Peripartum cardiomyopathy

Solomon Sulei Danbauchi; Albert I Oyati; Mohammad S Isa; Mohammed A Alhassan

doi:10.4103/0189-7969.142084

Users Online: 801

REVIEW ARTICLE

Year : 2014 | Volume : 11 | Issue : 2 | Page : 66-73

Peripartum cardiomyopathy

Solomon Sulei Danbauchi, Albert I Oyati, Mohammad S Isa, Mohammed A Alhassan
Department of Medicine, Ahmadu Bello University Teaching Hospital, Zaria, Nigeria

Date of Web Publication

3-Oct-2014

Correspondence Address:
Solomon Sulei Danbauchi
Department of Medicine, Ahmadu Bello University Teaching Hospital, Zaria
Nigeria

Source of Support: None, Conflict of Interest: None

Check

DOI: 10.4103/0189-7969.142084

Abstract

Peripartum cardiomyopathy is cardiovascular disorder that is seen only in females in third trimester to 6 months post delivery. It is a diagnosis of exclusion. The syndrome is still seen in Nigeria more especially Northern Nigeria where the largest cohort of patients were described in the early 70s. The longest follow up (30-35) years of the syndrome was also done in Zaria, Northern Nigeria. The etiology of the syndrome is unknown but from different parts of the world clinicians have associated the syndrome to different risk factors. The authors did a Medline, AJOL and other search to review write ups on this syndrome. Of the 27 publications on the syndrome from Nigeria, 90% came from the Northern Nigeria. In Nigeria the syndrome was associated with the famous Wakan Jeko which composes of a triad of hot baths, ingestion of pap (kunun kanwa) which is made with lake salt that has high levels of sodium (Na ⁺ ). Other authors have associated it with hypertension, myocarditis, use of tocolytics and deficiency of trace elements like selenium. Recently the South Africans have also proposed the possibility by products of stress on Prolactin leading to cardiac damage/Peripartum cardiomyopathy has maternal and child health implications in Nigeria, sometimes it does lead to maternal mortality so also infant mortality. Patients have been reported to have developed recurrent Peripartum cardiac failure if they did not take heed to the advice regarding avoiding the wakan jeko. Some of these patients have gone on to develop hypertension and presented with hypertensive cardiac failure or cerebrovascular accident. Peripartum cardiomyopathy etiology is still an enigma. A coordinated national and international effort is required to do a comprehensive research on this syndrome to put to rest or uphold some of the theories regarding etiology.

Keywords: Cardiomyopathy, peripartum, review

How to cite this article:
Danbauchi SS, Oyati AI, Isa MS, Alhassan MA. Peripartum cardiomyopathy. Nig J Cardiol 2014;11:66-73

How to cite this URL:
Danbauchi SS, Oyati AI, Isa MS, Alhassan MA. Peripartum cardiomyopathy. Nig J Cardiol [serial online] 2014 [cited 2023 May 30];11:66-73. Available from: https://www.nigjcardiol.org/text.asp?2014/11/2/66/142084

Introduction

Cardiovascular disorders are the leading causes of morbidity and mortality worldwide. It is estimated that in 2020 that the burden of cardiovascular disease in sub-Saharan Africa will double and a large proportion will be middle age. ^[1],[2] One of the cardiovascular disorders that we manage in sub-Saharan Africa is peripartum cardiac failure (PPCF), which is otherwise referred to as peripartum cardiomyopathy (PPCM) after the patient has presented with cardiac failure around partum. Based on a recent report from the National Heart, Lung, and Blood Institute, PPCM is defined by the presence of four criteria. ^[3] These include: (i) Development of cardiac failure in the last month of pregnancy or within 5 months of delivery; (ii) absence of an identifiable cause for cardiac failure; (iii) absence of recognizable heart disease prior to the last month of pregnancy; and (iv) left ventricular (LV) systolic dysfunction demonstrated by echocardiographic criteria such as depressed ejection fraction. ^[3] Peripartum failure is a relatively rare, but the life-threatening disease. It was first recognized by World Health Organization as reported by the technical committee to classify cardiomyopathy in 1980/81. ^[4] The initial definition was cardiac failure in the last trimester of pregnancy and 5 months postdelivery with known causes excluded. With the advent of more knowledge in echocardiography, the definition was modified as below. ^[5]

Criteria for the diagnosis of PPCM, which leads PPCF:

Development of cardiac failure in the last month of pregnancy or within 5-6 months of delivery
Absence of an identifiable cause for the cardiac failure
Absence of a recognizable heart disease prior to the last month of pregnancy
LV systolic dysfunction demonstrated by classic echocardiographic criteria that is, LV ejection fraction <45%, or reduction in fractional shortening (SF) <30%. In addition, LV dilatation with LV end-systolic dimension >2.7 cm/m ² .

Epidemiology

The incidence of PPCF varies widely with rates ranging from 1/1300 ^[6] to 1/15,000 live births ^[7] has been reported although the currently accepted incidence is approximately 1/3000-1/4000 live births. ^[8] Zaria in Northern Nigeria is known to have reported the highest incidence in the world of 1%. ^[4] Recently, the South Africans have also made some further strides in trying to defining the etiology of PPCF.

Possible etiologies

Many authors from different countries and even within the same country have alluded to different probable etiologies as being behind the syndrome of PPCF. Identified risk factors for peripartum failure include advanced maternal age, multiparty, obesity, multiple gestation, preeclampsia, chronic hypertension, and black race. ^[8],[9] These are findings from different reports or publications, but recent reports have shown younger age rather than older women and also primigravida being affected. ^[10]

What stood out mainly is either the association of high blood pressure or dilated heart. This had made experts to think or propose that hypertension might be an etiology or that this group of individual might be prehypertensive and have problems handling salt load from kunun kanwa. ^{[11],[12],[13]}

Wakan Jeko

As part of the earlier reports from Zaria, below is a sample of lake salt or potash that is usually consumed by a lady that has delivered and undergoing traditional practice of "Wakan Jeko." "Wakan Jeko" is composed of hot baths, ingestion of pap made with kanwa (lake salt) and hot bed, which can go on for up to 3 months, which with modernization has been reduced to 2-4 weeks. ^[11]

Prolactin

The other twist to the etiology of PPCF is the report from South Africa ^[14] that have observed increase in prolactin products (fragments) in the serum of patients that present with PPCF. It is proposed that these fragments lead to damage of the myocardium. These findings have not been replicated by other researchers in other countries. Currently, recent evidence in an animal (mice) model suggests a role for a 16 kDa prolactin derivative produced by proteolytic breaking of prolactin, which is a sequel to unbalanced oxidative stress present during late pregnancy and early puerperium. ^[15] This derivative has been found to have cardiotoxic, antiangiogenic, proapoptotic and proinflammatory properties, which can potentially damage or impair metabolism and contractility of cardiomyocytes. ^{[16],[17],[18]} This theory is supported by some few clinical reports of postpartum women with PPCF responding (recovery from PPCF) when treated with medicines causing a reduction of prolactin secretion from posterior pituitary gland or working as a D2 receptor antagonist such as bromocriptine and carbergoline. ^{[19],[20],[21]} As plausible this theory is, will the oxidative stress leading to these products, which affects the myocardium also explain the high proportion of raise blood pressure, which normalizes with treatment of the syndrome that has been seen with the syndrome in Zaria and other parts of Nigeria. Why is the syndrome rare in the Western world compared to Africans, because in the US, the syndrome is more common in the African American than its Caucasian counterpart? Is it that the Caucasian heart is resistant to damage byproducts of oxidative stress or the African heart is more susceptible to these products of prolactin?

Work like this should be replicated in other parts of the world where the syndrome has been described in large numbers so that it will be established whether it is a peculiar phenomenon like that of the famous "Wakan Jeko" and the syndrome in Zaria as reported or it is universal.

Myocarditis

Extensive research into the underlying etiology have been put in, but it is still not clear exactly how it occurs, this still makes PPCF to be regarded as a disease of unknown etiology. ^[10] However, many studies have suggested the idea of an inflammatory pathology leading to myocarditis, ^[22],[23] due to either a viral infection ^[24],[25] or an autoimmune response in pregnancy against maternal myocardium provoked by the release of fetal antigen into maternal blood or by some, as yet, unknown agents. ^{[23],[26],[27]} Again, it has to be asked whether the theory of myocarditis will also explain the blood pressure changes in this syndrome. None of these proposed mechanisms are strongly supported by clinical evidence, as there has been great variability in the results of endomyocardial biopsies and in the finding of autoantibodies against myocardium. Endomyocardial biopsies of the reported cases have shown features of myocarditis ranging between 9% and 78%. ^{[23],[25],[26],[27],[28]} However, there may be a role for proinflammatory cytokines such as tumor necrosis factor ^[29] and interleukins (IL-1, IL-6) in the etiology as well. ^[26],[30]

Trace elements and micronutrients

Other theories include impaired cardiac microcirculation, programmed cell death (apoptosis), ^[31] micronutrients deficiency such as selenium, possible genetic links, and other environmental factors. ^{[30],[31],[32]} The factor of deficiency in selenium was investigated in our neighbors Niger republic. It was established that a sizeable proportion of the subjects had decreased selenium levels in their serum. ^[32] Indeed, in certain cultures where the incidence of PPCF is high, certain cultural practices performed during the puerperium such as consuming lake salt or rock salt (known as "kanwa," which has a particularly high sodium content) to promote the flow of breast milk and the heating of the body by sitting/lying on a clay bed with a fire beneath to keep warm (a belief felt to keep off infection) have both been suggested as contributory factors in its development as well from different countries. ^{[32],[33],[34]}

Overall it appears that there is a multifactorial etiology albeit currently unknown. However, whatever the initial trigger or combination of initiating processes, myocardial biopsy in PPCM shows damage to the myocardium with progressive death of cardiomyocytes and destruction of the cytoskeleton of the heart, resulting in progressive loss of heart muscle, ultimately leading to clinical heart failure. ^[35]

Hypertension/tocolytics

While it is possible use of tocolytic agents or the development of preeclampsia and pregnancy-induced hypertension (PIH) may contribute to the worsening of heart failure, they do not cause PPCF; the majority of women have developed PPCF who neither received tocolytics neither had preeclampsia nor PIH. ^[36],[37]

Familial

Familial clustering in PPCF was noted, thus a genetic etiology could be playing a role, but in the Zaria experience this has not been observed. ^{[11],[12],[13],[34]} In the 35 years follow-up studies, there was no familial clustering except for the fact there was a positive family history of hypertension or cardiovascular events. ^[38]

Over all, PPCF in any woman may occur independent of any racial (more African descent) background, at any age during reproductive years, and in any pregnancy. ^[39]

Magnitude of the problem of peripartum cardiac failure in nigeria

Peripartum cardiac failure was first described in Nigeria in the 70's and first largest cohort of patients in the world was from Zaria center, it was made up of 224 patients. ^[34] The syndrome was noted mainly in where there is the predominance of Hausa and Fulani and where the custom of "Wakan Jeko" is practiced. The minority tribes in the north were also noted to be in the PPCF map or distribution in Nigeria, but this was when they engaged in the "Wakan Jeko." It is estimated that the highest incidence in the world is in Hausa land in Nigeria where it is 1.100 births. ^[11] After the report of the syndrome from Zaria, reports also came from Katsina, Sokoto, Kano, Abuja, etc., It is a maternal problem that is all over the north and affects to a small extent south western Nigeria. Though the syndrome described from Ibadan was thought to be precipitated by hypertension, which is a different observation from that of Zaria.

The syndrome does affect the last trimester of pregnancy and puerperal period, which calls for well-coordinated and effective maternal care. Invariably the syndrome in Zaria is mainly a postpartum presentation with various lengths of period postdelivery.

The first cohort of patients described from came from virtually every nook and cranny of the north, not <14 tribes have been represented (PPCF map). ^[34] It could be explained that in those days Ahmadu Bello University Teaching Hospital being the only reference center up north, so the representation of different tribes. Even with this, other practitioners have reported same syndrome from general hospitals from different parts of the north where predominantly in habited or influenced by the Hausas.

Effective and efficient antenatal care should identify subjects at risk, manage preeclampsia and treat it, which is thought to be one of the risk factors. A good postnatal care cannot be over emphasized; this will help identify subjects who have developed symptoms of cardiac failure. Postnatal care or clinics should be made compulsory even when a woman delivered at home, they should be made to have a postnatal care in the nearest comprehensive health center.

On Medline, meds cape, and AJOL search, it were noted that about 2290-3870 papers or articles mentioned PPCF in Nigeria. Of these papers 25 reports were based in Nigeria. In the reports from Nigeria, 90% of it was from Northern Nigeria of which about 70-80% are from Zaria center (Ahmadu Bello University Teaching Hospital). Nearly, all papers/reports were clinical descriptive studies. Few were had some molecular studies, assessing the atrial natriuretic peptides in a cohort of patients.

In Nigeria, incidence of 1 in 100 is related to local Hausa custom, could this have been based on over estimation because the diagnosis was mainly clinical? Zaria reported traditional hot baths, lying or sitting on the hot bed and kunun kanwa as precipitants. Other reports from Katsina, Sokoto, Kano and Abuja alluded that traditional hot practices stands out as a common factor and Northern Nigeria has the highest incidence, Zaria/Sokoto. Kanwa (30 g) that is lake salt contains 450 mmol of sodium (Na ⁺ ), this usually consumed per day [Figure 1].

Figure 1: Local lake salt (kanwa) that contains a lot of sodium. (Davidson N M and Parry EHO. Q J Med 1974;74:473)

Click here to view

The 35 years follow-up studies from the Zaria center have shown that education is a good tool in the prevention of this syndrome among women in Nigeria. When women are informed of the detrimental effects of the custom practice "Wakan Jeko" and they avoided it, in subsequent delivery they don't develop PPCF. Some women have even cut down the period of the practice, from what was 3 months to 1 month and in some cases as low as 2 weeks. The aspect of lying on the hot bed has virtually disappeared in the "Wakan Jeko" triad.

The other lesson from the 35 years follow-up studies is that the first cohort of patient described can be divided into four, (i) Those who had a single episode got over not developed the syndrome again, (ii) those have had recurrent PPCF (iii) those that have gone to develop cardiac failure chronically even outside pregnancies, and (iv) those who have gone on to develop hypertension and subsequently had a stroke or hypertensive cardiac failure.

Is the syndrome still seen in the northern part of Nigeria? The answer is affirmative yes; it is with us, especially in the rural areas. They are mainly seen in rural general hospitals. This is a personal experience in some of the general hospitals in the state we work (Kaduna).

Clinical presentation

Peripartum cardiac failure presentation is similar to that of LV heart failure due to other causes. Women at late pregnancy (third) trimester or puerperium, some even beyond these periods, but with duration of symptoms back dating to 5-6 months postdelivery, will present with shortness of breath on exertion subsequently at rest, body swelling, palpitations, and cough. Physical examination will confirm signs of congestive cardiac failure.

Diagnosis is usually that of exclusion, the common causes of cardiac failure in the environment should be excluded. The diagnosis has some challenges because women with normal pregnancy at a late stage will experience symptoms suggestive of cardiac decompensation, which means clinical examination is very important [Figure 2]. ^[5]

Figure 2: Map of Nigeria showing the shaded area as peripartum cardiac failure (PPCF) zone. Shaded area is where PPCF is very common. Other tribes include Higi, Bura, Bachama, Nupe, Kanuri, Tiv, Iggbira, Idoma, Igala, Tangale, Kilba, Margi, Lunguda, Gwari. (Davidson NM, Trevitt L and Parry EHO. Bull World Health Organ 1974;51:203-8)

Click here to view

Peripartum cardiac failure and maternal health in nigeria

It is estimated that the incidence of PPCF in the United States is between 1 in 1300 and 4000 live births. ^{[5],[36],[40]} While it can affect women of all races, it is more prevalent in some countries; for example, estimates suggest that PPCF occurs at rates of 1 in 1000 live births in South African Bantus, and as high as 1 in 300 in Haiti. ^[39],[41]

Some studies assert that PPCF may be slightly more prevalent among older women who have had higher numbers of live born children and among women of older and younger extremes of childbearing age . ^[40],[41] However, a quarter to a third of PPCF patients are young women who have given birth for the first time. ^{[36],[39],[43],[44],[45]}

Peripartum cardiac failure can occur in any woman of any racial background, at any age during reproductive years, and in any pregnancy. ^[39] The fact that it is more prevalent in the African and more so the Hausas or those that indulge in the customary practices postdelivery cannot be overemphasized.

Specific management during pregnancy and labor

As PPCF poses high risks to both mother and fetus, intense fetal and maternal monitoring is required during delivery when the syndrome occur in the third trimester of pregnancy.

If pregnancy is preterm (<37 weeks), the heart failure is well-tolerated, the patient is responding to medical treatment and with a stable cardiac status, the pregnancy should be allowed to go to term (i.e. 37 weeks) with elective induction and vaginal delivery thereafter. However, for mothers with a new diagnosis of PPCF at term, labor should be induced, or a cesarean section planned if LV function is poor or deteriorating rapidly. ^{[29],[46],[47]} Vaginal delivery is preferred over cesarean section because of the increased risk of pulmonary emboli and endometritis after cesarean section. ^[48]

During vaginal delivery, the second stage of labor and labor pain cause maximum hemodynamic and oxidative cardiac stress, which can be minimized by using appropriate regional anesthetics and reducing the duration of the second stage of labor? To relieve pain, continuous epidural or spinal anesthetic is preferred ^[48],[49] and the second stage of labor can be shortened by application of a vacuum device or forceps. ^{[42],[46],[50]} This helps to prevent acute cardiac decompensation during parturition. However, cesarean section should be performed if there is an obstetric indication or the patient is not responding to optimal medical treatment and is in acute cardiac decompensation or expected to progress to acute cardiac decompensation during parturition. ^[8] In other words, the presence of PPCF in the third trimester of pregnancy calls for a multidisciplinary approach to management. It involves the obstetrician and the cardiologist. The pediatrician is also a big partner because the health of the baby expected is very important.

In postpartum-onset PPCF, medical management remains the same as for pregnancy-onset PPCF. However, angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers can be used as after load reduction, as they have been shown to improve mortality in all heart failure patients with LV systolic improvement. ^[15],[51] Warfarin can also be used for anticoagulation, but should not be started until 5-7 days postnatally to reduce complications of delayed postpartum hemorrhage. In the interim between delivery and the start of warfarin, low-molecular-weight heparin should be prescribed. It should be noted that heparin and warfarin, β-blockers, digoxin and some ACE inhibitors (namely captopril and enalopril) are safe during breast feeding.

It is imperative to give contraceptive advice, as patients should not become pregnant again for at least a year or until LV function has returned to normal. Progestogenic methods of contraception, in particular, the Mirena intrauterine system and Implanon are the most efficacious and safe methods of contraception for women who have had PPCF. They also have the added advantage of reducing menstrual loss, which is often increased in patients receiving warfarin. The combined oral contraceptive pill is contraindicated because of its thrombogenic potential. Barrier methods have a high failure rate.

Prognosis of the syndrome

It's been noted that the following factors contribute to worst prognosis that is, the patient is most likely going to do badly. ^[52]

Older patients (≥30 years)
High parity (≥3 pregnancies)
Late onset of symptoms following delivery (≥7.6 weeks)
High echocardiography end diastolic volume (7.0 cm)
High pulmonary arterial pressure (≥38 mmHg) and arterial wedge pressure
Conduction defects on surface electrocardiograph
Persistence of cardiomegaly on chest radiograph 6-12 months posts the onset of the symptoms.

In the United States of America, mortality is about 25-50% and most deaths occur in the 1-3 months because of progression in pump failure, arrhythmias and thromboembolic events. ^[53] This observation is similar to our experience in Zaria center.

About 30-50% of patients with PPCF recover without complications with their baseline LV function at rest returning to normal. ^[54] Non return to normal at 6-12 months indicates irreversible cardiomyopathy and indicates worst prognosis. LV end systolic dimension of 5.5 or less and ejection fraction >27% have shown to predict LV function retuning back to normal after pregnancy. ^[55] LV internal diameter in diastole of >6 cm and SF of <20% at the time of diagnosis indicate more than three-fold higher risk of progression to persistent LV dysfunction. ^[56]

Adesanya et al. in a 10-year follow-up study reported 52% improving without an episode of PPCF, 26% with recurrence, 13% with cardiac failure unrelated to pregnancy and 9% progressing to a picture of dilated cardiomyopathy. In this same cohort of women 87% had transient hypertension on admission, and 45% later in 10 years. ^[57] The report also noted that echocardiography abnormalities may persist for 10 years and mortality rate was 11% in the 1 ^st year. Some authors have reported recurrence rate with additional pregnancies at 50-100%. ^[10] Bültmann et al. have reported 2/3 of PPCF patients have improved LV function. ^[58] Future pregnancy puts the PPCF woman with persistent LV dysfunction at high-risk of complications and death. ^[56] Such patients should be advised to avoid future pregnancies unless a successful cardiac transplant.

Public related issues in the management

The experience of Zaria on PPCF revealed several public related issues associated with the syndrome. It spans from sociocultural, religious, and political aspects. It also relate to good health care system, involving secondary care, and even tertiary.

On the sociocultural area, as far as the syndrome seen in the Nigerian women, are some believes attached to "Wakan Jeko." It is believed that engaging in the practices helps the women produce more breast milk. The second area is that of cleansing of the woman both physically spiritually. It believed that "Wakan Jeko" cleanses the woman from the bad blood and fluid that would have accumulated postdelivery (35 years follow-up in Zaria). Before believe was held that a woman should not deliver in hospital because they will discouraged from doing the customary practice. It is also believed that doing the "Wakan Jeko" the woman also gets spiritual cleansing. These are teachings that are deep rooted and the elderly women in the community are the custodians, sometimes it reaches the form of even bullying the young woman who has just delivered to succumbing to the threats to perform the practice.

Prevention of peripartum cardiac failure

The state of our health care delivery at the three tiers is very important. A good antenatal care is very important. It involves simple things like blood pressure measurement at every visit with a reliable machine, a urine deep stick for proteins. This can help identify women who are at risk especially when there is evidence of preeclampsia. There are instruments that can be used to identify women who are about to go into cardiac failure or at risk. ^[59] The personnel at the primary health care level should also know his or her limit. Some will need to be referred to secondary health care or tertiary care center.

The way forward

Public health campaigns

Going by the Zaria experience and the risk factors identified in the reports, it is very important to engage in an aggressive health campaigns on detrimental aspects of the some traditional practices. This can be done at antenatal care centers right from primary health care to secondary and tertiary care centers. It also involves community level meeting where the elderly women are invited to participate.

The mass media is another area; both print and electronic should be involved in the campaign. The radio has a wide coverage and large audience. Since there is a religious dimension to the some of the practices that is noted to precipitate the syndrome, the religious clerics must be engaged. The traditional rulers are also very important this project because they are the custodians of the community traditions and they can be best heard than a stranger coming from outside. The campaign should not take the form of blame rather whether we can do something better and avoid things that can cause harm to us.

Good primary health care system

A good and efficient primary health care system is very important pillar in the prevention of the syndrome in Nigeria. This hinges in the pedestal that a primary health care center should do a good blood pressure for antenatal women and refer those that require attention forward to a secondary care. The program of midwifes by Federal Government to help reduce maternal mortality should also in cooperate the prevention of PPCF in Nigeria. This will require some training of midwifes to detect women at-risk and refer them to secondary or tertiary centers.

Antenatal and postnatal care

A simple, accessible, efficient and friendly antenatal care at different tiers of health care delivery is absolutely very important. This will help in education of the pregnant woman, help detect women that are at-risk and manage them accordingly. Women that happen to deliver at home should be encouraged to attend postnatal care, this can also help detect women that have already develop symptoms of cardiac decompensation early.

Interdisciplinary collaboration in secondary and tertiary centers be enhanced, which will have a positive impact on management of the patients, prevention of the syndrome.

Further research on peripartum cardiac failure in Nigeria

Literature review has shown that the etiology of PPCF is still unsettled; it is usually a diagnosis of exclusion. The etiology has gone from malnutrition molecular level where it is thought that can be genetic or prolactin fragments products. In Nigeria, the strongest correlate is traditional practices "Wakan Jeko" and high blood pressure. It was concluded after the 35 years follow-up studies that these women could have been prehypertensives. In view of the reports from South Africa on prolactin fragments effect, we need to know the role of prolactin in our own patients, are we dealing with same or different the precipitants of the syndrome. Are these women prehypertensive then angiotensin genotype should done on these women, compared with that of hypertensives and normal individuals in the community? We need to establish whether "Wakan Jeko" is coincidental occurrence or the culprit behind the syndrome so that preventive measures are done based on established facts.

Conclusion

Peripartum cardiac failure is a syndrome of undefined etiology. Different authors from different countries and regions of the world have proposed varying etiologies spanning cultural practices (Wakan Jeko) to molecular abnormalities.

The syndrome is one of risk factors for poor maternal health, which goes on affect child health and mortality. The syndrome present as cardiac failure from other causes.

Prevention of the syndrome (PPCF) entails addressing some sociocultural believes, good and efficient maternal care in antenatal and postnatal care, involvement of mass media and the clergy.

References

1.	Murray CJ, Lopez AD, editors. The Global Burden of Disease: A Comprehensive Assessment of Mortality and Disability from Diseases, Injuries, and Risk Factors in 1990 and Projected to 2020. Boston, Mass: Harvard School of Public Health; 1996.
2.	The World Health Report. Making a Difference. Geneva: World Health Organization; 1999.
3.	Hibbard JU, Lindheimer M, Lang RM. A modified definition for peripartum cardiomyopathy and prognosis based on echocardiography. Obstet Gynecol 1999;94:311-6.
4.	Cardiomyopathies. Report of a WHO Expert Committee - WHO Technical Report Series No. 697. Heartbeat, No. 2, June 1981. Geneva: WHO; 1984.
5.	Pearson GD, Veille JC, Rahimtoola S, Hsia J, Oakley CM, Hosenpud JD, et al. Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review. JAMA 2000;283:1183-8.
6.	Seftel H, Susser M. Maternity and myocardial failure in African women. Br Heart J 1961;23:43-52. [PUBMED]
7.	Cunningham FG, Pritchard JA, Hankins GD, Anderson PL, Lucas MJ, Armstrong KF. Peripartum heart failure: idiopathic cardiomyopathy or compounding cardiovascular events? Obstet Gynecol 1986;67:157-68. [PUBMED]
8.	Brar SS, Khan SS, Sandhu GK, Jorgensen MB, Parikh N, Hsu JW, et al. Incidence, mortality, and racial differences in peripartum cardiomyopathy. Am J Cardiol 2007;100:302-4.
9.	Ansari AA, Fett JD, Carraway RE, Mayne AE, Onlamoon N, Sundstrom JB. Autoimmune mechanisms as the basis for human peripartum cardiomyopathy. Clin Rev Allergy Immunol 2002;23:301-24.
10.	Elkayam U, Akhter MW, Singh H, Khan S, Bitar F, Hameed A, et al. Pregnancy-associated cardiomyopathy: clinical characteristics and a comparison between early and late presentation. Circulation 2005;111:2050-5.
11.	Davidson NM, Parry EH. Peri-partum cardiac failure. Q J Med 1978;47:431-61. [PUBMED]
12.	Sanderson JE, Adesanya CO, Anjorin FI, Parry EH. Postpartum cardiac failure - heart failure due to volume overload? Am Heart J 1979;97:613-21. [PUBMED]
13.	Fillmore SJ, Parry EH. The evolution of peripartal heart failure in Zaria, Nigeria. Some etiologic factors. Circulation 1977;56:1058-61. [PUBMED]
14.	Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet 2006;368:687-93.
15.	Lok SI, Kirkels JH, Klöpping C, Doevendans PA, de Jonge N. Peripartum cardiomyopathy: the need for a national database. Neth Heart J 2011;19:126-133.
16.	Corbacho AM, Martínez De La Escalera G, Clapp C. Roles of prolactin and related members of the prolactin/growth hormone/placental lactogen family in angiogenesis. J Endocrinol 2002;173:219-38.
17.	Hilfiker-Kleiner D, Kaminski K, Podewski E, Bonda T, Schaefer A, Sliwa K, et al. A cathepsin D-cleaved 16 kDa form of prolactin mediates postpartum cardiomyopathy. Cell 2007;128:589-600.
18.	Tabruyn SP, Sorlet CM, Rentier-Delrue F, Bours V, Weiner RI, Martial JA, et al. The antiangiogenic factor 16K human prolactin induces caspase-dependent apoptosis by a mechanism that requires activation of nuclear factor-kappaB. Mol Endocrinol 2003;17:1815-23.
19.	de Jong JS, Rietveld K, van Lochem LT, Bouma BJ. Rapid left ventricular recovery after cabergoline treatment in a patient with peripartum cardiomyopathy. Eur J Heart Fail 2009;11:220-2.
20.	Habedank D, Kühnle Y, Elgeti T, Dudenhausen JW, Haverkamp W, Dietz R. Recovery from peripartum cardiomyopathy after treatment with bromocriptine. Eur J Heart Fail 2008;10:1149-51.
21.	Hilfiker-Kleiner D, Meyer GP, Schieffer E, Goldmann B, Podewski E, Struman I, et al. Recovery from postpartum cardiomyopathy in 2 patients by blocking prolactin release with bromocriptine. J Am Coll Cardiol 2007;50:2354-5. [PUBMED]
22.	Warraich RS, Sliwa K, Damasceno A, Carraway R, Sundrom B, Arif G, et al. Impact of pregnancy-related heart failure on humoral immunity: clinical relevance of G3-subclass immunoglobulins in peripartum cardiomyopathy. Am Heart J 2005;150:263-9.
23.	Marín Huerta E, Erice A, Fernández Espino R, Navascués I, Martín de Dois R. Postpartum cardiomyopathy and acute myocarditis. Am Heart J 1985;110:1079-81.
24.	Zimmermann O, Kochs M, Zwaka TP, Kaya Z, Lepper PM, Bienek-Ziolkowski M, et al. Myocardial biopsy based classification and treatment in patients with dilated cardiomyopathy. Int J Cardiol 2005;104:92-100.
25.	Fett JD. Inflammation and virus in dilated cardiomyopathy as indicated by endomyocardial biopsy. Int J Cardiol 2006;112:125-6. [PUBMED]
26.	Ansari AA, Fett JD, Carraway RE, Mayne AE, Onlamoon N, Sundstrom JB. Autoimmune mechanisms as the basis for human peripartum cardiomyopathy. Clin Rev Allergy Immunol 2002;23:301-24.
27.	Bozkurt B, Villaneuva FS, Holubkov R, Tokarczyk T, Alvarez RJ Jr, MacGowan GA, et al. Intravenous immune globulin in the therapy of peripartum cardiomyopathy. J Am Coll Cardiol 1999;34:177-80.
28.	Rizeq MN, Rickenbacher PR, Fowler MB, Billingham ME. Incidence of myocarditis in peripartum cardiomyopathy. Am J Cardiol 1994;74:474-7.
29.	Witlin AG, Mabie WC, Sibai BM. Peripartum cardiomyopathy: an ominous diagnosis. Am J Obstet Gynecol 1997;176:182-8.
30.	Ladwig P, Fischer E. Peripartum cardiomyopathy. Aust N Z J Obstet Gynaecol 1997;37:156-60.
31.	Veille JC, Zaccaro D. Peripartum cardiomyopathy: summary of an international survey on peripartum cardiomyopathy. Am J Obstet Gynecol 1999;181:315-9.
32.	Cénac A, Simonoff M, Moretto P, Djibo A. A low plasma selenium is a risk factor for peripartum cardiomyopathy. A comparative study in Sahelian Africa. Int J Cardiol 1992;36:57-9.
33.	Trevitt L. Attitudes and customs in child birth among Hausa women in Zaria City. Savanna 1973;2:223-6.
34.	Davidson NM, Trevitt L, Parry EH. Perpartum cardiac failure. An explanation for the observed geographic distribution in Nigeria. Bull World Health Organ 1974;51:203-8. [PUBMED]
35.	Fett JD. Understanding peripartum cardiomyopathy, 2008. Int J Cardiol 2008;130:1-2. [PUBMED]
36.	Fett JD, Christie LG, Carraway RD, Murphy JG. Five-year prospective study of the incidence and prognosis of peripartum cardiomyopathy at a single institution. Mayo Clin Proc 2005;80:1602-6.
37.	Sliwa K, Förster O, Libhaber E, Fett JD, Sundstrom JB, Hilfiker-Kleiner D, et al. Peripartum cardiomyopathy: inflammatory markers as predictors of outcome in 100 prospectively studied patients. Eur Heart J 2006;27:441-6.
38.	Ford L, Abdullahi A, Anjorin FI, Danbauchi SS, Isa MS, Maude GH, et al. The outcome of peripartum cardiac failure in Zaria, Nigeria. QJM 1998;91:93-103.
39.	Elkayam U, Tummala PP, Rao K, Akhter MW, Karaalp IS, Wani OR, et al. Maternal and fetal outcomes of subsequent pregnancies in women with peripartum cardiomyopathy. N Engl J Med 2001;344:1567-71.
40.	Mielniczuk LM, Williams K, Davis DR, Tang AS, Lemery R, Green MS, et al. Frequency of peripartum cardiomyopathy. Am J Cardiol 2006;97:1765-8.
41.	Desai D, Moodley J, Naidoo D. Peripartum cardiomyopathy: experiences at King Edward VIII Hospital, Durban, South Africa and a review of the literature. Trop Doct 1995;25:118-23.
42.	Sliwa K, Fett J, Elkayam U. Peripartum cardiomyopathy. Lancet 2006;368:687-93.
43.	Sliwa K, Förster O, Libhaber E, Fett JD, Sundstrom JB, Hilfiker-Kleiner D, et al. Peripartum cardiomyopathy: inflammatory markers as predictors of outcome in 100 prospectively studied patients. Eur Heart J 2006;27:441-6.
44.	Sliwa K, Skudicky D, Bergemann A, Candy G, Puren A, Sareli P. Peripartum cardiomyopathy: analysis of clinical outcome, left ventricular function, plasma levels of cytokines and Fas/APO-1. J Am Coll Cardiol 2000;35:701-5.
45.	Midei MG, DeMent SH, Feldman AM, Hutchins GM, Baughman KL. Peripartum myocarditis and cardiomyopathy. Circulation 1990;81:922-8.
46.	Lampert MB, Hibbard J, Weinert L, Briller J, Lindheimer M, Lang RM. Peripartum heart failure associated with prolonged tocolytic therapy. Am J Obstet Gynecol 1993;168:493-5.
47.	Heider AL, Kuller JA, Strauss RA, Wells SR. Peripartum cardiomyopathy: a review of the literature. Obstet Gynecol Surv 1999;54:526-31.
48.	Velickovic IA, Leicht CH. Peripartum cardiomyopathy and cesarean section: report of two cases and literature review. Arch Gynecol Obstet 2004;270:307-10.
49.	Zangrillo A, Landoni G, Pappalardo F, Oppizzi M, Torri G. Different anesthesiological management in two high risk pregnant women with heart failure undergoing emergency cesarean section. Minerva Anestesiol 2005;71:227-36.
50.	Task Force on the Management of Cardiovascular Diseases During Pregnancy of the European Society of Cardiology. Expert consensus document on management of cardiovascular diseases during pregnancy. Eur Heart J 2003;24:761-81. [PUBMED]
51.	Murali S, Baldisseri MR. Peripartum cardiomyopathy. Crit Care Med 2005;33:S340-6.
52.	Amos AM, Jaber WA, Russell SD. Improved outcomes in peripartum cardiomyopathy with contemporary. Am Heart J 2006;152:509-13.
53.	Sutton MS, Cole P, Plappert M, Saltzman D, Goldhaber S. Effects of subsequent pregnancy on left ventricular function in peripartum cardiomyopathy. Am Heart J 1991;121:1776-8.
54.	Whitehead SJ, Berg CJ, Chang J. Pregnancy-related mortality due to cardiomyopathy: United States, 1991-1997. Obstet Gynecol 2003;102:1326-31.
55.	Duran N, Günes H, Duran I, Biteker M, Ozkan M. Predictors of prognosis in patients with peripartum cardiomyopathy. Int J Gynaecol Obstet 2008;101:137-40.
56.	Chapa JB, Heiberger HB, Weinert L, Decara J, Lang RM, Hibbard JU. Prognostic value of echocardiography in peripartum cardiomyopathy. Obstet Gynecol 2005;105:1303-8.
57.	Adesanya CO, Anjorin FI, Adeoshun IO, Davidson NM, Parry EH. Peripartum cardiac failure. A ten year follow-up study. Trop Geogr Med 1989;41:190-6.
58.	Bültmann BD, Klingel K, Näbauer M, Wallwiener D, Kandolf R. High prevalence of viral genomes and inflammation in peripartum cardiomyopathy. Am J Obstet Gynecol 2005;193:363-5.
59.	Fett JD. Validation of a self-test for early diagnosis of heart failure in peripartum cardiomyopathy. Crit Pathw Cardiol 2011;10:44-5. [PUBMED]