Cardiovascular

Pathology Cases SYSPATH EXERCISE

Compassionate Group
Ausejo I Ca-at I Caballes I Demegillo I Malayag I Mangudadatu I Pa-alisbo I Salipoden
 Each case includes:
01 02 03
The Case History Diagnosis Etiology

04 05 06
Pathogenesis Gross and Pathophysiology
Histologic of Clinical
Morphology Manifestations
CASE No. 25
 Clinical History

A 9 year old female had two previous attacks of

rheumatic fever. She entered the hospital for the
third time with painful swollen joints, fever, and
pulmonary edema. She died with signs of
progressive heart failure.
DIAGNOSIS:Rheumatic heart disease
 Etiology and Pathogenesis
Etiology

Single or repeated attacks of rheumatic fever

that results in rigidity and deformity of valve
cusps, the fusion of the commissures, or
shortening and fusion of the chordae
tendineae

Pathogenesis

Group A Beta hemolytic streptococcal

pharyngeal infection -->antibody
cross-reactivity (Type II hypersensitivity) --> B
cells present the bacterial antigen to CD4-T
--> plasma cells induce the production of
antibodies against
Streptococcus-->antibodies also react against
the myocardium and joints -->cardiac
symptoms of rheumatic fever
 Gross Morphology
Gross

Left figure shows a pericardium

with Clear, straw-colored,
protein-rich exudate containing a
small number of inflammatory cells.

Right figure shows Left ventricle cut

open to display the characteristic
severe thickening of the mitral
valve,thickened chordae tendineae,
and hypertrophied ventricle
.MacCallum's patch in the left
atrium
 Histologic Morphology
Histologic

Figure above shows entire

thickness of the myocardium

Figure below shows high and

medium power view of
myocardium. Note the black dots
which represents Aschoff nodule
which is an interstitial aggregate of
macrophages and lymphocytes,
with necrotic collagen, in an area of
interstitial fibrosis.
Histologic Morphology
Histologic Morphology
 CASE No. 195
(Micro Case 4)
 Clinical History
A 67 year old male had rheumatic heart disease
for thirty years. Three months prior to death he
began to have episodes of fever and chills
accompanied by signs of worsening congestive
heart failure. Splinter hemorrhages and purpuric
skin rashes were noted three weeks before death.
DIAGNOSIS: INFECTIVE ENDOCARDITIS
 Etiology
Main underlying cause of native valve endocarditis:
● Rheumatic valvular disease
● Congenital heart disease
● Mitral valve prolapse
● Degenerative Heart disease

Most cases are caused by:

● viridans streptococci
● Streptococcus gallolyticus
● Staphylococcus aureus, coagulase-negative staphylococci
● HACEK organisms (Haemophilus, Aggregatibacter, Cardiobacterium,
Eikenella, Kingella)
● Enterococci
Pathogenesis & Pathophysiology
Rheumatic heart valve
produces turbulent blood
flow causing endothelial
injury where the bacteria
colonize forming a biofilm
and vegetation
 Gross Morphology
Splinter hemorrhages were
observed at digit tips. Blood
cultures grew alpha-hemolytic
streptococci. The alpha hemolysis
on blood agar typical of
Streptococcus viridans is shown.
Gram stain shows gram positive
cocci in chains.

Splinter hemorrhage - gross

 Gross Morphology
The heart weighed 400
grams. There was thickening
of the mitral valve leaflets
and the chordae tendineae.
Many friable calcified
pink-gray granular verrucae
were present on the valve.
In addition, a large
vegetation of the same type
was found on the left
auricular endocardium.
Heart - gross
 Microscopic Findings
The section represents a
portion of mitral valve, left
atrium and left ventricle. The
valve is greatly thickened
and damaged. It is infiltrated
with acute and chronic
inflammatory cells, and
shows a zone of necrosis and
fibrosis in the central portion
of the valve. The
Gram stain myocardium shows slight
focal fibrosis, and focal acute
inflammatory infiltration in
Blood agar plate
some sections.
 Histologic Morphology

Normal heart tissue sections demonstrate no evidence of fibrosis or hemorrhage.

Cardiac myocytes have moderately sized centrally located nuclei. Normal myocytes
are not brightly eosinophilic. Normally no inflammation is seen. Normal cardiac
myocytes do not show hypertrophy.
Clinical Manifestations
CASE No. 31
 Clinical History
This 45 year old man had been well until he was
awakened by chest pain that radiated to both arms and
neck and was associated with diaphoresis. His blood
pressure was 160/110. He was treated with diuretics
(Lasix), but he continued to gain weight. He developed a
friction rub. Two days after the onset of the chest pain
he had a cardiac arrest and died.
 Diagnosis

Acute Myocardial Infarct

Colloquially known as “heart attack”
 Etiology
Coronary Major independent
artery disease risk factors
Occlusion of coronary
01 02 Smoking, hypertension,
artery Diabetes mellitus, etc.

Predisposing Possible risk

risk factors factors
Physical inactivity,
03 04 Fibrinogen, C-reactive
obesity, family history, protein, homocysteine,
ethnicity, psychosocial elevated Lp(a)
factors
Gross Morphology
The heart was slightly enlarged.
There was severe atherosclerosis
of all the major coronary arteries
with recent thrombotic occlusion
of the proximal left anterior
descending coronary artery.
A recent transmural infarct was
present in the left ventricle that
involved the interventricular
septum and the papillary muscle.
Normal Heart Histology
Normal cardiac muscle in longitudinal
section shows a syncytium of myocardial
fibers with central nuclei. Faint pink
intercalated discs cross some of the
fibers. Red blood cells are seen in single
file in capillaries between the fibers.
Normal heart tissue sections
demonstrate no evidence of fibrosis or
hemorrhage. Cardiac myocytes have
moderately sized centrally located nuclei.
Normal myocytes are not brightly
eosinophilic. Normally no inflammation is
seen. Normal cardiac myocytes do not
show hypertrophy.
 Histologic Morphology

Heart, myocardium (low, med, high)

The slide includes a transmural section of the left ventricle. Nearly the entire section is involved by infarct.
However, there is a thin rim (5 to 10 cell layers) of endocardial myocytes which have survived because of
diffusion of oxygen and nutrients from the ventricular cavity. Other viable myocytes can be found around
larger blood vessels within the section. The intense hypereosinophilia of the necrotic myocytes can best be
appreciated by comparing the thin rim of lighter staining subendocardial myocytes with the deeper cells. Note
also the karyolysis that is characteristic of coagulation necrosis. In some areas there is little inflammatory
response. This observation is explained by microvascular necrosis which does not allow access of circulating
leukocytes to these areas.
 Histologic Morphology

Heart, epicardium (low, high)

In the epicardial half of the infarct, there is an intense acute inflammatory response. Many intact neutrophils
can be seen. In addition, there are many nuclear fragments from lysed neutrophils. Macrophage activity is
not evident. These features of the inflammatory response indicate that the infarct was approximately three to
four days old. Note also that the inflammation extends to the epicardial surface and that there are deposits
of fibrin on the epicardium (fibrinous pericarditis). The granular grey material seen within some blood
vessels is barium sulfate, which was injected to permit post-mortem study of the coronaries by radiography.
Pathogenesis
Pathophysiology
The pathophysiology of myocardial
infarction manifests the signs and
symptoms of the patient
(diaphoresis, chest pain radiating
to the neck and upper extremities).

Also, the appearance of a friction

rub in the first 2 or 3 days after MI
is associated with a larger infarct
size, lower ejection fraction, more
frequent anterior location of the MI,
and increased in-hospital and
1-year mortality rates.
Clinical Manifestations
CASE No. 286
 Clinical History

This 64 year old male had two episodes of

myocardial infarction followed by
congestive heart failure during the eight
months prior to death. Death was
preceded by arrhythmia.
DIAGNOSIS:
Myocardial
Infarction
 Etiology

Smoking 01 02 Diabetes
mellitus

Hypertension 03 04 Sedentary
lifestyle
Dyslipidemia Lack of fruits and
05 06 vegetables
consumption

Abdominal
Alcohol
obesity 07 08
consumption
waist /hip ratio :
> 0.90 for males
> 0.85 for females
 Etiology of Reperfusion Injury
Blood flow is
significantly decreased,
and ischemia occurs
when >75% of the luminal
surface area is lost.
Necrosis of the
myocardium follows
when complete loss of
blood flow occurs for >20
mins.
(PDF) Myocardial Infraction: Etiology, Risk Factors, Pathophysiology, Diagnosis and Management (researchgate.net)
Pathogenesis

Myocardial ischemia occurs when

blood flow to the myocardium is
obstructed by a partial or complete
blockage of a coronary artery by a
buildup of plaques or
atherosclerosis. Then, if the plaques
rupture, this can lead to myocardial
infarction or heart attack in lay
man’s term.
 Gross Morphology

As shown in the figure, the heart is hypertrophied and dilated. Marked

coronary atherosclerosis is seen with an old occlusion of the left
anterior descending vessel. A healed infarct involved the anteroseptal
and apical region of the left ventricle.
 Reviewing the Normal Histology

The figures show normal heart tissue sections that do not demonstrate
fibrosis or hemorrhage. Cardiac myocytes have moderately sized centrally
located nuclei. Normal myocytes are not brightly eosinophilic. No
inflammation is seen. Normal cardiac myocytes do not show hypertrophy.
 Histopathologic Morphology

The slide includes a transmural section of the anterior free wall and anterior portion of the
interventricular septum. Seen in the figure is a broad band of dense, highly collagenized scar tissue
replacing the middle layer of myocardium; patchy scarring interspersed with hypertrophied cardiac
myocytes is present on either side of this dense scar. The endocardium is markedly thickened and
there is organizing mural thrombus between cardiac trabeculae and extending into the lumen. Some
myocytes in the subendocardial layer show sarcoplasmic vacuolization, a chronic degenerative change
called "myocytolysis".
Pathophysiology of Clinical Manifestations
Clinical Manifestations
 References
● Arackal, A., Alsayouri K. (2022). Histology, Heart. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing. Available from: https://www.ncbi.nlm.nih.gov/books/NBK545143/
● Khadse, Neha & Wankhade, Anjali & Gaiki, Ajit. (2020). Myocardial Infraction: Etiology, Risk Factors,
Pathophysiology, Diagnosis and Management. American Journal of PharmTech Research. 10.
10.46624/ajptr.2020.v10.i1.014.
● Ojha N, Dhamoon AS. Myocardial Infarction. [Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK537076/
 Compassionate Group

Andrei Ausejo Julieen Rose Ca-at Adrian Joe Caballes

 Compassionate Group

Kathleen Faith Demegillo Jay-R Malayag Myrah Mangudadatu

 Compassionate Group

Rose Ann Pa-alisbo Samera Salipoden

 REFLECTION ON CHAPTER
Let's remember that cardiovascular disease is one of the leading cause of death globally.In
addition to morbidity and mortality, they are costly to the health system. I think it is important
for us to focus on the preventive measures focusing on controlling risk factors such as obesity,
sedentary lifestyle, and smoking in addition to early and correct treatment.As a future doctor, It
is really important for us to implement this kind of measures through education,
disseminating knowledge of chronic diseases and their risks to the population, and
collaboration for health promotion.

People living in low- and middle-income countries like the Philippines often do not have the
benefit of primary health care programmes for early detection and treatment of people with
risk factors for CVDs. People in low- and middle-income countries who suffer from CVDs and
other noncommunicable diseases have less access to effective and equitable health care
services which respond to their needs. As a result, for many people in these countries detection
is often late in the course of the disease and people die at a younger age from CVDs and other
noncommunicable diseases, often in their most productive years.
Education must be used to empower individuals to change their lifestyle and thus reduce their
cardiovascular risks. By applying these measures, we give autonomy to patients so that they
start to actively participate in healthcare, becoming authors of their outcome.
Thank You!
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