Heart

Exam 2
Just as we said the Blood Vessel chapter was 1) atherosclerosis and 2) everything else
We can now say the heart chapter is 1) ischemic heart disease and 2) everything else
Remember 1.5 cm is considered to be the
AVERAGE LV wall thickness, RV is 1/3 that,
and atria are ½ RV.
This is a section from “Shotgun Histology”, in other words, the terms on the left describe the entire myocardium. Atrial
natriuretic peptide (ANP), atrial natriuretic factor (ANF), atrial natriuretic hormone (ANH), or atriopeptin, is a powerful
vasodilator, and a protein (polypeptide) hormone secreted by heart muscle cells. It is involved in the homeostatic control of
body water, sodium, potassium and fat (adipose tissue). It is released by muscle cells in the upper chambers (atria) of the
heart (atrial myocytes), in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the
circulatory system, thereby reducing blood pressure.
STRIATIONS

NUCLEUS

DISCS

SARCOLEMMA

SARC. RETIC.

MITOCHONDRIA

ENDOTHELIUM

FIBROBLASTS

GLYCOGEN

A.N.P.
 S.A. NodeAV NodeBundle of HIS L. Bundle, R. Bundle

The specialized myocytes of the heart’s conduction system, Purkinje fibers, running sub-
endocardially, have this unique appearance.
I do not recall any pathologist ever pinpointing an EKG abnormaility to a specific histopathologic
abnormality of a Purkinje fiber.
Whichever artery winds up
supplying the posterior
interventricular septum is
said to be “DOMINANT”.
A thrombosis of WHICH
coronary artery would
usually result in sudden
death? Ans: MAIN left
coronary artery.
AX Anterior
Lateral
Posterior
Septal

VLA

The myocardial
perfusion is a
good test of
HLA coronary artery
and myocardial
function.
VALVES
• AV:
– TRICUSPID 13 cm
– MITRAL 11 cm
• SEMILUNAR:
– PULMONIC 8 cm
– AORTIC 6 cm
Note: R>L

These features are seen so commonly in autopsies of elderly

people no matter what they died from. Also keep in mind that
most people who do not die ACUTELY, die in cardiac failure.
Also keep in mind that even though atherosclerosis is NOT
considered normal aging, many of the atherosclerotic changes
cannot be completely separated from “normal” aging, because
it is so common.
 Sinotubular junction calcific deposits

Atherosclerotic plaque

< - BROWN

ATROPHY, HEART
LIPOFUCSIN
The pigment which accumulates with age is called lipofucsin, and caused the heart to appear “browner” than
normal. This is called “brown” atrophy of the heart. Lipofucsin is another typical example of a golden brown,
slightly refractile, INtrinsic pigment, which looks like hemosiderin, melanin, or bile, but accumulates, as a rule, on
opposite poles of the myocyte nucleus. It is also called, appropriately, AGING pigmernt.
It appears to be the product of the oxidation of unsaturated fatty acids.
 LVH, how do you know this is probably NOT a
cardiomyopathy? Ans: Thickening limited to LV

Note that not only is the FIBER thick, but

so are the nuclei. Note squaring off of the
nuclei, so called “BOXCAR” effect.
LEFT Heart Failure
Dyspnea
Orthopnea
PND (Paroxysmal Nocturnal Dyspnea)
Blood tinged sputum
Cyanosis
Elevated pulmonary “WEDGE”
pressure (PCWP) (nl = 2-15 mm Hg)
Can you understand why all of these findings
can be related to LEFT sided heart failure?
Ans: YES, primarily PULMONARY.
RIGHT Heart Failure
FATIGUE
“Dependent” edema
JVD
Hepatomegaly (congestion)
ASCITES, PLEURAL EFFUSION
GI
Cyanosis
Increased peripheral venous pressure
(CVP) (nl = 2-6 mm Hg)
Can you understand why all of these findings can be related
to RIGHT sided heart failure? Ans: YES, primarily STSTEMIC.

Malformation
Ventricular septal defect
Atrial septal defect
Pulmonary stenosis
Patent ductus arteriosus
Tetralogy of Fallot
Coarctation of aorta
Do the NAMES of these congenital heart
conditions adequately describe the pathology?
Ans: YES
Why have I highlighted the “D”s and the “T”s?
Ans: D = LR shunt, T= RL shunt (cyanosis,
or “blue” babies).
# kinds of Congenital heart diseases
1)LR shunts
2)RL shunts
3)Stenoses of Aorta or Pulmonary Artery

Atrioventricular septal defect

Aortic stenosis

Transposition of great arteries

Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid atresia
LEFT to RIGHT SHUNTS, NON-cyanotic
 VSD <- CLASSICAL
“TETROLOGY” of
FALLOT:
1) VSD, large
2) OBSTRUCTION to
RV flow
3) Aorta OVERRIDES
the VSD
4) RVH, including
subpulmonic
(causing stenosis to
Pulmonary Artery)

AVSD
TGA (TRANSPOSITION of GREAT ARTERIES

In TRUNCUS ARTERIOSUS,
the embryological structure known
as the truncus arteriosus fails to
properly divide into the pulmonary
trunk and aorta
 Tricuspid Atresia ->

Can ATRESIA be thought of, anatomically, as

being SEVERE stenosis? Ans: YES

CHRONIC plaque PLUS acute thrombosis = Acute

coronary syndromes. ↓
 Coronary Artery Pathology in Ischemic Heart Disease
Plaque
Syndrome Stenoses Disruption Plaque-Associated Thrombus
Stable angina >75% No No
Unstable angina Variable Frequent Nonocclusive, often with thromboemboli
Transmural myocardial Variable Frequent Occlusive
infarction
Subendocardial Variable Variable Widely variable, may be absent,
myocardial infarction partial/complete, or lysed
Sudden death Usually Frequent Often small platelet aggregates or thrombi
severe and/or thromboemboli
IHD “spectrum”
It is NOT unusual for the stenosis of stable angina to be MORE than the stenosis of an acute
coronary syndrome on which there is plaque disruption!
 Progression of Necrosis

Why does the necrosis spread from the endocardium to the pericardium (i.e., epicardium)? Ans: Because the
subendocardium is the LEAST well perfused by the subepicardial arteries. The “furthest away” theory, BOTH furthest away
from the artery and furthest away from the base.
The APEX of the myocardium is like the FOOT of a human being, it is the most likely to receive the brunt of ischemic and
infarctive phenomena, no matter WHERE along the course of the artery the disease occurs. The apex therefore the most
common site of wall motion abnormalities, logically.
NOTE: In ischemia, NO
gross or microscopic
findings are seen, visible
changes are seen only
with INFARCTION. You
cannot see ISCHEMIA!!!
When might myocardial
rupture occur? Why?
 Coagulative necrosis is PALE early. Or
purple.
Yellow when macrophages chew up
the dead tissue.
Sometimes red and soft again with
organization or neovascularation.
White and firm with fibrosis.

1 day (pyknosis, “waviness”)

3-4 days (neutrophils)
7 days (macrophages)
Weeks (organization)
Months (fibrosis)
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
LV should be no more than 1.5 cm.
 HISTOPATHOLOGY
• INCREASED FIBER (MYOCYTE) THICKNESS
• INCREASED nuclear size with increased
“blockiness” (boxcar nucleus)

Oh naulit na to ah. Baka mamali

pa tayo (hahaha)
 CLINICAL
• EKG in LVH
Summary of LVH Criteria
1) R-I + S-III >25 mm
2) S-V1 + R-V5 >35 mm
3) ST-T depr. in L lead
4) R-wave in L lead >11 mm
5) LAE + other criteria Positive
Criteria: 1=possible 2=probable
3=definite

ATRIAL FIBRILLATION Why?*

CHF, cardiac dilatation, pulmonary venous
congestion and dilatation
*Answer: owing to left atrial enlargement (i.e.,
dilatation, i.e. “stretching”)
Is this LV primarily hypertrophic,
or dilated? What is an EDV?
Diseases of the Pulmonary Parenchyma Disorders Affecting Chest Movement
Kyphoscoliosis
Chronic obstructive pulmonary disease Marked obesity (pickwickian syndrome)
Diffuse pulmonary interstitial fibrosis Neuromuscular diseases

Pneumoconioses
Cystic fibrosis
A reasonably logical way of looking at COR
Bronchiectasis PULMONALE, or RIGHT HEART FAILURE

Diseases of the Pulmonary Vessels

Disorders Inducing Pulmonary Arterial
Recurrent pulmonary thromboembolism Constriction
Metabolic acidosis
Primary pulmonary hypertension
Hypoxemia
Extensive pulmonary arteritis (e.g., Wegener Chronic altitude sickness
granulomatosis) Obstruction to major airways
Idiopathic alveolar hypoventilation
Drug-, toxin-, or radiation-induced vascular
obstruction
Extensive pulmonary tumor microembolism
AORTIC STENOSIS
2X gradient pressure
LVH (but no hypertension), ischemia
Cardiac decompensation, angina, CHF
50% die in 5 years if angina present
50% die in 2 years if CHF present
LVH is almost a reflex knee jerk conclusion to AS, but in this case
there may be NO systemic hypertension.
The LV extra work is at the aortic level, not the arteriolar level!
 MITRAL ANNULAR
CALCIFICATION
• Calcification of the
mitral “skeleton”
• Usually NO dysfunction
• Regurgitation usually,
but Stenosis possible
• F>>M

Idiopathic
“Myxomatous” degeneration? Describe it.

MYXOMATOUS degeneration of the mitral

valve
Associated with connective tissue disorders
“Floppy” valve
ACUTE:
-Inflammation
-Aschoff bodies
-Anitschkow cells
-Pancarditis
-Vegetations on chordae
tendinae at leaflet junction

CHRONIC:
THICKENED VALVES
Granuloma:Giant Cell::Aschoff
COMMISURAL FUSION
Body:Anitschkow Cell
THICK, SHORT, CHORDAE
TENDINAE
 CLINICAL FEATURES
• Migratory Polyarthritis
• Myocarditis
• Subcutaneous nodules
• Erythema marginatum
• Sydenham chorea

A GREAT classical Sydenham chorea (St. Vitus

“Dance”) can be seen at
www.youtube.com/watch?v=RnxqqW_nH0k
The great BRIDGE between infectious
and autoimmune diseases!
Also note this is a PAN-carditis, i.e., :
1) Endocardium
2) Myocardiom
3) Pericardium
 VEGETATIONS
• INFECTIVE >5mm Vegetations: 1) rheumatoid = small, at chordae
tendinae junction, 2) infectious = big (>5
• NON-Infective <5mm mm), 3) lupus (Libman-Saks) = BOTH sides
4) NBTE = non-bacterial thrombotic
endocarditis (<5 mm)
Splinter hemorrhages, Janeway lesions (palms, soles), Osler’s “nodes” (raised), Roth’s spots
(eye).
Do you think that for every skin lesion you see there may be 10 visceral lesions which you do
NOT see? Ans: Yes, I believe so!
 Carcinoid Heart Disease

Artificial Valves
A “restrictive” cardiomyopathy is a wall which
is NOT thickened or dilated necessarily, but
RIGID in diastolic relaxation, i.e., loss of
“compliance”. EF=1/EDV
 DCM
(Dilated Cardiomyopathy)

Path:
4 chamber dilatation
Hypertrophy, also 4 chambers
Interstitial Fibrosis
 Arrhythmogenic Right Ventricular Cardiomyopathy
(Arrhythmogenic Right Ventricular Dysplasia)

This is an uncommon dilated cardiomyopathy predominantly RIGHT ventricle.

So is NAXOS syndrome.

Wooly Hair Palmoplantar keratoderma

A genetic disease
LYMPHOCYTIC INFILTRATES are the USUAL pattern of ALL myocarditis, but eosinophils,
giant cells, and even trypanosomes can be seen occasionally
The “bread and butter” pericarditis is
classically and most often described in uremia
or pericardial infections.
What is the exudate? Ans: Fibrin
“Bread and butter” pericarditis = fibrinous
pericarditis.
 FIBROELASTOMAS (valvular,
usually papillary)

RHABDOMYOMA (Most
common cardiac tumor in
children)
 MYXOMA
Left atrium most common
CARDIAC TRANSPLANT
HVG
PATHOLOGY (heart and great vessels)