1.

INTRODUCTION
Peripartum cardiomyopathy (PPCM) is an uncommon condition with an
estimated frequency 1 in 1000 live births worldwide. This condition is linked to
high maternal-newborn morbidity and mortality. PPCM affects women with no
history of heart failure and manifests as acute or slow-progressing left ventricular
(LV) systolic dysfunction (LV ejection fraction less than 45 percent) during
pregnancy, after delivery, or in the first postpartum months. Patients with PPCM
exhibit various risk factor profiles, suggesting that several processes are involved
in the etiology of the disease.1
A small percentage of patients with PPCM present during the end of the
third trimester. Most PPCM symptoms appear in the postpartum period,
frequently in the first week after delivery. The most common symptoms include
palpitations, new-onset orthopnea, dyspnea, an unexplained cough, edema, and
abnormal weight gain during pregnancy. Physical examination signs are
consistent in a patient with heart failures, such as tachycardia, jugular venous
distension, pulmonary rales, peripheral edema, a third heart sound, and a displaced
apical impulse. Echocardiography and clinical complaints are the main diagnostic
criteria.2
The treatment follows the accepted guidelines for other systolic heart
failure forms, including bromocriptine, oral heart failure treatments,
anticoagulants, vasodilators, and diuretic agents.3 The prognosis of this disease
depends on the time of management. The mortality and morbidity rate of PPCM
in the first 6 months ranges from 2 – 12%, while the outcome after 6 months was
12 – 14%. The outcome is influenced by race and patient demographics.4
Here we report a patient with PPCM who delivered 10 months ago, and we
discuss the clinical symptoms, therapy, and the probability of conceiving in the
future for this patient.
2. CASE REPORT
A 39-years-old woman from Lhoksukon, working as a pharmacist, came to
the cardiology outpatient department at Cut Meutia Hospital on Tuesday, July
26th. The patient presented with 2 days history of worsening dyspnea before
admission. Dyspnea was exacerbated by exertion, e.g., climbing stairs or lifting
heavy drugs box during working as a pharmacist. The patient claimed dyspnea
diminished with rest. The patient claimed to experience fatigue easily and
swelling of the limb. A brief review of palpitation, chest discomfort and orthopnea
was denied. Based on the history taken, the patient gave birth through cesarean
section 10 months ago at 38 – 39 weeks of pregnancy (G1P1A0) when the patient
was 38 years old. During pregnancy, antenatal care (ANC) was routinely
performed every month by the midwife. Based on the ANC report, there was no
preeclampsia, infection, or abnormal physical examination of the heart during
pregnancy, but the patient claimed her weight had gained by 10 kg throughout the
pregnancy. The patient was giving birth to a female baby with 2500 gr of weight
and was treated in the Neonatal Intensive Care Unit of Sakinah Hospital for a few
days and the patient confirmed there was no congenital disease profound in her
baby. A history of diabetes mellitus was found 2 years ago. No chronic diseases
were recorded in her family, e.g., diabetes mellitus and heart disease.
Physical examination showed the patient in compos mentis state, blood
pressure 130/100 mmHg, heart rate (HR) 71 beats per minute (bpm), respiration
rate 19 times per minute, temperature 36,8 ⁰C, and oxygen saturation (SpO 2) was
99%. Chest auscultation revealed an S3 sound heard at the apex and normal breath
sound in all areas of the chest.
Laboratory investigations were within normal ranges, besides there was an
increased level of fasting blood glucose at 216 mg/dL and HbA1C at 8,9%.
 Figure 1. Thirty-nine years old woman with PPCM

Electrocardiography (ECG) on this patient showed sinus rhythm, heart rate

100 bpm, normal axis, normal P wave, ST changes in 12-leads were not found,
but there was T wave inversion in V5 and V6. The conclusion of this ECG was
sinus rhythm with lateral ischemia.

Figure 2. Thrity nine years old woman with cardiomegaly

Chest x-ray showed cardiomegaly with cardiothoracic ratio (CTR) about

>50%, aortic and pulmonary segments were normal, the cardiac wedge was not
found, and bronchovascular pattern looks increased in two segments. The
conclusion was cardiomegaly.

Figure 3. Thirty-nine years old woman with PPCM

Echocardiography finding was ejection fraction 41%, mild to moderate

mitral regurgitation (MR), mild tricuspid regurgitation (TR), dilatation of all
chambers, global hypokinetic and TAPSE 10.
Based on the physical and supporting examination, the diagnosis of
peripartum cardiomyopathy can be established. The patient was prescribed several
drugs including diuretics (Furosemide), mineralocorticoid receptor antagonist
(Spironolactone), angiotensin II receptor blocker (ARB) (Candesartan), and beta-
blocker (Concor), sacubitril valsartan sodium hydrate (Uperio), oral hypoglycemic
medication (Metformin), and proton-pump inhibitor (Omeprazole).
3. DISCUSSION
Peripartum cardiomyopathy (PPCM) is a form of heart failure due to
systolic dysfunction, characterized by low left ventricle ejection fraction (LVEF)
<45%, with no specific reversible cause, that present in late pregnancy towards to
several months postpartum period, and affects women with no history of heart
disease. The cause of this condition is unknown, but there are possible
mechanisms, including the imbalance of inflammatory, angiogenic processes, and
vascular damage. The activity of several biological factors, 16-kDa prolactin and
soluble fms-like tyrosine kinase 1 (sFlt1), were suspected of initiating and
promoting the development of PPCM. Several predisposing factors were
associated with PPCM, including multipara, certain ethnicity (African women),
smoking, diabetes mellitus, preeclampsia, malnutrition, and advanced or
pregnancy at a younger age.4
Patients with PPCM can experience various symptoms during pregnancy
or postpartum period. Most patients will present symptoms of heart failure, like
dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, fatigue, and
edema of the lower extremities.5 Dyspnea results from failure of cardiac filling
and increased pulmonary venous pressure, and it will disturb the balance of
hydrostatic and oncotic pressure. The slight change of hydrostatic and oncotic
pressure will favor the movement of the capillary fluid to accumulate in the
interstitium of the lung (alveoli), resulting dyspnea in patients with heart failure. 6,7
The disturbance of hydrostatic and oncotic pressure balance in blood vessel
extremities will result edema in lower extremities.8
This theory supports the finding in our patient, who experiences two
days of worsening dyspnea before admission. Dyspnea was exacerbated by
exertion and diminished with rest. The patient claimed to experience fatigue
and swelling of the limb.
Age is a key factor in the prevalence of PPCM. Even though the disease
can affect women of any age, >50% of cases affect those over 30.9 Both
preeclampsia and hypertension significantly increase the risk of PPCM. Up-
regulation of sFlt-1 has been demonstrated to cause preeclampsia by causing
endothelial dysfunction, lowering capillary density, and preventing VEGF
(vascular endothelial growth factor)-induced vasodilatation, which results in
hypertension, proteinuria, and edema. Women with PPCM have also been found
to have elevated levels of sFlt-1 and a decreased ratio of sFlt-1 to placental growth
factor (a type of VEGF). Increased sFlt-1 levels have also been observed in DM
patients.10 Although 70% of PPCM occurred in pregnant women with
normotensive blood pressure.11,12 The pathogenesis of PPCM may involve the
inflammation process. Patients with PPCM have higher levels of serum
inflammatory markers, such as the soluble death receptor sFas/Apo-1, C-reactive
protein, interferon-gamma (IFN-), and IL-6.13
This theory supports our findings. Based on the history taken, the
patient gave birth through cesarean section 10 months ago at 38 – 39 weeks
of pregnancy (G1P1A0) when the patient was 38 years old. During
pregnancy, ANC was routinely performed every month by the midwife.
Based on the ANC report, there was no preeclampsia, infection, or abnormal
physical examination of the heart during pregnancy. Our patient has had a
history of diabetes mellitus since two years ago.
Physical examination of patients with PPCM frequently reveals LV
dilatation, including the third heart sound and misplaced apical impulse, which is
occasionally but less frequently noticed since PPCM can occur even without LV
enlargement.14
Physical examination showed the patient in compos mentis state,
blood pressure 130/100 mmHg, heart rate (HR) 71 beats per minute (bpm),
respiration rate 19 times per minute, temperature 36,8 ⁰C, and oxygen
saturation (SpO2) was 99%. Chest auscultation revealed an S3 sound heard
at the apex and normal breath sound in all areas of the chest.
Laboratory blood testing is a standard assessment procedure for
individuals with cardiomyopathy or heart failure, including those with PPCM.
These Tests evaluate the function of the renal, hepar, and thyroid, as well as tests
to evaluate the electrolytes. A complete blood count is also performed to check for
anemia or signs of infection. In addition, cardiac stress and damage indicators can
determine the amount of risk, such as troponin and B-type natriuretic peptides.
Although BNP is frequently increased, no specific abnormalities are found in
laboratory tests for patients with PPCM.15,16
Laboratory investigations in our patient were within normal ranges,
besides there was an increased level of fasting blood glucose at 216 mg/dL
and HbA1C at 8,9%.
According to several studies, the 12-lead ECG of most PPCM patients will
be normal. However, this hypothesis does not completely rule out the likelihood
of abnormal ECG results in PPCM patients. Inverted T waves and ST depression
are the most frequent ECG abnormalities. Reduced left ventricular systolic
function was the reason for the abnormal result.17
ECG on our patient showed sinus rhythm, heart rate 100 bpm,
normal axis, normal P wave, ST changes in 12-leads were not found, but
there was T wave inversion in V5 and V6. 
Echocardiography is the primary diagnostic method for determining the
degree of cardiac dysfunction in PPCM. The ejection fraction in patients with
PPCM is often below 45 percent.18 The echocardiography may show left and right
ventricular dilatation, mitral and/or tricuspid regurgitation, pulmonary
hypertension, and left atrial or biatrial enlargement.19
Echocardiography in our patient showed mild to moderate mitral
regurgitation, mild tricuspid regurgitation, dilatation of all chambers,
TAPSE 0, and global hypokinesia with an ejection fraction 41%.
A chest x-ray can reveal other causes of dyspnea in all PPCM patients.
Cardiomegaly, pulmonary venous congestion, and pleural effusions are a few
radiological signs of heart failure that could be seen in PPCM.1,5,20
Chest x-ray in our patient revealed cardiomegaly.
Based on the theory, the therapy given to PPCM patients is similar to
therapy for heart failure patients. The therapy was (i) decongestive therapy using
vasorelaxants, diuretics, and non-invasive ventilation to minimize organ
dysfunction and improve symptoms; (ii) neuro-humoral therapy using beta-
blockers, ACE inhibitors, and mineralocorticoid receptor antagonists as oral heart
failure therapies to improve LV recovery and outcome; (iii) device therapy for a
subset of patients to minimize symptoms and improve outcomes; (iv)
anticoagulation; and (v) bromocriptine.3,21
Our patient was given several drugs, including diuretics (Furosemide
1x40 mg), mineralocorticoid receptor antagonist (Spironolactone 1x20 mg),
angiotensin II receptor blocker (ARB) (Candesartan1x8 mg), and beta-
blocker (Concor 1x2,5 mg), sacubitril valsartan sodium hydrate (Uperio 1x1),
oral hypoglycemic medication (Metformin 2x500), and proton-pump
inhibitor (Omeprazole 2x1).
Patients with PPCM are likely to get pregnant again, but the patient should
be informed of the possibility of PPCM in the subsequent pregnancy. Patients
who want to get pregnant again must ensure that their heart function returns to
normal, by carrying out several examinations such as stress echocardiography. If
the stress echocardiography results show augmentation within normal limits, the
patient can plan to get pregnant but have to monitor their vital signs (e.g., blood
pressure or HR), as well as signs and symptoms of heart failure. However, if the
results of stress echocardiography show poor augmentation, then pregnancy is not
recommended, and it is advised to undergo a follow-up check-up after a year.22,23

4. Summary
We report a case of a woman thirty-nine years old with PPCM after 10
months giving birth. The patient came with dyspnea on exertion, fatigue easily,
and limb swelling. Physical examination showed an S3 sound at the apex,
cardiomegaly was found in chest X-Ray examination, we got T inversion in V5
and V6 in ECG, echocardiography examination showed EF 41%, mild to severe
MR, mild TR, and all chamber dilatation.
We prescribed several medications, including diuretics (Furosemide),
mineralocorticoid receptor antagonist (Spironolactone), angiotensin II receptor
blocker (ARB) (Candesartan), and beta-blocker (Concor), sacubitril valsartan
sodium hydrate (Uperio), oral hypoglycemic medication (Metformin), and proton-
pump inhibitor (Omeprazole). Based on clinical findings and supporting
examination, we do not advise the patient to get pregnant again.