By : Rizki Amalia

0807101010112
Peripartum cardiomyopathy is a life-threatening
condition of unknown cause that occurs in previously
healthy women during the peripartum period. It is
characterized by left ventricular dysfunction and
symptoms of heart failure that can arise in the last
trimester of pregnancy or up to 5 months after
delivery.

The National Hospital Discharge Survey (19902002)
estimated that it occurs in 1 in every 2,289 live births in
the United States.

The disease appears to be more common in African
American women.

The rate varies in other populations : it is highest in Haiti,
with 1 case in 300 live births, which is nearly 10 times
higher than in the United States.
What causes PPCM? Contributing factors and specific
mechanisms remain unclear.
Although various hypotheses have been proposed, so
far no cause has been clearly identified. It is likely that
PPCM is a heterogenous disorder, with a multifactorial
etiology and complex biopathological processes.
Dyspnea and fatigue (90%),tachycardia (62%), and
peripheral edema (60%) persistent nocturnal dry
cough,orthopnea, paroxysmal nocturnal dyspnea
NYHA class III or IV functional status seem to be the
most common initial presentation

Other non-specific signs and symptoms include
dizziness, non-specific praecordial pain (50%),
abdominal discomfort, palpitations, most frequently
due to tachycardia or supraventricular tachiarryhtmias
PPCM was based on the following criteria :
1. Development of congestive heart failure during
pregnancy or the first 5 months after delivery ;
2. Absence of an identifiable cause for cardiac failure;
3. Absence of recognizable heart disease before
pregnancy ; and
4. Left ventricular systolic dysfunction with left
ventricular ejection fraction (LVEF)<45%.




How to optimize the diagnosis? Early involvement of a
cardiologist is needed for a timely diagnosis.

The rapid onset of heart failure symptoms in the
peripartum period may distinguish this difficult entity,
only if other causes of cardiomyopathy are excluded. A
screening clinical self-test for early recognition of
PPCM is now proposed. Cardiac MRI is also suggested
to have a great diagnostic and prognostic potential.
A score 5 has always been associated with LV systolic
dysfunction.
A score > 4 suggests the need for further investigation.
In this case, a blood BNP test and an echocardiography
are recommended.
If the score is < 4 the patient should be monitored for
BNP and C-reactive protein levels. If increased levels,
echocardiography should be performed.
The author emphasizes that this test is not diagnostic
for PPCM, but encourages an expanded use, because it
may be a useful tool for early recognition of the new
onset heart failure.
Exclusion of peripartum cardiomyopathy in the breathless
woman towards the end of pregnancy/early post-partum.

How to treat better? The current medical strategies are
not always safe enough for maternal prognostic.

There is no clear evidence for the beneficial effect of
standard therapy on the recovery of cardiac function in
patients with PPCM. As the cause of PPCM is still
unknown, no specific therapy has been established to
treat this condition.
Angiotensin-converting enzyme-inhibitors and
angiotensin-II receptor blockers. Angiotensin-
converting enzyme (ACE)-inhibitors and angiotensin-
II receptor blocker (ARB) are contraindicated because
of serious renal and other fetal toxicity
Hydralazine and long-acting nitrates. It is believed
that this combination can be used safely, instead of
ACE-inhibitors/ARBs, in patients with PPCM.
-Blockers. These have not been shown to have
teratogenic effects. b-1-selective drugs are preferred
because b-2 receptor blockade can, theoretically, have
an anti-tocolytic action.
Diuretics should be used sparingly as they can cause
decreased placental blood flow.
Furosemide and hydrochlorothiazide are most
frequently used.
Aldosterone antagonists. Spironolactone is thought to
have antiandrogenic effects in the first trimester.
Because the effects of eplerenone on the human foetus
are uncertain, it should also be avoided during
pregnancy.
Antithrombotic therapy. Fetotoxicity of warfarin needs
to be considered in all patients with PPCM and LVEF
,35%. Unfractionated or low-molecular-weight heparin
can be used. Fetotoxicity of warfarin needs to be
considered.





CASE REPORT
Identity Of Patient:
Name : Mrs. A
Umur : 38 Years Old
Sex : Female
Address : Baitussalam, Aceh Besar
Occupation : Housewife
Religion : Islam
Syllable : Aceh
Status : Menikah
Registration number : 0-95-51-30
Hopitalized : 24 Juni 2013
Examination day : 24 Juni 2013

The chief complaint: shortness of breath
Extra complaint : nausea, vomitus, and weakness




History of present illness:
A 38 years old female brought to the Emergency
Installation RSUDZA with complaints of shortness
of breath since 1 weeks ago, and worsen last
night. This complain felt continously., until now.
Patient must sleep with two pillows. It is worsen
with activity like go to bathroom, and recovery
with rest. Patient complain weakness, vomitus,
nausea, and doent have appetite to eat. This
occurs 3 months after delivery the fourth baby.
This symptomp occurs in mei with weakness,
palpitation, that day in day heavier.

History of past ilness:
The patient has been treated in the ICCU with the same complaints 1
weeks ago.

Family history
No one in her family suffering the same disease.

History of medicine:
Furosemide, Captopril, Spironolacton, Aspilet 1x80 mg, Concor, Digoksin,
Laxadyn syr

Social history:
Never smoking, and never consume alcohol.


Status Present
Conscious : Compos mentis
Blood Pressure : 90/60 mmHg
Heart Rate : 94 x/menit
Respiratory Rate : 24 x/menit
Temperatur : 36,5
0
C (axila)

Eyes : Conjungtiva palpebra inf pucat (+/+)
Ear/nose/mouth : normal
Neck : TVJ R-2 cmH
2
O
Thorax : Normochest, retraction (-), Vesiculer
(+/+), Rhonki (+/+), Wheezing (-/-)
Cor :
Inspection : Ictus Cordis (-)
Palpation : Ictus Cordis at ICS V linea midclavikula
sinistra
Percution : Upper at ICS III
Right side at di ICS IV linea parasternal
dextra
Left side at ICS V linea midclavikula
sinistra
Auskultation : BJ I > BJ II, reguler, murmur (-), gallop (-)



Ekstremitas superior inferior
pale (-/-) (-/-)
edema (-/-) (-/-)

Ht : 26 %
Hb : 8,7
Leukosit : 10,2
Trombosit : 330
Ur/ Cr : 25 / 0,7 mg/dl
KGDS : 130



CTR : 80%
Cor : Jantung tampak besar
Pulmo : perselubungan inhomogen pada paru
kanan dan kiri di bagian basal
Aorta : elongasi (-), dilatasi (-)
Pinggang jantung : (+)
Kesimpulan : Kardiomegali dengan CTR
80%.

Irama : Irama Sinus
Heart rate : 107 x/i
Regularitas : regular
Interval PR : 0,2 s
Axis : RAD
Morfologi
Gel P : durasi 0,04 s, amplitudo 1 mV
Kompleks QRS : QRS durasi 0,04 s
Segmen ST :
ST elevasi : -
ST depresi : -
Gelombang T : -
Q patologis : -
VES : (+)

Dimention, heart chamber : LA-LV dilatation
LVH (-)
Contractility RV decrease, tapse 1,6 cm
Global hipokinetik severe
Valve : MR severe and TR mild
Doppler :35 mmHg

PPCM NYHA fc IV
Bed Rest semifowler
O2 2-4 L/menit
Diet Jantung II 1500 kkal
Iv furosemide 1 amp/8 jam
Tab captopril 3x6,25 mg
Tab spironolakton 1x25 mg
Laxadyn syr I x CII





THANK YOU