Last edited: 1/24/2022

DILATED CARDIOMYOPATHY
Dilated Cardiomyopathy Medical Editor: Aldrich Christiandy

OUTLINE
I) OVERVIEW
II) CAUSES
III) PATHOPHYSIOLOGY
IV) COMPLICATION
V) DIAGNOSIS
VI) TREATMENT
VII) APPENDIX
VIII) REVIEW QUESTIONS
IX) REFERENCES

I) OVERVIEW

(A) DEFINITION (C) CAUSES

Cardiomyopathy is there some type of disease or there The most common cause of someone developing dilated
is something that is causing problems with the cardiomyopathy is idiopathic
myocardium of the heart o We don’t really know why
o There are issues where there’s decreased function There may be some suspicion that there’s genetic
of the myocardium of the heart involvement
o Usually, it’s not due to ischemic cause or valvular o 50% of cases that have dilated cardiomyopathy is
disease usually due to idiopathic
(B) TYPES  Maybe there’s some kind of familial relationship

Types of cardiomyopathies [Brieler, Jay et al., 2017]

o Arrhythmogenic (ARVD/C)
o Dilated
o Hypertrophic
o Restrictive

II) CAUSES

OVERVIEW

Figure 1. Causes of dilated cardiomyopathy

Causes of dilated cardiomyopathy

Idiopathic
o TTN gene
Autoimmune o Cocaine or methamphetamine
o Systemic lupus erythematosus o Doxorubicin, trastuzumab

Infection Tachycardia-induced
o Cox-B o Atrial fibrillation (AFib)
o HIV o High PVC burden
o Parvo B-19 Metabolic
o Trypanosoma cruzi o Adrenal medulla cancer (pheochromocytoma)
Stress-induced o Vitamin B1 deficiency
o High emotional stress o Thyroid gland cause
o Pregnancy

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 (A) GENETIC DEFECTS

Figure 2. Genetic defect

Most common (50% of the cases)

Etiology Pathophysiology
Probably affects TTN gene If there’s genetic defect in the sarcomere
o Controls different proteins that are connecting o Decrease in the sarcomere function → decrease
different parts of the sarcomere proteins ventricular contractility
 Sarcomere is the structural and functional unit of o Reduction in cardiac output
the actual muscle Reduction in cardiac output causes ventricles trying to
Remember sarcomere is the structural and functional unit come up with
of the actual muscle o Dilating the ventricles
o Trying to make their ventricles a little bit thinner
(B) AUTOIMMUNE

Figure 3. Autoimmune
Etiology Pathophysiology
Systemic lupus erythematosus (SLE) Develop certain types of autoantibodies and cause
particular destruction of the actual myocyte
Polyarteritis nodosa (PAN) o Destroy myocyte → destroy functional unit of the
cardiac muscle
o Decrease in the contractility of the muscle →
reduction in cardiac output
(C) INFECTIONS

Figure 4. Infections
Etiology Trypanosoma cruzi
Coxsackie B virus (Cox-B) High yield material
HIV Nasty bug that leads to the disease called Chagas
Parvovirus B19 disease
Trypanosoma cruzi
Clinical vignette that may present
Pathophysiology
Patient went traveling maybe in South America or Africa
May actually cause myocarditis and came back
o Inflammation of the myocardium → decrease the Having these conditions
function of the myocardium o Low-grade fever
o Decrease in contractility
o Periorbital swelling
o Having difficulty swallowing
o Mega esophagus
o Had difficulty being able to eliminate feces
 Because they have a mega colon
o Chest pain or cardiomyopathy

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 (D) STRESS-INDUCED

Figure 5. Stress-induced
Etiology Peripartum cardiomyopathy
High emotional stress → Takotsubo cardiomyopathy Around the time periods of pregnancy can put a lot high
o E.g., due to emotional stressor or loss of a loved one degrees of stress on the body
Pregnancy → Peripartum cardiomyopathy o Particularly third trimester up to about six months
o Particularly third trimester up to about six months postpartum
postpartum Pathophysiology
Takotsubo cardiomyopathy Put a lot of stressors on sympathetic nervous system
o Sympathetic nervous system on high activation due
to high stress state
o Increase the release of norepinephrine
Norepinephrine stimulates adrenal medulla to increase
the secretion of epinephrine that works on the heart
o Puts tons of stress on the heart
o Increase the contractility of the heart and heart rate
Overtime increase stress on the heart for a long time
(acute intense stress on the heart)
Figure 6. Takotsubo cardiomyopathy o Heart starts to go into a failure state
(A) ventriculogram (B) takotsubo pot [Buttner, R., & Burns, E., 2021]
This cardiomyopathy is named after the takotsubo pot
due to LV appearance like this pot [Buttner, R., & Burns, E., 2021]

(E) CARDIOTOXINS

Figure 7. Cardiotoxins
Etiology Doxorubicin / daunorubicin / trastuzumab
Chemotherapeutic agent → kill cancer cells
Cocaine or methamphetamine usage Trastuzumab is a breast cancer drug
Doxorubicin / daunorubicin /trastuzumab
Clinical vignette
Alcohol abuse
Too much alcohol can put a lot of stress on the heart o Taking some type of medication for their chemo and
Those toxins can put a lot of destruction to the actual start developing dilated cardiomyopathy
cardiac cells o Think about these agents
o Less cardiac tissues to maintain enough contractility
o Decrease in contractility
o Decrease in the cardiac performance overall
Cocaine or methamphetamine
Similar effect to sympathomimetic surge
Lots of norepinephrine and epinephrine causes
o Vasoconstriction
o Increase contractility
o Increase heart rate
These puts lots of stress for the heart

DILATED CARDIOMYOPATHY CARDIOVASCULAR PATHOLOGY: Note #1. 3 of 15

 (F) TACHYCARDIA-INDUCED

Etiology “Hey, I can’t maintain this high degree of stress that

SA node firing excessively or there’s some type of you’re continually requiring of me. I’m gonna have to
ectopic focus start slowing down”
o Regardless there’s lots of electrical activity going on This tachycardia overtime can lead to tachycardia-
throughout this conduction system induced cardiomyopathy
Pathophysiology May see this condition in patients with
Super high heart rate put a lot of stress on the heart Atrial fibrillation
o Reduce diastolic filling o With a rapid ventricular rate
o Less time for the myocardium to get perfusion
High PVC burden
Reduction in coronary perfusion causes o If someone has tons of PVCs over a long period of
o Reduce O2 delivery to the myocardium time
o This gives lots of stress on the myocardium  Put lots of stress on myocardium
Stress over long periods of time  Over time reduce contractility
o Cause myocardium to just tuck up and give up

(G) METABOLIC

Vitamin B1 (Thiamine) deficiency

Remember thiamine is needed to stimulate pyruvate
dehydrogenase
o Convert pyruvate to Acetyl-CoA
No pyruvate dehydrogenase → can’t generate Acetyl-
CoA
o Pyruvate starts shunting into making lots of lactate
o Lactate causes vasodilation
Vasodilating vessels leads to AV shunting
o Remember blood flowing from arteriole to venule has
to go through capillary bed
Figure 8. Metabolic cause o If we vasodilate them → blood runs through those
capillary bed really fast
Etiology
 Doesn’t get enough time to be able to dribble off
Adrenal medulla cancer → pheochromocytoma some O2
Heart has to work harder to be able to pump more blood
Thyroid gland cause
to those tissue
Adrenal medulla cancer (Pheochromocytoma) o Because we’re just shunting the blood so quickly
o We’re not giving enough time for O2 delivery
Adrenal medulla cancer that pumping out tons of
epinephrine and norepinephrine Heart doesn’t know that → keeps working harder and
o High amount of epinephrine and norepinephrine harder → eventually tuck out
increase the stress on myocardium Thyroid gland
Effects
Pumping tons of thyroid hormone → increases basal
o Increase contractility
metabolic rate
o Increase afterload
These causes lots of stress → heart will tuck out o Increase sympathetic nervous system
o Reduced contractility o This gives more stress to heart
o Long period of stress → dilated cardiomyopathy
(H) MNEMONIC
A Bunch of stuffs Can Cause Cardiac Dilation
o Alcohol abuse
o Beri-beri (wet)
 Vitamin B1 deficiency
o Coxsackie B myocarditis
o Chronic cocaine use
o Chagas disease
 Caused by Trypanosoma cruzi
o Doxorubicin & daunorubicin
Figure 9. Dilated cardiomyopathy causes mnemonic

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 III) PATHOPHYSIOLOGY
OVERVIEW

Figure 10. Pathophysiology of dilated cardiomyopathy

When we have a patient who has this issue

o They have reduced contractility
This is due to putting lots of stress onto the heart from the different things mentioned earlier
o Work harder overtime → heart isn’t able to maintain that demand → cardiac contractility drops
o Reduction in contractility → potentially reduce stroke volume → reduce cardiac output → drops blood pressure
o Remember that
𝐶𝐶𝐶𝐶 = 𝐻𝐻𝐻𝐻 𝑥𝑥 𝑆𝑆𝑆𝑆

𝐵𝐵𝐵𝐵 = 𝐶𝐶𝐶𝐶 𝑥𝑥 𝑇𝑇𝑇𝑇𝑇𝑇

This causes heart compensation → compensates in a way we don’t like it → dilated cardiomyopathy

(A) FACTORS AFFECTING STROKE VOLUME

Figure 11. Factors affecting stroke volume

Contractility Afterload
Patient with dilated cardiomyopathy won’t be able to Afterload is altered by renin-angiotensin-aldosterone
pump much blood out of ventricle → high systolic system (RAAS)
volume o Low cardiac output → drops blood pressure
o More blood that’s staying within the ventricles o Low BP stimulate RAAS → increase afterload
even after the ventricles contract One thing that heart tries to fix
Ventricles are starting to get filled with blood because
can’t pump enough it out
Preload
Heart does this stuff
Preload is amount of blood that gets into the heart o “Okay, I’m gonna try to increase my preload. So in
during the diastolic process order for me to be able to increase my preload, I’m
o Whenever heart is relaxing → more blood coming it going to dilate my ventricle”
→ more preload
Right and left ventricles are dilated
If we need to increase preload → need to make o Whole point of being dilated is to accommodate
ventricles bigger more volume
o Bigger lumen diameter of the ventricle o This increase preload
o Causes ventricular and possibly atrial dilation o Then increase stroke volume
Unfortunately, this can work to disadvantage

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 (B) CARDIAC REMODELING

Figure 12. Cardiac remodeling – eccentric hypertrophy

What happens next is, we go through a process called (i) High volume stress
remodeling process
o Causes ventricular dilation If we put the actual muscle cells under high degree of
volume stress
The thought o Sarcomeres are added in series
Increase the actual ventricle
o Increase preload → increase stroke volume
Problem Figure 14. Sarcomeres are added in series

Increase preload a little bit too much This causes them to go through a special type of
hypertrophy → eccentric hypertrophy
Remember Frank Starling’s law o Causes the ventricles to become thin
o “As you stretch the sarcomere, if you get it to the o And allow for the actual lumen of the left ventricle to
optimal stretching point, the contraction increases” dilate to accommodate these high volume
o Basically
 Increase stretch → increase contraction Disease
o Dilated cardiomyopathy
If you stretch the sarcomere too much beyond their
point of optimal contractility (ii) High pressure stress
o Contractility goes down If we put the actual muscle cells under high degree of
Because ventricles dilate, myocardium has to go through pressure stress
remodeling process o They have to be able to work hard against a high
o Myocardium has to actually accommodate all of these degree of pressure
higher volume o Sarcomerse are added in parallel
o The actual ventricular walls will actually start to be
thinner
o This drops the actual contractility even more
Cardiac remodeling type
Figure 15. Sarcomeres are added in parallel
This causes them to go through a special type of
hypertrophy → concentric hypertrophy
o In this condition, causes the ventricle to get thicker →
myocardium thickness will increase
Disease
o Left ventricular hypertrophy in condition due to
 Hypertension
 Aortic stenosis
Quick recap – Dilated cardiomyopathy
Reduction in contractility
o Ventricles trying to remodel by increasing preload
o Get volume overloaded
Figure 13. Cardiac remodeling type o Dilate the lumen of the ventricle
Put the myocardium cells under a high degree stress Ventricle walls get thin due to eccentric hypertrophy →
because of these two situations contractility drops
o High volume state
o High pressure state
We have two of these sarcomeres in a line

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 (C) LAPLACE’S LAW
Formula Problem within this patient
2𝑇𝑇
𝑃𝑃 = Diameter of the ventricle really increased
𝑅𝑅
Because the ventricular walls get really thin →
Symbol Explanation contractility and the tension, the force that they can
generate drops
Collapsing pressure of ventricle
𝑷𝑷
Pressure to pump the blood out Interpretation

Tension If the tension drops → collapsing pressure drops

𝑻𝑻 Represents contractility (force that the o Imagine this ventricle had to collapse and push
myocardium generate) blood out
 This is the pressure and a way to think about this
𝑹𝑹 Ventricle lumen diameter
If the radius goes up → collapsing pressure drops
These put a person into a situation where they aren’t able
to eject enough blood → systolic dysfunction

IV) COMPLICATION

Figure 16. Complications of dilated cardiomyopathy

(A) BIVENTRICULAR FAILURE

Overview These puts a lot of actual stress on the pulmonary
circulation
Dilated cardiomyopathy can cause biventricular failure
o Right ventricle has to work harder → over time
o Often starts with the left ventricular failure
right ventricle starts to fail
 Produces right ventricular failure
Can’t pump blood outward to the pulmonary
Left ventricle failing because now it is unable to generate
circulation
enough pressure
o Causes blood back up to the atria
o To eject the blood out to the systemic circulation
 Then down to inferior vena cava
Pathophysiology  Or up into superior vena cava
Blood starts accumulating in the left ventricle (i) Superior vena cava
o Backs up into the left arteria
o Backs up into the pulmonary circulation Up to the superior vena cava → brachiocephalic →
 Backs up into the pulmonary capillary area jugular vein plumps
o Causes jugular venous distension

(ii) Inferior vena cava

This causes fluid to start accumulating in the interstitial

spaces → pulmonary edema Accumulate fluid around the liver → hepatomegaly

Common symptoms
Difficulty of breathing
Dyspnea
Crackles or rales
o Via auscultation Back up into the lower extremities → pedal edema
Hypoxia
Table 1. Quick recap for right and left-sided heart failure
Maybe even cough
Low blood pressure Right-sided failure Left-sided failure
o Small degree of hypotension Jugular vein distension Hypotension
Hepatomegaly Pulmonary edema
Pedal edema

DILATED CARDIOMYOPATHY CARDIOVASCULAR PATHOLOGY: Note #1. 7 of 15

S3 heart sound Pathophysiology

Now whenever left ventricle tries to go through the

systolic process and pump blood up
o But the anulus is stretched
The blood will kind of like regurgitate back into the atria
Whenever we have systolic dysfunction on both places
o Imagine left ventricle is very stretchy o Mitral regurgitation murmur (MR)
o Because it’s very stretchy → high amount of o Tricuspid regurgitation murmur (TR)
compliance
We give the term holosystolic murmur (MR + TR)
Whenever blood is coming from the atria into ventricle
through the diastolic filling process
o It can fill until whenever we get to that maximum
filling process → boom!
It causes pathological heart sound because of the
maximum compliance of the ventricle → S3 sound
o High yield for patients with dilated cardiomyopathy
So, we have biventricular failure
o With additional S3 heart sound Whenever the person is through the systolic
(B) HOLOSYSTOLIC MURMUR period/contractile phase
o From the S1 and the way to S2
Anulus rings and valves structure o We’ll be able to hear the whooshing sound
 Where blood is going through the actual valves
We have particular ring where our valves are → anulus
back into the atria
type of ring
o It’s kind of a fibrous skeleton that’s a kind of (C) ELECTRICAL REMODELING
separation structure between the atria and ventricle
When our ventricle stretches, anulus ring also
stretches
o Remember tricuspid and mitral valve hangs off the
anulus rings

With these actual atria and ventricle

o They’re both stretching
Whenever this all remodeling process occur because
blood is backing up into the atria
Figure 17. Anulus ring and valve structure
o Atria undergo a remodeling process to accommodate
larger volume
Structures when we zoom in  Atria also can undergo dilation process
o Anulus
o Valve flaps Atria undergo electrical remodeling
o Chordae tendinea connected to the papillary muscle
“Atria don’t like being stretched”
Normal physiology
If the left ventricle is accumulating blood When we stretch those atria cells
o Ventricle contracts → underwent systole process o They get ticked off and alter the electrical activity →
o Valves close and block blood from coming back into o This lead to atrial arrhythmia
the atria
 No type of regurgitation Atrial arrhythmia
Atrial fibrillation
o More common
o High risk of forming thrombi in the left ventricle
 Because of decreased systolic function
o They form thrombus in their left atrium because
ventricle isn’t contracting
 While blood’s sitting within that area → increased
risk of embolizing
Supraventricular tachycardia

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 V) DIAGNOSIS

OVERVIEW

Figure 18. Diagnosis of dilated cardiomyopathy

Things to diagnose dilated cardiomyopathy They may present with
o Echocardiogram o Chest pain
o Chest X-Ray o Dyspnea / shortness of breath
o 12-lead EKG o Palpitation
o Lab
o Medical history We want to rule out certain type of cardiopulmonary
causes such as
Anytime a patient comes in and they see us o Full blown
o We don’t automatically think of “Oh, this is dilated o Acute decompensated heart failure
cardiomyopathy for sure” o Myocardial infarction (MI)
o They present with symptoms that we want to rule o Pulmonary process going on
out the more significant fatal deadly causes

(A) CHEST X-RAY

Get chest X-ray if the patient present with
o Short of breath
o Crackles or rales on auscultation
Findings from CXR
Pulmonary edema
o They got fluid all up in the lung
o Because left ventricular systolic failure is causing
fluid to back up
Pleural effusion
Cardiomegaly
o Nonspecific signs
o This sometimes would make us think “Oh, they got a
heart failure”
 Sometimes this is the common symptom of
patients with dilated cardiomyopathy Figure 19. Chest X-Ray findings (nonspecific) [Dixon, 2010]

(B) 12-LEAD EKG

We should always get 12-lead EKG if patients are having
o Shortness of breath
o Chest pain
o Palpitation
Findings from 12-lead EKG
Dilating atria → shows atrial fibrillation
Shows some type of supraventricular tachycardia
o These are not tests that are going to tell me anything
about dilated cardiomyopathy
o It’s just helping to rule out other particular causes
Figure 20. Example of dilated cardiomyopathy 12-lead EKG
[Buttner, R., & Burns, E., 2021]

Table 2. Diseases that Chest X-Ray and 12-lead EKG rule out on diagnosing dilated cardiomyopathy
Chest X-Ray rules out 12-lead EKG rules out
Pneumonia Any type of ischemia
ARDS ST segment elevation
Pneumothorax MI

DILATED CARDIOMYOPATHY CARDIOVASCULAR PATHOLOGY: Note #1. 9 of 15

 (C) ECHOCARDIOGRAM

Figure 21. Echocardiogram

Parameters that we check with echo Ejection fraction
Definitive test
Systolic function is decreased
Diameter Expect ejection fraction would be reduced → HFrEF
Increased diameter of the left ventricle o Heart failure reduced ejection fraction
o Or also potentially right ventricle if they have They may have akinesia or hypokinesia (global)
biventricular failure o Entire left ventricle would just not produce a lot of
contractility
Wall thickness
o Because all of their left ventricle is super thinned
Really thin/decreased wall thickness
o Because of the ventricular dilation → myocardium had
to go undergo the eccentric hypertrophy
 To allow for the volume overload state

(D) LABS

Figure 22. Labs

Rule out the etiology/cause of someone having a dilated
Toxicology screening
cardiomyopathy
Most common cause → idiopathic Rule out any type of alcohol abuse or cocaine,
o We’re not doing any genetic testing in this patient methamphetamine usage
 It’s not going to really going to yield a lot of
Viral panel
information
Coxsackie B virus not really necessary
HIV test necessary
Autoimmune disease
Check for
o ANA
o Rheumatoid factor (RF)

(E) PATIENT HISTORY

Stress states We might not need labs to really determine this
o Takotsubo cardiomyopathy→ ask about any kind of o Sometimes it’s looking through the medical history
emotional stressor
o Postpartum cardiomyopathy If we want to test for certain disease
 Pregnant o Think about those causes and things that we could
• Within their third trimester at least less than 6 order to determine those causes
months postpartum

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 VI) TREATMENT

OVERVIEW

Figure 23. Treatment for dilated cardiomyopathy

Quick recap
Reduction in cardiac contractility
o Lead to reduction in cardiac output → reduction in blood pressure
o Stimulate RAAS → lead to increase in cardiac remodeling → left ventricular dilation
 Ventricle walls super thin → ejection fraction drops
o RAAS also leads to increase in afterload → angiotensin II causes vasoconstriction of the arterial
• If we constrict the arteriole → increase the pressure within the arteries → puts lots of stress on left ventricle
o Heart tries to increase preload → dilate the ventricle too much
Frank Starling’s law
o Increased preload → increased stretch → increased contractile force at optimal length
o Stretch out the ventricle beyond optimal length → drop contractile force
Treatment
Table 3. General condition and treatment for dilated cardiomyopathy
Condition Treatment
Increased preload Give drugs to reduce preload and lifestyle change
Will cause ventricles to stretch way too
much
Reduce contractile force
High afterload Give drugs to reduce afterload
Decreased contractility Give drugs to increase the contractility of the ventricles
Remodeling Give drugs to reduce cardiac remodeling
Atrial fibrillation and systolic function Give anticoagulants
drops
High risk of clots
Thinning atria and ventricles Give antiarrhythmic drugs or AICD
Put them at risk for ventricular
tachycardia, ventricular fibrillation

(A) REDUCE PRELOAD (B) REDUCE AFTERLOAD

This also reduces venous return High afterload due to high amount of RAAS activity
Achieve less fluid/less volume within the blood o Give drugs that inhibit this → ACE-I and ARB
o Fluid and sodium restriction Vasodilate arteries and reduce afterload
o Get rid of the fluid → diuretics o Hydralazine
 Treatment is similar with heart failure o Isosorbide dinitrate
Nitroglycerin
o It causes vasodilation → less pressure to push up (C) INCREASE CONTRACTILITY
blood into atria and ventricle → less venous return Increase the inotropic action → digoxin
Inhibit angiotensin II o Positive inotropic → increase contractility
o Remember angiotensin II causes arterial Negative chronotropic
vasoconstriction, venoconstriction o Reduce heart rate
o Give them ACE-I and ARB o Useful in patient with atrial fibrillation

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 (D) INHIBIT CARDIAC REMODELING (ii) Atrial fibrillation
Dependent upon RAAS and sympathetic nervous Dilate the atria → causes them to electrical remodeling
system process
Reduce activity of RAAS o Increase risk of AFib → increase the risk of thrombi
Because they don’t have very good contractility in the
ACE-I and ARB
atria → blood starts accumulating
Aldosterone antagonist
o Same process as previous
o Spironolactone, eplerenone
Consider anticoagulants
Reduce activity of sympathetic nervous system
Warfarin
Remember high sympathetic nervous system activity→
o If they have valvular issue like they have mechanical
increase heart rate to increase blood pressure
heart valve
𝜷𝜷-blockers
o Metoprolol, esmolol DOAC
o Rivaroxaban, apixaban, dabigatran
Consider calcium channel blocker
o Not the best thing to do These will prevent them from developing embolic
o Avoid especially if they have very decompensated stroke
heart failure
(F) REDUCE RISK OF ARRHYTHMIA
(E) ANTICOAGULANT Consider 𝜷𝜷-blocker
Forming of clots o Atrial fibrillation benefit from this
Consider calcium channel blocker
(i) Systolic dysfunction o With the ventricular dilation
Due to systolic dysfunction → reduction in contractility o Can also stretch those ventricles → become irritated
o Not able to push as much blood out of the heart → electrically remodeled → lead to VTac, VFib
 Can cause someone to go into sudden cardiac
Remember volume of blood that sits in the heart after
death
systolic → systolic volume
More blood sitting in the heart → blood not moving → AICD
o Increases risk of stasis of blood flow o Automatic implantable cardiac defibrillator
o Certain situation where patient is having
Virchow’s triad
 Arrhythmia that are high risk of ventricular
o Increase stasis → increase the risk of clots
tachycardia, ventricular fibrillation
o Increase the risk of forming thrombi → can quickly
 Left ventricular ejection fraction < 35%
break off and form emboli
o We don’t want to waste any time
 Reduce the risk of going into VTac, VFib and
actually having a sudden cardiac death
o Whenever they go into VTac or VFib
 It will shock them to prevent them from going into
a sudden cardiac that type of issue

VII) APPENDIX
Table 4. Summary of causes of dilated cardiomyopathy
Causes Pathophysiology
Decrease in the sarcomere function → decrease ventricular
contractility
Idiopathic TTN gene o Reduction in cardiac output
o Dilating the ventricles
o Trying to make their ventricles a little bit thinner
Develop certain types of autoantibodies and cause particular
Systemic lupus destruction of the actual myocyte
Autoimmune erythematosus o Destroy myocyte → destroy functional unit of the cardiac muscle
Rheumatoid arthritis o Decrease in the contractility of the muscle → reduction in cardiac
Polyarteritis nodosa output
Coxsackie B virus Inflammation of the myocardium → decrease the function of the
(Cox-B) myocardium
Infection HIV Decrease in contractility
Parvovirus B19
Trypanosoma cruzi
Put a lot of stressors on sympathetic nervous system
o Sympathetic nervous system on high activation due to high stress
o Increase the release of norepinephrine
High emotional Norepinephrine stimulates adrenal medulla to increase the secretion of
stress → Takotsubo epinephrine that works on the heart
Stress—induced cardiomyopathy o Puts tons of stress on the heart
Pregnancy → o Increase the contractility of the heart and heart rate
Peripartum
cardiomyopathy Overtime increase stress on the heart for a long time (acute intense
stress on the heart)
o Heart starts to go into a failure state
o Decrease in contractility

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 Alcohol abuse
Put a lot of destruction to the actual cardiac cells
o Less cardiac tissues to maintain enough contractility
Alcohol abuse o Decrease in contractility
Cocaine or o Decrease in the cardiac performance overall
methamphetamine
Cardiotoxic usage Cocaine or methamphetamine
Doxorubicin / Similar effect to sympathomimetic surge
daunorubicin / Lots of norepinephrine and epinephrine causes
trastuzumab o Vasoconstriction
o Increase contractility
o Increase heart rate
These puts lots of stress for the heart
Super high heart rate put a lot of stress on the heart
o Reduce diastolic filling
o Less time for the myocardium to get perfusion
Tachycardia- Atrial fibrillation Reduction in coronary perfusion causes
induced High PVC burden o Reduce O2 delivery to the myocardium
o Gives lots of stress on the myocardium
Stress over long periods of time
o Cause myocardium to just tuck up and give up
Adrenal medulla cancer (Pheochromocytoma)
Adrenal medulla cancer that pumping out tons of epinephrine and
norepinephrine
o High amount of epinephrine and norepinephrine increase the stress
on myocardium
Effects
o Increase contractility
o Increase afterload
These causes lots of stress → heart will tuck out
o Reduced contractility
Adrenal medulla Vitamin B1 (Thiamine) deficiency
cancer
Metabolic (pheochromocytoma) Pyruvate starts shunting into making lots of lactate
Vitamin B1 deficiency o Lactate causes vasodilation
Thyroid gland cause Vasodilating vessels leads to AV shunting
Heart has to work harder to be able to pump more blood to those tissue
o Because we’re just shunting the blood so quickly
o We’re not giving enough time for O2 delivery
Heart keeps working harder and harder → eventually tuck out
Thyroid gland
Pumping tons of thyroid hormone → increases basal metabolic rate
o Cells have to work harder
o Increase sympathetic nervous system
o This gives more stress to heart
o Long period of stress → dilated cardiomyopathy

DILATED CARDIOMYOPATHY CARDIOVASCULAR PATHOLOGY: Note #1. 13 of 15

Table 5. Condition, pathophysiology, and treatment for dilated cardiomyopathy
Condition Pathophysiology Treatment
Drugs to reduce preload and
lifestyle change
ACE-I
Increased preload ARB
Diuretics
Nitroglycerin
Restrict fluid and sodium intake
Drugs to reduce afterload
ACE-I
Increased afterload ARB
Hydralazine
Isosorbide dinitrate
Drugs to increase the contractility
Decreased contractility of the ventricles
Digoxin
Reduce cardiac remodeling
ACE-I
ARB
Aldosterone antagonist
o Spironolactone
Remodeling o Eplerenone
𝛽𝛽-blockers
o Metoprolol
o Esmolol
Calcium channel blockers
Anticoagulants
Warfarin
High risk of atrial fibrillation and DOAC
systolic function drop o Rivaroxaban
o Apixaban
o Dabigatran
Antiarrhythmic drugs, IACD
Thinning atria and ventricle 𝛽𝛽-blockers
Calcium channel blockers

Formulas
o Cardiac output o Blood pressure
𝐶𝐶𝐶𝐶 = 𝐻𝐻𝐻𝐻 𝑥𝑥 𝑆𝑆𝑆𝑆 𝐵𝐵𝐵𝐵 = 𝐶𝐶𝐶𝐶 𝑥𝑥 𝑇𝑇𝑇𝑇𝑇𝑇

Symbol Explanation Symbol Explanation

Cardiac output Blood pressure
𝑩𝑩𝑩𝑩
𝑪𝑪𝑪𝑪 Amount of blood that’s being pumped out Pressure exerted by blood to artery wall
from the heart per minute
Cardiac output
Heart rate 𝑪𝑪𝑪𝑪 Amount of blood that’s being pumped out
𝑯𝑯𝑯𝑯
Beats per minute from the heart per minute
Stroke volume Total peripheral resistance
𝑻𝑻𝑻𝑻𝑻𝑻
Amount of blood that’s being pumped out Affects afterload
𝑺𝑺𝑺𝑺 from the heart per beat
Equals venous return/preload
o Amount of blood that comes back to
the heart per beat
o LaPlace’s Law – With wall thickness [Nadruz, 2015]

2𝑇𝑇 𝑥𝑥 ℎ
𝑃𝑃 =
𝑅𝑅
Symbol Explanation
Collapsing pressure of ventricle
𝑷𝑷
Pressure to pump the blood out

Tension
𝑻𝑻 Represents contractility (force that the
myocardium generates)
𝑹𝑹 Ventricle lumen diameter
𝒉𝒉 Ventricle wall thickness
14 of 15 CARDIOVASCULAR PATHOLOGY: Note #1. DILATED CARDIOMYOPATHY
 6) What other signs that you expect to find in this
VIII) REVIEW QUESTIONS patient with further examination? (May choose more
than 1)
1) What is the most common cause of dilated
a) Reduced ejection fraction
cardiomyopathy?
b) Increased thyroid hormone
a) Autoimmune
c) Hypotension
b) Coxsackie B virus
d) Jugular venous distension
c) Idiopathic
e) Hepatomegaly
d) Pregnancy
f) Thinning of the ventricle wall
g) Hypokinesia of ventricle
2) Which option below that contributes to stress-
induced dilated cardiomyopathy?
7) What would you like to do next in order to ensure
a) Destruction of the cardiomyocytes
your diagnosis or decide treatment plant for this
b) Ischemia due to coronary blood vessel occlusion
patient?
c) Renin-angiotensin aldosterone system
a) Activate cath lab
d) Sympathetic nervous system activation
b) Ask question about previous emotional stressors
c) Ask question about past medication
3) Biventricular failure can be found in patient with d) Ask question about syncope history
dilated cardiomyopathy because left ventricle failure e) Echocardiogram
that causes pulmonary edema and eventually causes f) MRI
right ventricular failure g) Trypanosoma cruzi serology
a) True h) HIV screening
b) False i) 24-h Holter monitoring

This scenario is used to answer question no. 4-9 8) In order to ensure the condition of the patient, you
A 35-year-old female patient present with chest pain and want to order echocardiogram. Echocardiogram
palpitation. She also has difficulty of breathing. She shows increased diameter of the left ventricle with
reported to have difficulty swallowing and eliminating thinning of the ventricular wall. The patient’s ejection
feces. She denies contacting person with similar situation fraction was 45%. What is your now current
as her. She studied abroad in an African country around differential diagnosis?
10 years ago and came back 6 years ago. During a) Heart failure with preserved ejection fraction
physical examination, S3 heart sound, holosystolic b) Heart failure with reduced ejection fraction
murmur, and crackles were heard with auscultation. The c) Myocardial infarction
other physical examination findings are unremarkable. d) Pneumonia
12-lead EKG shows atrial fibrillation and signs of LV e) Dilated cardiomyopathy
hypertrophy based on Sokolow-Lyon criteria with no ST- f) Hypertrophic cardiomyopathy
elevation. Lab result shows no elevation in troponin and g) Myocarditis
unremarkable toxicology screening result. CXR shows h) Rheumatoid arthritis-associated cardiomyopathy
signs of enlarged heart with pulmonary edema.
9) Assume that we’ve treated the underlying cause,
4) What are the more probable causes this condition in what is another treatment plan for this patient? (May
this patient? (May choose more than 1) choose more than 1)
a) Adrenal medulla cancer a) To reduce preload → lifestyle change by restricting
b) Alcohol abuse fluid and sodium intake
c) Autoimmune b) To increase afterload → administer epinephrine via
d) Emotional stressor IV
e) Endurance exercise c) To inhibit cardiac remodeling → prescribe ARB
f) Infection by Trypanosoma cruzi d) Reduce risk of thromboembolism events →
g) Total occlusion of coronary artery vessels prescribe rivaroxaban
h) Resistance exercise e) Reduce the risk of VTach and VFib → Implant AICD

5) Based on the information given, what are the IX) REFERENCES

differential diagnosis for this patient? (May choose ● Brieler, J., Breeden, M. A., & Tucker, J. (2017).
more than 1) Cardiomyopathy: An Overview. American family physician, 96(10),
a) Heart failure with preserved ejection fraction 640–646.
● Buttner, R., & Burns, E. (2021, April 29). Takotsubo
b) Heart failure with reduced ejection fraction cardiomyopathy. Life in the Fast Lane • LITFL. Retrieved January
c) Myocardial infarction 23, 2022, from https://litfl.com/takotsubo-cardiomyopathy-ecg-
d) Pneumonia library/
● Burns, E., & Buttner, R. (2021, July 18). Dilated cardiomyopathy
e) Dilated cardiomyopathy (DCM). Life in the Fast Lane • LITFL. Retrieved January 23, 2022,
f) Hypertrophic cardiomyopathy from https://litfl.com/dilated-cardiomyopathy-dcm-ecg-library/
g) Myocarditis ● Dixon, A. Dilated cardiomyopathy with pulmonary edema. Case
study, Radiopaedia.org. (accessed on 23 Jan 2022)
h) Rheumatoid arthritis-associated cardiomyopathy https://doi.org/10.53347/rID-10666
● Nadruz, W. Myocardial remodeling in hypertension. J Hum
Hypertens 29, 1–6 (2015). https://doi.org/10.1038/jhh.2014.36
● Akashi, Y. J., Yoshihiro J. Akashi From the Division of
Cardiology, Goldstein, D. S., David S. Goldstein From the Division
of Cardiology, Barbaro, G., Giuseppe Barbaro From the Division of
Cardiology, Ueyama, T., Takashi Ueyama From the Division of
Cardiology, & Akashi, C. to Y. J. (2008, December 16). Takotsubo
cardiomyopathy. Circulation. Retrieved January 24, 2022, from
https://www.ahajournals.org/doi/10.1161/circulationaha.108.767012

DILATED CARDIOMYOPATHY CARDIOVASCULAR PATHOLOGY: Note #1. 15 of 15