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  Table of Contents 
Year : 2020  |  Volume : 21  |  Issue : 1  |  Page : 4-9

Peripartum cardiomyopathy – An insight

Department of Anaesthesia, ABVIMS and Dr. RML Hospital, Delhi, India

Date of Submission09-Sep-2019
Date of Decision18-Dec-2019
Date of Acceptance23-Dec-2019
Date of Web Publication13-Feb-2020

Correspondence Address:
Dr. Aanchal Kakkar
Department of Anaesthesia, ABVIMS and Dr. RML Hospital, Delhi
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/TheIAForum.TheIAForum_65_19

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Peripartum cardiomyopathy (PPCM) is a potentially life-threatening disease. However, timely intervention and early detection can save lives. It presents in peripartum period as left ventricular dysfunction and heart failure. Although the disease is relatively rare, its incidence is rising. Previous research states vascular dysfunction, triggered by late-gestational maternal hormones such as abnormal prolactin and many other causes may lead to the development of PPCM. We have reviewed here the known epidemiology, pathophysiology, clinical presentation, management, and anesthesia concerns of PPCM.

Keywords: B-type natriuretic peptide, cardiac failure, chimerism, dobutamine, peripartum cardiomyopathy

How to cite this article:
Saraswat N, Virmani P, Kakkar A, Gupta A, Kaur M. Peripartum cardiomyopathy – An insight. Indian Anaesth Forum 2020;21:4-9

How to cite this URL:
Saraswat N, Virmani P, Kakkar A, Gupta A, Kaur M. Peripartum cardiomyopathy – An insight. Indian Anaesth Forum [serial online] 2020 [cited 2021 Jun 20];21:4-9. Available from: http://www.theiaforum.org/text.asp?2020/21/1/4/278187

  Introduction Top

Although peripartum cardiomyopathy (PPCM) was recognized as early in 1800 by Virchow and others.[1],[2] However. In 1937, the first large case series was published in New Orleans when Gouley et al. noticed that seven pregnant females during later months of pregnancy developed features of severe heart failure (HF) along with dilated cardiomyopathy, which persisted after delivery.[3] The syndrome remained poorly defined until 1971 when Demakis and Rahimatoola published data on 27 patients and first introduced the term “peripartum cardiomyopathy (PPCM).” They also established standard clinical criteria for the diagnosis of PPCM.[4],[5] In 1995, Lampert and Lang added the fourth criteria for the definition of PPCM, which includes echocardiographic demonstration of impairment in the left ventricular (LV) systolic function.[6] Following which in 1999 by a national heart, lung, and blood institute workshop on PPCM,[7] the criterion of ejection fraction (EF) <45% was introduced. Then, the European Society of Cardiology (ESC) provided an updated operational definition of PPCM.[8]

A search of literature published in English on PPCM was conducted. PPCM was put as a keyword search in PubMed and around 360 articles reflected of which relevant articles were evaluated, other materials scrutinized were selected references, relevant books and internet articles using Medline and Google scholar were critically reviewed.

  Definition Top

The workshop held by the National Heart Lung and Blood Institute and the Office of Rare Diseases states that it must develop during the past month of pregnancy or within 5 months of delivery.

In 2010, the working group on PPCM of the ESC defined PPCM is an idiopathic cardiomyopathy presenting with HF secondary to LV systolic dysfunction toward the end of pregnancy or in the months following delivery, where no other cause of HF is found. It is a diagnosis of exclusion. The LV may not be dilated, but the EF is nearly always reduced below 45%.[8]

The echocardiographic criteria proposed for peripartum cardiomyopathy are as follows[9]

  1. EF <45% or fractional shortening <30%
  2. End-diastolic dimension >2.7 cm/m2.

  Epidemiology Top

The precise incidence in India is not known, an incidence of one case per 1374 live births has been reported from a tertiary care hospital from South India.[10] The incidence of PPCM in the United States ranges from ≈1 in 1000 to 4000 live births.[11] A study of national hospital discharges from 1990 to 2002 showed increasing incidence from 2.3 to 4.5 per 10,000 live birth.[12] A recent national inpatient database analysis of 64 million discharge hospital records from 1000 hospitals in the United States identified 34,219 cases of PPCM, with an incidence of 1 in 968 births.[13] The incidence increased from 8.5 to 11.8 per 10,000 live births in 8 years between 2004 and 2011.

The increase in awareness, diagnostic ability, rising maternal age, and multiple pregnancies could have contributed to increase in the incidence of PPCM. In a population study conducted during 2002 and 2006 in California about maternal cardiovascular deaths, PPCM was the leading cause (23%).[14] However, the higher incidence was reported in developing countries, perhaps due to environmental, cultural puerperal and post puerperal practices. The incidence reported was 1 in 300 live births from Haiti,[15] and of 1 in 100 from Nigeria.[16]

  Associated Risk Factors Top

Nutritional deficiency (low selenium and zinc levels), advanced maternal age, multiple gestations, twin pregnancy, Afro-American race, preeclampsia and gestational hypertension, diabetes, obesity. Use of tocolytics, high sodium salt, and smoking, cocaine, alcohol abuse during pregnancy[17] are associated risk factors for PPCM.

  Etiopathogenesis Top

The etiology of PPCM is still unknown. The proposed pathogenesis factors are oxidative stress leading abnormal prolactin metabolism, abnormal immune response to pregnancy, abnormal response to increased hemodynamic burden of pregnancy, hormonal abnormalities, malnutrition, inflammation and apoptosis, viral myocarditis.

  Abnormal Prolactin Metabolism Top

It plays a fundamental role in the pathogenesis of PPCM as shown by experimental evidence. The proposed mechanism is unbalanced oxidative stress leads to the cleavage of full length 23 kDa prolactin to an angiostatic and proapoptotic 16 kDa form. The cleaved proapoptotic 16 kDa form destroys the cardiac microvasculature, reducesin vivo cardiac function and promotes ventricular dilatation. It also inhibits vascular endothelial growth factor (VEGF)-induced proliferation and migration of endothelial cells, induces apoptosis, dissociation of capillary structures, impairs NO-mediated vasodilatation, and cardiomyocyte function.[18] Most recently, experimental work has demonstrated the development of PPCM in female mice with a cardiomyocyte-specific deletion of the STAT3 protein. This increases oxidative stress and results in increased expression and proteolytic activity of cardiac cathepsin D. The resulting cleavage of prolactin into the 16-kDa form leads to detrimental effect on the myocardial microvasculature resulting in myocardial hypoxemia and apoptosis, and the development of PPCM. A blockade of prolactin with bromocriptine has been shown to prevent PPCM in experimental models.[18]

  Angiogenic Imbalance Top

Studies[19],[20] suggest mice that lack cardiac Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1alpha, a regulator of proangiogenic factors such as VEGF, develop severe PPCM. During late gestation, the human placenta secretes VEGF inhibitors such as soluble fms-like tyrosine kinase (sFLt1), which also damage the vasculature, with higher levels seen with multiple gestation or preeclampsia.[20] Among women with preeclampsia, subclinical cardiac dysfunction (as detected by the myocardial performance index) correlates with sFlt1 levels.[19] Exogenous sFlt1 alone caused diastolic dysfunction in wild type mice, and profound systolic dysfunction in mice lacking cardiac PGC-1α. Finally, plasma samples from women with PPCM contained abnormally high levels of sFlt1. These data strongly suggest that PPCM is in large part a vascular disease caused by excess anti-angiogenic signaling in the peripartum period.[19]

  Viral Myocarditis Top

Several investigators have suggested viral infection as a cause of myocarditis in PPCM.[21],[22] Bültmann et al. found parvovirus B19, human herpesvirus, Epstein–Barr virus, and cytomegalovirus DNA in endomyocardial biopsy specimens from 8 (31%) of 26 patients with PPCM.[21] Tsintsof et al. reported a case of a 12-year-old schoolgirl with HF due to varicella myocarditis and cardiac transplantation was performed 2 weeks later. Endomyocardial biopsy changes consistent with myocarditis were documented 6 days after the start of HF.[23]

  Inflammatory Cytokines Top

The cytokines that are elevated in PPCM compared to controls include tumor necrosis factor (TNF)-alpha and interleukin-6.[24],[25] In addition, Fas/Apo1, an apoptosis signaling receptor, and C-reactive protein are associated with more severe disease.[25]

  Chimerism Top

There is a mixture of genotype, sometimes provoking an immune response. An abnormal immune response may be produced after previous exposure immunization from prior pregnancy, or previous exposure to paternal major histocompatibility antigens the serum from patients with PPCM has been found to contain autoantibodies in high titers, which are not present in serum from patients with idiopathic cardiomyopathy. Most of these antibodies are against normal human cardiac tissue proteins of 37, 33, and 25 kD.[17] Autoantibodies are associated with increased levels of cytokines (TNF-alpha, interleukin-6, and soluble Fas receptors), and are correlated with dilatation of LV and systolic dysfunction.[24],[25]

  Clinical Features Top

Symptoms are the same as those with nonpregnamt systolic dysfunction. During later pregnancy or in the postpartum period, any new or rapid onset of the symptoms requires prompt evaluation: Fatigue, palpitations, orthopnea, paroxysmal nocturnal dyspnea, nocturia, dyspnea, pedal edema, and postural hypotension. However, these symptoms can be difficult to differentiate from common complaints in late pregnancy and postpartum period, making the diagnosis challenging.

Physical examination often reveals tachycardia, blood pressure may be normal or reduced, elevated jugular venous pressure, pulmonary crepitations. Arrhythmias are commonly found, which may be responsible for embolic phenomenon peripheral or pulmonary. In some patients, small-to-moderate pericardial effusion may be found. Overall clinical presentation and hemodynamic changes are indistinguishable from those found in other forms of dilated cardiomyopathy.[26]

  Diagnosis Top

It is a diagnosis of exclusion which can be further supported by investigations.

X-ray chest may reveal cardiomegaly and pulmonary venous congestion.

Electrocardiogram - Sinus tachycardia, nonspecific ST-T changes, conduction abnormalities, arrhythmias commonly atrial fibrillation.

Echocardiography - It remains a mainstay in the diagnosis of PPCM. The echocardiogram generally reveals a global reduction in LV systolic function with LVEF nearly always <45%. The left ventricle is frequently but not always dilated.[8] Other possible echocardiographic findings include enlargement of left atrium, left ventricle or left atrial thrombus, dilated right ventricle, right ventricular hypokinesis, mitral and tricuspid regurgitation, and rarely small pericardial effusion.[27] It is recommended to evaluate candidates of PPCM under treatment in 6 weeks, 6 months, and annually.[8]

  Biomarkers Top

Till date no specific diagnostic biomarkers are available for PPCM. Biomarkers such as brain natriuretic peptide and troponin are not or mildly elevated during the peripartum period; however, they are typically elevated in PPCM.

Supported by a study done in 38 patients with PPCM, it was found that NT-proBNP levels were approximately five times higher in patients with PPCM than control group.[28]

A study conducted by Kamiya et al. on 102 patients with PPCM. He found that only four patients had a B-type natriuretic peptide (BNP) under 100 pg/mL, and a mean serum BNP of 1258 pg/mL.[29] Thus although a mild elevation of BNP can be expected with normal pregnancy, higher elevations of BNP have been reported with PPCM.

Recent work has suggested that microRNAs, specifically miR146a, may serve as a novel biomarker for PPCM.[30]

  Management Top

The aim of treatment is to decrease preload, afterload and to improve cardiac contractility. This will optimize cardiac output and improve oxygenation, ultimately improving both fetal and maternal outcome. Treatment is similar to that of systolic HF resulting from other etiologies. First and foremost aim is to maintain ABC, i.e., airway, breathing, and circulation.

PPCM should be treated in accordance with the current ESC guidelines for HF.[31] Intravenous loop diuretics, mostly furosemide, thiazide diuretics may cause neonatal hyponatremia and bleeding diathesis. Vasodilators such as nitrates and hydralazine are used for preload and afterload reduction. Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are used in postpartum period however contraindicated during pregnancy because of serious renal and other fetal toxicity.[32] Beta-Blockers are avoided in acute decompensated HF but have an established role in chronic decompensation. These have not been shown to have teratogenic effects.[33] Beta-1 selective drugs are preferred because Beta-2 receptor blockade can, theoretically, have an anti-tocolytic action. Metoprolol is the agent of choice. Pregnancy and puerperium are hypercoagulable states thus antithrombotic therapy is warranted in all patients with LVEF - 35%, mural thrombi, and atrial fibrillation. Fetotoxicity of warfarin needs to be considered. Unfractionated or low-molecular-weight heparin can be used. Inotropic support, preferably dobutamine is provided in cardiogenic shock. In case of pulmonary edema morphine is advocated along with diuretics and vasodilators. Mechanical ventilation has to be initiated when required. Vasopressors may be considered in critically ill patients after weighing benefit against the risks of increased systemic vascular resistance which can further impair cardiac output and uteroplacental blood flow.[34]

Role of bromocriptine and cabergoline

Most recently few studies have suggested the role of prolactin breakdown products in the etiology of PPCM. Prolactin secretion can be reduced with bromocriptine and cabergoline which had beneficial effects in a small study.[18],[35]

Immune modulating therapy

With proposed inflammatory nature of PPCM, the use of immunosuppressive and immune-modulatory has been utilized. Intravenous immunoglobulin,[36] plasmapheresis, immunoadsorption improved the EF in several studies and also markedly reduced the levels of inflammatory cytokines.

Other interventions and devices

Likewise other dilated cardiomyopathies, PPCM is also prone for ventricular arrhythmias. No antiarrhythmic agent is completely safe during pregnancy quinidine and procainamide should be tried first because of their higher safety profile.[37] Beta-blockers may be useful, for atrial arrhythmias digoxin may be considered.[38] Consideration of an implantable cardioverter-defibrillator is warranted if ventricular tachycardia with hemodynamic compromise occurs because of the potential for a fatal recurrence.

Due to its highly recoverable nature, the temporary use of an intra-aortic balloon pump or LV assist devices may help in stabilizing critical patients.[8] Extracorporeal membrane oxygenation has been tried successfully in some patients as a bridge to recovery.[39] The final resort is cardiac transplantation. There are prognostic indicators of recovery from acute stage, baseline EF, patients with worse baseline EF, presence of LV dilatation (defined as LV end-diastolic diameter 6 cm or greater), and LV thrombus[40] have been associated with worse outcomes.

Markers of inflammation (Fas/apo-1),[25] elevated troponin, and NT-proBNP[28] levels are associated with poor outcomes.

  Lactation Top

Delivery and anesthesia

PPCM requires a multidisciplinary approach requiring combine effort of obstetrician, cardiologists, anesthesiologists, intensivists, and neonatologist. Team discussion is necessary regarding time and mode of delivery for better fetal and maternal outcome. Early delivery is not required if the maternal and fetal conditions are stable. The vaginal delivery needs to be done with continuous hemodynamic monitoring and even invasive monitoring has been advocated according to the patient's profile.[8] Pain and anxiety associated with labor increases sympathetic activity that can be detrimental to already diseased heart. It will also decrease uteroplacental outflow, thus jeopardizing an already compromised fetus.[41] Effective labor analgesia decreases sympathetic outflow and decreases plasma catecholamine levels in the mother and causes a decrease in cardiac preload and afterload which is beneficial in patients with PPCM.[38] Continuous spinal-epidural analgesia is recommended for labor analgesia which can be continued for cesarean section if required, as the hemodynamic stability may be more easily maintained.[42],[43],[44]

GA is advised for patient on anticoagulants or with cardiac decompensation and also preferred with borderline cardiac decompensation as an already dyspneic patient may not be amenable to the procedure of RA. In such a patient, even minor degrees of sympathetic blockade associated with RA may lead to fulminant cardiac failure.[41] Strict hemodynamic control, intraoperative fluid management, and meticulous cardiovascular monitoring is the necessity for better maternal and fetal outcome.

  Conclusion Top

PPCM is an uncommon but potential life-threatening cardiac failure of unknown etiology, possess devastating consequences; hence, it should be suspected, promptly identified and treated. Prognosis is linked to the recovery of LV functions. Patients with normal cardiac function on echo evaluation subsequent pregnancy may be considered under close multidisciplinary supervision and whose LV function does not improve even six months after puerperium subsequent pregnancies are associated with a very high mortality.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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