HEART DISEASE
Ed Friedlander, M.D., Pathologist
scalpel_blade@yahoo.com

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Welcome to Ed's Pathology Notes, placed here originally for the convenience of medical students at my school. You need to check the accuracy of any information, from any source, against other credible sources. I cannot diagnose or treat over the web, I cannot comment on the health care you have already received, and these notes cannot substitute for your own doctor's care. I am good at helping people find resources and answers. If you need me, send me an E-mail at scalpel_blade@yahoo.com Your confidentiality is completely respected. No texting or chat messages, please. Ordinary e-mails are welcome.

I am active in HealthTap, which provides free medical guidance from your cell phone. There is also a fee site at www.afraidtoask.com.


If you have a Second Life account, please visit my teammates and me at the Medical Examiner's office.

Freely have you received, give freely With one of four large boxes of "Pathguy" replies.

I'm still doing my best to answer everybody. Sometimes I get backlogged, sometimes my E-mail crashes, and sometimes my literature search software crashes. If you've not heard from me in a week, post me again. I send my most challenging questions to the medical student pathology interest group, minus the name, but with your E-mail where you can receive a reply.

Numbers in {curly braces} are from the magnificent Slice of Life videodisk. No medical student should be without access to this wonderful resource.

I am presently adding clickable links to images in these notes. Let me know about good online sources in addition to these:

Freely have you received, freely give. -- Matthew 10:8. My site receives an enormous amount of traffic, and I'm still handling dozens of requests for information weekly, all as a public service.

Pathology's modern founder, Rudolf Virchow M.D., left a legacy of realism and social conscience for the discipline. I am a mainstream Christian, a man of science, and a proponent of common sense and common kindness. I am an outspoken enemy of all the make-believe and bunk that interfere with peoples' health, reasonable freedom, and happiness. I talk and write straight, and without apology.

Throughout these notes, I am speaking only for myself, and not for any employer, organization, or associate.

Special thanks to my friend and colleague, Charles Wheeler M.D., pathologist and former Kansas City mayor. Thanks also to the real Patch Adams M.D., who wrote me encouragement when we were both beginning our unusual medical careers.

If you're a private individual who's enjoyed this site, and want to say, "Thank you, Ed!", then what I'd like best is a contribution to the Episcopalian home for abandoned, neglected, and abused kids in Nevada:

I've spent time there and they are good. Write "Thanks Ed" on your check.

Help me help others

My home page
More of my notes
My medical students

Especially if you're looking for information on a disease with a name that you know, here are a couple of great places for you to go right now and use Medline, which will allow you to find every relevant current scientific publication. You owe it to yourself to learn to use this invaluable internet resource. Not only will you find some information immediately, but you'll have references to journal articles that you can obtain by interlibrary loan, plus the names of the world's foremost experts and their institutions.

Alternative (complementary) medicine has made real progress since my generally-unfavorable 1983 review. If you are interested in complementary medicine, then I would urge you to visit my new Alternative Medicine page. If you are looking for something on complementary medicine, please go first to the American Association of Naturopathic Physicians. And for your enjoyment... here are some of my old pathology exams for medical school undergraduates.

I cannot examine every claim that my correspondents share with me. Sometimes the independent thinkers prove to be correct, and paradigms shift as a result. You also know that extraordinary claims require extraordinary evidence. When a discovery proves to square with the observable world, scientists make reputations by confirming it, and corporations are soon making profits from it. When a decades-old claim by a "persecuted genius" finds no acceptance from mainstream science, it probably failed some basic experimental tests designed to eliminate self-deception. If you ask me about something like this, I will simply invite you to do some tests yourself, perhaps as a high-school science project. Who knows? Perhaps it'll be you who makes the next great discovery!

Our world is full of people who have found peace, fulfillment, and friendship by suspending their own reasoning and simply accepting a single authority that seems wise and good. I've learned that they leave the movements when, and only when, they discover they have been maliciously deceived. In the meantime, nothing that I can say or do will convince such people that I am a decent human being. I no longer answer my crank mail.

This site is my hobby, and I do not accept donations, though I appreciate those who have offered to help.

During the eighteen years my site has been online, it's proved to be one of the most popular of all internet sites for undergraduate physician and allied-health education. It is so well-known that I'm not worried about borrowers. I never refuse requests from colleagues for permission to adapt or duplicate it for their own courses... and many do. So, fellow-teachers, help yourselves. Don't sell it for a profit, don't use it for a bad purpose, and at some time in your course, mention me as author and KCUMB as my institution. Drop me a note about your successes. And special thanks to everyone who's helped and encouraged me, and especially the people at KCUMB for making it possible, and my teaching assistants over the years.

Whatever you're looking for on the web, I hope you find it, here or elsewhere. Health and friendship!

PicoSearch
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More of Ed's Notes: Ed's Medical Terminology Page

Perspectives on Disease
Cell Injury and Death
Accumulations and Deposits
Inflammation
Fluids
Genes
What is Cancer?
Cancer: Causes and Effects
Immune Injury
Autoimmunity
Other Immune
HIV infections
The Anti-Immunization Activists
Infancy and Childhood
Aging
Infections
Nutrition
Environmental Lung Disease
Violence, Accidents, Poisoning
Heart
Vessels
Respiratory
Red Cells
White Cells
Coagulation
Oral Cavity
GI Tract
Liver
Pancreas (including Diabetes)
Kidney

Bladder
Men
Women
Breast
Pituitary
Thyroid
Adrenal and Thymus
Bones
Joints
Muscles
Skin
Nervous System
Eye
Ear
Autopsy
Lab Profiling
Blood Component Therapy
Serum Proteins
Renal Function Tests
Adrenal Testing
Arthritis Labs
Glucose Testing
Liver Testing
Porphyria
Urinalysis
Spinal Fluid
Lab Problem
Quackery
Alternative Medicine (current)
Preventing "F"'s: For Teachers!

Medical Dictionary

Courtesy of CancerWEB

KCUMB Students
"Big Robbins" -- Heart
Lectures follow Textbook

QUIZBANK

{08187} Heart within the pericardium

ekg What's a 'double-blind study'? Two pathologists trying to read an EKG!

A simple rule to follow, whatever you do: If you're not having fun, you're not in the right place.

Once I had brains, and a heart also; so having tried them both, I should much rather have a heart.

Does CPR work better if you do your compressions with a toilet plunger? The great controversy, including a frank admission that CPR....: JAMA 273: 1299, 1995.

A talking monitor-defibrillator now exists that tells resuscitation teams how well they are doing and how well they are complying with guidelines. It clearly helps teams do things right, and after 1586 uses had no demonstrable impact at all on any outcome measure (BMJ 342: d512, 2011).

Out-of-hospital CPR survivors do twice as well (i.e., after you exclude those that were already obviously hopeless, maybe 6% of them are alive without obvious brain damage a month later) if you DON'T do the mouth-to-mouth stuff...: Lancet 369: 920, 2007.

Your instructor's personal decision not to allow CPR to be performed on him is not to be taken as rejection of the work that has gone into developing or practicing the technique, or a denial that some folks are saved by it and leave good quality lives afterwards. We can chat about this if you like.

According to the British, the United States of America now spends 0.5-1% of our ENTIRE gross national product on the critical care unit, with the vast majority of the patients not living long (Lancet 376: 1273, 2010).

Blood Vessels and Heart
Taiwanese pathology site
Good place to go to practice

Cardiovascular
Surgical Pathology Atlas
Nice photos, hard-core

Heart Slides
Iowa Virtual Microscopy
Have fun

Cardiovascular
Utah cases for path students
Juliana Szakacs MD

Cardiovascular Diseases
First Section
Chaing Mi, Thailand

Cardiovascular Diseases
Second Section
Chaing Mi, Thailand

Cardiovascular Diseases
Third Section
Chaing Mi, Thailand

Cardiovascular
Photos, explanations, and quiz
Indiana U.

Cardiovascular Pathology
Photo Library of Pathology
U. of Tokushima

Cardiovascular
Brown Digital Pathology
Some nice cases

Heart Transplant Pictures
Great site
Transplant Pathology Internet Services

Myocardium Exhibit
Virtual Pathology Museum
University of Connecticut

Heart and Vessel Pathology
Photomicrograph collection
In Portuguese

Cardovascular Pathology
Sampurna Roy, MD
Lots of photos and good text

Normal Heart
WebPath photo

Normal aortic valve
WebPath photo

Normal tricuspid valve
WebPath photo

Normal coronary artery
WebPath photo

Heart Histology
Ed's Histology Notes

Normal myocardium
WebPath photo

Myocardium
Slide from Andrea McCollum MD
Cuyahoga County Coroner's Office

Normal heart
Textbook-perfect
KCUMB Team

LEARNING OBJECTIVES

Define and use the following terms:

Describe the changes in the myocardium in a trained aerobic athlete, and recognize that these are desirable rather than harmful.

Review the general pathology of congestive heart failure. You should probably already know this from your earlier studies of cardiac physiology and the pathology of the body fluids.

Describe the clinical spectrum of atherosclerotic coronary artery disease.

Tell how the various kinds of angina pectoris arise. Explain how myocardial infarcts occur, why they are so serious, and what the pathologist will see at autopsy under varying circumstances. Tell how subendocardial infarcts occur. Describe the typical picture of chronic ischemic cardiac disease. Tell what a pathologist will find in classic coronary "sudden death", and when the diagnosis can and cannot be made.

Mention the other causes of ischemic heart disease, and tell about how they operate. Tell about the other causes of sudden death.

Define and use the following terms:

    atresia
    clubbing
    concentric hypertrophy
    congenital heart disease
    cor triloculare biatriatum
    cyanotic congenital heart disease ("blue baby")
    dilatation
    Eisenmenger's syndrome
    endocarditis
    hypertensive heart disease
    jet lesion
    late cyanosis
    paradoxical embolus
    polycythemia
    pressure overload
    reperfusion injury
    shunt
    transposition

Astronaut Alan Shepard gets auscultated

Alan Shepard
Astronaut

Recall the upper limit of normal weight of the sedentary adult's heart, left ventricular thickness, and right ventricular thickness.

List the minimal anatomic criteria for hypertensive heart disease. Describe the role of pressure overload (clear) and chronic catecholamine stimulation (probable) as causes of this hypertrophy. Describe the gross and microscopic changes typical of the hypertensive's heart. Appreciate that this is a very common finding, both clinically and at autopsy. Explain the difficulty of making the diagnosis when left ventricular failure confuses the picture.

Distinguish cor pulmonale from right heart enlargement caused by left ventricular failure or by congenital malformations. Recognize pulmonary embolization as the only setting for true "acute cor pulmonale". Describe the hypoxic vascular response, and describe how the shape of the right ventricle on cross section differs from normal in this setting. Recognize cor pulmonale as a sufficient explanation for sudden death cases coming to autopsy. Appreciate the tremendous clinical importance of cor pulmonale in many settings.

Tell what we know about causes of serious congenital heart disease. Recall the incidence per thousand live births, and the risk of recurrence. List the problems common to all these children, and the hazards presented by jet lesions.

List tetralogy of Fallot (most common), transposition of the great arteries, persistent truncus arteriosus, and tricuspid atresia as the four most important forms of congenital cyanotic heart disease, and clearly explain the abnormal anatomy and physiology of each. Explain the seriousness of the right-to-left shunt, the most dreaded consequences of paradoxical embolization, and other problems faced by these patients.

Diagram tetralogy of Fallot, listing the four features that define the syndrome.

Describe the usual pattern in transposition of the great arteries, and how a septal defect permits survival after birth. Distinguish "corrected transposition".

Define truncus arteriosus, and recall that it leads eventually to pulmonary hypertension.

Recall ventricular septal defect, atrial septal defect, and patent ductus arteriosus as the major causes of congenital left-to-right shunt. Explain the associated hazards, and especially why cyanosis develops weeks to years after birth in patients with left-to-right shunts.

Recall the location of most ventricular defects. Explain the reason that a "VSD" is unwholesome. Give the meaning of "Roger's disease" and the spontaneous closure rate.

Describe the usual clinical course in atrial septal defect, and tell why these are so seldom recognized in youth. Distinguish ostium primum ("endocardial cushion"), ostium secundum, and sinus venosus atrial septal defects. Recognize ostium primum as the usual form in Down's syndrome, as ostium secundum as most common in other people.

Locate the normal ductus arteriosus and define its function and fate. Identify prostaglandin E as maintaining the patency of the normal ductus. Recognize that in congenital heart disease with impaired blood flow to the lungs, it is good for the ductus to remain open.

Describe patent ductus arteriosus, mentioning its relationship to other defects and to Turner's syndrome, and its most common location. Tell why preductal coarctation can cause right sided heart failure in utero. Describe how it causes hypertension, and mention clinical findings that would alert the pediatrician to post-ductal coarctation. Mention the reasons for getting it fixed surgically.

Recognize pulmonary stenosis with intact interventricular septum as a common, serious cardiac malformation.

Describe the problems caused by a bicuspid aortic valve. Describe the aortic valve in congenital valvular aortic stenosis, and the defect in congenital sub-valvular stenosis. Explain why aortic stenosis commonly produces sudden death.

Give a short account of each:

Relate dextrocardia, Kartagener's syndrome, immotile cilia, and situs inversus totalis.

Remember that mitral stenosis is virtually always caused by scarring from rheumatic fever.

List the important causes all eight valvular syndromes.

List the three important causes of acquired aortic valve stenosis. Sketch a normal (three cusp) aortic valve with calcific stenosis, mention the age of onset, and explain why the process is so serious. Sketch a bicuspid valve with the same thing, and mention which kind of valve is more prone to this.

Describe Barlow's "syndrome" of the mitral valve. Tell how prevalent the disease is, describe the relationship to Marfan's syndrome, and tell what makes the mid-systolic "click". Describe the four complications (bacterial endocarditis, mitral insufficiency, rhythm disturbances, and cardiac neurosis) that can result.

Describe the essential pathogenesis of rheumatic fever and rheumatic pancarditis, and the typical time of onset. List the six principal findings, and describe the changing incidence of the disease in the U.S. and globally. Mention the recurrence rates cited after repeat strep throat. Describe a typical Aschoff body, and tell where it is located. Explain why rheumatic endocarditis is considered more serious in the long run than the myocarditis or pericarditis, and describe the locations of the lesions on the valves in the acute illness.

Describe the pathologic anatomy in chronic mitral valve deformity and chronic aortic valve deformity following rheumatic fever.

Explain why infective (i.e., bacterial) endocarditis is so serious. Tell ways in which the blood becomes seeded with microbes, and times and places where the fibrin-platelet thrombi form inside the heart. Describe acute infective endocarditis, the types of valves that may be involved, its usual cause, and the fatality rate. Name the bacterium most often responsible for subacute bacterial endocarditis. Tell what you will see grossly and microscopically. Tell what valve are most often involved in IV drug-users and in other people. Mention why bacterial endocarditis might be "culture negative". Describe the dread complications of bacterial endocarditis in some detail, and mention clues to the diagnosis. Tell what healed bacterial endocarditis looks like.

Describe typical settings for nonbacterial thrombotic endocarditis ("marantic endocarditis"). Describe the gross and microscopic lesions.

Describe calcification of the mitral annulus as seen in some older individuals, and describe its clinical significance.

Describe the gross, microscopic, and functional lesions in carcinoid syndrome, and explain why we think that the lesions usually occur only on the right side.

Recognize the five complications of valve replacement.

Give a short account of each:

Distinguish "myocarditis" (i.e., inflammatory, i.e., autoimmune or infection) and "cardiomyopathy" (i.e., a noninflammatory disorder).

Describe the gross and microscopic pathology and clinical course of a typical case of myocarditis. Recall viruses, especially Coxsackie A & B and parvovirus B19 as the most important causes of significant acute myocarditis, and that this is (fortunately) rare. Mention why we think much of the damage is immune-mediated. Explain why we think many cases of "idiopathic dilated cardiomyopathy" ("Barney Clark's disease") result from Coxsackie myocarditis.

Given a cardiomyopathy, subclassify it as dilated ("flabby heart"), hypertrophic ("muscle-bound heart"), or restrictive-infiltrative-obliterative (i.e., amyloid, "stiff heart").

Recall "dilated-congestive" cardiomyopathy as an end-stage of various longstanding cardiac injuries, and describe the way this heart looks and functions. Describe the histology, and why mural thrombi form.

Cite the clinical features of alcoholic cardiomyopathy, and relate it to cobalt toxicity and beriberi. Recognize alcohol itself as a controversial cause of cardiomyopathy.

Mention the typical setting for peripartum cardiomyopathy, and explain why we suspect a nutritional deficiency.

Recall that disarray of the myocardial fiber arrangement as the typical, though not invariable, feature of hypertrophic cardiomyopathy. Recognize "asymmetric septal hypertrophy" and "idiopathic hypertrophic subaortic stenosis" as the classic hypertrophic cardiomyopathy in which the septum is primarily involved. Recognize "obstructive hypertrophic cardiomyopathy" as the feared consequence of an over-thick septum, and describe this syndrome. Cite the gene responsible for many of these cases.

Briefly describe the heart disease seen in sarcoidosis and systemic amyloidosis, and recall the prevalence of minor amyloid deposits in the hearts of the elderly.

Describe endomyocardial fibrosis as seen in the apices of hearts of young Africans. Describe Loeffler's endocarditis ("with eosinophils") clinically and histologically. Describe endocardial fibroelastosis as seen in U.S. infants, both grossly and clinically.

Describe cardiac damage from anthracyclines (adriamycin and its relatives), and from cocaine.

Recall ruptured MI, penetrating injury, and backwards rupture of an aortic dissection as the only common causes of hemopericardium.

Tell how much fluid is required to produce cardiac tamponade, and under what circumstances it must accumulate.

Recognize the causes of pericarditis from table 13-9 of "Big Robbins". Mention the classic posture assumed by patients with pericarditis. Mention some of the organisms (TB, viruses) that may come from a serous pericardial effusion.

Recognize myocardial infarcts, uremia, radiation, lupus, rheumatic fever and trauma as the causes of fibrinous pericarditis, describe the origin of the distinctive physical sign, give the gourmet comparisons, and mention the anatomic progression and clinical prognosis.

Describe the causes and outcome of purulent (suppurative) pericarditis. List the significant causes of hemorrhagic pericarditis (i.e., TB and cancer) and caseous pericarditis (TB).

Recognize the cancers that tend to metastasize to heart. Be aware of the problems that such metastases can cause, and the difficulty of making the diagnosis.

Recall atrial myxomas ("wrecking balls") as the only common primary tumors of the heart. Tell where they arise and how they cause problems. Recognize their gross and microscopic appearances.

Recognize any good example of each of the types of lesions depicted in the videodisc series.

Say "REE-nin", not "RENN-in", when talking about that important hormone from human physiology. Rennin is from a calf's stomach and you use it to make cheese.

The heart has its reasons of which Reason knows nothing. -- Blaise Pascal

The heart weeps for what is has lost; the spirit rejoices for what it has found. -- Sufi Proverb

{03467} normal histology

INTRODUCTION

* THE PROARRHYTHMIAS FIASCO

Pacemaker wire
WebPath photo

Hypertrophied heart
Ed Lulo's Pathology Gallery

Cardiac Hypertrophy
From Chile
In Spanish

Myocardial hypertrophy
Boxcar nuclei and thick fibers
KCUMB Team

ATHLETE'S HEART (is good: Eur. Heart. J. 17: 127, 1996; making the call Prog. Card. Dis. 54: 387, 2012).

Athletic heart
Tom Demark's Site

BIG HEARTS

CONGESTIVE HEART FAILURE ("CHF"; update Lancet 373: 941, 2009)

Left ventricular hypertrophy
Perhaps from hypertension
KU Collection

Hypertrophied hypertensive heart
WebPath photo

Hypertrophied hypertensive heart
WebPath photo

ISCHEMIC HEART DISEASE

Coronary Artery Exhibit
Virtual Pathology Museum
University of Connecticut


Pathology of Myocardial Infarction
WebPath Tutorial

Syndrome X

Acute myocardial infarct
Great labels
Romanian Pathology Atlas

Healing myocardial infarct
Great labels
Romanian Pathology Atlas

Acute myocardial infarct
Pittsburgh Pathology Cases

Large infarct
WebPath photo

Massive anteroseptal infarct
WebPath photo

Enzyme diagnosis of acute MI
Pittsburgh Pathology Cases

Myocardial Infarcts I
From Chile
In Spanish

Myocardial Infarcts II
From Chile
In Spanish

Mycardial Infarcts III
From Chile
In Spanish

Acute Myocardial Infarct
Text and photomicrographs. Nice.
Human Pathology Digital Image Gallery

Myocardial Infarct, Healed
Text and photomicrographs. Nice.
Human Pathology Digital Image Gallery

{03476} atherosclerosis, coronary artery
{06531} ruptured plaque with thrombus

Atherosclerotic coronary artery
Serial sections
WebPath photo

Coronary thrombus
Great labels
Romanian Pathology Atlas

Ruptured plaque with thrombus
WebPath photo

Ruptured plaque with thrombus
WebPath photo

Coronary with atherosclerosis
Decide yourself about obesity
WebPath photo

Coronary with severe atherosclerosis


Normal coronary artery
WebPath photo

Atherosclerotic coronary artery
WebPath photo

Severe atherosclerosis with calcium
WebPath photo

Severe atherosclerosis of a coronary artery
WebPath photo

Fresh coronary thrombus
WebPath photo

Fresh coronary thrombus
WebPath photo

Hemorrhage into a plaque
WebPath photo

Fresh coronary thrombus
WebPath photo

Recanalized thrombus
WebPath photo

{06569} polyarteritis nodosa of a coronary artery
{06587} aspergillus infection of a coronary artery

Kawasaki disease
Article and photos
AAFP

Epstein-Barr coronary aneurysm
Advanced students
Yutaka Tsutsumi MD

{03525} syphilis. Nice plasma cells.

{06575} coronary artery dissection

{03386} coronary artery amyloidosis
{06584} amyloid (special stain)
{17483} amyloid myocardium

Contraction bands
WebPath photo

Early MI
WebPath photo

Early MI
WebPath photo

Infarct, ~3-4 days
WebPath photo

Infarct, 1-2 weeks
WebPath photo

Healed subendocardial infarct
WebPath photo

Old MI, scar
WebPath photo

Myocardial infarct
Karyorrhectic neutrophils
KU Collection

Myocardial ischemic scar
Slide from Andrea McCollum MD
Cuyahoga County Coroner's Office

Subendocardial ischemic scar
Slide from Andrea McCollum MD
Cuyahoga County Coroner's Office

Subendocardial scar
Healed watershed infarct
KCUMB Team

Subendocardial scar
Healed watershed infarct
KCUMB Team

{10103} myocardial infarct, acute
{06639} very early MI (bottom only)
{06428} myocyte degeneration (hydropic change)
{06431} myocyte degeneration (hydropic change)
{06642} contraction bands
{06651} contraction bands
{06645} necrosis and polys
{06630} subendocardial MI
{06654} good necrosis and polys (NOTE: the myocyte nuclei are homogenized rather than pyknotic; that still means "dead")
{06443} road-kill, lots of polys, fibers very dead; good contraction bands remain
{06446} nice granulation tissue
{06663} nice granulation tissue
{06666} nice granulation tissue (left)
{06449} nice scar
{06338} nice scar
{06455} nice scar (trichrome)

Ruptured MI
Dino Laporte's PathosWeb

Ruptured MI
WebPath photo

Ruptured MI
WebPath photo

{03614} ruptured wall
{07141} hemopericardium
{03617} ruptured septum
{53285} ruptured septum

{06323} myocardial ventricular aneurysm

Old MI
WebPath photo

Aneurysm of ventricle
WebPath photo

Ventricular aneurysm with thrombus
WebPath photo

{11489} old rheumatic fever, mitral valve
{11492} acute rheumatic fever
{49008} acute rheumatic fever, vegetations
{18809} Aschoff nodule
{28587} Aschoff nodule
{28590} Aschoff nodule
{53304} Aschoff nodule
{46305} Aschoff nodule
{46481} Aschoff nodule, great caterpillar chromatin
{06467} old rheumatic fibrosis of mitral valve
{06845} old rheumatic mitral stenosis
{06847} old rheumatic mitral stenosis
{06850} old rheumatic mitral stenosis, large left atrium
{06815} old rheumatic aortic valve disease with insufficiency
{11549} old rheumatic aortic valve disease, good fusion of cusps
{11486} old rheumatic aortic valve stenosis

Rheumatic fever

Yutaka Tsutsumi MD

Acute rheumatic fever
Urbana Atlas of Pathology

Rheumatic fever verrucae
Classic drawing
Adami & McCrae, 1914

Aschoff nodule
WebPath photo

Rheumatic fever
Caterpillar cell ("Anitschkow myocyte")

Acute rheumatic fever
Verrucae
WebPath photo

Old rheumatic fever
WebPath photo

Old rheumatic mitral valve
WebPath photo

Old Rheumatic Fever
Australian Pathology Museum
High-tech gross photos

Mitral Stenosis (old rheumatic fever)
CDC
Wikimedia Commons

Rheumatic aortic valve
CDC
Wikimedia Commons

Old rheumatic mitral valve
CDc
Wikimedia Commons

Splinter hemorrhages
Supposedly from endocarditis
WebPath photo

More credible endocarditis splinter
WebPath photo

Pulmonic valve endocarditis producing
lung abscesses; great photos
Dr. Warnock's Collection

Endocarditis
Urbana Atlas of Pathology

MRSA endocarditis

Yutaka Tsutsumi MD

Infective Endocarditis
Australian Pathology Museum
High-tech gross photos

Torulopsis glabrata endocarditis
Advanced students
Yutaka Tsutsumi MD

Meningococcal endocarditis

Yutaka Tsutsumi MD

Bacterial endocarditis
Severe valve damage
KU Collection

Trichosporon beigelii endocarditis
Advanced students
Yutaka Tsutsumi MD

Bacterial Endocarditis
From Chile
In Spanish

Bacterial endocarditis, aortic valve
Classic drawing
Adami & McCrae, 1914

Bacterial endocarditis
CDC
Wikimedia Commons

{06563} acute bacterial endocarditis
{08458} acute bacterial endocarditis
{38563} bacterial endocarditis
{03293} bacterial endocarditis, aortic valve cusp perforation
{03413} bacterial endocarditis, gross
{06986} bacterial endocarditis
{06989} bacterial endocarditis

Bacterial endocarditis
WebPath photo

Bacterial endocarditis
WebPath photo

Endocarditis
Fistula formation

Bacterial endocarditis
WebPath photo

Bacterial endocarditis
WebPath photo

Mozart

{06326} Non-bacterial thrombotic endocarditis
{06965} Non-bacterial thrombotic endocarditis
{53315} Non-bacterial thrombotic endocarditis
{53317} Non-bacterial thrombotic endocarditis

Aortic valve vegetations
Probably marantic thrombi
KU Collection

Non-bacterial thrombotic endocarditis
WebPath photo

Non-bacterial thrombotic endocarditis
WebPath photo

Non-bacterial thrombotic endocarditis
WebPath photo

Non-bacterial thrombotic endocarditis
WebPath photo

{06962} Libman-Sacks endocarditis

Libman-Sacks Endocarditis
Thailand

{08044} carcinoid heart disease (trust me; look for the white fibrous stuff)
{08047} carcinoid heart disease (pulmonic valve, trust me)

{10739} endocardial fibroelastosis

{53323} Bjork-Shiley "toilet seat"/"disk" valve

{03626} infection on prosthetic valves
{07732} prosthetic valve endocarditis
{07723} worn-out prosthetic valve

Pig valve
WebPath photo

Toilet seat valve
WebPath photo

Birdcage valve
WebPath photo

MYOCARDITIS (Lancet 379: 738, 2012)

Myocarditis I
From Chile
In Spanish

Myocarditis II
From Chile
In Spanish

Viral myocarditis
Great labels
Romanian Pathology Atlas

Viral myocarditis

Yutaka Tsutsumi MD

Myocardial microabscess
WebPath photo

Myocardial microabscess
WebPath photo

{24946} coxsackie B myocarditis
{03461} myocarditis, microscopic
{15753} Chagas' disease
{26582} Chagas' disease
{53320} toxoplasmosis

Chagas disease

Yutaka Tsutsumi MD

Coxsackie B myocarditis
WebPath photo

Chagas cardiomyopathy
CDC
Wikimedia Commons

{07946} sarcoid heart

Giant cell myocarditis

KU Collection

Idiopathic giant cell myocarditis
Pittsburgh Pathology Cases

CARDIOMYOPATHIES: Non-inflammatory, non-ischemic heart muscle disease. (Call the heart transplant team!) Review (still good): Br. Med. J. 315: 1529, 1997.

Arrhythmogenic Right Ventricular Dysplasia
Tabib's paper from circulation
Dramatic transillumination photo

Arrhythmogenic Right Ventricular Dysplasia
Essay and good photos

Arrhythmogenic Right Ventricular Dysplasia
Indian Journal
Essay and great photos

Arrhythmogenic Right Ventricular Dysplasia
JACC
Essay and photos

Arrhythmogenic Right Ventricular Dysplasia
National Registry
Essay and one really good gross photo

Arrhythmogenic Right Ventricular Dysplasia
Imaging -- worth a look
Radiographics journal

Arrhythmogenic Right Ventricular Dysplasia
Wikimedia
Shows its importance

{03629} dilated cardiomyopathy vs. normal
{03632} dilated cardiomyopathy
{07769} dilated cardiomyopathy
{11555} dilated cardiomyopathy

Dilated heart
Urbana Atlas of Pathology

Dilated cardiomyopathy
WebPath photo

Dilated cardiomyopathy
WebPath photo

Dilated cardiomyopathy
Most myocytes replaced by scar

Dilated Cardiomyopathy
CDC
Wikimedia Commons

{07811} hypertrophic cardiomyopathy
{07814} hypertrophic cardiomyopathy
{07799} hypertrophic cardiomyopathy
{07820} hypertrophic cardiomyopathy, microscopic
{11561} hypertrophic cardiomyopathy, microscopic
{07823} hypertrophic cardiomyopathy, electron micrograph

Hypertrophic cardiomyopathy
WebPath photo

{07937} amyloid heart
{07940} amyloid heart
{07943} amyloid heart

Amyloid
WebPath photo

Amyloid
Congo Red birefringence
WebPath photo

{07039} von Gierke's disease
{07958} hemochromatosis
{07967} Fabry's
{08053} pheochromocytoma heart
{08078} radiation atherosclerosis
{08081} radiation pericarditis

Hemochromatosis
WebPath photo

* CADAVERIC SPASM

PERICARDIAL DISEASE (Lancet 363: 717, 2004)

Pericarditis
From Chile
In Spanish

{18719} fibrinous pericarditis

Fibrinous pericarditis
Classic gross appearance
KU Collection

Fibrinous pericarditis
Great labels
Romanian Pathology Atlas

Fibrinous pericarditis
Fibrin strands on right
KU Collection

Fibrinous pericarditis
WebPath photo

Fibrinous pericarditis
WebPath photo

Fibrinous pericarditis
WebPath photo

Fibrinous pericarditis
WebPath photo

{03659} constrictive non-calcific pericarditis

Hemorrhagic pericarditis
WebPath photo

Hemorrhagic pericarditis
WebPath photo

CARDIAC TUMORS are rare.

{07975} myxoma
{07982} myxoma

Atrial myxoma
WebPath photo

Cardiac myxoma
WebPath photo

Atrial Myxoma
AFIP
Wikimedia Commons

Atrial myxoma embolus
AFIP
Wikimedia Commons

Atrial myxoma
AFIP
Wikimedia Commons

{08029} lipomatous hypertrophy ("lipoma") of atrial septum

LAST PHOTOS

{17416} tiger-stripes of fatty change in extreme anemia; remember this one?
{11480} thromboembolus caught in heart

PULSUS PARADOXUS OVERSIMPLIFIED

BIBLIOGRAPHY / FURTHER READING

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reset Jan. 30, 2005:

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Teaching Pathology

EXAMINING THE LIVING CARDIOVASCULAR SYSTEM
Correlations with Pathology
Ed Friedlander MD "the pathology guy"

A group of you asked, in lieu of continuing into "lung", to integrate pathology and the changes you have learned about on physical exam. Pathologists are the big integrators and "why"-folks in most medical schools, so here goes....
0. Turn off the TV 1. Inspect 2. Palpate 3. Percuss 4. Auscultate
Valsalva: Reduces, then increases, preload
Leg lift: Increases preload
Handgrip: Increases afterload

Inspection! Apex impulse. Where? How big? Any others? Dextrocardia / situs inversus. Cyanosis? Jugular venous distention? (For a great review on the physical examination of the jugular veins, see Am. Heart. J. 136: 6 & 10, 1998. More than 3 cm vertically above sternal angle, high CVP.) Anything else?

Jugular venous pulse peaks demystified (see also South. Med. J. 100: 1022, 2007....

Big "A"'s: think of high pulmonary vascular resistance ("pulmonary hypertension", why?
Big "V"'s: Tricuspid regurgitation (why)?

Estimating CVP is very helpful. Be sure you can recognize Kussmaul's sign in the neck veins in tamponade (and explain how it happens -- nice case Lancet 371: 1810, 2008)

Palpation! Right ("sternal") lift or heave. Big apex beat is "left lift" or "left heave". Thrill -- palpable murmur. Feel PMI and carotids simultaneously. Position of PMI can be measured; duration has most to do with actual hypertrophy.

Percussion!: Bring your sharpie marker. Don't expect this to tell you as much or as well as a chest x-ray.

Auscultation!: Bell (S3 and S4; mitral stenosis) vs. diaphragm (everything else). The Littman diaphragm, lightly applied, supposedly hears the low pitches as well as the bell. You decide. "I can't tell you, professor, I am listening to diastole!" Inching along. Sitback and put your elbows on your knees. Roll over on your left side and lean back against me.
S1. What is it? Can anybody hear T1?
S2. What is it? P2 is delayed a bit during inspiration. Learning to tell if a sound is split. Exaggerated split (i.e., P2 is always a little too late): increased pulmonary vascular resistance (why?), left-to-right shunt (why?), right bundle branch block (why?) Paradoxical split (i.e., A2 is always a little too late and/or P2 a bit early); left bundle branch block (why?), some normal folks. Loud A2: systemic hypertension. Loud P2: Pulmonary hypertension.
S3: Waves-in-the-wall, the heart as kettledrum? "Tennessee". When do you hear it? Why?
S4: Atrial sound. "Kentucky". When do you hear it? Why?

Ejection click: Little wiggles in the aortic and/or pulmonary valve leaflets as they open.
Opening snap: Litle wiggles in the stiff leaflets of a tight mitral valve. Midsystolic click: Barlow posterior leaflet being pulled tense, less when you increase preload.
Murmurs mean turbulence. Volume of sound is proportionate to force and volume of turbulent flow.


Systolic murmurs:

Diastolic murmurs: always deserve your serious attention.

Continuous murmurs: patent ductus (why?), fistulas (why?), mammary souffle (why?)

Friction rub: Fibrin-coated surfaces of epicardiumon pericardium (or visceral on parietal pleura). Ephemeral.

Blood pressure: Korotkoff sounds. "Auscultatory gap", and why you need to have a finger on the pulse of the wrist. Wide cuffs for big arms (avoids factitious hypertension).

Pulses: Rhythm. "Respiratory arrhythmia" -- often the pulse is slower on inspiration than on expiration. Regularly irregular or irregularly irregular. Pulsus alternans (easiest to detect using a cuff, "the heart rate suddenly doubled!") bespeaks left CHF, why? Absent doralis pedis. Carotid bruits. Other bruits. Jerky pulse (think hypertrophic cardiomyopathy, why?) Hyperkinetic. Waterhammer (Corrigan) pulse. Thready pulse. "Pulsus paradoxus" (everybody has a slight decrease, >10 torr is abnormal, how to measure it). Capillary refill (2 sec. rule). Check those leg veins to detect coarctation of the aorta. Why you don't want to use your thumb to palpate a pulse.

Other stuff: Barrel chest. Marfanoids. Ehlers-Danlos. Pectus. Erythema marginatum. Xanthomas. Osler's nodes. Roth spots. Vessel changes (narrowed light reflex, AV nicking, copper wires, silver wires) of (hyaline) arteriolar sclerosis. Splinter hemorrhages (uh huh...) Hepatojugular reflux. Edema (+1 pit goes away fast, +2 5 sec +3 1 min +4 5 min, or thereabouts). Non-pitting edema (lymph, real vein trouble). Homan's sign. Varicose veins; Trendelenberg test, tourniquet test.
Pathological Chess


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