Cardiovascular Pathology Case-based_Gross and Microscopic

Marc Imhotep Cray, M.D.
Photo: Photograph of chordae tendineae attached to papillary muscles of a ventricle. From Seeley’s Anatomy & Physiology. 10th ed. New York, NY: McGraw-Hill 2010.
Prepared and presented by:
Cardiovascular Pathology
Gross and Microscopic
An Integrated & Case-based Learning Sequence
Companion: Cardiovascular Pathology Interactive Questions and Answers

Cardiovascular Disease (CVD)
Classification Schemas
CVD can be classified as:
 Vascular
 Inflammatory/Autoimmune
 Anatomic
 Degenerative
 Traumatic/Emergency
 Infectious
 Congenital
 Neoplastic
CVD is a class of diseases that involve the heart and/or blood vessels.
CVD includes:
 CAD such as AP and MI
 CVA
 Heart failure
 Hypertensive heart disease
 Rheumatic heart disease
 Cardiomyopathy
 Arrhythmias
 Congenital heart disease
 Valvular heart disease
 Myocarditis
 Aortic aneurysms and dissection
 Peripheral Artery Disease(PAD)
 Thromboembolic Disease
 Venous Thrombosis

3
Baron SJ and Lee CI. Lange Pathology Flash Cards. New York: McGraw-Hill, 2009..

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Baron SJ and Lee CI. Lange Pathology Flash Cards. New York: McGraw-Hill, 2009..

Learning Objectives
5
1. Define and classify arteriosclerosis.
2. List the risk factors and explain the pathogenesis of
atherosclerosis and describe the morphology of atheromatous
lesions.
3. Enumerate the complications of atherosclerosis.
4. Explain the pathogenesis of essential hypertension and
describe the cardiac and vascular pathology and complications
that it produces.
5. List the causes of secondary hypertension
6. Compare in a table form between benign and malignant
hypertension.

Learning Objectives (2)
6
7. Define and classify aneurysms and describe their clinical
effects.
8. Define and classify vasculitis.
9. Describe the pathogenesis of vasculitis in general, and
pathogenesis, morphology and clinical features of polyarthritis
nodosa and giant cell arteritis in particular.
10. List the causes of congestive heart failure and describe its
pathogenesis.
11.Tabulate the differences between right vs. left heart failure.
12. Classify ischemic heart disease and describe its
pathogenesis.

7
13. Explain the pathogenesis, morphology, fate, and
complications of myocardial infarction.
14. Explain the pathogenesis of acute rheumatic fever and
rheumatic heart disease.
15. Describe the morphologic changes of acute and
chronic rheumatic heart disease.
16. Define infective endocarditis.
17. Describe the pathogenesis and morphologic changes
of acute and subacute infective endocarditis and their
cardiac and extra-cardiac complications.
18. Define myocarditis, list its causes and describe its
morphology and list its complications.

8
19. Define and classify congenital heart diseases and
describe their pathogenesis.
20. List the causes of pericarditis and describe the
morphology of acute and chronic pericarditis.
21. List the tumors of the heart and relate their location and
morphology to the clinical features that they produce.
22. Describe the morphology of tumors of blood vessels
with emphasis on benign vs malignant.
23. Hemangiomas and Kaposi sarcoma and its various
types with their associations.
24. Define primary and secondary varicose veins. List their
causes, risk factors, and complications.

Presentation Topical Outline
• Overview of Heart and Vascular Diseases
• Normal Heart: Anatomy and Physiology
• Atherosclerotic Cardiovascular Disease
• Angina Pectoris
• Myocardial Infarction
• Aortic Aneurysm & Arterial Dissection
• Infective Endocarditis
• Pericarditis
• Myocarditis and ARF & RHD
• Neoplasm
• Congenital Heart Disease
• Cardiomyopathies
• Arterial (Hypertension) and Venous Diseases
• Congestive Heart Failure

Overview of Heart and
Vascular Diseases
10

The Six Principal Mechanisms of
Heart Disease
11
Although a wide range of diseases can affect CVS,
pathophysiologic pathways that result in a “broken”
heart distill down to six principal mechanisms:
1. Failure of the pump
2. Obstruction to flow
3. Regurgitant flow
4. Shunted flow
5. Disorders of cardiac conduction
6. Rupture of the heart or major vessel

Mechanisms of Heart Disease:
1. Failure of the pump
12
 In most common situation, cardiac muscle
contracts weakly and chambers cannot empty
properly so-called “systolic dysfunction”
 In some cases, muscle cannot relax sufficiently to
permit ventricular filling, resulting in diastolic
dysfunction

2. Obstruction to flow
13
 Lesions that prevent valve opening (e.g., calcific
aortic valve stenosis) or
 Lesions that cause increased ventricular chamber
pressures (e.g., systemic hypertension or aortic
coarctation) can overwork myocardium which has
to pump against the obstruction

3. Regurgitant flow
14
 Valve pathology that allows backward flow of
blood results in increased volume workload and
may overwhelm pumping capacity of affected
chambers

4. Shunted flow
15
 Defects (congenital or acquired) that divert
blood inappropriately from one chamber to
another, or from one vessel to another, lead to
pressure and volume overloads

5. Disorders of cardiac conduction
16
 Uncoordinated cardiac impulses or blocked
conduction pathways can cause
arrhythmias that slow contractions or
prevent effective pumping altogether

6. Rupture of heart or major vessel
17
 Loss of circulatory continuity (e.g., a gunshot
wound through thoracic aorta) may lead to
massive blood loss, hypotensive shock, and death

Heart failure
18
 Heart failure, often referred to as congestive heart failure
(CHF), is the common end point for many forms of cardiac
disease and typically is a progressive condition with a poor
prognosis
 In the United States alone, over 5 million individuals are
affected, resulting in well over 1 million hospitalizations
annually, and a financial burden in excess of $32 billion
 Roughly one half of patients die within 5 years of receiving a
diagnosis of CHF, and 1 in 9 deaths in the United States
include heart failure as a contributory cause

Vascular diseases
19
 Vascular diseases are responsible for some of the most
common and lethal conditions afflicting mankind
 Although most clinically significant disorders involve arterial
lesions, venous pathologies also can wreak havoc
 Vascular disease develops through two principal
mechanisms:
1. Narrowing or complete obstruction of vessel lumina,
occurring either progressively (e.g., by atherosclerosis)
or acutely (e.g., by thrombosis or embolism)
2. Weakening of vessel walls, causing dilation and/or
rupture

Normal Heart:
Anatomy and Physiology
20
Essential Normal Heart A&P Videos
(Parent Folder)
 Location of the heart
 Pericardium
 Conduction System of the Heart
 Control of Heart Rate
 Coronary Arteries
 The Cardiac Cycle

Normal heart, gross
• This is external appearance of
a normal heart
• Epicardial surface is smooth
and glistening
• Amount of epicardial fat is
usual
• Left anterior descending
coronary artery extends down
from the aortic root to the apex
21

Normal tricuspid valve, gross
22
• This is the tricuspid
valve
• Leaflets and thin and
delicate
• Just like mitral valve,
leaflets have thin
chordae tendineae that
attach leaflet margins to
papillary muscles of
ventricular wall below

Normal coronary artery,
microscopic
23
• This is a normal coronary
artery
• Lumen is large, without
any narrowing by
atheromatous plaque
• Muscular arterial wall is of
normal proportion

Normal myocardium, medium power
microscopic
24
• This is normal appearance
of myocardial fibers in
longitudinal section
• Note central nuclei and
syncytial arrangement of
fibers, some of which have
pale pink intercalated
disks

Physiologic Principles of Cardiac Output
25
Cardiac Output (CO)
• CO is equal product of stroke volume (SV) and heart rate (HR); thus,
changes in either SV or HR cause a change in CO
• SV is dependent upon contractility, preload, and afterload
Contractility (inotropism)
• Increases with sympathetic stimulation, increased intracellular calcium
concentrations, decreased extracellular sodium concentrations, and
administration of digitalis
• Decreases with parasympathetic stimulation, heart failure, acidosis,
hypoxia, and hypercapnia.
Preload
• Preload is ventricular end-diastolic volume and is related to right atrial
pressure.
• Increases with increased venous return caused by exercise, blood
transfusion, and sympathetic stimulation
• Venous dilators (eg, nitroglycerin) work by decreasing preload

Physiologic Principles of CO (2)
26
Starling Curve (Illus.)
• Starling curve relates preload (or
ventricular end-diastolic) volume with
CO (or SV)
• It shows that force of contraction is
proportional to initial length of cardiac
muscle fiber
• An increase in preload will cause a
corresponding increase in CO
Afterload
• Afterload is diastolic arterial pressure and is proportional to peripheral
resistance.
• LV afterload corresponds to aortic pressure and RV afterload corresponds
with pulmonary artery pressure.
• Vasodilators (eg, hydralazine) work by decreasing the afterload.
First Aid for the USMLE Step1, 2020, Pg.285.

Mean arterial pressure (MAP)
27
• Mean arterial pressure (MAP) is determined by how much
blood heart pumps into arterial system in a given time
(cardiac output [CO]) and how much resistance arteries have
to this input (total peripheral resistance [TPR])
• Mathematically, this is expressed as MAP = CO X TPR
o Consequently all drugs that lower BP work by
affecting either CO or TPR (or both)
Important Note:
• Primary determinant of SBP is CO, whereas
• Primary determinant of DBP is TPR
• B/C approximately one third of cardiac cycle is spent in
systole and two thirds in diastole, MAP can be calculated
as MAP=1/3 SBP + 2/3 DBP

Blood pressure regulation
28
Kumar V; Abbas AK; Aster JC. Robbins Basic Pathology, 10th ed. Philadelphia: Elsevier, 2018; Fig. 10.3, Pg.365.
Blood pressure is determined by vascular resistance and cardiac output. Vascular resistance is regulated at the level of the
arterioles, influenced by neural and hormonal inputs. Cardiac output is determined by heart rate and stroke volume, SV is
strongly influenced by blood volume. Blood volume in turn is regulated mainly by renal sodium excretion or reabsorption.
Renin, a major regulator of BP, is secreted by the kidneys in response to decreased BP in afferent arterioles. In turn, renin
cleaves angiotensinogen to angiotensin l; subsequent peripheral catabolism (ACE) produces angiotensin Il, which regulates
BP by increasing vascular SMC tone and by increasing adrenal aldosterone secretion, which consequently increases renal
sodium reabsorption.

Physiology of Blood Vessels
29
Arteries
• Thick walled vessels under high pressure that carry stressed
volume
• Divided into three types: (1) large, elastic arteries (eg,
aorta); (2) medium-sized, muscular arteries comprising
branches of aorta; and (3) small arteries within tissues and
organs
• Atherosclerosis affects elastic and muscular arteries
Arterioles
• Smallest branches of arteries
• Principal sites of physiologic blood flow resistance
• Site of highest reduction in blood pressure and velocity
• Hypertension affects small muscular arteries and arterioles

Physiology of Blood Vessels (2)
30
Capillaries
• Arise from arterioles and comprise largest total cross-
sectional area and surface area in cardiovascular system
• Lined by endothelial cells and supported by a thin basement
membrane of note, tunica media is absent
• Slow flow, high surface area, and thin walls allow rapid
exchange of materials betw. blood and tissue.
Veins
• Large-caliber, thin-walled vessels under low pressure
• Contain highest proportion of blood in cardiovascular system,
and carry unstressed volume
• Have poor support and are predisposed to compression,
dilatation, and invasion by tumors and inflammation

Structure of Blood Vessels
(a) arteries and (b) veins share
same general features, but walls
of arteries are much thicker b/c of
higher pressure of bld that flows
through them
(c) micrograph shows relative
differences in thickness (LM ×160)
https://opentextbc.ca/anatomyandphysiology/chapter/
20-1-structure-and-function-of-blood-vessels/
 Resistance vessels =small arteries,
arterioles, and precapillary sphincters
 Capacitance vessels =sm. and lg.
veins
• Have great capacity to distend
• For a similar rise in pressure,
capacitance vessels may
accommodate 20 times more bld
than resistance vessels

Regional vascular specializations. Although all vessels share the same general constituents, the
thickness and composition of the various layers differ as a function of hemodynamic forces and
tissue requirements
32
Kumar V; Abbas AK; Aster JC. Robbins Basic Pathology, 10th ed. Philadelphia: Elsevier, 2018; Fig. 10.1, Pg.362.

Basal and activated endothelial cell states. Normal blood pressure, laminar flow, and stable growth factor
levels promote a basal endothelial cell state that maintains a nonthrombotic surface and appropriate vascular
wall smooth muscle tone. Injury or exposure to certain mediators results in endothelial activation, a state in
which endothelial cells develop adhesive, procoagulant surfaces and release factors that lead to smooth muscle
contraction and/or proliferation and matrix synthesis.
33
Kumar V; Abbas AK; Aster JC. Robbins Basic Pathology, 10th ed. Philadelphia:
Elsevier, 2018; Fig. 10.2, Pg.363.

Endothelial Cell Properties and Functions
34
Kumar V; Abbas AK; Aster JC. Robbins Basic Pathology, 10th ed. Philadelphia: Elsevier, 2018; Table. 10.1, Pg.3

Vascular Structure and Function
Key Points
35
 All vessels are lined by endothelium; although all ECs share certain
homeostatic properties, ECs in specific vascular beds have special features
that allow for tissue-specific functions (e.g., fenestrated ECs in renal
glomeruli)
 Relative SMC (smooth muscle cell) and ECM (extracellular matrix) content
of vessel walls (e.g., in arteries, veins, and capillaries) varies according to
hemodynamic demands (e.g., pressure, pulsatility) and functional
requirements
 EC function is tightly regulated in both basal and activated states
 Various physiologic and pathophysiologic stimuli induce endothelial
activation and dysfunction that alter EC phenotype (e.g., procoagulative
versus anti-coagulative, proinflammatory versus anti-inflammatory,
nonadhesive versus adhesive)

Atherosclerotic
Cardiovascular
Disease
36

Clinical Vignette 1
37
A 40-year-old white man presents to your office complaining of
pressure-like chest pains radiating to his shoulder during
strenuous physical activities. On further questioning, he
indicates that he has painful muscle cramps in his legs when
climbing stairs. Both his chest pains and leg cramps are
relieved by rest. Family history reveals his father died of an MI
in his early 50s and two paternal uncles experienced the same
fate. Physical examination is notable for yellow nodules under
both eyelids. You send him for laboratory studies including
triglyceride and cholesterol levels to confirm your diagnosis.
What is the Diagnosis?

Atherosclerosis Capsule
38
Very Common: Disease of elastic arteries and large- and medium-sized
muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol
plaques in intima
Location: Abdominal aorta > Coronary artery > Popliteal artery > Carotid
artery > circle of Willis.
Risk Factors: Modifiable: smoking, hypertension, dyslipidemia (inc. LDL, dec.
HDL), diabetes; Non-modifiable: age, sex (inc. in men & postmenopausal
women), family history
Symptoms: Angina, claudication, but can be asymptomatic
Progression: Inflammation important in pathogenesis: endothelial cell
dysfunction macrophage and LDL accumulation foam cell formation fatty
streaks smooth muscle cell migration (involves PDGF and FGF),
proliferation, and extracellular matrix deposition fibrous plaque complex
atheromas calcification (calcium content correlates with risk of
complications)
Complications: Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus,
emboli
Platelet-derived growth factor (PDGF)
Fibroblast growth factor (FGF)

Atherosclerosis
39
 Etiology:
 Risk factors include smoking, HTN, diabetes, hypercholesterolemia
(increased LDL), positive family history, old age, male gender,
postmenopausal status in women, hyperuricemia, and oral
contraceptive use
 Pathology:
 Artery: Progresses from fatty streaks (lipid-laden foam cell
accumulations in intima) to proliferative plaques to complex atheromas
 Atheroma: Central core of cholesterol and foam cells (lipid-laden
macrophages) covered by fibrous cap
o atheromas may be complicated by overlying thrombus formation,
ulceration, or calcification of plaque;
o usually present in elastic arteries and medium/large muscular
arteries

Atherosclerosis (2)
40
Clinical Manifestations: Often asymptomatic; can present w
angina or claudication (pain in muscles during exercise,
relieved by rest)
 Complications include aneurysms, MI, stroke, bowel ischemia, renal
artery ischemia, peripheral vascular occlusive disease, and emboli of
overlying thrombus or of plaque itself
Treatment: Lipid-lowering agents (eg, HMG-CoA reductase
inhibitor)=Statins
Note: Xanthomas are yellow plaques or nodules of skin
composed of lipid-laden macrophages and are assoc. w
hypercholesterolemia

Arteriosclerosis
41
Arteriosclerosis is a general term
for several disorders that cause
thickening and loss of elasticity
in the arterial wall
 Atherosclerosis, the most
common form, is also most
serious b/c it causes coronary
artery disease and
cerebrovascular disease
Atherosclerosis is patchy intimal plaques (atheromas)
in medium-sized and large arteries
 Plaques contain lipids, inflammatory cells, smooth
muscle cells, and connective tissue
Coronary artery with atherosclerotic
narrowing, microscopic

Atherosclerosis Pathogenesis
43
First Aid for the USMLE Step1 , 2020, Pg.302.
Endothelial cell injury → macrophages/platelets adhere to damaged endothelium
and release cytokines → smooth muscle hyperplasia/migration of cells to the
tunica intima → macrophages form foam cells plus smooth muscle → fibrous cap
develops → fibrous cap (plaque) calcifies dystrophically and ulcerates →
platelets adhere to the ulcer, causing vessel thrombosis

44
Atherosclerosis
Pathogenesis (2)
First Aid for the Basic Sciences- Organ Systems, Pg. 47.

Pathobiology of Atherosclerosis
45
GROSS/MICRO BIOLOGY
 Fatty streaks are flat and yellow and on
microscopy contain foam cells (lipid-laden
macrophages)
 Fibrous plaques are elevated white plaques
that contain a necrotic core of cholesterol,
lipids, foam cells, and debris surrounded by
a fibrous cap of collagen, smooth muscle,
and lymphocytes
COMPLICATIONS
 Plaque rupture unstable angina, MI,
death, stroke, aneurysm formation due to
artery wall degeneration, TIAs, renal artery
ischemia, peripheral vascular occlusive
disease (PVD), impotence, claudication,
proximal renal thrombosis → RAAS
activation and hypertension
First Aid for the Basic Sciences- Organ
Systems, Pg. 47.
Fibrous plaque.

Atherosclerosis Complication (MI)
46
 Symptoms develop when
growth or rupture of plaque
reduces or obstructs blood
flow
 Diagnosis is clinical and
confirmed by angiography,
ultrasonography, or other
imaging tests
 Treatment includes risk
factor and dietary,
modification, physical
activity, antiplatelet drugs,
and antiatherogenic drugs
Heart and LAD coronary artery w recent thrombus
 Anterior surface of heart demonstrates an opened left
anterior descending coronary artery
 Within lumen of coronary can be seen a dark red recent
coronary thrombosis
 Dull red color to myocardium as seen below glistening
epicardium to lower right of thrombus is consistent with
underlying myocardial infarction

Risk Factors for Atherosclerosis
47
Risk factors are divided into major and minor
categories:
 Major: Hyperlipidemia, hypertension, smoking,
diabetes, and obesity
 Minor: Male gender, oral contraceptives / decreased
estrogen (Postmenopausal), increased age, sedentary
lifestyle, stress, elevated homocysteine level, family
history, and infections (Chlamydia pneumoniae) [See
https://www.nature.com/articles/nrmicro796]

Coronary artery with atherosclerotic
narrowing, microscopic
• Coronary artery shown here
has narrowing of lumen due to
build up of atherosclerotic
plaque
• Severe narrowing can lead to
angina, ischemia, and infarction
48

Coronary artery with recanalized
thrombosis, microscopic
• This section of coronary artery
demonstrates remote thrombosis
w recanalization to leave only two
small, narrow channels
49

Coronary artery with calcific
atherosclerosis, microscopic
50
• There is a severe degree of
narrowing in this coronary
artery
• It is "complex" in that there is
a large area of calcification
on lower right, which appears
bluish on this H&E stain
• Complex atheroma have
calcification, thrombosis, or
hemorrhage
• Such calcification would
make coronary angioplasty
difficult

Aortas demonstrating various
degrees of atherosclerosis, gross
51
• These three aortas
demonstrate mild, moderate,
and severe atherosclerosis
from bottom to top
• At bottom, mild
atherosclerosis shows only
scattered lipid plaques
• Aorta in middle shows many
more larger plaques
• Severe atherosclerosis in
aorta at top shows extensive
ulceration in plaques

Diagnostic Classifications of CAD
52
 Anatomic (Pathologic) Dx= Atherosclerosis (ASHD)
 Etiologic Dx= Coronary Heart Disease (CHD, IHD,
CAD)
 Physiologic Dx=AP, Arrhythmia MI, SCD, Related
arterial diseases, Over time CAD can lead to heart
failure
 Functional Dx= Stable vs Unstable Angina vs ACS

Coronary heart disease (CHD) Defined
(Etiologic Dx)
53
 Coronary heart disease (CHD) is a condition in which
proper circulation of blood and oxygen are not provided to
heart and surrounding tissue
 Result is due to a narrowing of small blood vessels, which
normally supply heart w blood and oxygen
 CHD, one type of cardiovascular disease, is leading cause
of death for both men and women in United States

Causes (Anatomic Dx)
54
 The typical cause of CHD is atherosclerosis, which
takes place w plaque and fatty build up on artery walls,
narrowing the vessels

55
Kumar V and Abbas AK. Robbins and Cotran Pathologic Basis of
Disease, 9th ed. Philadelphia: Saunders, 2015, Fig. 12-19, p 550.
Schematic for causes and
outcomes of ischemic heart
disease (IHD) showing
interrelationships among:
 Coronary artery disease
(CAD),
 Acute plaque change,
 Myocardial ischemia,
 Myocardial infarction(MI),
 Chronic IHD,
 congestive heart failure
(CHF), and
 Sudden cardiac death
(SCD)

Coronary artery, mild atherosclerosis, gross
56
• A coronary artery has been
opened longitudinally
• Coronary extends from left to right
across middle of picture and is
surrounded by epicardial fat
• Increased epicardial fat correlates
with increasing total body fat
• There is a lot of fat here,
suggesting one risk factor for
atherosclerosis
• This coronary shows only mild
atherosclerosis, with only an
occasional yellow-tan lipid plaque
and no narrowing

Coronary artery, severe atherosclerosis,
gross
57
• This is left coronary artery from
aortic root on left
• Extending across middle of
picture to right is anterior
descending branch
• This coronary shows severe
atherosclerosis w extensive
calcification
• At far right, there is an area of
significant narrowing

Coronary artery, hemorrhage into
plaque, gross
58
• Coronary atherosclerosis with
complication of hemorrhage
into atheromatous plaque, seen
here in center of photograph
• Such hemorrhage acutely may
narrow arterial lumen

Heart and LAD coronary artery with
recent thrombus, gross
• Anterior surface of heart
demonstrates an opened left
anterior descending coronary
artery
• Within lumen of coronary can be
seen a dark red recent coronary
thrombosis
• Dull red color to myocardium as
seen below glistening epicardium
to lower right of thrombus is
consistent with underlying
myocardial infarction
59

Angina Pectoris
60

Clinical Vignette 2
61
During a routine physical examination, a 60-year-old man
mentions to you that he occasionally experiences chest
discomfort that radiates to his left shoulder. He describes that
discomfort as a “weight on his chest” and notes that the pain
tends to come on after he shovels his driveway and dissipates
with rest. He denies any chest pain at rest. You schedule him
for an exercise stress test, write him a prescription for
nitroglycerin, and warn him against performing any strenuous
exercise until further consultation with a cardiologist.

Angina Pectoris (AP)
62
 Etiology:
 Stable angina: Caused by atherosclerosis
 Prinzmetal (variant) angina: Associated with coronary
artery vasospasm
 Unstable (crescendo) angina: Caused by disruption of
atherosclerotic plaque w partial thrombosis in coronary
artery
o angina pectoris that is irregular
o classified as a type of acute coronary syndrome (ACS)
o difficult to distinguish unstable angina from non-ST elevation
(non-Q wave) myocardial infarction (NSTEMI)
 Pathophysiology: All types of angina are caused by
transient ischemia resulting in inadequate myocardial
oxygenation

Angina Pectoris (2)
63
Clinical Manifestations:
 Stable: Precordial chest discomfort associated w
exertion; pain is relieved by rest and
nitroglycerin; nonspecific ST-T changes on ECG
 Prinzmetal: Episodic chest pain occurring at rest;
may see ST elevation on ECG
 Unstable: Progressively frequent chest pain
initially occurring with activity but later occurring at
rest; considered indication for acute MI in near
future; may see ST depressions on ECG

Angina Pectoris (3)
64
Treatment:
 Stable: Nitrates; β-blockers; statins; aspirin
 Prinzmetal: Vasodilators (nitrates, calcium
channel blockers [CCBs])
 Unstable: β-blockers; statins; aspirin; coronary
evaluation w catheterization in near future;
consider heparin treatment
Of note: Angina pectoris may be clinically silent in
diabetics

Angina Pectoris Overview
65
Angina, or angina pectoris
(AP), is a gripping (vice-like
or pressure-like) pain felt in
the center of the chest that
may radiate to the neck,
jaw, and arms and is caused
most often by exercise;
emotion, eating, and cold
weather are other causes

CAD Risk Factors
66
Certain conditions are considered to put an individual at
greater risk for coronary heart disease
The following are some risk factors:
(same as for atherosclerosis in general)
 Diabetes
 High blood pressure
 High bad cholesterol (LDL)
 Smoking
 Genetics (heredity)
 Age (particularly 50+)
 Increased levels of C-reactive protein, fibrinogen,
or homocysteine
 Lack of sufficient physical activity
 Low good cholesterol (HDL)
 Menopause
 Obesity

Angina Pectoris (Chest Pain)
67
• When supply of O2 and
nutrients in bld is insufficient to
meet demands of heart heart
muscle “cries out in pain”
• Heart demands a large supply
of oxygen to meet demands
placed on it
• In CAD patients demands on
the heart require O2 supply
that can’t be meant

68
Raff RB, Rawls SM, Beyzarov EP. Netter's Illustrated
Pharmacology, Updated Edition. Philadelphia: Sanders,
2014.
 Angina, or angina pectoris, is
a gripping pain felt in chest that
may move to neck, jaw, and
arms and is caused most often
by exercise; emotion, eating,
and cold weather are other
causes
 AP occurs when heart
receives deficient oxygen b/c
of blood vessel narrowing,
which results mainly from
atherosclerosis due to aging ,
cigarette smoking, HTN, high
cholesterol levels, obesity, and
diabetes

Diagnosis
69
DX of CHD may be accomplished by a variety
of means:
Coronary angiography
Coronary arteriography
Coronary CT angiography
Echocardiogram
Electrocardiogram (ECG)
Electron-beam CT (EBCT)
Exercise stress test
Magnetic resonance angiography
Nuclear scan

Treatment
70
Coronary heart disease treatment methods may include:
(depends on presenting Physiologic Dx)
1. Angioplasty with stenting
2. Coronary artery bypass surgery (CABG)
3. Medication
4. Minimally invasive heart surgery
5. Proper diet and exercise
6. Quitting smoking
7. Treatment of other comorbidities, HTN, DM, Obesity, LDL

Myocardial Infarction
71

Clinical Vignette 3
72
A 60-year-old man presents to the emergency department
complaining of 2 hours of crushing substernal chest pain that
radiates to his left shoulder and jaw. He appears fatigued and
is breathing heavily and sweating profusely. You order an ECG,
which demonstrates ST elevations across the precordium. You
immediately activate the cardiac catheterization laboratory in
the hopes of minimizing tissue damage caused by his
condition. You worry that this patient may be at significant risk
for ventricular rupture in 5–7 days

Myocardial Infarction
73
Etiology: Caused by vasospasm, embolus, or
atherosclerotic thrombus resulting in coronary artery
occlusion
 Risk factors include increasing age, hypertension,
smoking, diabetes, male gender, postmenopausal women,
and hyperlipidemia
Pathology
 Heart: Progression from wavy fibers w edema and
hemorrhage (4-12 hours) to coagulative necrosis w
muscle hypereosinophilia and neutrophilic infiltration
(12-36 hours) to macrophage infiltration w phagocytosis
of dead cells and formation of granulation tissue (5-10
days) to scar formation (10 days to 2 months)
(See USMLE Step 1 First Aid, 2020, Pgs. 305-7)

Myocardial Infarction (2)
74
Clinical Manifestations: Crushing, substernal chest pain with
radiation to jaw and left arm; dyspnea; nausea; diaphoresis
 Complications: include cardiac arrhythmia (can cause sudden death
within first few days), fibrinous pericarditis (within 3-5 days), pulmonary
edema, CHF, shock, thromboembolism, rupture of ventricular free
wall or septum (VSD) (within 7-10 days), rupture of papillary muscle
leading to mitral regurgitation, and Dressler syndrome (autoimmune
fibrinous pericarditis several weeks post-MI)
 Lab findings: Diagnosis with ST elevation (STEMI) and permanent Q
wave on ECG (within hours); elevated cardiac troponin (seen within 4
hours to 10 days); elevated CK-MB, LDH-1, and AST
 Tx: Thrombolytic therapy and/or coronary angioplasty for early MI

Cardiac and vascular function curves:
MI causes decrease contractility (Inotropy)
75
 Inotropy: Changes in contractility altered SV altered CO/VR and RA
pressure (RAP)
 Catecholamines, digoxin, exercise ⊕
 HF w reduced EF, narcotic overdose, sympathetic inhibition ⊝
To learn more see: Ppt. Presentation, Relationships Betw. CO and VR
First Aid for the USMLE Step1 , 2020, Pg.289.

Heart, left ventricle, acute
myocardial infarction, gross
76
• This is left ventricular wall
which has been sectioned
lengthwise to reveal a large
recent myocardial infarction
• Center of infarct contains
necrotic muscle that appears
yellow-tan
• Surrounding this is a zone of
red hyperemia
• Remaining viable myocardium
is reddish- brown

Heart, left ventricle and septum,
myocardial infarction, gross
• This cross section through
heart demonstrates left
ventricle on left
• Extending from anterior portion
and into septum is a large
recent myocardial infarction
• Center is tan with surrounding
hyperemia
• Infarction is "transmural" in
that it extends through full
thickness of wall
77

Heart, transmural myocardial infarction with
rupture and hemopericardium, gross
78
• One complication of a transmural
myocardial infarction is rupture of
myocardium
• This is most likely to occur in first
week between 3 to 5 days following
initial event, when myocardium is
softest
• White arrow marks point of rupture
in this anterior-inferior myocardial
infarction of left ventricular free wall
and septum
• Note dark red blood clot forming
hemopericardium can lead to
tamponade

Heart, left ventricular aneurysm, gross
• A cross section through heart
reveals a ventricular aneurysm
with a very thin wall at arrow
• Note how aneurysm bulges out
• Stasis in this aneurysm allows
mural thrombus, which is
present here, to form within
aneurysm
79

80
How it Works Book of the Human Body, Sixth Edition. Imagine Publishing Ltd, 2016.
Learn more: Myocardial infarction_ Causes, Symptoms, Diagnosis,
Treatment, and Pathology. Dr. Cray Ppt. Presentation

81
How it Works Book of the Human Body, Sixth Edition. Imagine Publishing Ltd, 2016.

Aortic Aneurysm
and
Arterial Dissection
82

Aortic aneurysm
83
 Localized pathologic dilation of
aorta
 May cause abdominal and/or back
pain, which is a sign of leaking,
dissection, or imminent rupture

Abdominal aortic aneurysm
84
 Usually assoc. w atherosclerosis
 Risk factors include history of
tobacco use, inc. age, male sex,
family history
 May present as palpable
pulsatile abdominal mass
 Most often infrarenal (distal to
origin of renal arteries)
CT Scan (arrows point to outer dilated
calcified aortic wall, with partial crescent-
shaped non-opacification of aorta due to
flap/ clot)

Aorta, atherosclerotic aneurysm, gross
• Here is an example of an
atherosclerotic aneurysm of aorta
in which a large "bulge" appears
just above aortic bifurcation
• Such aneurysms are prone to
rupture when they reach 6 to 7 cm
in size
• They may be felt on PE as a
pulsatile mass in abdomen
• Most are located below renal
arteries so that surgical resection
can be performed w placement of
a dacron graft
85

Thoracic aortic aneurysm
86
 Assoc. w cystic medial
degeneration (necrosis)
 Risk factors include
hypertension, bicuspid
aortic valve, connective
tissue disease (eg, Marfan
syndrome)
 Also assoc. w 3° syphilis
(obliterative endarteritis
of vasa vasorum)
 Aortic root dilatation
may lead to aortic valve
regurgitation
A contrast enhanced CT showing a
large thoracic aneurysm of about 7 cm
which has ruptured
Black arrow is aorta, white arrow is bld in thorax

Abdominal aortic aneurysm, CT scan
with contrast
• This abdominal high
speed CT scan w contrast
demonstrates an AAA
approx. 6 cm in diameter
• At this size, there is
increased risk for rupture
87
Clinical: Master of Surgery Video_Abdominal Aortic Aneurysm Repair

Clinical Vignette 4
88
A 30-year-old man with Marfan syndrome presents to the
emergency room with severe, sudden, tearing chest pain
radiating to the abdomen and back. The pain has
progressively shifted downward over the last several hours.
On physical examination, he is found to have asymmetric
pulses and a pericardial friction rub. ECG studies are normal
and angiography shows an ascending aortic abnormality. You
schedule the patient for immediate surgical repair.

Aortic Dissection
89
 Etiology: Associated with hypertension, trauma, Marfan
syndrome, Ehlers-Danlos syndrome*, coarctation
of the aorta, bicuspid aortic valve, and last trimester of
pregnancy; there is no (direct) assoc. with atherosclerosis
 Pathology:
 Gross: Tear in aortic intima allowing formation of
intramural hematoma; possible presence of cystic medial
necrosis (lesion predisposing to aortic dissection
characterized by separation of elastic and muscular
elements of media)
*Ehlers–Danlos syndromes (EDS) are a group of genetic connective tissue disorders;
Symptoms may include loose joints, joint pain, stretchy velvety skin, and abnormal scar
formation; Can be noticed at birth or early childhood; Complications may include aortic
dissection, joint dislocations, scoliosis, chronic pain, or early osteoarthritis.

Types of Aortic Dissection
90
Two types:
Stanford type A (proximal):
involves ascending aorta
 May extend to aortic arch
or descending aorta
 May result in acute aortic
regurgitation or cardiac
tamponade
Stanford type B (distal):
involves only descending
aorta (Below left subclavian
artery) First Aid for the USMLE Step1 , 2020, Pg.303.

91
Osmosis Aortic Dissection video graphic capture 1

92
Osmosis Aortic Dissection video graphic capture 2

Aortic Dissection cont’ed.
93
Clinical Manifestations: Presents with sudden, severe,
tearing left chest pain, often radiating through back; pain
shifts downward with time
 Complications include aortic rupture causing
hemopericardium, cardiac tamponade, and death
Treatment:
Stanford type A Surgical repair if dissection involves
ascending aorta or if there is significant branch artery
involvement;
Stanford type B Strict HR and BP control with β-blockers,
and vasodilators or CCBs

Aorta, dissection with tear in arch,
gross
• There is a tear (arrow)
located 7 cm above aortic
valve and proximal to great
vessels in this aorta with
marked atherosclerosis
• This is an aortic dissection
94

Hemopericardium with cardiac
tamponade, gross
• An aortic dissection may lead to
hemopericardium when blood
dissects through media proximally
• Such a massive amount of
hemorrhage leads to cardiac
tamponade (prevents heart from
filling properly in diastole)
• Presents w dyspnea and tachypnea
PE Beck's triad = distended neck
veins, hypotension, distant heart
sounds, and pulsus paradoxus (drop
in systolic blood pressure ≥10 mm
Hg on inspiration)
95

Aorta, dissection, gross
• This aorta has been opened
longitudinally to reveal an area
of fairly limited dissection that is
organizing
• The red-brown thrombus can be
seen in on both sides of section
as it extends around aorta
• Intimal tear would have been at
left
• This creates a "double lumen"
to aorta
• This aorta shows severe
atherosclerosis which, along
with cystic medial necrosis
and hypertension, is a risk factor
for dissection
96

Aorta, dissection, microscopic
• Here, dissection went into
muscular wall
• Aortic dissection is an extreme
emergency and can lead to
death in a matter of minutes
• Blood can dissect up or down
aorta
• Blood dissecting up around
great vessels can close off
carotids
• Blood can dissect down to
coronaries and shut them off
97

Carotid artery, dissection with
compression, gross
• Right carotid artery is
compressed by blood dissecting
upward from a tear with aortic
dissection
• Blood may also dissect to
coronary arteries thus pts. w
AD may have Sx of severe chest
pain (for distal dissection) or
may present with findings that
suggest a stroke (w carotid
dissection) or myocardial
ischemia (w coronary dissection)
98

Infective Endocarditis
99

Clinical Vignette 5
100
A 30-year-old man presents to the emergency room with
sudden high fever and shaking chills. A new murmur localized
to the mitral valve is heard. The patient has bilateral nail-bed
hemorrhages, painful nodules on the tips of his fingers and
toes, an erythematous rash on his palms and soles, and
white spots surrounded by hemorrhage in his retina. You
immediately begin the patient on broad spectrum antibiotics
and order blood cultures and an echocardiogram to confirm
the diagnosis.

Acute and Subacute Endocarditis
101
 Etiology:
 Acute: Often caused by Staphylococcus aureus
 Subacute: Often caused by viridians streptococci (eg, S
mutans); often occurs after dental procedures
 Pathology:
 Acute: Large vegetations consisting of fibrin, inflammatory
cells, and bacteria on previously normal valves
 Subacute: Small vegetations consisting of fibrin, chronic
inflammatory cells, and fibrosis on abnormal valves (mitral
and aortic)

Acute and Subacute Endocarditis (2)
102
 Acute: Sudden high fever with chills; new onset of murmur
 Subacute: Insidious onset with low-grade fever
 Both types can present w Osler nodes (painful nodules on
digit pads), Janeway lesions (red rash on palms and
soles), Roth spots (white spots on retina with surrounding
hemorrhage), nail-bed splinter hemorrhages, and
bacteremia
 Complications include chordae tendineae rupture,
perforation of valvular leaflet, heart failure, suppurative
pericarditis, and septic emboli

Acute and Subacute Endocarditis (2)
103
Treatment:
 Acute: Broad spectrum antibiotics; may need surgical
treatment if severe
 Subacute: Broad spectrum antibiotics; prophylaxis of
SBE with antibiotics in susceptible individuals before
dental procedures
Note:
 Tricuspid valve endocarditis is assoc. w IV drug use
 Nonbacterial thrombotic endocarditis (NBTE or marantic
endocarditis) is assoc. w sterile emboli and seen w
cancer metastasis or renal failure, SLE (Libman-Sacks
endocarditis) [which demonstrates vegetation on both
sides of valve] , DIC, or carcinoid syndrome

Aortic valve, infective endocarditis,
gross
• This is infective endocarditis
• Aortic valve demonstrates a
large, irregular, reddish tan
vegetation
• Virulent organisms, such as
Staphylococcus aureus,
produce an "acute" bacterial
endocarditis,
• While some organisms such as
Streptococcus viridans
produce a "subacute" bacterial
endocarditis
104

Infective endocarditis spreading to
myocardium, gross
• In this case, infective
endocarditis
demonstrates how
infection tends to spread
from valve surface
• Here, vegetations can be
seen on endocardial
surfaces, and infection is
extending into to
underlying myocardium
105

Infective endocarditis, microscopic
106
• Microscopically, valve in
infective endocarditis
demonstrates friable
vegetations of fibrin and
platelets (pink) mixed with
inflammatory cells and
bacterial colonies (blue)
• Friability explains how
portions of vegetation can
break off and embolize

Heart, microabscesses, gross
107
The epicardial surface
of the heart is smooth
and glistening, but there
are small scattered
pinpoint yellowish
microabscesses
(Higher magnification in next photo).

Heart, microabscess, gross
108
• This magnification of the preceding
photograph shows the small yellowish
pinpoint microabscesses on the
epicardial surface
• Microabscesses may appear in
persons who are septic
• They may also represent emboli from
an infective endocarditis in which small
portions of a vegetation have
embolized out coronary arteries

Heart, microabscess, microscopic
109
• Microscopic
appearance of a
microabscess is
shown here
• Center consists of blue
bacterial colonies and
is surrounded by acute
inflammatory cells

Pericarditis
110

Clinical Vignette 6
111
A 35-year-old woman presents with acute chest pain and a
nonproductive cough. Review of systems reveals a history
of malar rash, fatigue, and migratory polyarthritis. On
physical examination, she is found to have a friction rub and
distant heart sounds and she complains of increased pain
when supine. An increased jugular venous pressure is
noted with inspiration and diffuse ST elevations are seen on
most ECG leads. You initiate therapy with corticosteroids
and refer her to a rheumatologist and a cardiologist.

112
Heart Wall Layer Anatomical Relationships,
Including Pericardium
Pericardium Anatomy Explained _Video

Pericarditis
113
 Etiology:
 Acute:
o Can be serous (caused by SLE, RA, scleroderma,
renal failure, viral infection, or tumors),
o fibrinous (caused by renal failure, MI, ARF, radiation,
or postsurgical trauma),
o hemorrhagic (caused by TB or malignancy), or
o suppurative (caused by bacteria such as TB,
Staphylococcus, or Pneumococcus)
 Constrictive (Chronic): Previous history of acute
pericarditis

Pericarditis (2)
114
Pathology and Pathophysiology:
 Acute:
(1)Serous: protein-rich exudate in pericardial space w
inflammatory rxn on tissue surfaces;
(2)Fibrinous: fibrin-rich exudate in pericardial space, which
may resolve or organize into scar;
(3)Suppurative: purulent exudate w massive inflammatory
rxns on tissue surfaces, which usually organizes into scar;
(4)Hemorrhagic: fibrin-rich exudate w assoc. hemorrhage in
pericardial space
 Constrictive: Heart encased by fibrous scar w loss of
pericardial space reduced cardiac contraction and
venous return

Pericarditis (3)
115
 Clinical Manifestations:
 Acute: Chest pain worsening w inspiration and supine
position; friction rub; pulsus paradoxus; distant heart
sounds; fever; nonproductive cough; Kussmaul sign
(increased JVP with inspiration)
Lab findings: Diffuse ST elevations in most ECG leads
and normal CK-MB
 Constrictive: Quiet heart sounds; Kussmaul sign; S3;
may mimic right-sided heart failure
 Treatment:
 Acute: Treat any underlying causes if known; NSAIDs;
corticosteroids if necessary
 Constrictive: Pericardiectomy

Fibrinous pericarditis, gross
• A window of adherent
pericardium has been opened
to reveal surface of heart
• There are thin strands of
fibrinous exudate that extend
from epicardial surface to
pericarial sac
• This is typical for a fibrinous
pericarditis
116

Hemorrhagic pericarditis, gross
• Pericarditis here not only has
fibrin, but also hemorrhage
thus, this is called a
"hemorrhagic pericarditis"
• It is really just fibrinous
pericarditis with hemorrhage
• Without inflammation, blood in
the pericardial sac would be
called "hemopericardium”
117

118
Check-Up Question
(UWorld, 2015. Cardiology / Pathology # 36):
A 34-year-old Caucasian male presents to the emergency
department with recent-onset dyspnea and fatigue. There is no
significant past medical history except for a mild respiratory
illness one week ago. His blood pressure is 80/60 mmHg. His
pulse is 120 beats per minute, regular, but weak. The pulse
becomes undetectable to palpation during each inspiration.
The jugular veins are distended The lungs are clear to
auscultation. Which of the following do you most suspect in this
patent?
A. Acute fibrinous pericarditis
B. Acute myocardial infarction
C. Septic shock
D. Constrictive pericarditis
E. Cardiac tamponade
F. Tension pneumothorax

119
Explanation:
Jugular venous distension (JVD) is key here. JVD indicates that
there is elevation central venous pressure (CVP) in the superior
vena cava. The combination of acute-onset CVP elevation (>15
cm H20) with hypotension and tachycardia can occur with cardiac
tamponade or tension pneumothorax. No history of chest trauma
and no abnormalities on lung auscultation make tension
pneumothorax is unlikely. Given the history of an antecedent
respiratory illness, the most likely diagnosis is cardiac tamponade
due to a serous viral pericarditis and a significant acute
pericardial effusion.
NB: Observation of Beck's triad on PE hypotension,
distended neck veins, and distant or muffled heart sounds on
auscultation - as well as tachycardia, are together indicative of
tamponade.

120
Myocarditis
and
Acute Rheumatic Fever
&
Rheumatic Heart
Disease

Clinical Vignette 7
121
A 20-year-old man from Panama presents to your clinic
complaining of dyspnea, orthopnea, bilateral leg swelling, and a
bloated belly. He denies any history of a congenital heart
disease, rheumatic fever, or valvular disease. As you prepare to
admit him to the hospital for further testing and treatment, you
wonder if a parasitic disease may be causing his condition.

Myocarditis
122
 Etiology and Epidemiology: Usually caused by viruses (ie,
Coxsackievirus A, Coxsackievirus B), or Trypanosoma cruzi
(Chagas disease); other causes include fungi (eg, Candida),
helminthes (eg, trichinosis), parasites (eg, toxoplasmosis),
bacteria (eg, Lyme disease), postviral syndrome, SLE, drug
hypersensitivity, hyper/hypothyroidism, and sarcoidosis
 Seen most commonly in young men
 Pathology:
 Gross: Hemorrhages visible on ventricular myocardium
 Microscopic: Diffuse myocardial degeneration and
necrosis with mononuclear inflammatory infiltrate

Myocarditis (2)
123
 Clinical Manifestations: May be asymptomatic or may
present as biventricular heart failure, fever, dyspnea,
fatigue, new onset of systolic murmur, palpitations, or
pleuropericardial pain
Complications include arrhythmias or sudden death
 Treatment: Usually supportive

Interstitial viral myocarditis,
microscopic
124
• Interstitial lymphocytic
infiltrates shown here are
characteristic for a viral
myocarditis=most common
type of myocarditis
• Many of these cases are
probably subclinical
• Some may be a cause for
sudden death in young
persons
• Most common viral agent is
Coxsackie B

Clinical Vignette 8
125
A 10-year-old girl presents to the clinic with fever, malaise,
migratory polyarthritis, and a blanching erythematous ring-
shaped rash over her proximal extremities. On further
questioning, you find out that she suffered from a severe
sore throat 2 to 3 weeks ago. Serum studies demonstrate
an ESR of 100 and a positive anti–streptolysin O titer. You
worry that she may suffer from valvular heart disease during
her adult years as a result of her current condition.

Acute Rheumatic Fever and
Rheumatic Heart Disease
126
 Etiology:
 Acute rheumatic fever (ARF): Antibodies formed against
group A β-hemolytic streptococci cross-react against
patient’s tissues; usually presents in children 5-15 years of
age
 Rheumatic heart disease (RHD): Late sequelae of acute
rheumatic fever; presents 20+ years after ARF
 Pathology:
 ARF: Presence of Aschoff bodies (inflammatory foci
surrounded by lymphocytes) and Anitschkow cells
(macrophages which may become multinucleated)
producing a pancarditis in heart tissue; serofibrinous
pericardial exudate
 RHD: Mitral stenosis with fish-mouth deformity; may also
affect aortic valve

ARF and RHD (2)
127
 ARF: Onset of symptoms 2-3 weeks after streptococcal
pharyngitis; major Jones criteria include carditis,
migratory polyarthritis, chorea, erythema marginatum
(blanching, ring-shaped rash), and subcutaneous
nodules; minor Jones criteria include fever, arthralgia, or
evidence of previous streptococcal infection (positive
anti–streptolysin O [ASO] titer)
Lab findings: Elevated ESR
 RHD: Presents with valvular heart disease (usually mitral
stenosis, but aortic stenosis as well); valvular disease
may lead to hypertrophy of heart, arrhythmias, and HF
Treatment: Penicillin for streptococcal infection; salicylates
for fever and arthritis; endocarditis prophylaxis if indicated

Acute rheumatic carditis,
microscopic (1)
128
• Microscopically, acute
rheumatic carditis is marked
by a peculiar form of
granulomatous inflammation
with so-called "Aschoff
nodules" seen best in
myocardium
• These are centered in
interstitium around vessels as
shown here
• The myocarditis may be
severe enough to cause
congestive heart failure

Acute rheumatic carditis, micro. (2)
129
• Here is an Aschoff nodule at
high magnification
• Most characteristic component
is the Aschoff giant cell
• Several appear here as large
cells with two or more nuclei
that have prominent nucleoli
• Scattered inflammatory cells
accompany them and can be
mononuclears or occasionally
neutrophils

Acute rheumatic carditis, micro. (3)
130
• Another cell seen w
acute rheumatic carditis
is Anitschkow cell
(myocyte)
• This is a long, thin cell
with an elongated
nucleus

Chronic rheumatic valvulitis,
gross
131
• In time, chronic rheumatic
valvulitis may develop by
organization of acute
endocardial inflammation along
with fibrosis, as shown here
affecting the mitral valve
• Note shortened and
thickened chordae tendineae

Neoplasia
132

Clinical Vignette 9
133
A 40-year-old woman presents to the emergency room
complaining of dyspnea on exertion and fainting spells.
Physical examination is significant for a low-grade fever and
a regurgitant murmur localized in the left atrium near the
mitral valve. Two-dimensional echocardiography shows
a tumor near the mitral valve that moves with the cardiac
cycle. You schedule surgery to excise the lesion.

Cardiac Neoplasms (Atrial Myxoma
and Rhabdomyoma)
134
Etiology and Epidemiology:
 Myxomas: Etiology unknown although 10% of cases are
caused by autosomal dominant trait; seen in adults
 Rhabdomyomas: Associated with tuberous sclerosis;
seen in infants and young children
Pathology:
 Myxoma: Usually found in LA near fossa ovalis; often in
pedunculated form; composed of globular myxoma cells
and smooth muscle cells in a mucopolysaccharide ground
substance
 Rhabdomyoma: Grayish myocardial mass that protrudes
into ventricle; composed of spider cells (polygonal cells w
glycogen-laden vacuoles separated by cytoplasmic
strands)

Cardiac Neoplasms (2)
135
 Myxoma: Presents when mitral valve function is
compromised by ball-valve obstruction causing dyspnea
or syncope, when a stroke occurs b/c of an embolus, or
when a regurgitant valvular murmur is found on physical
examination; systemic manifestations includes fever,
wasting, arthralgias, malaise, and anemia
 Rhabdomyoma: Presents with symptoms of obstruction of
cardiac chamber
Treatment: Myxomas are usually benign and can be surgically
excised
Note:
 Metastasis is most common cause of cardiac tumor
 Cardiac sarcomas are rare, but when they occur malignant
tumors that often metastasize

Heart, rhabdomyoma, gross
• This two year old child
died suddenly
• At autopsy, a large firm,
white tumor mass found
filling left ventricle
• This is a cardiac
rhabdomyomas
• Such primary tumors of
heart are rare
136

Heart, atrial myxoma, gross
137
• Left atrium has been opened to
reveal most common primary
cardiac neoplasm--an atrial
myxoma
• These benign masses are most
often attached to atrial wall, but can
arise on a valve or in a ventricle
• Can produce a "ball valve" effect
by intermittently occluding AV valve
orifice
• Embolization of fragments of tumor
may also occur
• Myxomas are easily Dx by
echocardiography

Heart, epicardium, metastases, gross
• Primary tumors of heart are
uncommon
• Metastases to heart are more
common, but rare overall (only
about 5 to 10% of all malignancies
have cardiac metastases)
• Seen over surface of epicardium
are pale white-tan nodules of
metastatic tumor
• Metastases may lead to a
hemorrhagic pericarditis
138

Congenital Heart
Disease
139

Congenital Heart Disease
Type of Defect Mechanism
140
Capsule:
Cyanosis (early; less common) Tetralogy of Fallot,
transposition of great vessels, truncus arteriosus, total
anomalous pulmonary venous return, tricuspid atresia
Late cyanotic shunt (uncorrected left to right becomes right
to left) Eisenmenger syndrome (caused by ASD, VSD,
PDA; results in pulmonary hypertension/polycythemia)
Frequency: VSD > ASD > PDA
Right-to-Left shunts: Early cyanosis
Left-to-Right shunts: “Later” cyanosis

(Acyanotic)
141
Acyanotic heart defects without shunting include:
• Pulmonary stenosis (a narrowing of pulmonary valve)
• Aortic stenosis
• Coarctation of the aorta
• Ventricular Septal Defect (VSD) There is a hole within membranous
or muscular portions of intraventricular septum that produces a left-
to-right shunt, more severe with larger defects
• Atrial Septal Defect (ASD) A hole from a septum secundum or
septum primum defect in interatrial septum produces a modest left-
to-right shunt
• Patent Ductus Arteriosus (PDA) Ductus arteriosus, which normally
closes soon after birth, remains open, and a left-to-right shunt
develops

Early cyanosis
142
“Blue Babies” Often diagnosed prenatally or become
evident immediately after birth. Usually require urgent
surgical treatment and/or maintenance of a PDA
• Tetralogy of Fallot Pulmonic stenosis results in right ventricular
hypertrophy and a right-to-left shunt across a VSD, which also has an
overriding aorta
• Transposition of Great Vessels Aorta arises from right ventricle and
pulmonic trunk from left ventricle; A VSD, or ASD with PDA, is needed
for extrauterine survival
o There is right-to-left shunting
• Truncus Arteriosus There is incomplete separation of aortic and
pulmonary outflows, along w VSD, which allows mixing of oxygenated
and deoxygenated bld
o There is right-to-left shunting

Heart, tetralogy of Fallot, diagram
143
 Diagram depicts features of
Tetralogy of Fallot:
 Ventricular septal defect;
 Overriding aorta;
 Pulmonic stenosis;
 Right ventricular hypertrophy
 Obstruction to right ventricular
outflow creates a right-to-left
shunt that leads to cyanosis

Heart, transposition of great vessels, diagram
144
 In diagram, transposition of great
vessels is shown occurs when
trunco-conal septum does not spiral
down Instead, it descends straight
down As a result outflow of right
ventricle is into aorta and outflow from
left ventricle is into pulmonic trunk
 In order for this system to work, there
must be a connection betw. system
and pulmonic circulations
Sometimes this is through a VSD or
an ASD In diagram, this is through a
patent ductus arteriosus

145
• Hypoplastic Left Heart Syndrome There are varying
degrees of hypoplasia or atresia of aortic and mitral
valves, along with a small to absent left ventricular
chamber
• Coarctation of Aorta Either just proximal (infantile
form) or just distal (adult form) to ductus is a narrowing
of aortic lumen leading to outflow obstruction
• Total Anomalous Pulmonary Venous Return
(TAPVR) pulmonary veins do not directly connect to
left atrium drain into left innominate vein, coronary
sinus, or some other site leading to possible mixing
of blood and right-sided overload

Heart, atrial septal defect, gross
• In region of foramen ovale on
inter-atrial septum is a small
atrial septal defect, as seen in
this heart opened on t right
side
• Here defect is not closed by
septum secundum, so a shunt
exists across from left to right
146

Heart, ventricular septal defect, gross
• This is heart of a premature
stillborn w Trisomy 13 in
which a ventricular septal
defect is visible in
membranous septum
• About 90% of VSD's are in
membranous septum and
10% in muscular septum
147

Aorta, coarctation, gross
• This portion of aorta was
resected from a patient
with a coarctation
• The aorta narrows
postductally here to
about a 3 mm opening
148

Aorta, coarctation, gross
• Aorta is opened
longitudinally here to reveal
a coarctation
• In region of narrowing,
there was increased
turbulence that led to
increased atherosclerosis
149

Congenital cardiac defect associations
150
Disorder Defect
Alcohol exposure in utero
(fetal alcohol syndrome)
VSD, PDA, ASD, tetralogy of Fallot
Congenital rubella PDA, pulmonary artery stenosis, septal defects
Down syndrome AV septal defect (endocardial cushion defect),
VSD, ASD
Infant of diabetic mother Transposition of great vessels, VSD
Marfan syndrome MVP, thoracic aortic aneurysm and dissection,
aortic regurgitation
Prenatal lithium exposure Ebstein anomaly
Turner syndrome Bicuspid aortic valve, coarctation of aorta
Williams syndrome Supravalvular aortic stenosis
22q11 syndromes Truncus arteriosus, tetralogy of Fallot
USMLE Step 1 First Aid, 2020, Pg. 300.

Cardiomyopathies
151

Clinical Vignette10
152
A 20-year-old college football player suddenly collapses and
dies during a practice session. His father had suffered a
similar fate in his early 30s. On autopsy, he is found to have a
hypertrophied heart with an enlarged intraventricular septum.
On histologic examination of the myocardium, you see
disoriented, tangled, hypertrophied myocardial fibers and you
suspect that his death was related to an autosomal dominant
condition resulting in a mutation of beta-myosin heavy chain
protein gene.

Cardiomyopathy
153
Etiology:
 Dilated: Most common cardiomyopathy (90%); causes
include alcoholism, chronic ischemia, wet beriberi
(vitamin B1 deficiency), postmyocarditis, cocaine abuse,
doxorubicin toxicity, peripartum cardiomyopathy, and
muscular dystrophies
 Hypertrophic: Idiopathic or resulting from autosomal
dominant mutation in β-myosin heavy chain gene
 Restrictive: Can be idiopathic or caused by radiation,
sarcoidosis, amyloidosis, Hemochromatosis, Löffler
endomyocardial fibrosis, systemic sclerosis, radiation
and endocardial fibroelastosis

Cardiomyopathy (2)
154
 Dilated: Dilation of all chambers; hypertrophy of muscle
cells; interstitial fibrosis; results in systolic dysfunction
 Hypertrophic: Hypertrophy of interventricular septum and
myocardium; banana-shaped LV lumen; haphazard
arrangement of hypertrophied myocytes; results in LV
outflow tract obstruction and impaired diastolic filling
leading to decreased CO
 Restrictive: Bi-atrial dilation; diffuse interstitial fibrosis;
results in decreased ventricular compliance with
decreased diastolic filling and decreased CO

Cardiomyopathy (3)
155
 Dilated: Signs of CHF
Imaging: CXR demonstrates balloon heart
 Hypertrophic: Dyspnea; angina; syncope w exertion;
palpitations; sudden death
 Restrictive: Dyspnea; exercise intolerance; weakness;
edema
Treatment:
 Dilated: ACEIs; anticoagulants; diuretics; transplant
 Hypertrophic: β-blockers; refrain from strenuous exercise
 Restrictive: Treatment of underlying cause

Capsule of CMP Findings
156
• Dilated (Congestive)= Most common cardiomyopathy
(90% of cases) All four chambers are dilated, and there is
also hypertrophy
o Most common cause is chronic alcoholism, though some may be the
end-stage of remote viral myocarditis
• Hypertrophic = most common form is idiopathic
hypertrophic subaortic stenosis (IHSS) results from
asymmetric interventricular septal hypertrophy resulting in
left ventricular outflow obstruction
• Restrictive Myocardium is infiltrated with a material that
results in impaired ventricular filling
• Most common causes are postradiation fibrosis, amyloidosis and
hemochromatosis

Heart, dilated cardiomyopathy, gross
157
• This very large heart has a
globoid shape b/c all of the
chambers are dilated
• It felt very flabby, and
myocardium was poorly
contractile
• This is an example of a
cardiomyopathy
• This term is used to denote
conditions in which
myocardium functions poorly
and heart is large and dilated,
but there is no specific
histologic finding

Heart, dilated cardiomyopathy, [XRAY]
• This chest radiograph
demontrates marked
cardiomegaly, with t left
heart edge appearing far
to left
158

Heart, cardiomyopathy, micro.
• Microscopically, heart
demonstrates hypertrophy
of myocardial fibers
(which also have
prominent dark nuclei)
along w interstitial fibrosis
159

Heart, hypertrophic cardiomyopathy,
explanted heart, gross
160
• There is marked left ventricular
hypertrophy, w asymmetric
bulging of a very large
interventricular septum into left
ventricular chamber
• About half of these cases are
familial, though a variety of
different genes may be
responsible for this disease
• Both children and adults can be
affected, and sudden death can
occur
• Seen here is explanted heart
Pacemaker wires enter right
ventricle

161
Dilated cardiomyopathy Hypertrophic Obstructive cardiomyopathy
 Dilated cardiomyopathy will result in systolic dysfunction b/c heart
becomes so massively enlarged that it cannot pump adequately
In contrast,
 Hypertrophic cardiomyopathy will result in diastolic dysfunction
because there is so much extra myocardium that the chambers
cannot fill with an adequate quantity of blood

Arterial and Venous
Diseases
162

Clinical Vignette 11
163
A 45-year-old obese white man presents to the clinic for an
annual checkup. He has no complaints other than occasional
headaches. During the history, you find that he is a smoker and
has a family history of heart disease. His physical examination
is significant for mild obesity and a blood pressure of 160/100.
You suggest lifestyle changes including weight loss, a low-salt
diet, and smoking cessation, and you also prescribe
hydrochlorothiazide to treat his condition.

Essential and Secondary Hypertension
164
Etiology and Epidemiology:
 Primary (idiopathic) (90%): Risk factors include old age,
race, diabetes, smoking, obesity, and positive family history
 Secondary (10%): Caused by renal parenchymal disease,
renovascular disease, Conn syndrome, Cushing syndrome,
pheochromocytoma, Obstructive sleep apnea (OSA), and
drug reactions (OCP, NSAIDS, steroids)
 Microscopic: Hyaline thickening of vessels; atherosclerosis
 Pathophysiology: Primary (essential) HTN has been
associated with increased cardiac output and
increased total peripheral resistance

Hypertension (2)
165
 Clinical Manifestations: Usually asymptomatic; can be
associated with occasional headaches or palpitations
Complications include
 CAD
 MI
 CVA
 CHF
 Peripheral vascular disease
 Aortic dissection
 Retinopathy
 Renal failure

Hypertension (3)
166
Treatment:
 Reduce blood pressure to < 140/90 mm Hg with lifestyle
changes and antihypertensive therapy; treat underlying
causes of secondary hypertension
 Lifestyle changes: Weight loss, exercise, reduce salt
intake, smoking cessation, and moderate alcohol intake
 Pharmacologic agents: ACE inhibitors, calcium
antagonists, β-blockers, thiazide diuretics, α-blockers
Note: Hypertensive renal disease can present with nephritic
syndrome and is assoc. w overstimulation of RAAS

Heart, hypertension with left
ventricular hypertrophy, gross
167
• This left ventricle is very
thickened (slightly over 2 cm in
thickness), but the rest of the
heart is not greatly enlarged
• This is typical for hypertensive
heart disease
• The hypertension creates a
greater pressure load on the
heart to induce the
hypertrophy

Heart, concentric hypertrophy
with hypertension, gross
• Left ventricle is markedly
thickened in this patient w
severe hypertension that
was untreated for many
years
• Myocardial fibers have
undergone hypertrophy
168

169
Concentric hypertrophy is assoc. w increased left ventricular wall thickness
whereas
Eccentric hypertrophy is characterized by dilatation of left ventricular chamber;
however increase in overall size of cardiomyocytes under both conditions

Eccentric vs Concentric Hypertrophy
Key Points (1)
170
 Dilated cardiomyopathy Leads to systolic HF
 Dilated cardiomyopathy displays eccentric hypertrophy
(sarcomeres added in series)
 Systolic HF reduced EF (nml 55% to 70%); Incr.
EDV or volume overload ; decr. Contractility often 2°
to ischemia/MI or dilated cardiomyopathy
• Ejection Fraction (EF) is an index of ventricular
contractility (decr. in systolic HF; usually normal in
diastolic HF)

Eccentric vs Concentric
Hypertrophy Key Points (2)
171
Hypertrophic Obstructive Cardiomyopathy Leads to
Diastolic HF*
 Marked by ventricular concentric hypertrophy (sarcomeres
added in parallel) often septal predominance (see slide 159)
 Myofibrillar disarray and fibrosis
 Physiology of HOCM—asymmetric septal hypertrophy
and systolic anterior motion of mitral valve outflow tract
obstruction Sx dyspnea, possible syncope
 Other causes of concentric LV hypertrophy: Chronic
Hypertension, Friedreich ataxia
*Diastolic dysfunction—preserved EF, normal EDV; decr.
compliance (incr. EDP or pressure overload) often 2° to
myocardial hypertrophy

Eccentric vs Concentric
Hypertrophy Key Points (3)
172
 CHF due to DCM or chronic IHD is characterized by
dilatation of 1 or both ventricles and contractile
(systolic) dysfunction
 Diastolic dysfunction occurs in hypertensive heart
disease, which causes concentric ventricular hypertrophy
and decreased left ventricular chamber size
 Asymmetric septal hypertrophy and dynamic
ventricular outflow tract obstruction are characteristics of
hypertrophic cardiomyopathy

Check Up Question
173
1. A 56-year-old man is admitted to a tertiary care center after being
involved in a high-speed motor vehicle accident. He was thrown from his
vehicle and suffered severe head trauma along with multiple fractures
involving his ribs and extremities. Despite aggressive treatment, he dies
from massive cerebral edema and brain herniation the following day.
Autopsy shows increased thickness of the left ventricular wall and
decreased left ventricular cavity size. The structural changes observed in
this patient’s heart are most likely associated with which of the following
conditions?
A. Atrial septal defect
B. Hemochromatosis
C. Longstanding hypertension
D. Mitral insufficiency
E. Normal aging
F. Recent myocardial infarction
G. Wolff-Parkinson-White syndrome

Answer
174
Educational objective:
Concentric hypertrophy results in a uniform thickening of the ventricular
wall and narrowing of the ventricular cavity with the outer dimensions of
the ventricle remaining virtually unchanged. This form of hypertrophy is
often seen with increased ventricular afterload (pressure overload).
Eccentric hypertrophy results in dilatation of the ventricle with an
associated increase in chamber size. It is typically caused by volume
overload.
The changes in this patient's left ventricle (LV) are consistent with concentric
hypertrophy due to hypertensive heart disease. Concentric hypertrophy uniformly
thickens the ventricular wall with the outer dimensions of the ventricle remaining
almost unchanged, resulting in a narrowed ventricular cavity size. Concentric
hypertrophy results from chronic elevation of ventricular pressures during systole
(pressure overload). It can be caused by longstanding hypertension and aortic
stenosis, both of which increase LV afterload.
Cardiac Pathology Questions and Answers_UWorld #1

175
A 30-year-old African American man presents with recent-onset
headaches, blurred vision, and dyspnea. On physical
examination, he appears very ill and has difficulty concentrating
and answering your questions. You see cottonwool spots on a
funduscopic examination, a displaced forceful heart beat, and a
blood pressure reading of 190/130. You immediately place the
patient on IV sodium nitroprusside treatment.

Malignant Hypertension
176
Pathology Arteriole: Hyperplastic
arteriosclerosis (concentric, laminated
onionskin thickening of arterial walls
accompanied by necrotizing arteriolitis
[fibrinoid deposition in arteriole walls w
necrosis and inflammation])
 Can result in other pathologic
conditions including
o LV hypertrophy and failure and
o Malignant nephrosclerosis (ruptured
glomerular capillaries causing flea-bitten
kidney) renal failure  ESRD
o CVA
Etiology and Epidemiology: Results from an accelerated
course of essential or secondary HTN
 More common in young African American men

Malignant Hypertension (2)
 Presents w headache, altered mental status, blurred vision,
and dyspnea
 PE shows displaced forceful cardiac apex beat, presence
of S4, papilledema, retinal hemorrhages and exudates, and
marked DBP inc. (> 120 mm Hg)
Treatment and Prognosis: Initial lowering of BP w IV agents
(Nipride, hydralazine, labetalol) followed by strict BP control w
oral agents
 Often can result in an early death
A 59-year-old African American man presents to the ER with severe headache
and blood pressure of 200/110. On physical examination, he has papilledema
and fundal hemorrhages. What is the diagnosis?

Renal arteriole, fibrinoid necrosis with
malignant hypertension, microscopic
• One complication of hyperplastic
arteriolosclerosis with malignant
hypertension is fibrinoid necrosis,
as seen here in a renal arteriole
178

179
 Hypertensive emergency-also known as malignant hypertension
symptoms of end-organ involvement (blurred vision, headache, retinal
hemorrhages, exudates, and papilledema) as well as a significantly
elevated blood pressure
• Hypertensive emergency is primarily used as a specific term for a
“hypertensive crisis” w a DBP≥ 120 mmHg or SBP ≥ 180 mmHg
• A patient w malignant hypertension (hypertensive emergency) always
has retinal papilledema as well as flame-shaped hemorrhages and
exudates on ophthalmic exam
 Hypertensive urgency is primarily used as a specific term of a less
serious and less urgent condition (no evidence of acute end organ
damage)
• Term hypertensive crisis is most often used in this sense (so called
severe asymptomatic hypertension)
Hypertensive emergency (Malignant hypertension)
vs Hypertensive urgency

180
• This muscular artery seen
above and below shows a
more severe vasculitis with
acute and chronic
inflammatory cell infiltrates,
along with necrosis of
vascular wall
• This is classic polyarteritis
nodosa (PAN), a form of
vasculitis involving mainly
small to medium-sized
arteries anywhere in body,
but more often renal and
mesenteric arteries
Muscular artery, polyarteritis nodosa, micro.

181
 There are two other forms of
arteriosclerosis (hardening of
arteries) in addition to atherosclerosis:
1) arteriolosclerosis and 2) medial
calcific sclerosis (Monckeberg's)
 Arteriolosclerosis is typically seen in
kidneys one form--called hyaline
arteriolosclerosis-- markedly
thickened arteriole to lower right this
glomerulus with PAS stain
Hyaline arteriolosclerosis, high power micro.
 Hyaline arteriolosclerosis is seen in elderly, but more advanced
lesions are seen in persons with DM and/or w HTN

182
• Seen in this artery to right of
thyroid tissue
• Occurs most often in elderly
• Does not have serious
pathologic consequences b/c
arterial lumen is not
compromised
• Small muscular arteries in
pelvis, neck, & breast regions
affected
Monckeberg's medial calcific sclerosis
Medial calcific sclerosis is a type of arteriosclerosis that
typically has no significant clinical impact
• Can also be seen involving extremities in assoc. w
autonomic neuropathy in DM

183
• This fibrin and platelet
thrombus in a small
peripheral artery in heart
is characteristic for
thrombotic
thrombocytopenic purpura
(TTP)
• For this reason, pts w
TTP may die from heart
failure
Thrombus in small artery with thrombotic
thrombocytopenic purpura (TTP), micro.

184
Temporal artery, giant cell arteritis, low power
microscopic
• Temporal arteritis  one
manifestation of giant cell
arteritis, which can affect
mainly branches of external
carotid artery, but
sometimes also great
vessels at aortic arch and
coronaries
• There is granulomatous
inflammation of media
• Shown here is extensive
inflammation in temporal
arterial wall leading to a
markedly narrowed lumen

185
Temporal artery, giant cell arteritis, HP micro.
• Giant cell (temporal) arteritis
occurs after age 50
• Erythrocyte sedimentation
rate (ESR) is often markedly
elevated (100 mm/hr or
more)
• C-reactive protein (CRP) is
elevated, driven by incr. in
interleukin-6 (IL-6)
• 50% develop polymyalgia
rheumatica
• focal granulomatous
inflammation with narrowed
arterial lumen is seen here at
high magnification

186
Temporal artery, giant cell arteritis, gross
• Patients with giant cell
arteritis may have a
visible firm, palpable,
painful temporal artery
that courses over surface
of the scalp

Varicose veins, gross
187
 Prominent veins shown here
on lower leg are varicosities
 Varicose veins are a common
problem with aging venous
valves become incompetent
 There may be muscular
atrophy with less tone to
provide a massage effect on
large superficial veins, and skin
becomes less elastic with time
 Hydrostatic pressure from
standing for long periods
exacerbates problem

Comparison of healthy and varicose veins
188

189
Comparison of healthy and varicose veins (2)

Varicose veins
190
 Risk factors: Obesity, not
enough exercise; Other
related factors are pregnancy,
menopause, aging
 Symptoms: None, fullness or
pain in area
 Complications: Bleeding,
superficial thrombophlebitis
 Treatment: Compression
stockings, exercise, surgery

Congestive Heart
Failure
191

192
A 55-year-old woman presents to your clinic complaining of
ankle swelling and increasing shortness of breath with
exertion. Upon directed questioning, she reveals that she also
experiences shortness of breath when she is lying down.
Physical examination reveals marked hepatosplenomegaly,
distended neck veins, and pedal edema. A chest x-ray is
suggestive of cardiomegaly. You start the patient on an ACE
inhibitor, diuretic, and a low-sodium diet and you refer her to a
cardiologist.

Congestive Heart Failure
193
Etiology
 Left-sided (LS): Ischemic heart disease (especially MI);
hypertension; aortic/mitral valve disease;
cardiomyopathies; myocarditis
 Right-sided (RS): Left-sided heart failure; mitral
stenosis; cor pulmonale; cardiomyopathies;
myocarditis; tricuspid/pulmonary valve disease

Congestive Heart Failure (2)
194
 LS: Hypertrophied and dilated LV; dilated LA; pulmonary
congestion w hemosiderin-laden macrophages or “heart
failure” cells
 RS: Hypertrophied and dilated RV; usually hypertrophied
and dilated LV; hepatic congestion (nutmeg liver) w
centrilobular necrosis; congested spleen
 Pathophysiology for both left- and right-sided failure:
o LV failure leads to decreased cardiac output, resulting in dyspnea;
Pulmonary edema results from LV failure to keep up w RV output,
leading to increased fluid transudation from pulmonary vessels
o RV failure leads to increased central venous pressure, causing
hepatomegaly and peripheral edema

Common causes of nonvalvular
heart failure
195
Etiology Ventricular
wall
thickness
Ventricular
cavity size
Contractile
function
Diastolic
function
Ischemic
heart disease Normal or
decreased
Increased Decreased NormalDilated
cardiomyopathy
Hypertensive
heart disease
Increased
globally Decreased Normal Decreased
Hypertrophic
cardiomyopathy
Increased
septal
thickening
Redrawn after USMLE World 2016, Cardiology (Pathology), Question # 14.
See: Dumitru, I. Etiology of Heart Failure. Medscape, May, 2018.
Accessed April, 2020. Available at https://emedicine.medscape.com/article/163062-overview#a4

196
See :Congestive heart failure (CHF) - systolic, diastolic, left side, right side, & symptoms_Osmosis

Congestive Heart Failure (3)
197
 LS: Dyspnea; orthopnea; paroxysmal nocturnal
dyspnea (PND); pleural effusion; cerebral anoxia; salt
and water retention
 RS: Fluid retention and peripheral edema;
hepatosplenomegaly; ascites; distention of neck
veins
Treatment: Diuretics; low-sodium diet; ACE inhibitors;
nitrates; beta-blockers; digoxin
Note: Cor pulmonale refers to isolated right-sided heart
failure caused by chronic pulmonary hypertension

A man with CHF and marked jugular venous distension.
External jugular vein marked by an arrow
198https://www.wikiwand.com/en/Jugular_venous_pressure

Severe peripheral (pitting) edema
199https://www.wikiwand.com/en/Edema

CHF CXR Findings
200https://www.wikiwand.com/en/Heart_failure

Siderophages =
hemosiderin-laden macrophages
201
https://www.wikiwand.com/en/Heart_failure

Companion Video Learning Series:
Heart Failure_Lecturio
202
Model of a normal heart, with contracted muscle (left); and a weakened heart, with over-stretched
muscle (right) https://www.wikiwand.com/en/Heart_failure

203
THE END
See next side for sources and further study.

Sources:
 Baron SJ; Lee, CI. Lange Pathology Flash Cards, 2nd Ed. New York, NY: Mc Graw-
Hill, 2009.
 Buja, LM; Krueger GR. Netter’s Illustrated Human Pathology 2nd Ed. Illustrations
by Frank H. Netter, MD. Philadelphia, PA: Saunders- Elsevier, 2014.
 Kumar V; Abbas AK; Aster JC. Robbins Basic Pathology, 10th ed. Philadelphia:
Elsevier, 2018.
 Le, T; Bhushan, V. First AID for the USMLE Step 1 2020. Mc Graw-Hill, 2020.
 WebPath Online: Cardiovascular Pathology Image Plates
Further Study:
 Cardiovascular Pathology Rapid Review Notes
 Cardiac Pathology Questions and Answers_UWorld
 Cardiovascular Pathophysiology High Yield Cases_w Questions;
Answers-Discussion
 Video Edu: Cardiovascular Pathology & Pathophysiology_Osmosis

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