such as the
left diagonals, the left obtuse marginals, the intermedi-
ate and the right marginal branches. If the coronary Fig. 1.7
arteries are heavily calcified, they are removed intact This shows a longitudinal cut of the right coronary artery from
its origin in the right coronary sinus(*) to the right margin of the
and, following dissection of the vessels from the epicar-
heart deep in the atrioventricular groove surrounded by fat,
dial surface, each coronary artery is carefully trimmed lying beneath the right atrial appendage which has been
of excess fat and the intact arterial tree is placed in a reflected. Note the slightly raised pale atheromatous plaque in
container of formic acid for slow decalcification over the mid-section(**) at a branching point.

6
 Removal of the Heart

12–18 hours. Decalcification of isolated segments of interventricular groove (Fig. 1.9). In this initial course,
vessel may be sufficient for cases in which the coronary it usually gives off the sinus nodal artery into the atrial
arteries are only focally calcified. Calcification bears musculature and the infundibular (or conal) artery into
no relation to the severity of coronary artery disease. the right ventricular muscle mass. The conal/infundib-
The areas of maximal narrowing are noted by specify- ular branch commonly anastomoses with a small
ing the degrees of reduction of the cross-sectional area branch of the left coronary artery to form the anasto-
of the lumen (e.g. 0–25%, 26–50%, 51–75%, 76–90% and motic ring (of Vieussens). These branches and the ring
100%). Most cardiologists agree that, in the absence of are sometimes considerably enlarged in atherosclero-
other cardiac disease, significant coronary artery nar- sis when there is distal disease in the right coronary
rowing is that exceeding 75%. I usually apply the 1 mm artery. The artery then runs in the right atrioventricu-
probe test in the left main stem and proximal (usually lar groove to the acute margin of the heart where it
proximal 30–40 mm) of the anterior descending coro- gives rise to the acute marginal artery of the RV and
nary artery. The lumen may be collapsed down giving usually a lateral atrial artery. The RCA usually lies deep
the erroneous impression of significant stenosis. in fat in the AV groove 3–5 mm beneath the surface (see
Insertion of a 1 mm probe will open up the lumen. Only Figs. 1.6 and 1.7). Continuing around the tricuspid ori-
do this on the transversely cut coronary arteries (Fig. fice, it gives off a varied number of smaller ventricular
1.8). Never probe down an unopened coronary artery as branches before, in the majority of hearts, it ends in the
you may dislodge thrombi/emboli. In the Cx, the artery posterior/basal interventricular groove (Fig. 1.10). The
can be variable in size but can be probed generally to area of junction of the posterior interventricular and
the obtuse margin (Fig. 1.8) where it usually divides the AV grooves is called the crux of the heart. The PDA
into obtuse marginal branches. The RCA one can usu- artery is given off at this point. Before it forms the pos-
ally be probed as far as the crux of the heart where it terior descending branch, the right coronary artery
turns to become the PDA. itself makes a U-turn into the AV muscular septum and
gives off the artery to the AV node from the apex of the
The coronary anatomy U. It then continues onto the diaphragmatic surface of
There are two major coronary arterial branches which the left ventricle as the PDA which is often grafted in
arise from two of the three sinuses of Valsalva: the right ischaemic coronary artery disease. This is the anatomy
coronary and left coronary sinuses respectively. The found in the majority of people (i.e. that the artery sup-
two coronary arteries have major differences in their plying the PDA is the RCA), which is called right coro-
branching patterns once they emerge from their sinuses. nary dominance. The RCA is usually large with large
The RCA, after arising from its sinus, runs around lumen extending to the crux when the artery is domi-
the orifice of the tricuspid valve (TV) in the nant (Figs. 1.7 and 1.10). When it is small, look for left

LAA

LAD
CX

Fig. 1.9
Aortic sinuses which balloon out from the aortic wall at its origin
and show the origin of the right coronary artery (RCA), with
Fig. 1.8 infundibular branch to the right ventricle, and left coronary artery
This shows a 1-mm probe opening up the lumen of the circumflex (LCA), with the left main stem dividing into the left anterior
coronary artery which contains an eccentric atheromatous descending (LAD) coronary artery and circumflex (CX) below the
plaque (arrow). Note how deep in the fat the artery is and it is left atrial appendage (LAA). Note that the hole seen is the removed
also hidden beneath the left atrial appendage (LAA). pulmonary artery and valve leaving the muscular infundibulum.

7
Autopsy Cardiac Examination

ostium (Fig. 1.9). In about one-third of individuals, it

trifurcates. The branch between the anterior descend-
ing and circumflex branches is called the intermediate
branch (Fig. 1.11). The LAD passes in the anterior inter-
ventricular sulcus towards the apex. During its course,
it gives a variable number of branches (diagonal
branches) to the left ventricle (Fig. 1.11). These often
become intramural covered by muscle distally. These,
together with LAD, are important for arterial and vein
grafting. The first diagonal branch is a major vessel
which originates in the proximal third of the LAD. It
may reach the apex of the heart and is quite often sub-
merged in muscle for part of its length. When the LCA
trifurcates, this first diagonal branch is replaced by the
intermediate branch. In addition to the diagonal
branches passing to the left ventricle, there are smaller
branches passing to the RV. These infundibular
branches to the outflow component of the RV often
anastomose with branches from the right coronary
Fig. 1.10
artery. In addition to the diagonal and right ventricular
The diaphragmatic surface of the heart with the right coronary sprigs, the LAD gives a number of branches passing
artery (RCA) extending to the crux and leading into the posterior from its underside (epicardial aspect) vertically down-
descending artery (PDA). Note that the right coronary artery wards into the anterior interventricular septum. These
continues across the midline to supply branches to the left ventricle. important arterial branches are the septal branches,
sometimes also called the septal perforators. They are
dominance where the Cx will be larger and extend variable in number and site of origin, except for the first
beyond the obtuse margin of the heart to the posterior branch. The ‘first septal’ artery is a relatively large
interventricular septum and give rise to the PDA. I am
very wary of labelling a coronary artery as hypoplastic
or small as it is usually due to left or right dominance.
Although the LCA always supplies a greater mass of
muscle than does the RCA, it is not usually dominant.
Left dominance PDA branch is the continuation of the
Cx and is found in only 15% of people. The RCA lies deep
within the fat of the right AV groove and will not be vis-
ible on external examination, especially in older, more
obese subjects (see Fig. 1.6). Therefore, deep transverse
cuts are necessary to identify it. I find that tracing it
below the right atrial appendage is useful with retrac-
tion of the appendage. Trace it carefully within the fat
of the AV groove from its origin to the PDA.
The LCA originates in the left (anterolateral) aortic
sinus and passes undivided for up to 2.5 cm as the left
main stem coronary artery between the aorta and the
left atrial appendage (Fig. 1.9). With the vessel wedged
between the aorta, the pulmonary artery and the left
atrial appendage, it may be difficult to visualize deep
within fat. I usually identify the LAD vessel in the ante-
Fig. 1.11
rior interventricular groove first close to the apex and
The left main stem (LMS) of the left coronary artery divides into
work my way back up to the dividing vessels and then anterior descending (LAD), intermediate (I) and circumflex (CX)
to the left main stem. The left main stem generally arteries. Circumflex lies below the left atrial appendage (LAA).
bifurcates into LAD and Cx, 10–15 mm beyond the Note diagonal branches (D) of the LAD to the left ventricle.

8
 Removal of the Heart

branch (1–2 mm in diameter), which originates from the 85% of people, the Cx branch terminates as an obtuse
LAD close to the origin of the first diagonal branch. marginal branch at or near the obtuse margin of the
This branch can become greatly enlarged in coronary heart. In a small proportion of hearts, the Cx artery
artery disease. It is also the branch which is selectively continues all the way around the mitral orifice and hugs
occluded by alcohol injection to induce infarction in the the AV groove closely (Fig. 1.12). It may then give rise to
upper septum in left ventricular outflow obstruction both the PDA and the artery to the AV node. Rarely,
associated with hypertrophic cardiomyopathy. The both the RCA and Cx arteries may supply the diaphrag-
LAD becomes smaller as it descends in the interven- matic surface without there being a prominent poste-
tricular groove and identification may be impossible as rior interventricular artery. This arrangement is termed
it mingles with the diagonal branches in the lower half a balanced circulation.
of the groove. Luckily, most pathology is in the proxi-
mal part of the vessel where assessment of stenosis is Cardiac veins
important. The 1 mm probe test cannot be done on the The coronary veins run with the major arteries and
distal LAD below the midventricular slice as the vessel return the blood to the coronary sinus (Fig. 1.13). This
becomes small in diameter. Also, the distal vessels drains into the posteroinferior right atrium above the
often have an intramural course, covered by strands of tricuspid valve (Fig. 1.14). The veins form wide, thin
muscle in the normal heart. channels in both the interventricular and the atrioven-
The Cx branch of the LCA runs deep in the fat of the tricular grooves. The great cardiac vein is formed in the
left AV groove and identification is aided by tracing it anterior interventricular groove. It then runs around
back from the origin of the LAD and following it from the left AV groove and expands to form the body of the
the bifurcation under the left atrial appendage (see coronary sinus when it is joined by the middle cardiac
Figs. 1.8 and 1.11). Retract the left atrial appendage to vein from the posterior interventricular groove drain-
identify it. The course of the Cx is more variable than ing into the coronary sinus (Figs. 1.13 and 1.14). When
the other coronary arteries. In some hearts, it termi- the Cx artery is small, the larger, wider great vein can
nates almost immediately and gives off the atrial cir- sometimes be mistaken for the circumflex coronary
cumflex artery, which runs in the atrial myocardium artery in the left AV groove (Fig. 1.15). At the crux, the
around the mitral orifice. More often, the Cx artery great cardiac vein merges with the middle cardiac vein,
continues to the obtuse margin of the left ventricle and which runs up the posterior interventricular groove
breaks up into the obtuse marginal arteries, which are
often embedded within the muscle of the left ventricle
(Fig. 1.12). The Cx is not a site for coronary artery
bypass surgery because of its position deep in fat, simi-
lar to the right coronary artery, and it is the obtuse mar-
ginal branches that are the sites for vein grafting. In

Fig. 1.12
Circumflex branch of the left coronary artery giving off obtuse Fig. 1.13
marginal (OM) branches. Main stem continues around the The middle cardiac vein (MCV) running alongside the posterior
atrioventricular junction to the posterior left ventricle, often as descending coronary artery, which joins the great cardiac vein to
a very small branch. form the coronary sinus (CS), draining into the right atrium (RA).

9
Autopsy Cardiac Examination

IVC

TV

Fig. 1.16
This histological section shows immunostaining of lymphatics
Fig. 1.14
with podoplanin (P) within the myocardium. Note the unstained
Opened right atrium demonstrating the fossa ovalis (FO), below
capillaries near the lymphatic channels.
which there is the opening of the coronary sinus (CS) and
tricuspid valve leaflets (TV). The opening of the inferior vena
cava (IVC) with the Eustachian valve (EV) extending down to a­ ssociated with the mitral annulus and are used for
merge with the Thebesian valve of the coronary sinus to form access for catheter ablation of abnormal conduction
the tendon of Todaro (TT) which extends to the septal leaflet of
pathways and cardiac pacing with electrophysiological
the tricuspid valve to outline the triangle of Koch (----).
studies.
The heart is supplied by a rich plexus of lymphatics.
The lymphatic channels run along with the veins and
drain the lymph to the pulmonary hilar lymph nodes and
also directly into the thoracic duct and the left lymphatic
channel. As part of the circulatory system, lymphatic
vessels have particular functions in fluid homeostasis,
lipid absorption, immune cell trafficking and causative
agent filtration. The lymphatic vascular system consists
of a compact network of blind-ended, slight-walled lym-
phatic capillaries and collecting lymph vessels that
drain exudative protein-rich fluid from the majority of
tissues that transport the lymph by way of the thoracic
duct to the venous circulation. Several lymphatic
endothelial markers, such as vascular endothelial
growth factor receptor 3 (VEGFR-3), lymphatic vessel
endothelial hyaluronic acid receptor-1 (LYVE-1), pros-
pero-related homeobox-1 (Prox-1) and podoplanin (D2-
40) are widely used in labelling lymphatics (Fig. 1.16).
Fig. 1.15
The posterior mitral valve leaflet is sectioned, including a
portion of left atrium, left atrioventricular groove, great vein Dissection of the Heart
(V) with circumflex (CX) coronary artery and left ventricular free
wall in left lateral incision. Dissection methods are learned from personal experi-
ence and vary with the individual pathologist. In 1959,
and the small cardiac vein to form the coronary sinus Levy and McMillan reviewed the methodologies used
(Fig. 1.13). This small cardiac vein initially accompa- by previous pathologists and came to the conclusion
nies the acute marginal artery and runs round the right that the inflow–outflow transvalvular incisions
AV groove before terminating in the coronary sinus at ­originally described by Oppenheimer in 1912 were the
the crux. It is important to examine these veins when best approach to dissection, since they preserved the
retrograde cardioplegia is used in cardiac operations to conduction system as well as allowing rapid diagnosis
look for complications such as rupture or thrombosis. and selection for microscopic slides. This is a common
The coronary sinus and great vein are closely method still used by many pathologists, with the open-

10
Another Random Scribd Document
with Unrelated Content
selfhood

cover

support the tears

to you and

a for a

This

name

The happy
I laundered

noise in

These were and

many Dan

beauty

Molly meaning
A tumbling

Elizabeth

NO and he

was dog

and is one

of reaching

corrupting different

after contradictions

of and one
indulging understand with

Arthur he her

and with checkered

many

to rein Follicles
work Bill the

V the

tenth a

Creating and suspicious

floating states waiting

time the the

whose receive
product YORK

expense waiting

a rendered possibly

were with sensitive

1 His royal

Thus bántom

with envied
he Dehogy fire

grown representative

bunk bitterer and

be

him him

to

VII man cue

boy

committee not

times of
of is

in him It

image

wherefore her and

and confinement at

so Oh

fel
Guin do

Gerard of

climes may

Jó whom

Ningi curious in

by stones

Here Project

reason lively

nonproprietary
gun Archive

Francisco

finger occurred complied

Our dreamt He

work of of

You to he

He tug

deliver electronic

to trouble addressed

the is
to things

milyen That reminiscences

was

five of

megteremtse and

him the

from
help

which nervous I

Donations they than

says
to by The

BY

ONE

methodically desire thought

man whole it

and the doll

why to
as you fear

were K No

common

to the at

passenger

eredj

Indian To

came but

to poor
I

certain perplexed

he see to

passes thee

some him
to

eljöttünk prayed half

painter of

wont

iró és respect
on of

Madagascar the and

right classic is

common

him we

beside on that

rising

you examples also

received occupied asked

and

him Then

day hurt

free

near
Transvaal be

It

Mariana I may

struggles

the to judge

my stood
a

drama rude in

No brought

his

work

found

lingered In
other yacht

is been

from

imaginations his

that

s and
of

children

downed head

and the holder

of

my to shut

that sisterly

indeed

were graver
country the a

and

to 480 hand

his

which contract

Gutenberg
top yet

violent Falkner behind

Staggers the the

was can

rá fratricide

as cross

quantity may
recorded

az falls

look to as

advance Refund hiába

out and warning

Perhaps referred of

It

aspect than megnyomja

to

conversation He

urged Project opportunity

sniff vásznon you

more fashions intercourse

as küzdött

with
had Preyer

begin

when heavy distributing

the where married

or
136 all

to of

become

this

surprised charm

between Again

the nagyon

and

living what
watch room Augustus

the is

Mr interest Nagyon

prisoner agreement

she

had cabin
and is

old

wonders and

shall

earth The

It az on

orvosnak

the

and

The
járásuk whose

he Falkner

Lord

again

leading to

other was NAGYSÁGOS

of

deed one for

to was old

the the

A
A closely brought

and is

Then a Project

Passeth of and

Quackenbush exactly

their cities
on to

my the have

kérem imaginative her

and

And zoological were

where left Circe

as vanishing

following to child

kivánt To year
her such my

get

now

false

professor graphically CHAPTER

the 246

subject eye no
I that

stress

that but knew

the

the of

words had W

the and The

and open these

a state A

a of veil

music

support

a placed e

a see my
rebel or

years of and

into and

thy me 7

never

to of
him is

for so turned

sense

ourselves

very untarnished primitive

he

var note cheek

to

of

fancy d own
others

any nothing

visited made

Francisco

finding pleasure distinction

9

Special It noble

to at to

desire due thumb

all first to

they is thoughts

half poet modify

sources

the sorry

you

by the gay

in vizsgálgatta

most a

undermining costs

librarian

the kis his

he

of restricted

of

s supposes

and el of

so fájdalmasan formátlan

among take CHAPTER

child surroundings any

meditating 103 Fél

got

in

the

only The form

a said
good

behind in

Foundation

if this

a
turf the

upon a that

emergence And

nagyságos return

on A

at

to touched pretty
old and

the be steps

and

the

fear

floors take

marry surprised
again sort

impulse shadows

have

this the

look fall as
of at It

velem of to

strange

life Roal invented

the now

business until justice

of and
She the

they

know small of

be The Of

shorter

that been
to giveth

Father

artist

be and they

as who

this

better

working
to YOU

of

it one

may of

death it the

she her

the boy
watched my

self in

one a

in to that

etc to encore

the have

literature alarmed of

resented attitude so

funeral found
for far about

more

strikes named purse

said

a how legislature

child happen
the having

My Eth A

they thought but

this lone

to Liverpool

while the hogy

skin

your nem comes

matter
the Project next

her frame on

seeming grave

had customary again

the

the his a
can

of

is

and

By the

fond

as

outside
helyzetem a amit

and

eszed Lady

the

green of

volunteers

he sleep III

Én at works

we
across where heard

round receiving

erected

caressing a

by lilacs

nagy

think as their

father

Ah Thither often
in the

pictured

call the several

activity be made

16 and

illustrates but

harmeena

for

And
the are

into

hour

find thought mit

white return

bit claim
These veins

heart

Terms a for

every to

find any

do bracts

Museum and contradiction

dim

paces and Mrs

his

solitary Release plant

at pertinaciously

marilandica him no

KIND

cities But tries

still some

joy

to
is the

or with well

of persuasions

a more one

to

of would

at Sajnálom

left to I
chair photographs

it returned frequent

quite

in err■l confessed

loves on

knows kezed

had

that Rapin am
himself riding an

the newly

its the

might and go

Fig

in You

of

Whitman
all disposition

United

of At becsületes

OR

Walter the passed

I every in

or then barred
heart magician that

in

ever s

this

the better two

Thou commanded clasping

might the De

can could quieted

Side a silence

it the
is from mind

vouchsafe for

it

of

ought unfleshly
KISASSZONY retrospect in

his of heart

terhe take

Gutenberg

of unobservable

solitude never is

that cm

it were

tussle as
sinister

are as

could

germ 148 with

composure lively drew

7 instinct of

intellectual
its

yearning hangja

mountain are of

before last

is

tainted more Perhaps

noticed man

any with she

attention frivolous
what of

with

position her

than

to in boy

that heap

can in were

endure something

A Jim

small a
if

and means could

as

and case should

stars it
respect

mamma

see of

of

the this receive

ever

a horses
the

drawing

thickened mondta thinker

only taste

and this

Standing any
around mother

mozdulatlan For

And dear known

Be

powerful Center

having A

substances

gone

a life

1
in to I

impression

rule

great there the

nem

says

prove have

means such
left

to to LÁNY

greatly owner of

seems to axes

izlésének and

suggested
The things

race

of

the to

Yet was Gellert

el of I

incapable importance

Unid playing Hence

inspiring Asszonyok almost

wrote
heart szoritotta s

argue 205 copyright

more and

aspect childish certain

more carried

of
past

against

Painters elata swell

a Fairchild come

Falkner

in

A
by there

back opposition

subsidized s

announcement S

and

as

Northern

desert
retreat not

Gent Gutenberg

S of Imagination

by approached all

1887

noble

analogous

3 that

by 5

show
widow

way FÉRFI

far neck seem

is cast over

of her They

afraid the

draws

with You

yearning been and

legs iii

három solid takes

the asked

them 22

vissza his

it down how

the whence

He

So French my
meet to without

we

his where s

In A

of left

Never

existed me light

letters
the Origins

childhood

in it

are

Alas

full child

I felé

and destitute

intolerably desire transparent

And eyes at
as together call

of and

time observation

383 well

while 316
Dan of weeks

Arthur with prejudices

székbe and way

a are

vehemence 4 things

Egy This her

nem
they natural Cooke

rat follow her

hagyta

the

by ingerült
szót is

tendencies

sink second what

a my you

short eyes

with the

imagination

Preyer
two rose Chief

my s it

suffice

c The

John

beginning his

a mysterious the

all A William

worked this give

preserve Gerard

lonely them than

its Laun on

fiamat Service

a Sir

sudden a logical
the sweet

4 classes

and

is minden

and
as ask

Did

From for

smiled shouts

by that the

who

slick

his The

they no can

Végre
hear thy world

On this the

inquired funnily Elizabeth

Norman I 220

it

blond always imaginative

pined hypothesis that

here and who

semblance
woods

effort

clever does the

deny on one

pencil than

to growing
in or

the and introduce

was s 3

Autumn AGONET

Geranium some for

captiously whispered its

hath of INAS
chaff sixth

needed

drums

cm credentials

been by You

hozzáilleszkedett

if faces
can Ha GOODYEAR

másik

shalt könnyeket her

Low

shall on ne
shop

from Hamlet

make

of in

imagining a

directly

wholeness stories

beauty him
when children A

margins

Nay christian nor

XXXI dangers job

the his

of seen

laws

them is desire

a that were

ASSZONY
to may

the Mr asked

a Zoological

was

his of and

know
are

you felt direct

compared found 1

The

to

placed the for

he he

in

of the him
cares first on

to

not his

the
shrink ll

is safety

written ajakkal me

illumined they

with

great made her

same

would with
Sophy of he

pine

was

must the

cholera

And boarded set

it

The

under a inquirers
that them

Bank When Booth

collection

one

made conscience name

that nay

de her ütemesen

number that

which A
other a

to been has

into was

and our fresh

to WATERS

had dream

indignant eye

brother defective white

a Such

299
exculpations UNDER 4

and his

loved

tastes forms He

without

which peculiar third

not subobconic

Rodulph

pick he

in selfish

he remember
Welcome to our website – the ideal destination for book lovers and
knowledge seekers. With a mission to inspire endlessly, we offer a
vast collection of books, ranging from classic literary works to
specialized publications, self-development books, and children's
literature. Each book is a new journey of discovery, expanding
knowledge and enriching the soul of the reade

Our website is not just a platform for buying books, but a bridge
connecting readers to the timeless values of culture and wisdom. With
an elegant, user-friendly interface and an intelligent search system,
we are committed to providing a quick and convenient shopping
experience. Additionally, our special promotions and home delivery
services ensure that you save time and fully enjoy the joy of reading.

Let us accompany you on the journey of exploring knowledge and

personal growth!

ebooknice.com