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Peripartum Cardiomyopathy
Introduction
Peripartum cardiomyopathy (PPCM) is a rare cause of cardiomyopathy that occurs during late pregnancy or the early postpartum period. This condition can be life-threatening and is characterized by significant left ventricular dysfunction and heart failure.[1][2][3] However, PPCM has had various definitions. In 2000, The National Heart Lung and Blood Institute and The Office of Rare Diseases workshop established the following 4 criteria for PPCM, becoming the condition's first case definition:
- Cardiac failure in the last month of pregnancy or within 5 months of delivery
- Absence of a determinable etiology for the cardiac failure
- Absence of demonstrable structural cardiac disease before the last month of pregnancy
- Echocardiographic evidence of diminished left ventricular systolic function noted by one of the following:
- Left ventricular ejection fraction (LVEF) <45%
- Motion-mode fractional shortening <30%
- Left ventricular end-diastolic dimension exceeding 2.7 cm/m2
Then, the 2019 European Society of Cardiology Working Group used the following 3 key criteria:
- Development of heart failure toward the end of pregnancy or in the postpartum period
- Absence of another identifiable cause of heart failure
- Left ventricular systolic dysfunction with a left ventricle (LV) ejection fraction <45%; LV may or may not be dilated [4]
An expanded definition of PPCM has been proposed to include 2 additional categories: early PPCM, which is diagnosed from the first to the ninth month of pregnancy, and late PPCM, which is identified between 6 and 12 months after delivery. This broader framework acknowledges variations in the timing of disease onset and extends beyond the traditional postpartum focus.[5]
Patients with PPCM typically present with dyspnea, fatigue, cough, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, and hemoptysis, though clinicians may not promptly recognize the condition as these symptoms are nonspecific. The primary diagnostic studies used to assess whether peripartum patients meet the definition of PPCM are the electrocardiogram (ECG) and echocardiogram. Though peripartum cardiomyopathy is acutely treated similarly to other forms of systolic heart failure with pregnancy-safe therapies (eg, dietary sodium restriction, loop diuretics, beta-blockers, hydralazine or nitrates, and digoxin), the overall management of cardiomyopathy associated with pregnancy requires the collaboration of a multidisciplinary team to address the various aspects of patient care the condition affects including labor and delivery, lactation, contraception, and family planning.[6] Though many patients may recover depending on their left ventricular ejection fraction at the time of diagnosis, the condition is associated with many adverse outcomes, including brain injury, cardiopulmonary arrest, pulmonary edema, and death.[7] Therefore, prompt evaluation and treatment are essential to improving patient outcomes.
Etiology
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Etiology
The etiology behind PPCM is still unclear. Most experts believe the underlying mechanism is multifactorial, including autoimmune conditions, nutritional deficiencies, the hemodynamic stress of pregnancy, and a hormonally mediated vascular insult in patients with a genetic predisposition being potential contributors.[6]
Peripartum Cardiomyopathy Risk Factors
Other factors associated with a higher risk of PPCM include:
- Age older than 30 years
- African descent
- Pregnancy with multiple gestation
- Prior or concurrent preeclampsia, eclampsia, or postpartum hypertension
- Maternal cocaine abuse
- Oral tocolytic therapy with beta-adrenergic agonists (eg, terbutaline) >4 weeks
- Parity ≥4 [7]
Epidemiology
The incidence and prevalence of this condition vary widely, depending on race and geographic regions, and perhaps due to the misdiagnosis.[8] Despite this, the available information from multiple studies has shown that the incidence of PPCM varies geographically. In the United States, the incidence has been reported to be as low as 1 case per 4,000 live births compared to the higher incidence in Nigeria of 1 case in every 100 live births. Women older than 25 years, with a mean age of 30 years, were found to be more likely to develop PPCM. The incidence has also been reported to be 4 times higher in African American women than in Caucasian women; Hispanic women are the ethnicity with the lowest incidence.[9][10] PPCM is more prevalent in Asia and Africa.[11] Data shows that PPCM complicates 1 in 837 to 1 in 1,374 deliveries in South Asia.[12][13] This finding supports possible socioeconomic factors and suggests genetic contributions.
The incidence of PPCM has increased in the past few years, mainly due to the advent of new diagnostic techniques and greater awareness of the condition.[14] When considering the timing of diagnosing PPCM, around 19% of cases are identified in the final month of pregnancy, while the majority—approximately 75%—are detected within the first month postpartum. Notably, 45% of these postpartum diagnoses occur during the first week after delivery.
Pathophysiology
The pathophysiology of PPCM remains incompletely understood, though multiple interrelated mechanisms have been proposed. Pregnancy induces substantial hemodynamic changes, including increased blood volume, cardiac output, and myocardial mass. However, these changes alone do not fully account for PPCM, as heart failure typically manifests postpartum once hemodynamic stress subsides. While viral myocarditis has been considered a potential etiology—supported by findings of viral genomes, eg, echovirus, coxsackievirus, and parvovirus B19 in myocardial biopsies—evidence remains inconclusive, and myocarditis is rarely the primary cause.
Emerging research suggests vascular-hormonal mechanisms as a primary contributor. Hormonal imbalances during the peripartum period may predispose susceptible individuals to PPCM. Prolactin, a pituitary hormone, is implicated through its cleavage into a toxic 16-kDa fragment that damages cardiac vasculature, leading to systolic dysfunction. Additionally, elevated levels of vascular endothelial growth factor, soluble fms-like tyrosine kinase 1 (sFlt-1), and placental hormones—common in preeclampsia and multiple gestations—have been associated with cardiovascular damage and the pathogenesis of PPCM. Increased concentrations of progesterone, plasma brain natriuretic peptide, and activin A may further exacerbate myocardial vulnerability, whereas protective hormones (eg, relaxin-2) are often suppressed in affected individuals.[15]
Inherited predispositions have also been implicated in the etiology of PPCM, with approximately 15% to 20% of PPCM cases linked to mutations in genes associated with dilated cardiomyopathy, most notably TTN.[16] The TTN gene, located on chromosome 2 (2q31), encodes titin, the largest sarcomeric protein in the human body, essential for myocardial structural integrity and function. Evidence of a cluster of families with PPCM has been observed.[16] Truncating mutations in TTN, combined with environmental and hormonal stressors, are believed to contribute to PPCM pathogenesis. Consequently, genetic testing is increasingly recommended for patients diagnosed with PPCM.[7][6]
In addition to these primary mechanisms, several other hypotheses have been proposed as contributing factors to PPCM, including:
- Hemodynamic stress of pregnancy: Significant hemodynamic changes occur during pregnancy. There is an increase in preload secondary to the increase in red cell mass, blood volume, and cardiac output by 20% to 30% due to a 15% to 25% increase in heart rate and stroke volume. All these changes begin during the first and second trimesters when the patient with structural heart disease will develop symptoms. However, patients with PPCM typically have symptom onset during the peripartum. Therefore, hemodynamic stresses may not be the primary reason for PPCM.[17][10][18]
- Myocarditis: Due to viral genomes in the biopsy of patients with PPCM (eg, Echovirus, Coxsackie, and Parvovirus B19), myocarditis has been hypothesized as an underlying pathology. However, a discrepancy amongst other studies exists, so the specificity of these findings is poor, and further studies are necessary.[7][6][19]
- Late pregnancy hormonal effects: Studies have improved our understanding of the etiology of PPCM as the role of a toxic hormonal environment that generates in late pregnancy and the relationship with genetic factors that can contribute to the development of PPCM. Significant hormonal changes occur at the end of pregnancy. Prolactin levels increase during late pregnancy and in the puerperium stage. Studies investigating the effect of prolactin metabolism in the mouse model of PPCM demonstrated a knockout expression of STAT3, an enzyme found in the myocardium of patients with end-stage heart failure secondary to PPCM. STAT3 protects the heart from reactive oxygen species that, when increased, generate an angiostatic N-terminal 16 kDA prolactin fragment that promotes apoptosis in endothelial cells and cardiomyocytes, resulting in vascular and myocardial dysfunction.[7][6][20]
- Inflammation: A proinflammatory state might play a role in the development of PPCM. Increased levels of cytokines such as TNF-alpha and interleukin-6 have been found in patients with PPCM and heart failure.[7][6][21]
- Autoimmune processes: Concern for an autoimmune response as a possible cause of PPCM has been described, especially because high levels of antibodies against certain cardiac tissue could cause autoimmune myocarditis as the etiology behind PPCM. The evidence supporting this theory is based on the theory of immunosuppression during pregnancy, exposing the mother's body to antigens from the fetus that can cause the generation of an immune response after pregnancy when the immune system recovers.[7][6][22]
- Selenium deficiency: This nutritional deficiency has been associated with cardiomyopathy, particularly in malnourished populations such as regions in Nigeria.[23]
Histopathology
The diagnosis of PPCM is based on clinical presentation and echocardiographic findings. A myocardial biopsy is unnecessary. However, histopathology should demonstrate patchy fibrosis, myofiber hypertrophy, degeneration, and necrosis with inflammatory endomyocardial infiltrates when performed in rare cases. Viral genomes, eg, herpesvirus 6, parvovirus B19, and Epstein-Barr virus, are occasionally detected.[24]
Heart specimens found in the autopsy of women with a history of PPCM appear to be pale, heavier, and dilated. Mural thrombi have been discovered in the hearts with cardiac dysfunction. Inside the heart, the valves look normal, and the coronary vessels are often patent unless a known history of ischemia exists. Pericardial effusion is occasionally found. In the microscopic view of the heart, evidence of interstitial edema and cellular swelling, fibrosis, and hypertrophy is frequently seen in the myocardium, with areas of abundant collection of eosinophils. An increased number of glycogen and mitochondria is commonly found in myocardial cells evaluated with electron microscopy.[25]
History and Physical
Clinical Features
Pregnancy-associated cardiomyopathy typically presents after 36 weeks of gestation, and the majority of cases are seen in the first month after delivery. An earlier presentation can occur in patients with underlying cardiac comorbidities, including valvular or ischemic cardiomyopathy. Presentation of peripartum cardiomyopathy can vary depending on the degree of the disease at the moment of presentation. Symptoms related to heart failure and related to pregnancy are paroxysmal nocturnal dyspnea, pedal edema, orthopnea, and dyspnea on exertion. Other symptoms included a dry cough, palpitations, increased abdominal girth, lightheadedness, and chest pain, though clinicians may not promptly recognize the condition as these symptoms are nonspecific.[7][6]
Findings on physical exams frequently include jugular venous distentions, displaced apical impulse, third heart sound, and mitral regurgitation murmurs.[7][6] In severe cases, patients may present with acute respiratory failure or cardiogenic shock, requiring close monitoring in the intensive care unit.
Evaluation
Diagnosing PPCM requires a high index of suspicion based on the 3 clinical criteria because symptoms are similar to those related to physiopathologic changes secondary to pregnancy. PPCM is a diagnosis of exclusion, and detailed investigation is required to rule out other more common causes of cardiomyopathy.[1][26]
Laboratory Studies
Initial evaluation consists of routine blood work to evaluate for other causes of those symptoms, including anemia, electrolyte abnormalities, endocrine conditions (eg, thyroid disorders), and renal or liver dysfunction. Elevation of brain natriuretic peptide (BNP) is commonly found elevated in patients with heart failure and patients with PPCM.[6]
Imaging Studies
Chest radiography may be part of the initial evaluation, with findings consistent with cardiomegaly and pulmonary edema. These findings are nonspecific for PPCM but are generally suggestive of heart failure. The primary diagnostic studies utilized for PPCM are electrocardiograms and echocardiograms. Electrocardiographic findings can be nonspecific. Common findings are sinus tachycardia, supraventricular tachycardia, atrial fibrillation or flutter, and occasionally ventricular tachycardia. ST segment and T wave abnormalities have been reported but are also nonspecific. Despite these nonspecific findings, QRS prolongation >120 milliseconds is related to increased mortality in patients with PPCM.
Echocardiography is the main study utilized to evaluate the anatomy and functionality of the heart in patients with suspected PPCM. Evaluation of the left ventricular ejection fraction (LVEF) is critical to rule out PPCM, as part of the criteria requires an LVEF of <45%. PPCM may be diagnosed on echocardiography based on this LVEF, end-diastolic diameter >2.7 cm/m2, M-mode fractional shortening of <30%, or a combination of these features. Echocardiography also evaluates for other causes of heart failure (eg, valvular diseases or left ventricular hypertrophy). Typically, echocardiography is sufficient to differentiate PPCM from other causes of heart failure, demonstrating left ventricular dilatation of varying degrees, left ventricular systolic dysfunction, right ventricular and biatrial enlargement, mitral and tricuspid regurgitation, pulmonary hypertension, and intracardiac thrombus.[27] Dilation of the ventricles and atriums can be present, and LV thrombus or atrial thrombosis can also be found.[7][6]
Further cardiovascular testing can be done with cardiac magnetic resonance imaging (MRI); this modality helps diagnose other causes of the heart unrelated to PPCM and can determine the volume of the chambers and ventricular more precisely than echocardiography. A further role of cardiac MRI in PPCM is yet to be determined. Cardiac catheterization is a modality typically used only in selected patients. Left heart catheterization is indicated in patients with suspicion of ischemic cardiomyopathy. Right heart catheterization is less frequently used for the evaluation of PPCM. Echocardiographic parameters for chamber pressure can be used initially, and if further assessment is necessary or patient illness is severe and more accurate measurement is required, a right heart catheterization can help with these situations. Endomyocardial biopsy is not recommended and is mainly used to evaluate for infiltrative diseases (eg, giant cell myocarditis) that can cause a failing heart.[6]
Treatment / Management
Though peripartum cardiomyopathy is acutely treated similarly to other forms of systolic heart failure with pregnancy-safe therapies (eg, dietary sodium restriction, loop diuretics, beta-blockers, hydralazine or nitrates, and digoxin), the overall management of cardiomyopathy associated with pregnancy requires the collaboration of a multidisciplinary team to address the various aspects of patient care the condition affects including labor and delivery, lactation, and family planning.[7][6]
Pharmacological Management
Pharmacologic therapeutic considerations for this population may include arrhythmia management, anticoagulation therapy, mechanical support, and investigational therapies.[28][29][30] As part of the goal of treatment for patients with PPCM, optimizing the preload or volume status is done through appropriate diuresis and keeping a balance of intra- and extravascular volume. Fluid restriction is fundamental to achieving this goal. Prepartum PCCM has special considerations for treatment due to adverse effects of medication that might cross the placenta and affect the fetus. As an example, the use of diuretics during pregnancy should be done carefully and in very low doses, as they may impair the perfusion of the placenta and cause potential harm to the fetus. Both hydrochlorothiazide and furosemide are safe during pregnancy and lactation, with close monitoring for diuresis and at low doses. Insufficient data exist about potassium-sparing diuretics for PPCM during pregnancy.
Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) are contraindicated during pregnancy due to the well-known teratogenic effects if administrated during pregnancy. Both of these medications can be used after delivery, but breastfeeding is contraindicated. Beta-blockers can be used cautiously during pregnancy (beta-1 selective agents are preferred) and are contraindicated during breastfeeding because this is excreted in the breast milk. Carvedilol is a combined beta-blocker with an additional alpha-blockade effect that allows a decrease of the afterload and is effective in the treatment of PPCM. Hydralazine, a vasodilator, is safe during pregnancy. A nitroglycerin drip can be used to manage afterload in the acute setting. Nitroprusside is contraindicated during pregnancy for concern of cyanide's toxicity.[7][6]
In very ill patients with hemodynamic instability, inotropes might be necessary. Use of inotropes such as dobutamine, dopamine, and milrinone is restricted for this critical situation with close monitoring and with fast weaning off medication if possible. Digoxin is another drug that can be used to treat PPCM. It is safe during pregnancy and can be used when the ionotropic and chronotropic effects are necessary, especially in the setting of uncontrolled atrial fibrillation.
Novel heart failure medications, eg, sacubitril-valsartan and sodium-glucose cotransporter 2 (SGLT2) inhibitors, show promise in improving outcomes in other forms of heart failure. These medications may be used postpartum, although their safety during pregnancy and lactation remains uncertain. Cardiac resynchronization may be considered when medical therapy alone fails to improve ejection fraction or clinical outcomes.[31](B3)
Anticoagulation therapy in patients with PPCM is controversial. As a general recommendation, patients with PPCM without LV thrombus or atrial fibrillation should not be in anticoagulation. Anticoagulation is often necessary due to the heightened thrombotic risk in PPCM, particularly when the ejection fraction falls below 30% to 35% or atrial fibrillation is present. Patients with PPCM atrial fibrillation or LV thrombus should be anticoagulated according to the guidelines for anticoagulation and the trimester of pregnancy.[7][6]
Labor and Delivery Management
Because PPCM frequently presents in the last trimester, the timing and mode of delivery may be a significant management consideration. Interprofessional coordination of care is required, including cardiologists, obstetricians, maternal-fetal medicine specialists, anesthesiologists, pharmacists, and social workers. The primary goal of labor and delivery management is to mitigate maternal and fetal complications, with delivery as clinically indicated (eg, hemodynamic instability).[7][6]
Lactation Considerations
The risks to breastfeeding associated with medications used to treat PPCM are an essential consideration. Many medications are considered safe for lactation, and due to the benefits of breastfeeding, many authorities recommend breastfeeding to able women. Clinicians should ensure that any medications used in treatment are considered safe for lactation.[7][6]
Family Planning Considerations
Shared decision-making is required in patients who recover following a pregnancy complicated by PPCM. Clinicians should counsel women considering subsequent pregnancies on the increased risks (eg, miscarriage, persistent ventricular dysfunction, and maternal death). Closely monitored during pregnancy and for 6 months postpartum with serial echocardiograms is typically recommended in patients choosing to proceed with pregnancy. However, heart failure medications considered unsafe in pregnancy should be discontinued for 3 months before conception, and heart function reevaluated to confirm full recovery.[32]
To prevent pregnancy before reassessment has been performed and in those women not desiring additional pregnancies, clinicians should counsel patients on contraceptive options following delivery. In patients with severe LV dysfunction and an elevated thromboembolic risk, combination oral contraceptives should be avoided. Subcutaneous implants or intrauterine devices are recommended; however, injectable depot medroxyprogesterone acetate is not as effective and should be used as a second-line option. In patients who desire permanent contraception, tubal ligation and vasectomy may also be considered.[7][6]
Genetic counseling and testing are recommended even without a family history of cardiomyopathy. Variants in genes such as FLNC and DSP may increase the risk of ventricular arrhythmias in PPCM, and conditions like Danon disease or Duchenne muscular dystrophy can present as PPCM. Identifying genetic variants can guide family testing and reduce unnecessary monitoring during pregnancy for unaffected relatives.
Additional Therapies
Decisions regarding the use of an implantable cardioverter defibrillator (ICD) and cardiac resynchronization therapy in patients with PPCM should consider the natural history of these diseases, including the potential for the recovery of ventricular function. Mechanical circulatory support has been described in patients with fulminant PPCM. The placement of a left ventricular assistant device (LVAD) can be a bridge for transplant or recovery.
Experimental medications, eg, pentoxifylline, bromocriptine, IVIG, and immunosuppression, are still under investigation. Recent data suggest that increased oxidative stress during the peripartum period enhances the formation of abnormal 16-kDa prolactin, which induces toxic effects on cardiac myocytes. Bromocriptine, a dopamine receptor agonist with prolactin-blocking properties, reduces the impact of 16-kDa prolactin on cardiac myocytes and has been associated with better outcomes in small studies.[33](B3)
Differential Diagnosis
PPCM is a diagnosis of exclusion; therefore, consideration of other heart failure etiologies is necessary. Preexisting congenital cardiac conditions, valvular diseases, or cardiomyopathy can decompensate with the hemodynamic changes related to pregnancy, and further manifestation can be seen later in the pregnancy. Other conditions with overlapping manifestations include:
- Normal physiological effects of pregnancy
- Takotsubo cardiomyopathy
- Severe preeclampsia or eclampsia
- Pulmonary embolism
- Acute pulmonary edema from prolonged tocolysis or preeclampsia
- Cardiac dysfunction secondary to arrhythmia
- Amniotic fluid embolism syndrome [7]
Pertinent Studies and Ongoing Trials
Heart failure is a leading cause of maternal mortality and morbidity in the United States, with PPCM accounting for up to 70% of heart failure cases during pregnancy. The development of PPCM has been linked to cardiac angiogenic imbalance caused by cleaved 16kDa prolactin, leading to interest in prolactin inhibitors like bromocriptine for treatment. One systematic review and meta-analysis found that adding bromocriptine to standard guideline-directed medical therapy significantly improved LVEF and increased the likelihood of left ventricular recovery. However, no significant reduction was observed in all-cause mortality between the treatment groups.[34]
Prognosis
In women who recover, improved heart function typically occurs 3 to 6 months postpartum but has been described as occurring until 48 months after delivery. PPCM is a major contributor to maternal mortality in the United States and other parts of the world, accounting for approximately 60% of cardiogenic shock cases occurring during pregnancy or the early postpartum period. While over half of affected patients experience recovery of cardiac function, the condition still carries significant morbidity and mortality. Some patients may require advanced interventions, eg, LVAD placement or heart transplantation.
In the United States, Black women are twice as likely as White women to experience prolonged cardiac dysfunction; when recovery occurs, it takes twice as long. Mortality rates can reach 20%, with the highest rates observed among Black women in the United States and women in less developed regions. The condition can profoundly impact affected individuals, their families, and newborns during a critical life stage.
Favorable Prognostic Factors
Several factors are strong predictors of LV recovery and associated with a good prognosis, including:
- Small LV diastolic dimension (<5.5 cm)
- LVEF >30% to 35% and fractioning of shortening >20% at the time of diagnosis
- Absence of troponin elevation
- Absence of LV thrombus.
- Non-African American ethnicity
Poor Prognostic Factors
The following factors may be associated with a poor prognosis:
- LV diastolic dimension ≥ 6 cm
- LVEF <35%
- QRS >120 milliseconds
- Delayed diagnosis
- High NYHA class
- Multiparity
- African descent
Recurrence of PPCM in subsequent pregnancies is elevated, and the patient should be advised against further pregnancies and monitored closely.[35] Long-term outcomes are variable. About 50% of patients improve with standard medical treatment. However, 25% develop chronic heart failure, and the remainder die during the course of the disease.[36] Patients should be advised against future pregnancy if the ejection fraction remains low, as mortality is high in such cases. However, if pregnancy is desired, patients should wait at least 5 years after the ejection fraction has normalized.
Complications
The following complications have been associated with PPCM:
Consultations
Clinicians that may be consulted in the evaluation of peripartum cardiomyopathy include:
Deterrence and Patient Education
Deterrence and patient education play a crucial role in managing PPCM. Early recognition of symptoms, such as fatigue, shortness of breath, and edema, is vital for prompt diagnosis and treatment. Patients should be educated about the risks of PPCM, especially if they have a history of hypertension, preeclampsia, or multiple pregnancies, as these factors may increase the likelihood of developing the condition. Patients should be counseled on family planning and contraceptive options following delivery. Additionally, clinicians should advise women considering subsequent pregnancies on the increased risks (eg, miscarriage, persistent ventricular dysfunction, and maternal death). (Refer to "Family Planning Considerations" in the Treatment/Management section for more information.)
Counseling for women considering a subsequent pregnancy is challenging, as recurrence of PPCM occurs in 10% to 50% of cases, sometimes with worse outcomes. Although the lack of full recovery of systolic function before another pregnancy is linked to poorer outcomes, it is not a definitive predictor. Counseling should address these risks while considering the patient's strong desire to expand her family. Close monitoring by an interprofessional team during and after subsequent pregnancies is essential to improve outcomes.
Additionally, counseling on lifestyle modifications, including proper nutrition and weight management, is essential. Educating patients about the potential for recurrence in future pregnancies and the importance of early prenatal care and regular cardiac monitoring can help manage risks. Discussions about the safety of breastfeeding, potential treatment options like bromocriptine, and the importance of adherence to medications and follow-up visits are equally crucial for improving long-term outcomes. Educating patients can enhance adherence to care plans, minimize complications, and improve overall prognosis.
PPCM results in a significant financial strain on healthcare resources due to the increased disability-adjusted life years, especially in low- and middle-income countries. Resources may need to be directed to socially vulnerable communities to reduce disparities and mortality.
Pearls and Other Issues
PPCM is a condition that occurs in previously healthy women near the end of pregnancy or shortly after delivery and potentially leads to severe heart failure. Although recovery of heart function occurs in 45% to 50% of cases, the long-term mortality rate remains high at 20%. The incidence of PPCM is rising globally, and its exact cause remains unclear, involving factors like oxidative stress, inflammation, hormonal changes, and genetic mutations.
The 16-kDa prolactin, a product of oxidative stress, is recognized as the main trigger, damaging cardiomyocytes through microRNA-146a and the NF-κβ pathway. Bromocriptine, which inhibits prolactin, may help, though many cases do not respond, suggesting other underlying mechanisms. Current biomarkers, such as BNP, are not specific, and further research is needed to identify better diagnostic and prognostic molecular indicators.
Ongoing investigations into the disease’s pathophysiology, including microRNA and heat shock proteins, may improve diagnostics, treatment strategies, and outcomes.[37] An interprofessional approach is key, and patients should be closely monitored for complications such as arrhythmias and thromboembolism. While prevention remains elusive, early prenatal care and managing risk factors can help reduce the likelihood of PPCM. Women diagnosed with this condition should be counseled about the risks of recurrence in future pregnancies.
Enhancing Healthcare Team Outcomes
An interprofessional approach to PPCM is essential to enhancing patient-centered care, improving outcomes, and ensuring patient safety. Physicians, advanced practitioners, nurses, pharmacists, and other healthcare professionals must collaborate to facilitate early diagnosis and effective management. Obstetricians, prenatal nurses, and nurse practitioners must be vigilant in recognizing PPCM symptoms, as timely referral to cardiologists significantly impacts patient survival. ICU specialists and radiology teams play a crucial role in monitoring and diagnostic evaluations for severe cases. Additionally, pharmacists provide critical guidance on the safe use of cardiac medications, considering potential fetal toxicity and maternal health implications.
Care coordination between healthcare professionals strengthens team performance and optimizes patient care. Nurses are integral to ongoing patient education, reinforcing adherence to medical management and lifestyle modifications, while cardiologists tailor treatment plans to minimize complications. Open communication across disciplines ensures that delivery timing and postpartum monitoring are individualized to the patient’s needs. An interprofessional strategy allows for comprehensive care, reducing PPCM-related morbidity and mortality through a well-coordinated, patient-focused approach.
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