PATHOLOGY
4
Ischemic Heart Disease, Hypertensive Heart Disease,
Congestive Heart Failure, and Cor Pulmonale
Lecturer: Dr. Luis Cruz | December 4, 2018
Transcriber group: 3A
BLUE - additional notes from the handout and Robbins
ORANGE - from recording and 2020 trans
CONTENT OUTLINE
• Ischemic Heart Disease
• Ischemic Heart Syndrome
o Angina Pectoris
o Myocardial Infarction
o Chronic Ischemic Heart Disease
o Sudden Cardiac Death
• Acute Coronary Syndrome
• Myocardial Infarction
• Hypertensive Heart Disease
o Pulmonary Hypertensive Heart Disease
• Congestive Heart Failure
• Left Sided Heart Failure
• Heart Sided Heart Failure
• Inflammatory Heart Disease
o Rheumatic Heart Disease
o Infective Endocarditis
• Non-Bacterial Thrombotic Endocarditis
• RHD and Congenital Heart Diseases
• Endocarditis of Systemic Lupus Erythematosus
• Syphilitic Aortitis with Aortic Valve ring Dilatation
• Valvular Heart Diseases
o Mitral Valve Prolapse
o Calcific Aortic Valve Stenosis
o Calcification of the Mitral Annulus
ISCHEMIC HEART DISEASE
• Reduction or absence of blood supply to the heart
• Accounts for 80-90% of all heart disease mortality
• Caused by an imbalance between the myocardial
blood flow and the metabolic demand of the
myocardium
• Consequence of reduced coronary blood ︎flow
secondary to obstructive atherosclerotic vascular
disease
• CAUSES:
o Atherosclerosis – 90-95% of cases
o Vasospasm
o Thrombosis
o Stenosis of the coronary artery
o Inflammatory arteritis
• In all these causes, the main pathology will be the
decrease in the size of the caliber
FACTORS REDUCING CORONARY BLOOD FLOW
● Decreased aortic diastolic pressure
● Increased intraventricular pressure and myocardial
contraction
○ The more intraventricular pressure and
myocardial contraction, the more blood will flow
when ejected out from the left ventricle
● Coronary artery stenosis, which can be further
subdivided into the following etiologies:
5.
○ Fixed coronary stenosis
o Acute plaque change (rupture, hemorrhage)
o Coronary artery thrombosis – diameter of
thrombus can affect diameter of the vessel
Lumen
o Vasoconstriction
● Aortic valve stenosis and regurgitation
● Increased right atrial pressure
Note: ︎ “Thrombolytic ︎ therapy” ︎ with ︎ agents ︎ such ︎ as ︎
streptokinase or tissue plasminogen activators is often
used within the first 12 hours following onset of
symptoms and with ST-segment elevation to try and
lyse the thrombus.
ISCHEMIC HEART SYNDROMES
ANGINA PECTORIS (REVERSIBLE)
● ︎“chest ︎pain” ︎
● ︎3 ︎variants: ︎
A. Stable/typical angina (increase demand)
- Experience chest pain with exertion
- pain is described as a crushing or squeezing
substernal sensation that often radiates down
the left arm or to the left jaw (referred pain)
- relieved by rest
B. Prinzmetal/variant angina (vasospasm)
- occurs at rest and is caused by coronary artery
spasm
C. Unstable/crescendo angina (pre-infarction)
- characterized by increasingly frequent pain,
precipitated by less exertion or even occurring
at rest
MYOCARDIAL INFARCTION
● ︎Permanent ︎myocardial ︎damage ︎(coagulative ︎necrosis) ︎
due to irreversible myocardial ischemia
CHRONIC ISCHEMIC HEART DISEASE
● Post-infarction decompensation (CHF)
● aka ischemic cardiomyopathy ︎
● progressive heart failure secondary to ischemic
myocardial damage
● In most instances, there is a known clinical history of
previous MI. After prior infarction, chronic IHD
appears when the compensatory mechanisms (e.g.,
hypertrophy) of residual myocardium begin to fail.
SUDDEN CARDIAC DEATH
● Unexpected death from cardiac causes after or
without the onset of symptoms
● Congenital or acquired
● Fatal arrhythmia
○ usual mechanism of death in IHD
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 ○ unexpected death due to a lethal arrhythmia such o Rest angina
as asystole or sustained ventricular fibrillation o New-onset severe angina
(definition from Robbins) o Crescendo pattern of occurrence
2. Non-ST segment Elevation Myocardial Infarction
ACUTE CORONARY SYNDROME (NSTEMI)
● There is no ST-segment change but there is
SYNDROME PATHOLOGY
myocardial necrosis for release of a biomarker
3. ST segment Elevation Myocardial Infarction
STABLE ANGINA* Stenotic endothelialized
(STEMI)
atheromatous plaque
● There is St-segment elevation and myocardial
UNSTABLE ANGINA Ruptured atheromatous plaque necrosis with release of biomarker
with subocclusive thrombosis
MYOCARDIAL INFARCTION
• Produced most often by atherosclerosis leading to
VARIANT ANGINA Coronary spasm with or without thrombosis
atheromatous plaque • Ischemic coagulative necrosis of myocardial fibers
MYOCARDIAL Ruptured atheromatous plaque with loss of normal contractile and conductive
INFARCTION with occlusive thrombosis responses of affected myocardium
* STABLE ANGINA IS NOT INCLUDED IN ACUTE
CORONARY SYNDROME EPIDEMIOLOGY
• Age peak:
ATHEROSCLEROSIS TIMELINE o 55-64 yrs (males)
o 80’s ︎(females) ︎
o Estrogen stimulation is somewhat
protective for female
• Sex:
o 3:1, M:F
o Men are at greater risk than women
o In general, women tend to be protected against
MI during their reproductive years.
▪ menopause = less estrogen = exacerbation of
coronary artery disease
• Risk factors: HPN, hypercholesterolemia, cigarette
smoking, diabetes mellitus, sedentary lifestyle and
OCT

FACTORS AFFECTING THE LOCATION, SIZE AND

Figure 1. Atherosclerosis Timeline
Location, size, and morphology depends on:
From recording:
It starts with the deposition of foam cells in the vessel.
It will have fatty streaks and the presence of the fatty
streaks will produce endothelial dysfunction producing
atheroma which is the start of the plaque. The patient
can have fibrosis in the atheroma and the plaque can
either be complicated by either, fissuring or rupture.
Fissuring usually occurs in the boundary of the normal
intima of the artery as well as the plaque. Shear stresses
(e.g. increase fluid, sudden dilatation, or sudden
vasoconstriction due to neurohormonal effects) can lead
to fissures in the boundary between the plaque and
normal intima.
PATTERNS OF IHD WITH ACUTE CORONARY
SYNDROMES
1. Unstable angina
● There is no ST-segment change and there is no
sufficient myocardial damage for release of a
biomarker. There is one or more of the
following:
MORPHOLOGY OF MI
• Location, severity, and rate of occlusion
o Usually left side (the working portion of the
heart)
o Sudden occlusion = greater size, severe effect
o Chronic ischemia = heart can compensate by
producing collaterals
o Athletes have a higher vascular perfusion
• Size of vascular bed perfused by occluded vessel
• Duration of occlusion
o Sudden occlusion is worse than a slow,
progressive occlusion since blood vessels do
compensate for gradual changes
o Metabolic/oxygen demands of myocardium at risk
o Transmural or massive MI may affect the whole
heart
o Affected by blood pressure and heart rate
o Extent of collateral blood vessels
o Increased with exercise
o If a patient have a sedentary life,
collateralization of the coronaries will be less
o Less colateral = greater size of infarction
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o Presence, site, and severity of spasm
o Toxic metabolites occurring in the areas of
infarction can incite vasospastic phenomenon
that could affect other arteries of the heart and
is contributory to massive infarction of the
heart
o Alterations in BP, heart rate, cardiac rhythm
Figure 2. Heart with Myocardial Infarction. Typical color
of the heart is reddish-brown. An infarcted heart is seen
as white due to absence of blood.
EVOLUTION OF MORPHOLOGIC CHANGES IN MI
TIME OF
GROSS MORPHOLOGIC FINDINGS
ONSET
18-24 hrs Pallor of myocardium
24-72 hrs Pallor with some hyperemia
3-7 days Hyperemic border with central yellowing
10-21 Maximally yellow and soft with vascular
days margins
7 weeks White fibrosis
TIME OF
MICROSCOPIC FINDINGS
ONSET
Wavy myocardial fibers but no
1-3 hrs
inflammatory cells
Staining defect in myocardial fiber
2-3 hrs cytoplasm with tetrazolium or basic
fuchsin dye
Coagulation necrosis with loss of cross
striations, contraction bands, edema,
4-12 hrs
hemorrhage, and early neutrophilic
infiltrate
Continuing coagulation necrosis,
18-24 hrs pyknosis of nuclei, and marginal
contraction bands
Total loss of nuclei and cross striations
24-72 hrs
along with heavy neutrophilic infiltrate
Macrophage and mononuclear infiltration
3-7 days
begin, fibrovascular response begins
Fibrovascular response with prominent
10-21
granulation tissue containing capillaries
days
and fibroblasts
Fibrosis with dense collagenous
7 weeks
connective tissue and no inflammation
NOTE: The above gross and microscopic changes over
time can vary. In general, a larger infarct will evolve
through these changes more slowly than a small infarct.
CLINICAL MANIFESTATIONS (ACUTE MI)
o Ischemic Myocardial Damage
○ Chest pain
○ Dyskinetic precordial impulse
○ Fourth heart sound
○ Low grade fever
○ Leukocytosis / increased ESR
● ︎Autonomic ︎Disturbance ︎
○ Tachycardia
○ Sweating
○ Vomiting
○ Syncope
PATHOGENESIS
From handout:
• Occlusive intracoronary thrombus
o thrombus overlying a plaque causes 75% of
myocardial infarctions, with superficial plaque
erosion present in the remaining 25%
• Vasospasm
o with or without coronary atherosclerosis and
possible association with platelet aggregation
• Emboli
o from left sided mural thrombosis, vegetative
endocarditis, or paradoxic emboli from the
right side of heart through a patent foramen
ovale
From Robbins:
• Majority of MIs are caused by acute thrombosis
within coronary arteries.
• Disruption or erosion of preexisting atherosclerotic
plaque serves as the nidus for thrombus generation,
vascular occlusion, and subsequent infarction of the
perfused myocardium.
• In 10% of MIs, transmural infarction occurs in the
absence of occlusive atherosclerotic vascular
disease; such infarcts are mostly ascribed to:
o coronary artery vasospasm
o embolization from mural thrombi (e.g., in the
setting of atrial fibrillation)
o valve vegetations
• Severe fixed coronary atherosclerosis leads to
marginal perfusion of the heart. In this setting, a
prolonged period of increased demand (e.g., due to
tachycardia or hypertension) can lead to ischemic
necrosis of endomyocardium
• Ischemia without detectable atherosclerosis or
thromboembolic disease = caused by disorders of
small intramyocardial arterioles, including
vasculitis, amyloid deposition, or stasis, as in sickle
cell disease.
Coronary Artery Occlusion
• In a typical MI, the following sequence of events
takes place:
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 o atheromatous plaque is eroded or suddenly
disrupted by endothelial injury, intraplaque
hemorrhage, or mechanical forces, exposing
subendothelial collagen and necrotic plaque
contents to the blood.
o Platelets adhere, aggregate, and are activated,
releasing thromboxane A2, adenosine
diphosphate (ADP), and serotonin = causing
further platelet aggregation and vasospasm
o Activation of coagulation by exposure of tissue
factor and other mechanisms adds to the
growing thrombus. o Within minutes, the
thrombus can evolve to completely occlude the
coronary artery lumen.
Myocardial Response to Ischemia
• Within seconds of vascular obstruction, aerobic
metabolism ceases = drop in adenosine
triphosphate (ATP) = accumulation of potentially
noxious metabolites (e.g. lactic acid) in the cardiac
myocytes
• Functional consequence: rapid loss of contractility
• Prolonged ischemia lasting for 20 - 40 minutes =
irreversible damage and coagulative necrosis of
myocytes
o Irreversible injury first occurs in the
subendocardial zone
o WHY? (1) susceptible to ischemia because it is
the last area to receive blood delivered by the
epicardial vessels, and (2) it is exposed to high
intramural pressures which can impede the
inflow of blood.
Figure 3. Myocardial Infarction Consequences
PATHOLOGY
● Common location: left ventricle
● Gross morphologic appearance of MI can vary.
Patterns include (2 forms):
1. Transmural infarct
▪ More common type of MI because of occlusion of
coronary artery.
▪ Involves the full thickness of the left ventricular
wall from endocardium to epicardium, usually
the anterior free wall and posterior free wall and
septum with extension into the RV wall in 15-
30%.
▪ Isolated infarcts of RV and right atrium are
extremely rare.
▪ These infarcts are also called ST-︎ segment
elevated MIs (STEMIs).
2. Subendocardial
▪ Multifocal areas of necrosis confined to the inner
1/3-1/2 of the left ventricular wall.
▪ Do not show the same evolution of changes seen
in a transmural MI.
▪ Aka:”non–ST-segment elevated MIs” or
”NSTEMIs” ︎
▪ Decreases in oxygen delivery (as from
hypotension, anemia, or pneumonia) or
increases in oxygen demand (as with
tachycardia or hypertension) can cause
subendocardial ischemic injury
▪ Subendocardial affectation commonly involves
the purkinje bundles, which are located in the
same area which leads to distorted/erratic
contraction of the heart.
▪ Sometimes mistaken for epigastric pain
▪ Subendocardial area is the least perfused region
of the myocardium and most vulnerable to
reduction in blood flow
DISTRIBUTION OF ARTERIAL INVOLVEMENT AND
RESULTANT INFARCTION
● Left Anterior Descending Artery (LAD)
o 40-50%
o Anterior Wall of Left Ventricle
o Anterior ⅔ of Interventricular Septum
● Right Anterior Descending Artery (RAD)
o 30-40%
o Posterior Wall of Left Ventricle
o Posterior ⅓ of Interventricular Septum
● Left Circumflex Artery (LCA)
o 15-20%
o Lateral Wall of Left Ventricle
COMPLICATIONS OF MI
● cardiac arrhythmias (75-95% of complicated cases)
and ︎conduction ︎defects, ︎with ︎possible ︎“sudden ︎death”
○ MI contributes to arrhythmias by causing
electrical instability (irritability) of ischemic
regions of the heart.
● LV congestive heart failure (60%)
● cardiogenic shock (10-15%)
● rupture of free wall, septum or papillary muscle
(1-5%)
● thromboembolism (15-40%)
● OTHERS: pericarditis, ventricular aneurysms
From handout:
● Clinical complications of MI depend on the size and
location of the infarction, as well as pre-existing
myocardial damage. Complications can include:
o Arrhythmias and conduction defects, with
possible ︎"sudden ︎death” ︎
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 o Extension of infarction, or re-infarction
o Congestive heart failure (pulmonary edema)
o Cardiogenic shock
o Pericarditis
o Mural thrombosis, with possible embolization
o Myocardial wall rupture, with possible
tamponade
o Papillary muscle rupture, with possible valvular
insufficiency
Figure 6. Shows a black band pointing to the rupture of
o Ventricular aneurysm formation
a papillary muscle affecting the mitral valve.
(yung info sa handout and ppt parang ex mo lang, hindi
consistent 🙊 )

MICROSCOPIC FEATURES

"
Figure 7. Signs of Aortic Disease

Figure 4. Shown are sections of cardiac muscle tissue

with ︎ varying ︎ extent ︎ of ︎ myocardial ︎ damage. ︎ What’s ︎
important is to know that the ultramicroscopic changes
(loss of striation, variation in nuclei size, and location)
happen in about 6 hrs post-infarction. There will be
inflammatory infiltrates in the area of the infarct as a
consequence of decreased oxygen. Vascular damage,
hemorrhage, and inflammation and repair are also
evident.

Figure 8. Signs of Aortic Regurgitation. The heart is

suffering from papillary rupture. Usually involves
murmurs. Aortic regurgitation happens whenever there
is rupture.

Figure 5. Aneurysm with thrombus. In examining

gross specimens, the best gauge in order for it to be
"
considered hypertrophy is by weight. Enlarged or
Figure 9. Heart enveloped in pericardial sac: this will
termed, cardiomegaly, if it exceeds the normal value by
pinge in contraction and might lead to cardiac
weight (distinct character). In some instances, it can be
tamponade.
thin but heavy, so it is still considered cardiomegaly.
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Figure 10. Pericardial sac filled with blood that is clotted
(tamponade). Cardiac tamponade is when fluid in the
pericardium builds up and leads to its compression.
Figure 11. Time activity for enzymes released from the
infarcted myocardium. Serum enzyme activity is
expressed as multiples of the upper reference limit.
These enzymes were used before and is still
continuously used and accepted.
Figure 12. An ECG result showing abnormal readings in
relation to the time.
ADVERSE PROGNOSTIC FACTORS OF ACUTE MI
● Advance age
● Anterior transmural infarction
● Left bundle branch block
● Heart failure
● Systolic hypotension
● Complex ventricular arrhythmias occurring late after
myocardial infarction
● History of previous myocardial infarction
KILLIP CLASSIFICATION OF ACUTE MI
● used in predicting and stratifying the risk of mortality
in accordance with the examination results and the
development of heart failure.
● Individuals with a low Killip class are less likely to die
after a myocardial infarction than individuals with a
high Killip class.
● Killip class I
○ (-) no clinical signs of heart failure
● Killip class II
o (+) rales or crackles in the lungs
o (+) S3 gallop
o elevated jugular venous pressure
● Killip class III
○ (+) frank acute pulmonary edema
● Killip class IV
○ those in cardiogenic shock or hypotension
(measured as systolic blood pressure <90
mmHg)
○ evidence of low cardiac output (oliguria, cyanosis,
or impaired mental status)
LABORATORY DIAGNOSIS OF MI
BIOMARKERS (from handout)
● None is completely sensitive and specific for MI,
particularly in the hours following onset of
symptoms.
● Timing is important, as are correlation with patient
symptoms, electrocardiograms, and angiographic
studies
● biomarkers described in association with acute
myocardial infarction:
1. Troponins
- Troponin I and T are structural components of
cardiac muscle
- highly specific for myocardial injury (more specific
than CK-MB)
- begin to increase following MI within 3 to 12 hours,
about the same time frame as CK-MB
- remain elevated longer than CK--up to 14 days
✓ making troponins a superior marker for
diagnosing myocardial infarction in the recent
past
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 ✓ disadvantage of continued elevation: more
difficult to diagnose reinfarction or extension of
infarction
- Troponin T lacks specificity because elevations can
appear with skeletal myopathies and renal failure

2. Total Creatine Kinase (CK)

- simple, inexpensive, and readily available
- elevation in total CK is not specific for MI, because
most CK is located in skeletal muscle, and
elevations are also seen in non-cardiac conditions

3. Creatine Kinase - MB fraction

- CK can be subdivided into three isoenzymes:
✓ MM - present in both cardiac and skeletal
muscle
✓ MB - specific for cardiac muscle Figure 14. Cardiac Marker Testing and Triaging
✓ BB - in brain, bowel, and bladder Strategies
- increases within 3 - 4 hours of myocardial necrosis
- peak in a day and return to normal within 36 hours HYPERTENSIVE HEART DISEASE (HHD)
● ︎response ︎of ︎the ︎heart ︎to ︎ increased demands induced
- less sensitive than troponins
by systemic or pulmonary hypertension
- useful for diagnosis of reinfarction or extensive of
○ Systemic (left-sided) Hypertensive Heart Disease
an MI
○ Pulmonary Hypertensive Heart Disease

4. Myoglobin
- not specific for cardiac muscle and can be elevated
with any form of injury to skeletal muscle.
- rise in myoglobin can help determine the size of
infarction
- elevated even before CK-MB

5. B-type natriuretic peptide (BNP)

- released from ventricular myocardium
- marker of heart failure
- release can be stimulated by:
✓ systolic and diastolic left ventricular
dysfunction Figure 15. This figure shows the proportion of the
✓ acute and chronic right ventricular failure different causes of hypertension in which the essential
✓ acute coronary syndromes type was the most frequent cause of hypertension.
✓ stable coronary heart disease
MINIMAL CRITERIA FOR DIAGNOSIS OF
✓ valvular heart disease
SYSTEMIC HHD
✓ left and right ventricular hypertrophy ● ︎Left ︎Ventricular ︎Hypertrophy ︎(LVH) ︎in ︎the ︎absence ︎of ︎
secondary to arterial or pulmonary other cardiovascular pathology
hypertension
● ︎History ︎of ︎hypertension ︎

6. C-reactive protein (CRP)

PATHOLOGIC FEATURES
- acute phase protein elevated when inflammation is
● Concentric hypertrophy without dilatation
present
(compensated)
- reflect the extent of atheromatous plaque ○ If you examine the ventricle, it should be
formation and predict risk for acute coronary
concentric - equally / uniformly thickened
events
● Dilatation and thinning of wall (marks
- lacks specificity for vascular events decompensation)

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Figure 16. This figure shows typical concentric
hypertrophy (compensated) in a typical compensated
hypertensive heart disease
NOTES (from Robbins):
● essential feature of HHD is left ventricular
hypertrophy, typically without ventricular dilation
until very late in the process
● heart weight can exceed 500 g (normal for 60 to 70
kg individual = 320-360 g)
● left ventricular wall thickness can exceed 2.0 cm
(normal is 1.2 to 1.4 cm).
● With time, increased left ventricular wall thickness
imparts a stiffness that impairs diastolic filling and
can result in left atrial dilation.
● In long-standing systemic hypertensive heart
disease leading to congestive heart failure,
hypertrophic left ventricle typically is dilated.
Starling’s Law by Frank Starling
● The heart thickens and stretches and then will go
back to its original state.
Congestive Heart Failure
● However, if there is progressive hypertension, this
can overstretch the heart and will be unable to go
back to its original size and will not contract
anymore leading to Congestive Heart Failure
PULMONARY HYPERTENSIVE HEART DISEASE
(COR PULMONALE)
● Right ventricular enlargement secondary to
pulmonary hypertension (attributable to primary
disorders of the lung parenchyma or pulmonary
vasculature)
● Due to right ventricular pressure overload
● Because the pulmonary vasculature is the low
pressure side of the circulation, the right ventricle
has a thinner and more compliant wall than the left
ventricle
● Characterized by
o right ventricular hypertrophy
o dilatation
o potential failure secondary to pulmonary
hypertension
● Most frequent cause are disorders of the lungs,
especially chronic respiratory diseases such as
emphysema or primary pulmonary hypertension
TYPES OF COR PULMONALE
ACUTE COR PULMONALE
● There is marked dilatation of the right ventricle
without hypertrophy
○ right ventricle usually shows only dilation; if an
embolism causes sudden death, the heart may
even be of normal size (Robbins)
● There may be aneurysm with a very big thrombus
which may be dislodged and overhang the
pulmonary arteries (saddle thrombus)
● Usually brought about by thrombus coming from
the deep calf veins / leg muscle veins wherein the
thrombus lengthens and increases in size and can
be detached which may then extend from the leg up
to the Inferior Vena Cava
○ If thrombus is dislodged, it can ride on
pulmonary artery bifurcation occluding left and
right pulmonary arteries.
● Can follow massive pulmonary embolism
● Changes in right ventricle shape
○ Normal crescent shape to dilated ovoid
CHRONIC COR PULMONALE
● Results from right ventricular hypertrophy
secondary to prolonged pressure overload
● Usually due to lung diseases such as Intrinsic Lung
Diseases, COPD, Typical Pneumoconiosis as well as
Systemic Diseases which may affect the lung
● Right ventricular wall thickens
○ In extreme cases, thickness of the right
ventricular wall is comparable to or even
exceed that of the left ventricle
● Because chronic cor pulmonale occurs in the setting
of pulmonary hypertension, pulmonary arteries
often contain atheromatous plaques and other
lesions, reflecting long-standing pressure
elevations.
PATHOGENESIS
● Right ventricle enlargement due to pulmonary
hypertension caused by lung disorders:
○ COPD, DIP, ATELECTASIS, CYSTIC FIBROSIS
✓ Cystic Fibrosis is not a common disease
among Filipinos
o Pulmonary Embolism, Primary
o Pulmonary Hypertension
o Kyphoscoliosis, Pickwickian Habitus
o Metabolic Acidosis, Hypoxia
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Disorders Predisposing to Cor Pulmonale (from SCHEMA OF PATHOGENESIS OF COR PULMONALE
Robbins):

CONGESTIVE HEART FAILURE

● “pump ︎ failure” ︎ due ︎ to ︎ decreased myocardial
capacity to contract or myocardial capacity to fill
chambers with blood
○ rate is not sufficient to meet the metabolic
demands of the tissue
● common endpoint of all complications involving the
heart
● Theories:
o Backward failure - damming back of blood into
the venous side of the heart because of
inability to eject the blood (volume overload)
o Forward failure - failure to eject blood into the
circulation; with diminished flow to the tissues
(pressure overload)
● Definitions of CHF:
○ condition in which the heart fails to discharge
its contents (Thomas Lewis)
○ state in which the heart fails to maintain an
Figure 17. This figure shows papillary muscles in the
right ventricle demonstrating right ventricular adequate circulation for the needs of the body
hypertrophy despite a satisfactory filling pressure (Paul
Wood)
○ syndrome that arises when the heart is
chronically unable to maintain an appropriate
blood pressure without support (Peter Harris)
● common problem in old age as a result of
cardiovascular disease
● one of the common symptoms is congestion, which
takes the form of water retention and swelling
(edema):
o peripheral edema - swollen limbs and feet
Figure 18. Saddle Pulmonary Embolism. Shows a
o pulmonary edema - causing breathing difficulty
saddle thrombus wherein the pulmonary artery is
o ascites - swollen abdomen
dissected showing a very large thrombus occluding the
vessel lumina

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 ● Class I - no limitation on normal physical activity
but may have left ventricular dysfunction.
● Class II - mild symptoms on normal physical
activity.
● Class III - marked symptoms on less than normal
physical activity.
● Class IV - symptomatic even at rest.

MECHANISMS / CAUSES
● Mechanical Overload
o increased resistance to flow (afterload)
▪ systemic hypertension
▪ aortic stenosis
Figure 20. The relationship between cardiac output
o excessive flow load (preload)
and end diastolic pressure from a normal and failing
▪ septal defects with left to right shunts
heart.
● Diminished strength of contraction
● Diminished ventricular filling
MAJOR AND MINOR CRITERIA OF HF

Major Criteria Minor Criteria

Paroxysmal nocturnal Ankle edema

dyspnea

Neck vein distention Night cough

Rales, S3 gallop Dyspnea on exertion

Cardiomegaly Hepatomegaly

Acute pulmonary Pleural effusion

edema
Figure 22. The various unfortunate events that could
Increased venous Vital capacity reduced lead to heart failure.
pressure >16cm of by 1/3
H20

Hepatojugular reflux Tachycardia

NOTE: The ones in bold are also overt signs of heart

failure.

Figure 23. This diagram shows a possible scenario on

how congestive heart failure (CHF) may occur.

● Having hypertension, valvular disease or myocardial

infarction may increase workload of the heart and
stress in its walls.
● Changes in structure may occur and will result in its
dysfunction. These will be manifested as a decrease
Figure 21. Spectrum of Heart Failure. NYHA in cardiac output which may then decrease arterial
Functional Classification. blood volume.
● The condition is further aggravated when other
response such as the Renin-Angiotensin Aldosterone

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 System (RAAS) is activated, thus increasing plasma
volume causing edema.
" right sided HF
Figure 24. LUQ normal heart. RUQ left ventricular
hypertrophy. LLQ heart with MI. RLQ dilated heart.
LEFT-SIDED HEART FAILURE
● Causes:
o Ischemic Heart Disease
o Hypertension
o Aortic and Mitral Valve Disease
o Myocardial Infarction
● Morphologic Changes
o Lungs - congestion and edema
o Chronic Passive Congestion - “brown ︎induration” ︎
o Pleural effusion
o Kidneys - acute tubular necrosis
o Brain - hypoxic encephalopathy
● Backward failure of the left ventricle causes
congestion of the lungs' blood vessels
● Failure of the left side of the heart causes blood to
back up (be congested) into the lungs, causing
respiratory symptoms as well as fatigue due to
insufficient supply of oxygenated blood.
● Respiratory symptoms:
o increased rate of breathing and increased work
of breathing (non-specific signs of
respiratory distress)
o Rales or crackles, heard initially in the lung
bases
✓ when severe and heard throughout lung
fields =suggest the development of
pulmonary edema (fluid in the alveoli)
o Cyanosis = suggests severe low blood oxygen;
late sign of extremely severe pulmonary edema.
● Additional signs indicating left ventricular failure:
o laterally displaced apex beat (which occurs if the
heart is enlarged)
o gallop rhythm (additional heart sounds) -
marker of increased blood flow
o increased intra-cardiac pressure.
o Heart murmurs may indicate the presence of
valvular heart disease, either as a:
✓ cause of HF = aortic stenosis
✓ result of HF = mitral regurgitation
RIGHT-SIDED HEART FAILURE
● Causes:
o Left sided heart failure - most common cause of
o Intrinsic lung disease
o Cardiomyopathy and diffuse myocarditis
o Tricuspid or pulmonary valve disease
● Morphologic Changes:
o Liver - chronic passive congestion giving it an
appearance like a nutmeg
o Spleen - congestive splenomegaly
o Dependent edema / ascites
● Backward failure of the right ventricle leads to
congestion of systemic capillaries.
● What differs pure right-sided heart failure from left-
sided heart failure is that engorgement of the
systemic and portal venous systems typically is
pronounced and pulmonary congestion is minimal in
right-sided HF.
● Clinical findings:
o pitting peripheral edema
o nocturia
o ascites
o liver enlargement
✓ significant liver congestion may result in
impaired liver function (congestive
hepatopathy), jaundice and even coagulopathy
(problems of decreased or increased blood
clotting)
● Jugular venous pressure is frequently assessed as a
marker of fluid status, which can be accentuated by
eliciting hepatojugular reflux.
o If the right ventricular pressure is increased =
parasternal heave may be present, signifying
the compensatory increase in contraction
strength.
● Patients rarely present with an isolated right sided
heart failure. It typically presents as biventricular
CHF with symptoms reflecting both right-sided and
left-sided heart failure.
Figure 25. Frothy sputum
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Figure 26. Chronic Passive Congestion of Lungs
Figure 27. Chronic Passive Congestion of Liver
INFLAMMATORY HEART DISEASE
RHEUMATIC FEVER
● occurs ︎ after ︎ group ︎ A ︎ β-hemolytic streptococcal
infections (usually pharyngitis)
● Jones criteria: diagnosis of acute rheumatic fever
is made based on serologic evidence of previous
streptococcal infection in conjunction with one
major and one minor or two major
Major criteria: ︎
o migratory polyarthritis of large joints
✓ temporary migrating inflammation of the
large joints, usually starting in the legs and
migrating upwards.
o carditis
✓ inflammation of the heart muscle
(myocarditis) which can manifest as
congestive heart failure with shortness of
breath, pericarditis with a rub, or a new heart
murmur.
o subcutaneous nodules
✓ painless, firm collections of collagen fibers
over bones or tendons. They commonly
appear on the back of the wrist, outside
elbow, and front of the knees.
o erythematous annular rash (erythema
marginatum) in the skin
✓ reddish rash that begins on the trunk or arms
as macules, which spread outward and clear
in the middle to form rings
✓ rings continue to spread and coalesce with
other rings = taking on a snakelike
appearance
✓ typically spares the face and is made worse
with heat.
o Sydenham chorea
✓ a neurologic disorder characterized by
involuntary purposeless, rapid movements
(also called St. Vitus dance) ︎
Minor Criteria:
✓ fever (38.2-38.9oC)
✓ Arthralgia – joint pain without swelling
✓ Raised erythrocyte sedimentation rate of
CRP
✓ Leukocytosis
✓ ECG showing features of heart block
✓ Previous episode of rheumatic fever or
inactive heart disease
RHEUMATIC HEART DISEASE
● cardiac manifestation of rheumatic fever
● associated with inflammation of all parts of the
heart, but valvular inflammation and scarring
produce the most important clinical features.
● deforming fibrotic valvular disease which produces
permanent dysfunction and severe, sometimes fatal
cardiac failure decades later.
ETIO-PATHOGENESIS
● acute rheumatic fever is a hypersensitivity reaction
classically attributed to antibodies directed against
group A streptococcal molecules that cross-react
with host myocardial antigens
● heightened immunologic activity to strep antigen
● autoimmune reaction
● TARGETS:
o heart valve glycoproteins - hyalorunate capsule
o myocardial/smooth m. sarcolemma - Strep
membrane Ag
o cardiac myosin - strep. M-protein (virulence
factor)
MORPHOLOGIC LESIONS IN RHD
● Aschoff Bodies
o foci of fibrinoid necrosis surrounded by
lymphocytes, macrophages, plump activated
histiocytes ︎called ︎"Anitschkow ︎cells” ︎or ︎Aschoff ︎
cells (caterpillar cells)
o pathognomonic of rheumatic fever
● Pancarditis with sero-fibrinous pericardial exudate -
“bread ︎and ︎butter ︎pericarditis”
● Verruca - vegetations of fibrinoid necrosis w/in
cusps or along chordae tendinae
● McCallums plaques - irregular thickenings 20 to
subendocardial lesions brought about by
regurgitation jets in the left atrium
● Mitral valve lesions:
o leaflet thickening
o commissural fusion and shortening
o thickening and fusion of chordae tendinae
✓ Fibrous bridging across the valvular
commissures and calcification create “fish-
mouth” ︎or ︎“buttonhole” ︎stenoses.
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 CLINICAL COURSE Clinical Presentation of Mitral Regurgitation:
● Age incidence: children 5-15 yrs old ● Dyspnea
● Females more prone for valvular lesions o increased left atrial pressure, particularly during
● Attacks begin with migratory polyarthritis with fever exertion
● LVF
o Symptoms in all age groups typically begin 2 to 3
o contractile failure with severe ventricular
weeks after streptococcal infection and are
dilatation
heralded by fever and migratory polyarthritis
● RVF
● 50-75% of children have acute carditis
o passive consequence of increased left atrial
(arrhythmias) pressure and reactive pulmonary
o principal clinical manifestation is carditis vasoconstriction
● Reactivation with subsequent pharyngeal ● Systemic emboli
infections cumulative effects on the heart o atrial dilation and fibrillation
leading to decompensation
● Most important functional consequence of
rheumatic heart disease is valvular stenosis
and regurgitation; stenosis tends to
predominate

INFECTIVE ENDOCARDITIS
● Colonization or invasion of the heart valves or mural
endocardium by microbiologic agents leading to
formation of bulky, friable vegetations laden with
organisms

ACUTE INFECTIVE ENDOCARDITIS

● refers to tumultuous, destructive infections,
frequently involving a highly virulent organism
attacking a previously normal valve.
● leads to death in 50% of cases

SUBACUTE INFECTIVE ENDOCARDITIS

● refers to infections by organisms of low virulence
affecting a previously abnormal heart,
especially scarred or deformed valves.
● appears insidiously and even if untreated follows ︎ a
protracted course of weeks to months; most
patients recover after appropriate antibiotic
Causes of Mitral Regurgitation: therapy.
● mitral valve leaflet disease
o mitral valve prolapse MORPHOLOGIC LESIONS
o rheumatic disease ● BACTERIAL-LADEN VEGETATION
o endocarditis* o pathognomonic most commonly on heart valves
● subvalvular disease ● "RING ABSCESS" in acute endocarditis
o chordal rupture* ● petechiae
o papillary muscle dysfunction ● nail bed splinter hemorrhages
o papillary muscle rupture* ● “Roth" ︎spots ︎- retinal hemorrhages
● dilating LV disease ● Janeway lesions - painless palm or sole
o LVF ︎(‘functional’ ︎mitral ︎regurgitation) erythematous lesions
*these disorders produce acute mitral regurgitation ● Osler nodes - painful fingertip nodules

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 ● diagnosis is confirmed by positive blood cultures
and echocardiographic findings.

COMPLICATIONS
● Cardiac
o Valve insufficiency
o suppurative pericarditis
o dehiscence of prosthesis
o ring abscess
● Embolic
Janeway lesions Osler node
o cerebral abscess/infarct (left-sided lesions)
o pneumonia/pulmonary abscess (right-sided)
● Renal
o infarction
o glomerulonephritis (focal and diffuse)
✓ due to glomerular trapping of antigen antibody
complexes
● renal failure
Nail bed splinter hemorrhage Roth spots
NON-BACTERIAL THROMBOTIC ENDOCARDITIS
DUKE CRITERIA (NBTE)
1. 2 major ● aka ︎“Marantic ︎Endocarditis”
2. 1 major and 3 minor ● vegetative endocarditis in debilitated patients
3. 5 minor usually with cancer or sepsis
● sterile vegetations along line of closure of leaflets of
Pathologic criteria: microorganisms demonstrated by cusps composed of bland thrombus without
culture or histologic examination inflammatory reaction
● characterized by the deposition of sterile thrombi on
Major: cardiac valves typically in those with an ︎ underlying
✓ Blood culture “hypercoagulable ︎state” ︎
✓ Echocardiographic ID of valve-related or implant o hypercoagulable states are the usual precursor
related mass or abscess to NBTE
✓ Partial septation of a valve ● vegetations in NBTE are typically small (1-5 mm in
✓ New valvular insufficiency diameter) and valvular damage is NOT a
prerequisite.
Minor:
RHD AND CONGENITAL HEART DISEASES
✓ Predisposing heart condition
● Etiopathogenesis:
✓ IV drug use
o Acute - Staphylococcus aureus (20-30% of
✓ Vascular lesions (roth spots, osler nodes) cases)
o Subacute - Streptococcus viridans
CLINICAL COURSE
o Others: fungal, enteric bacteria, etc.
● fever is the most consistent sign of infective
● No bacteria can be cultured in 5-20% of cases
endocarditis
● In subacute disease (particularly in older adults):
ENDOCARDITIS OF SYSTEMIC LUPUS
o fever may be absent
ERYTHEMATOSUS
o only manifestations are nonspecific fatigue,
● Libman-Sacks endocarditis
weight loss, flulike syndrome, and
● Characterized by the presence of sterile vegetations
splenomegaly
on the valves of patients with SLE.
● By contrast, acute endocarditis often manifests
● Mitral and tricuspid valvulitis
with:
● Sterile vegetations on the undersurfaces of AV valves
o rapidly developing fever, chills, weakness, and
● “HEMATOXYLIN ︎BODIES” ︎– pathognomonic of SLE
lassitude
● In those who are not treated promptly, microemboli
SYPHILITIC AORTITIS WITH AORTIC VALVE
are formed, which can give rise to:
o petechiae RING DILATATION
o nail bed splinter hemorrhages ︎ ● Incompetence of valves leading to massive
o retinal hemorrhages (Roth spots) hypertrophy
o painless palm or sole erythematous lesions ● “COR ︎BOVINUM”
(Janeway lesions)
o painful fingertip nodules (Osler nodes)

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 VALVULAR HEART DISEASE Clinical: MR, arrythmias, infective endocarditis
MITRAL VALVE PROLAPSE
● “floppy ︎valve”, ︎Barlow’s ︎syndrome, ︎midsystolic click -END-
● Young ︎females, ︎Marfan’s ︎syndrome
● Unknown etiology, defect in connective tissues

Morphology:
- degeneration of zona fibrosa in leaflet
- ballooning or hooding of the leaflets
- later findings: fibrous thickening of leaflets
fibrous deposits on LV surface

REFERENCES:
● Robbin’s ︎Basic ︎Pathology ︎10th Ed
● Lec ppt and handout
● Recordings

TRANSCRIBED BY:
● GROUP 3A
● SUBTRANSHEAD: CB
Figure 28. Mitral Valve Prolapse ● TRANSHEAD: LFM
CALCIFIC AORTIC VALVE STENOSIS
Incidence: elderly, bicuspid valves
Cause: dystrophic calcification of valves
Morphology: heaped up calcific mass on cusps, LVH
Clinical features: angina, syncope, cardiac
decompensation

Figure 29. Calcific aortic valve stenosis

CALCIFICATION OF THE MITRAL ANNULUS

Incidence: elderly
Cause: Ca2+ deposits due to degenerative changes
(aging)
Morphology: stony-hard blading behind leaflets

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