Peripartum cardiomyopathy in an intensive care unit setting

Abstract

Managing pregnant patients in the coronary care unit and the intensive care unit has been a challenge for many clinicians, as they do not encounter those special populations on a routine basis. Peripartum cardiomyopathy (PPCM) is an uncommon but potentially life-threatening condition that occurs during the last month of pregnancy or within five months of delivery. It is associated with left ventricular systolic dysfunction, leading to reduced ejection fraction and heart failure. Although the exact etiology remains unclear, potential contributing factors can include factors such as myocarditis, abnormal immune responses, genetic predispositions, and hormonal imbalances. The future implications of PPCM are wide. Besides physical illness, mental illness can also limit functionality and impose health challenges. Additionally, subsequent pregnancies carry an increased risk of recurrence, especially if cardiac function remains poor. Ongoing research into the molecular and genetic underpinnings of PPCM may pave the way for different targeted therapies and strategies focusing on prevention. Increasing awareness, early detection, and advances in treatment can significantly reduce morbidity and mortality associated with PPCM. Multidisciplinary care is crucial in optimizing outcomes for women affected and their families. This mini review aims to help appraise healthcare providers and clinicians in addressing and managing this challenging condition.

Key Words: Hemodynamic decompensation; Hemodynamic stabilization; Mechanical circulatory support; Bromocriptine therapy; Peripartum cardiomyopathy

Core Tip: Early recognition of peripartum cardiomyopathy is critical, as symptoms mimic heart failure and other acute conditions. Management includes guideline-directed heart failure therapy tailored to pregnancy/lactation, individualized hemodynamic and respiratory support, and mechanical circulatory support if needed. Bromocriptine may be considered in severe cases to improve left ventricular recovery, with concurrent anticoagulation due to thrombotic risk. Long-term care requires serial echocardiography, natriuretic peptide monitoring, and counseling on future pregnancy risks, as residual cardiac dysfunction may persist.

INTRODUCTION

Peripartum cardiomyopathy (PPCM) is maternal heart failure with systolic dysfunction and an ejection fraction below 45%. It usually develops in the last month of pregnancy or within five months after delivery. The diagnosis requires exclusion of prior cardiac disease and other common causes of hemodynamic decompensation[1,2].

The incidence of PPCM varies widely worldwide, from 0.03 per 1000 live births in the United States[3] to rates nearly 200 times higher in parts of Haiti and Nigeria[4]. In the United States, Black women represent 43.9% of all PPCM hospitalizations despite comprising a smaller proportion of the population, and some studies report a six-fold higher mortality risk compared to White women. This hints towards the importance of high-quality health care and attention to genetic predispositions, especially in certain ethnic subgroups[5].

The onset of PPCM often coincides with other pregnancy complications that cause similar hemodynamic instability, such as preeclampsia or pulmonary embolism[6]. Pregnancy itself is a major hemodynamic stressor, and women with a familial predisposition to cardiomyopathy may develop the condition during this period[7]. These factors make diagnosis challenging. The disease has an unpredictable course, with sudden deterioration sometimes necessitating urgent intensive care unit (ICU) admission-about 30% of hospitalized patients require intensive care. As most deaths occur within 30 days of diagnosis, maintaining a high index of suspicion and initiating prompt evaluation are critical[8].

ETIOLOGY

Advanced maternal age is a recognized risk factor for PPCM, with the mean presentation age around 30–31 years, but higher rates and worse outcomes are seen in mothers over 40[9]. This is likely due to diminished cardiac reserve, accumulated comorbidities, and reduced adaptation to pregnancy-related changes[10]. Race and ethnicity also influence risk, with African American women experiencing a threefold higher incidence compared to White women[8]. Slower recovery rates and a greater likelihood of clinical deterioration after diagnosis compound this disparity. Hypertensive disorders of pregnancy, particularly severe preeclampsia, are among the strongest predictors, with over a 20-fold increase in risk[11]. Autoimmune factors, such as autoantibodies against cardiac proteins and receptors, are linked to more severe dysfunction and poorer recovery[4]. Nutritional factors, notably selenium deficiency, are associated with a higher incidence, and supplementation may improve symptoms and reduce mortality[12,13].

Additional risk factors include gestational diabetes, obesity, tocolytic therapy, viral myocarditis, and multiple gestation[4].

PATHOPHYSIOLOGY

The physiological expansion of maternal blood volume, combined with increased heart rate and cardiac output, raises myocardial workload during pregnancy. These adaptations promote structural and homeostatic remodeling of cardiovascular tissue, which can exacerbate cardiac stress in the presence of other vulnerabilities[14]. Interestingly, the incidence of PPCM peaks in the last trimester. This is a time when hemodynamic stressors begin to decline. Therefore, this suggests that there exist additional pathophysiological mechanisms, such as hormonal influences, that contribute to the disease process[15].

Another contributing factor is elevated soluble fms-like tyrosine kinase-1 (sFlt-1), a decoy receptor that inhibits VEGF’s vasodilatory and angiogenic effects[16,17]. Elevated sFlt-1 levels, also seen in multiple gestations and preeclampsia, may explain the shared vascular injury patterns between PPCM and preeclampsia[18]. A simplified illustration is depicted in Figure 1.

Figure 1 Factors contributing to the pathophysiology of peripartum cardiomyopathy. Orange dotted lines denote detrimental interactions among the depicted components.

GENETIC PREDISPOSITION

Genetic testing has shown that approximately 15%-20% of PPCM patients carry pathogenic truncating variants in genes linked to familial cardiomyopathy. The most common are TTN (titin) variants, found in 10%-15% of cases, followed by mutations in BAG3, FLNC, DSP, LMNA, MYBPC3, and SCN5A. About two-thirds of these variants are located in the A-band region of the TTN gene, mirroring the distribution seen in familial cardiomyopathy[19].

TTN truncating variants are associated with poorer outcomes, as carriers tend to have significantly lower ejection fractions at one year. This could be important to prognosticate recovery outcomes after discharge[20].

To differentiate between familial cardiomyopathy and PPCM, the timing of symptom onset may help. Women with genetic cardiomyopathy often present earlier, around the second trimester when hemodynamic stress peaks, whereas classic PPCM typically develops in the last month of pregnancy or postpartum[21]. However, current evidence suggests routine genetic testing for all PPCM patients as it could potentially help predict disease severity and manage resources[22].

CLINICAL FEATURES AND DIAGNOSIS

Clinical features of PPCM resemble typical heart failure symptoms, including dyspnea, orthopnea, peripheral edema, dizziness, and cough, usually presenting late in pregnancy or within months after delivery. However, these symptoms do not reveal the underlying cause of heart failure[22]. Heart failure may result from chronic conditions such as hypertension or from genetic defects affecting sarcomere function, as seen in familial cardiomyopathies[23]. Identifying the underlying cause is crucial, as it allows targeted management of risk factors that can influence disease progression[24].

Careful attention to clinical features is essential, as certain symptoms may suggest alternative diagnoses. For example, chest pain may shift suspicion from PPCM to conditions like pulmonary embolism or pregnancy-associated myocardial infarction[24]. Alongside clinical evaluation, basic imaging and laboratory tests provide valuable insights. Key investigations include chest X-ray and echocardiography[22].

In heart failure, a chest X-ray may reveal signs such as pulmonary edema, cardiomegaly, interstitial or alveolar infiltrates, and pleural effusions. It is also useful for excluding pulmonary conditions that can mimic or contribute to symptoms, such as chronic obstructive pulmonary disease, pneumonia, pulmonary fibrosis, and pneumothorax[22]. Echocardiography helps identify structural cardiac abnormalities such as valvular disease, congenital defects, or regional wall motion abnormalities as seen in myocardial infarction. Additionally, an electrocardiogram (ECG) is important to exclude ischemic causes of heart failure and detect arrhythmias that may contribute to decompensation[25]. Biomarkers such as NT-proBNP (> 300 pg/mL) and BNP (> 100 pg/mL) are useful for ruling out heart failure[26]. Troponins are sensitive markers of acute myocardial injury, such as MI or myocarditis[27].

Cardiac magnetic resonance (CMR) imaging plays a crucial role in the postpartum evaluation of patients presenting with heart failure or suspected PPCM. CMR offers high-resolution, tissue-characterizing capabilities that help differentiate PPCM from Takotsubo syndrome (TTS), myocarditis, and other causes of cardiomyopathy[28]. Maintaining a high index of suspicion is essential until all differential diagnoses are thoroughly ruled out.

In PPCM, CMR typically shows global or regional left ventricular (LV) systolic dysfunction with minimal or absent late gadolinium enhancement (LGE), suggesting non-ischemic, non-inflammatory injury[29].

In TTS, CMR may demonstrate transient apical or mid-ventricular ballooning with myocardial edema on T2-weighted imaging and no LGE, consistent with myocardial stunning rather than necrosis[30].

In myocarditis, CMR often reveals myocardial edema, subepicardial or mid-wall LGE, and regional wall motion abnormalities that follow a non-coronary distribution, helping to distinguish it from PPCM or ischemic injury[31,32].

Additionally, CMR is highly sensitive for detecting LV thrombus, especially when echocardiographic windows are suboptimal. Thrombi are best visualized using contrast-enhanced, delayed imaging[32].

It is worth noting that TTS should be clearly distinguished as a differential diagnosis in the peripartum period. Its presentation often overlaps with PPCM, including symptoms such as chest pain, dyspnea, and transient LV dysfunction. This is important because the treatment approach and prognosis differ between TTS and PPCM.

The RETAKO study (REcapTure of takotsubo cardiomyopathy in obstetric patients)[33] is a recent research effort focused on understanding the features, diagnosis, and management of TTS in the peripartum period. While PPCM and TTS can present with overlapping features, their underlying mechanisms, imaging characteristics, and management differ significantly. Treatment for TTS is primarily supportive, focusing on heart failure management, avoidance of catecholamines, and anticoagulation if apical thrombus is present. Most cases of TTS resolve within weeks, with full recovery of cardiac function expected in the majority of patients. In contrast, PPCM requires guideline-directed medical therapy for heart failure, with special consideration for pregnancy and lactation status, and may involve additional therapies.

ICU MANAGEMENT PRINCIPLES

Severe presentations of PPCM often require intensive care for hemodynamic stabilization, respiratory support, careful fluid and thromboembolic risk management, and, in a subset, mechanical circulatory support (MCS).

Hemodynamic stabilization

Acute hemodynamic support in PPCM aims to restore end-organ perfusion while minimizing further myocardial injury.

For cardiogenic shock, shortterm inotropic support is often used to augment contractility while vasoactive therapy stabilizes perfusion pressure. Dobutamine increases cardiac output primarily through beta1–mediated positive inotropy and modest chronotropy, with generally mild but unpredictable reductions in systemic vascular resistance due to beta2 vasodilation. Milrinone provides inotropy with added lusitropy and acts as an inodilator by reducing systemic and pulmonary vascular resistance. This can improve forward flow but also increases the risk of hypotension. Careful titration is therefore required for either drug. Choice and dosing should be individualized according to the patient's blood pressure, filling status, and arrhythmic risk. Regular reassessment with hemodynamics at the bedside is important[34,35].

Invasive monitoring: Arterial line placement is indicated for continuous blood-pressure monitoring in unstable patients and titration of vasoactive agents. Central venous access (and, in centers where available and appropriate, pulmonary artery catheterization or advanced hemodynamic monitoring) can help with fluid and inotropic management in complicated or refractory cases[34,35].

Avoidance of afterload reduction in hypotension. Although afterload reduction (e.g., with ACE inhibitors) benefits chronic systolic dysfunction, these agents are contraindicated in the setting of hypotension or cardiogenic shock. Afterload-reducing therapy can be deferred until the patient is hemodynamically stable and (in the postpartum) maternal/fetal concerns are addressed[34,35] (Table 1).

Table 1 Suggested intensive care unit hemodynamics order set.

Suggested ICU hemodynamics order set
Insert an arterial line and central venous catheter for unstable patients
Start norepinephrine if MAP < 65 mmHg with signs of hypoperfusion
Initiate inotrope for low-output states:
Dobutamine 2-5 μg/kg/minute, titrated every 30-60 minutes based on invasive measures
OR Milrinone 0.25-0.5 μg/kg/minute, titrate every 30-60 minutes based on invasive measures
Avoid nitroprusside or hydralazine in the presence of hypotension
Daily ECG
Daily electrolytes:
Maintain K+ > 4.0 mmol/L
Maintain Mg2+ > 2.0 mg/dL
Escalation checklist:
Persistent hypotension despite inotrope → Add vasopressor
Cardiac index < 2.0 L/minute/m2 after 2 hours → Consider mechanical circulatory support (see section E)
Lactate > 4 mmol/L or worsening acidosis → Activate advanced heart failure consult

ICU: Intensive care unit; MAP: Mean arterial pressure; ECG: Electrocardiogram.

Respiratory support

Respiratory dysfunction caused by pulmonary edema or respiratory muscle fatigue is seen in severe PPCM.

Oxygen and noninvasive ventilation (NIV). Supplemental oxygen and NIV are first lines for hypoxemia and alveolar edema if the patient can protect their airway. NIV can reduce the work of breathing and improve oxygenation while avoiding intubation in many patients.

Endotracheal intubation and mechanical ventilation. Indicated for persistent hypoxemia, inability to protect the airway, progressive respiratory fatigue, or when aggressive invasive hemodynamic support is required. Ventilator strategy should minimize cardiopulmonary interactions that worsen preload/afterload-avoid large tidal volumes and unnecessary positive end-expiratory pressures that may reduce venous return unless needed for oxygenation.

Pulmonary edema management. Optimize preload (see fluid management) and use diuretics and, when indicated, positive pressure ventilation to redistribute fluid and improve oxygenation. Rapid correction of hypoxemia and attention to left-sided filling pressures are priorities (Table 2).

Table 2 Suggested intensive care unit respiratory order set.

Suggested ICU respiratory order set
Oxygen via nasal cannula or HFNC; titrated to target saturation
NIV (CPAP 5-10 cm H2O) if hemodynamically stable and cooperative
Early intubation if PaO2/FiO2 < 150 or signs of fatigue
Daily chest X-ray and ABG for ventilated patients
Avoid high PEEP in preload-dependent patients
Escalation checklist
SpO2 < 88% despite HFNC/NIV → Prepare for intubation
Worsening pulmonary edema → Intensify diuresis and evaluate for MCS
Signs of ventilator-induced hypotension → Adjust PEEP and fluids cautiously

HFNC: High flow nasal cannula; NIV: Non-invasive ventilation; CPAP: Continuous positive airway pressure; ABG: Arterial blood gas; PEEP: Positive end expiratory pressure; MCS: Mechanical circulatory support.

Fluid management

Careful balancing of preload and perfusion is central to optimizing cardiac output without worsening pulmonary congestion.

Diuretics for volume overload. Loop diuretics (e.g., furosemide) are used to relieve pulmonary and systemic congestion. Diuresis frequently improves oxygenation and symptomatic status.

Avoid over diuresis in preload-dependent patients. Overly aggressive diuresis can precipitate hypotension and reduce cardiac output in patients who are dependent on higher preload; invasive monitoring or dynamic measures of volume responsiveness help guide therapy. Titrate diuretics to clinical response and hemodynamic data[34,35] (Table 3).

Table 3 Suggested intensive care unit fluid order set.

Suggested ICU fluid order set
Furosemide IV bolus (20-40 mg), repeat or switch to infusion if inadequate diuresis
Strict input/output monitoring; daily weights
CVP-guided diuresis in invasive monitoring patients
Hold diuretics if MAP < 60 mmHg or rising creatinine
Escalation checklist
Persistent volume overload despite high-dose loop diuretics → Add thiazide synergy
Rising creatinine > 0.3 mg/dL in 48 hours → Reassess fluid goals
CVP < 5 cmH2O and hypotension → Stop diuretics and reassess preload

ICU: Intensive care unit; CVP: Central venous pressure; MAP: Mean arterial pressure.

Anticoagulation

PPCM is at high risk of intracardiac thrombus and thromboembolism due to severe LV systolic dysfunction and peripartum prothrombotic state.

Indications. Anticoagulation is considered if LV ejection fraction (LVEF) is greatly reduced (< 30%) or when an LV thrombus is present. The decision must weigh against the risk of bleeding (including risk of postpartum hemorrhage) and be coordinated with obstetric management if delivery is near[34,35] (Table 4).

Table 4 Suggested intensive care unit anticoagulation order set.

Suggested ICU anticoagulation order set
Initiate unfractionated heparin infusion; target PTT 60-80 seconds
Daily CBC and coagulation profile
Transition to warfarin postpartum if stable and no planned procedures
Escalation checklist
New embolic event → Evaluate anticoagulation adequacy
Active bleeding → Hold anticoagulant and reverse if indicated

ICU: Intensive care unit; CBC: Complete blood count; PTT: Partial thromboplastin time.

Multiple expert sources recommend heparin prophylaxis-typically low molecular weight heparin (LMWH)-when bromocriptine is administered, due to its pro-thrombotic potential[36].

Need to balance with obstetric bleeding risk. Major reviews emphasize that anticoagulation should be initiated only after careful consideration of the bleeding risk, particularly in the peripartum context.

MCS

When pharmacologic therapy cannot maintain perfusion, early MCS consideration is lifesaving and can bridge to recovery or definitive treatment. Refractory cardiogenic shock despite optimized inotropes/vasopressors, progressive end-organ dysfunction, or severe arrhythmias may prompt escalation to MCS. Key triggers include:

Hemodynamic instability: Mean arterial pressure < 65 mmHg accompanied by signs of ongoing hypoperfusion (e.g., cool extremities, altered mentation, oliguria).

Metabolic derangement: Low cardiac output. Escalating support requirements: Increasing doses of inotropes and/or vasopressors to maintain perfusion.

End-organ hypoperfusion: Evidence of organ dysfunction such as elevated creatinine, liver enzymes, rising lactate, or oliguria.

These criteria correspond to the Society for Cardiovascular Angiography and Interventions cardiovascular shock. Stage C (classic) for standard hypoperfusion, D (deteriorating) if escalating despite therapy, and E (extremis) if in refractory shock or arrest-each stage warranting urgent MCS escalation[37].

Devices available in the ICU: A range of devices exist to offer cardiopulmonary support. Intra-aortic balloon pump-provides modest afterload reduction and coronary perfusion augmentation; may be used as a temporizing measure in selected patients. Percutaneous ventricular assist devices (e.g., Impella)-can unload the left ventricle and increase systemic flow.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO)-offers full cardiopulmonary support and is especially useful when combined with respiratory failure or refractory shock. LV unloading during VAECMO is advised when there is an elevated PCWP (commonly > 15-18 mmHg), absence of aortic valve opening or poor pulsatility, increasing LV dimension or pulmonary edema and spontaneous echocardiographic contrast or LV thrombus. LV unloading strategies include conservative approaches (e.g., optimizing ECMO flow, afterload, and preload). These are selected based on the patient's condition and the institution's capability. ECMO can serve as a bridge to recovery, durable mechanical support, or transplantation[34,38] (Table 5).

Table 5 Suggested intensive care unit mechanical circulatory support order set.

Suggested ICU MCS order set
Early heart team consult if escalating inotropes/pressors > 24 hours
Prepare femoral access for urgent IABP or ECMO
Daily echocardiographic monitoring while on support
Escalation checklist
MAP < 60 mmHg and lactate rising despite inotropes → Initiate MCS
Multiorgan failure progression → Reassess goals of care

ICU MCS: Intensive care unit mechanical circulatory support; ECMO: Extracorporeal membrane oxygenation; MAP: Mean arterial pressure; MCS: Mechanical circulatory support.

The selection of modality depends on local expertise, hemodynamic goals (unloading vs support), and the anticipated duration of support. Early consultation with a tertiary center experienced in MCS is recommended when deteriorating hemodynamics are expected.

Pharmacological therapy in the ICU

Medical therapy in PPCM combines standard heart-failure measures (modified for pregnancy/postpartum) with some disease-specific approaches.

Diuretics (furosemide): First-line for symptomatic congestion. Use with attention to hemodynamics and renal function.

Beta-blockers: Evidence-based guideline-directed beta-blockers are evidence-based in systolic heart failure, but their initiation in PPCM should be guarded and typically deferred until the patient is hemodynamically stabilized. Selective agents such as metoprolol are typically used once tolerated.

ACE inhibitors/ARBs: These agents improve remodeling and outcomes in systolic heart failure but are contraindicated during pregnancy. They are typically initiated postpartum once breastfeeding and maternal considerations are addressed.

Bromocriptine (prolactin-inhibition strategy): An emerging, disease-targeted therapy has been proposed based on the hypothesis that a cleaved 16-kDa prolactin fragment contributes to myocardial injury in PPCM. Small trials and registry data suggest bromocriptine added to standard heart-failure therapy may improve recovery of LVEF in selected patients; because bromocriptine can increase thrombotic risk, most protocols pair it with concurrent anticoagulation. Use of bromocriptine is not yet standard of care within institutions and must be reserved on a case-by-case basis and within multidisciplinary discussion. Breastfeeding and continued use of Bromocriptine should be approached on a case-by-case basis[29,39].

Inotropes and vasopressors: Use the lowest effective dose for the shortest duration. All agents cross the placenta to some degree; maternal stabilization takes priority.

Levosimendan: ESC guidelines mention it as an option where available (non-catecholamine inodilator, calcium sensitizer)-may be advantageous in PPCM with high catecholamine load, though safety data in pregnancy remain limited[40] (Table 6).

Table 6 Suggested intensive care unit pharmacotherapy order set.

Suggested ICU pharmacotherapy order set
Furosemide IV as above
Metoprolol succinate 125-25 mg daily once off inotropes for 24 hours
Lisinopril 25-5 mg daily postpartum if SBP > 90 mmHg
Bromocriptine with concurrent anticoagulation (UFH or LMWH)
Levosimendan 6-12 μg/kg over 10 minute (loading) 0.05-0.2 μg/kg/minute for 24 hours (maintenance). Limited data available in pregnancy. Not advisable during lactation
Escalation checklist
Hypotension after beta-blocker → Hold and reassess
Worsening renal function after ACEi → Stop and monitor

ACEi: Angiotensin converting enzyme inhibitor; UFH: Unfractionated heparin; LMWH: Low molecular weight heparin.

Obstetric considerations

As the pregnancy nears term, patients with PPCM require careful obstetric planning. This includes weighing maternal cardiac stability against fetal development and well-being. A team-based approach involving an obstetrician, maternal-fetal medicine, cardiology, critical-care, anesthesia, and neonatology has been shown to improve outcomes in the intrapartum period and prevent post-partum complications[15].

Timing of delivery

In women with compensated heart function, delivery is aimed at term (39-40 weeks) with the aim to ensure adequate fetal lung maturity and development. Refractory heart failure, increased mechanical, ionotropic support, and fetal distress are indications for urgent delivery. Thus, in worsening of disease status, maternal safety is prioritized over gestational age[41].

Mode of delivery

Individualized decisions on the method of delivery depend upon the hemodynamic state, with vaginal delivery and titrated epidural anesthesia being the preferred mode in a stable mother. It mitigates abrupt fluid shifts, and there is generally a lower risk of blood loss[42]. In women with significant heart failure (NYHA Class III-IV), shortening the second stage of labor with assistance from vacuum or forceps alleviates the stress of maternal Valsalva. The Cesarean mode is an option in such instances of heart failure where rapid hemodynamic control becomes necessary. It is also performed in stable mothers with standard obstetric indications like fetal distress, malpresentations, etc.[43]. Several studies, however, have shown that there is increased morbidity associated with sections due to a change in volume status and the use of central neuraxial anesthesia[44]. There must be continuous fetal and maternal monitoring with vigilance in volume status and necessary pain control, irrespective of the delivery mode.

Lactation

Breastfeeding post-delivery should be approached on a case-by-case basis, considering the caveat of heightened metabolic demand in heart failure in lactation, against the benefits that breast milk confers on the newborn. Lactating mothers have elevated Prolactin levels and increased cytotoxic T-cell activity, but studies have shown that in stable PPCM, breastfeeding is not inferior to non-breastfeeding mothers[45]. Bromocriptine, a D-2 agonist drug, has been shown to play a dual role in treatment by rapidly suppressing lactation and improving LVEF. In the ICU, doses begin at 2.5 mg twice a day, which can be titrated to 10-20 mg based on serum prolactin levels, with prophylactic anticoagulation. Therapy is continued on low-dose maintenance after the acute phase to prevent rebound lactation[35].

The 2025 ESC Guidelines for the Management of Cardiovascular Disease in Pregnancy highlight the importance of recognizing it as a life-threatening condition with significant implications for maternal morbidity and mortality[40]. Key recommendations include:

Counselling on recurrence risk and contraception: Every woman with PPCM should receive structured counselling about the risk of recurrence in future pregnancies, even if LV function normalizes. Guideline emphasize shared decision-making, involvement of multidisciplinary teams, and the importance of reliable contraception. Long-acting reversible contraceptives are often preferred in women with residual LV dysfunction due to its efficacy and reliability. Estrogen-containing methods should be avoided if LV dysfunction persists, as they may pose additional cardiovascular risks.

Bromocriptine as a disease-modifying therapy: Based on the prolactin-cleavage hypothesis, bromocriptine may be considered after delivery to improve LV recovery. However, prothrombotic risk is significant; thus, it should always be co-administered with at least prophylactic LMWH[46].

Continuation of guideline-directed medical therapy: Even in women who demonstrate apparent full recovery of LVEF, heart failure therapies (ACEi/ARB/ARNI, beta-blocker, MRA, and SGLT2i if tolerated) should be continued for at least 12 months. The rationale is the high rate of late relapses and the possibility of subclinical myocardial vulnerability. Tapering may be cautiously considered thereafter under close follow-up with cardiac imaging and biomarkers.

For women with PPCM and an LVEF < 35: Wearable Cardioverter-Defibrillator (WCD) can be considered in the vulnerable first 6 months within the postpartum period when arrhythmic risk is highest[47]. A WCD may be considered as a bridge while awaiting potential recovery. The guidelines stress that routine early ICD implantation should be avoided given the high chance of recovery in PPCM compared with other non-ischemic cardiomyopathies[48-50].

Recovery and follow-up

Some predictors of poor recovery include patients with cardiogenic shock with low EF (< 30%-35%) and LV dilation. Reduced right ventricular fractional area change (RVFAC < 31.4%), a sign of right ventricular dysfunction, and low left atrial volume are strong and independent predictors of mortality and morbidity[51,52]. The Presence of Preeclampsia is interestingly associated with improved LV recovery.

It is important to establish a close follow-up plan post-discharge. This includes serial echocardiograms and natriuretic peptides to track cardiac function during the first 6 months. Surveillance for arrhythmias with electrocardiogram and ambulatory rhythm monitoring is a regular practice[53]. Advanced cardiac imaging, such as magnetic resonance imaging, can be considered at 6 months to monitor signs of recovery or disease progression.

Medical treatment for heart failure should be continued and titrated step-wise for 12-24 months based on functional status, with reinforcement of adherence[54]. Studies determine that an LVEF of > 50%-55% is the cut-off to indicate recovered LV function[48]. Even when the LVEF has normalized, imaging often reveals residual cardiac abnormalities and reduced exercise capacity[50]. Preconception counseling should therefore include discussion of the potential pregnancy risks that remain despite apparent recovery, with strong recommendations to avoid subsequent pregnancies if there is evidence of prior adverse outcomes. A multidisciplinary team and shared decision-making process provide a collaborative framework to guide safe planning for any future pregnancy.

CONCLUSION

PPCM is a diagnosis of exclusion. It is marked by LV systolic dysfunction developing near term or postpartum. PPCM has a variable course that can deteriorate rapidly and carries an early mortality risk. Early escalation of diagnostics using echocardiography, biomarkers, and targeted imaging can help rule out more common causes of cardiac decompensation. Patients can deteriorate unexpectedly and require ICU-level care. Diligent optimization of hemodynamic, respiratory, and thromboembolic components is central to stabilizing patients and preventing organ injury. Bromocriptine represents a promising disease-targeted adjunct. However, it requires anticoagulation and multidisciplinary governance due to thrombotic risk and lactation effects. Obstetric planning prioritizes maternal stability, favors vaginal delivery only when feasible, and promotes vigilant peripartum monitoring to navigate fluid shifts. Recovery is heterogeneous but can be navigated with a structured followup plan. This includes serial echocardiography, rhythm surveillance, and sustained heartfailure therapy for at least 12-24 months. A coordinated, multidisciplinary approach across cardiology, critical care, and obstetrics is the key to improving maternal and neonatal outcomes.