“The strongest hearts

have the most scars.”

Jeff Hood
GENERAL
DATA37-year old, female,
37-year old,Roman
female Catholic Chest tightness
NEUROMUSCUL “Thus,
BURNIN
GASTROINTESTI Exertional
dyspnea and/or
PULMONAR dyspnea
chest discomfort
VASCULAR that CARDIAC
SHARP SHARP TIGHTN
AR appear during activity are characteristic of
NAL Y
G PLEURI
Orthopnea ESS
STABBI patients with heart disease,…” TEARIN
CHIEF COMPLAINT
NG
COLICK Ejection TIC
Fraction
Yet al. (2015). Harrison's
Kasper, D. L.,
30%
= G
Principles of Internal Medicine
PRESSU
RE
20/E (Vol.1 & Vol.2).
Pneumon Pulmonary
Costochondr Esophage CHEST PAIN embolism
itis ia
al spasm Spontaneous
Acute Heart Failure withPleuritis Reduced Ejection aortic Fraction
Jameson, J. L., et al. (2018). Harrison’s principles of internal medicine (20th ed.). New dissection
York: McGraw-Hill Education, p. 1787-8
CARDIOMYOPATH
ST-Elevation Myocardial
ST-Elevation Myocardial ENDOMYOCARDI
ST-ELEVATIONCOMPLETE LBBB
Y Infarction Infarction TIS

SGARBOSSA CRITERIA
1. ST-elevation of ≥1 mm and concordant with the QRS complex (5 points)
2. ST-segment depression ≥1 mm in lead V1, V2, or V3 (3 points)
Acute Heart
3. ST elevation Failure
≥5 mm with with
and discordant Reduced
the QRS Ejection Fraction
complex (2 points)
Wilner, B. et al. (2017). LBBB in patients with suspected mi: an evolving paradigm. American College of Cardiology.
 Acute Heart Failure with Reduced Ejection Fraction

CARDIOMYOPATH
Y

“In
“Themultivariable
unique adjusted models,
morphology of a history
stress-induced
“The apical ballooning syndrome, or stress-
TAKOTSUBO of irregular menses,
cardiomyopathy is parity,
apical and and
ballooning use the
of
induced cardiomyopathy, occurs typically
CARDIOMYOPATHY postmenopausal
relative hormone
compensatory replacement were
hypercontractility of
in older women after sudden intense
significantly associated This
the basal segments. with the onset of
phenomenon
emotional or physical stress.”
TTS.”
suggests that hemodynamics have an
important role.”

Dias, A., et al. (2019). Takotsubo syndrome: State-of-the-art review by an expert panel - part 1. Cardiovascular Revascularization Medicine, 20(1),
70-79
Jameson, J. L., et al. (2018). Harrison’s principles of internal medicine (20th ed.). New York: McGraw-Hill Education, p. 1790
Lee, J., & Kim, J. (2011). Stress-induced cardiomyopathy: the role of echocardiography. Journal of Cardiovascular Ultrasound, 19(1), 7-12
 Acute Heart Failure with Reduced Ejection Fraction

CARDIOMYOPATH
Y
• Heat intolerance and
• Ejection fraction = 30%
diaphoresis
• No tremors
TAKOTSUBO • Wide pulse pressure
THYROTOXIC • No diarrhea
CARDIOMYOPATHY • Tachycardia
CARDIOMYOPATHY
“The high
“The
“The mostcardiac
high common
cardiac outputcardiovascular
output produces
produces aa
manifestation
bounding
bounding is sinus
widened
widened pulse tachycardia
pressure.” often
pulsepressure.”
associated with palpitations”

Jameson, J. L., et al. (2018). Harrison’s principles of internal medicine (20th ed.). New York: McGraw-Hill Education, p. 2703-4
 Acute Heart Failure with Reduced Ejection Fraction

CARDIOMYOPATH ST-Elevation Myocardial ENDOMYOCARDI

Y Infarction TIS

“The main clinical symptoms and signs of

• •No
History
Kounis urticarial
of bronchial
Initially, rashes
chest painor
asthma
• Present with vasospasmassociated
syndrome are always
PRINZMETAL
KOUNIS SYNDROME • swollen
Peripheral
occurredoropharynx
eosinophilia
on exertion
EOSINOPHILIA with
• •No
subclinical,
Tachycardia
clinical,
• Patent coronary
hypotension
acute or chronic
arteries
andcoronary
diaphoresis by
allergicNo transient
reactions accompanied
59% [12.17 x 10 /L]
cardiacspasm
9
symptomatology.”
on angiography
“Urticaria and swollen
“PVA is caused oropharynx
by focal spasm of werean
the common coronary
“Prinzmetal
epicardial
“Coronary symptoms and signs
etangiography
al. described
artery awithatresultant
initialof
syndrome
demonstrates
presentation.”
severe ischemic
transmural
transient pain that
ischemia...”
spasm as usually occurs at
the diagnostic
rest…” of PVA…”
hallmark
Kounis, N. G., et al. (2018). Anaphylactic cardiovascular collapse and Kounis syndrome: systemic vasodilation or coronary
vasoconstriction?. Annals of Translational Medicine. 6(17), 332
Kounis,
Jameson,N. G., et al.
J. L., et (2011). Kounis
al. (2018). syndrome:principles
Harrison’s a new twistofon an old disease.
internal medicineFuture Cardiology,
(20th ed.). New7(6), 808-9
York: McGraw-Hill Education, p. 1871-2
 Acute Heart Failure with Reduced Ejection Fraction

CARDIOMYOPATH
EOSINOPHILIA ST-Elevation Myocardial ENDOMYOCARDI
Y x 109/L]
59% [12.17 Infarction TIS

• Asthmatic
No attacks pain,
vague abdominal
LOEFFLER • Peripheral
nausea, eosinophilia
vomiting, diarrhea
ENDOMYOCARDITIS • Trichuris
No fever trichiura eggs on
• No lip edema
fecalysis
• Eosinophil
Prevalencelevels expected range
of co-infections
from
with1.5 - 4.0 x 109 = 19.1%
A. lumbricoides

Belizario Jr., V. Y., & de Leon, W. U. (2013). Medical parasitology in the Philippines. Diliman, Quezon City: The University of the Philippines
Press, p. 130, 142, 143
O’Connell, et al. (2015). Eosinophilia in infectious diseases. Immunol Allergy Clin North Am, 35(3):493-522
 Acute Heart Failure with Reduced Ejection Fraction

EOSINOPHILIA ENDOMYOCARDI
59% [12.17 x TIS
109/L] • Severe eosinophilia
EOSINOPHILIC
LOEFFLER • More than 20% eosinophilia will start to
infiltrate the heart
ENDOMYOCARDITIS
“Three levels of severity of eosinophilia have
been defined as follows: mild, 0.5 to 1.5 x 109/L;
moderate, 01.5 to 5 x 109/L; and severe, greater
than 5 x 109/L.”

Masaki, N., et al. (2016). Echocardiographic changes in eosinophilic endocarditis induced by Churg-Strauss syndrome. Internal Medicine, 55(19),
2819-2823
Roufosse, F., & Weller, P. F. (2010). Practical approach to the patient with hypereosinophilia. The Journal of Allergy and Clinical Immunology, 1
26(1), 39-44
 EOSINOPHILIC ENDOMYOCARDITIS

IDIOPATHIC CHRONIC
CHURG-STRAUSS
“Eosinophilic myocarditis can be an important manifestation of the
HYPEREOSINOPHILI EOSINOPHILIC
hypereosinophilic syndrome, which in Western countries SYNDROME
is often considered
C SYNDROME LEUKEMIA
idiopathic, although in Mediterranean and African countries, is associated with
antecedent infection. It may also be seen with systemic eosinophilic syndromes
such as Churg-Strauss syndrome or malignancies.”

Jameson, J. L., et al. (2018). Harrison’s principles of internal medicine (20th ed.). New York: McGraw-Hill Education, p. 1787-8
 EOSINOPHILIC ENDOMYOCARDITIS

• Cardiac involvement in about

• 40-50%
Male predominance (9:1)
IDIOPATHIC • History of asthma
“Cardiovascular complications of HES are a
HYPEREOSINOPHILIC • Other causes
major of of
source eosinophilia may
morbidity and mortality in
SYNDROME be identified
these disorders. Whereas earlier studies
reported that up to 84% of HES patients
have issigns
“HES and symptoms
predominantly a disease of cardiac
of men
disease,
(MF more
ratio, recent
9:1) andreports suggest
is usually that the
diagnosed
between
frequency closer
theisages 20-50to years.”
40-50%.”

Al-Sanouri, B., Maslamani, Y. & Al-Sanouri, I. (2016). A  Fatal Case of Chronic Eosinophilic Leukemia Not Otherwise  Specified (CEL-NOS) in
a 19-Year-Old Male with Acute Transformation into  Blast Crisis. Case Reports in clinical Medicine, 5:528-540.
Ogbogu, P., Rosing, D.R., & Horne, M.K. (2007). Cardiovascular symptoms of Hypereosinophilic Syndromee. Immunol Allergy Clin North Am,
27(3):457-475.
 EOSINOPHILIC ENDOMYOCARDITIS

• Elevation of serum LDH that could be

secondary to high cellular turnover
• Organ damage primarily in the heart
d/t presence
The eosinophilicofdegranulation
conditions (atopic
CHRONIC
EOSINOPHILIC LEUKEMIA predisposition) that could otherwise
“Secondly, clinical and laboratory features
induce a reactive
can relate eosinophilia
to the leukaemic doesitself:
process
notsplenomegaly,
fulfill thelymphadenopathy,
WHO criteriacytopenias,
for
CEL.
raised lactate dehydrogenase (LDH) and
hyperuricaemia due to high cell turnover…”

Kumar, A., Sinha, S., & Tripathi, A. K. (2008). Chronic eosinophilic leukemia: a case report and review of literature. Indian journal of hematology
& blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion, 23(3-4), 112-5.
Sarah Fletcher, Barbara Bain; Eosinophilic leukaemia, British Medical Bulletin, Volume 81-82, Issue 1, 1 January 2007, Pages 115–127,
https://doi.org/10.1093/bmb/ldm008
 EOSINOPHILIC ENDOMYOCARDITIS

CHURG-STRAUSS SYNDROME

• Cardiomyopathy occurs in 60%

of patients
• Bronchial asthma exacerbations
“It is often manifested
“...classically
“Myocardial associated by
involvement may asthma
microscopic
with give rise to,
• Microscopic hematuria allergic rhinitis,
cardiomyopathy; lung infiltrates, peripheral
hematuria andthe heart
mild is involved
proteinuria in 60%
and, less
of patients and
hypereosinophilia
frequently, accounts
by the , for
andalmost
nephrotic half of
syndrome or
extravascular
the deaths
rapidly in the syndrome.”
progressive
necrotizing renal failure.”
granulomata.”
Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease. Philadelphia: Elsevier Saunders,
p. 511
Rosai, J. (2011). Rosai and Ackerman’s surgical pathology (10th ed.). New York: Mosby Elsevier, p. 1142
 EOSINOPHILI
PRODROME VASCULITIS
A

Bronchial asthma Peripheral blood Life-threatening

CHURG-STRAUSS
exacerbations eosinophiliaSYNDROME
vasculitis of the
small and medium
vessels
Eosinophilic
infiltration of
multiple organs

King, T. (2018). Clinical features and diagnosis of eosinophilic granulomatosis with polyangiitis. UpToDate.
 Focal Segmental

ESPIRAT
Glomerulosclerosis

PRODROME PHASE Microscopic Mild

hematuria proteinuria
2nd-3rd decades of life

RENA
• Nutritional status
Bronchial asthma • Negative acute phase reactant
exacerbations
Hypoalbuminemia

King, T. (2018). Clinical features and diagnosis of eosinophilic

Absence of mild proteinuria
Rosai, J. (2011). Rosai and Ackerman’s surgical pathology (10th ed.). New
granulomatosis with polyangiitis. UpToDate York: Mosby Elsevier, p. 1142
 HEART INFILTRATION

PERICARDIUM MYOCARDIUM ENDOCARDIUM

EOSINOPHILIC
DEGRANULATION
“...noted in our second case report.
“…diffuse thrombus deposits on the surface of
Pericarditis Pericarditis during CSS is rarely Thrombus
severe formation
the injured endocardium Fibrosis may mimic
Kumar, V., Abbas, A. K., & Aster, andJ. C. (2015).
cardiac Robbins and tamponade
Cotran pathologicis basis ofquite
myocardial thickening onSaunders,
echocardiography.”
disease. Philadelphia: unusual…”
Elsevier
Minimal Anterior
Masaki, N., et al. (2016). Echocardiographic changes in eosinophilic endocarditis induced
p. 511
Hypokinesia
by Churg-Strauss syndrome. Internal Medicine, 55(19), 2819-282 of IV
Myocardial
effusion stiffness Agard, C., et al. (2007). Churg-Strauss syndrome revealed by LVComplete
wall LBBB
thickening
granulomatous acute Septum
pericarditis: two case reports and a review of literature.
Seminars in Arthritis and Rheumatism, 36(6), 386-91
 HEART INFILTRATION
↓ Contractility
Degranulation of eosinophils
Pulmonary
↓ Ejection Fraction Congestion
Damage to myocytes

Chest HEART FAILURE Dyspnea

MYOCARDIAL NECROSIS ↑Orthopnea
LDH
pain

WHAT COULD HAVE CAUSED THE PATIENT’S

 Complete LBBB

ONTRAST-IND
FATAL ARRHYTh
Bundle branch
CONTRAST MEDIA re-entry
“Tachycardia with a left bundle
branch block pattern is associated with
phenomenon
“bundle branch re-entry” in 73%.”“…allergy, asthma, urticarial, or other
HYPERSENSITIVIT hypersensitivity showed 52% rate of
Ventricular
hypersensitivity reactions compared to
Y REACTION Tachycardia
patients without allergy history (7.1%).
Caceres, J., et al (1989). Sustained bundle branch
reentry as a mechanism of clinical tachycardia. Especially, asthma has been reported as a
Circulation, 79(2), 256-70
risk factor of severe reactions.”
Suh-Young, L., et al. (2014). Radiocontrast media Sudden Cardiac
hypersensitivity in the Asia Pacific Region. Asia Pacific
Allergy, 4(2), 119-125 Death
 FINAL DIAGNOSIS

Acute Heart Failure with Reduced Ejection Fraction

secondary to Eosinophilic Endomyocarditis
due to Churg-Strauss Syndrome
 CAUSE OF DEATH
• Immediate Cause:
Cardiogenic shock secondary to Fatal Arrhythmia
• Antecedent Cause:
Eosinophilic Endomyocarditis
• Underlying Cause:
Churg-Strauss Syndrome
DO NOT LET SUCCESS
GET INTO YOUR HEAD
DO NOT LET FAILURE
GET INTO YOUR
HEART -ANON
 REFERENCES
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Al-Sanouri, B., Maslamani, Y. & Al-Sanouri, I. (2016). A  Fatal Case of Chronic Eosinophilic Leukemia Not Otherwise
 Specified (CEL-NOS) in a 19-Year-Old Male with Acute Transformation into  Blast Crisis. Case Reports in
clinical Medicine, 5:528-540.
Belizario Jr., V. Y., & de Leon, W. U. (2013). Medical parasitology in the Philippines. Diliman, Quezon City: The
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