Peripartum cardiomyopathy

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Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy that is defined as deterioration in cardiac function presenting typically between the last month of pregnancy and up to five months postpartum. As with other forms of dilated cardiomyopathy, PPCM involves systolic dysfunction of the heart with a decrease of the left ventricular ejection fraction (EF) with associated congestive heart failure and an increased risk of atrial and ventricular arrhythmias, thromboembolism (blockage of a blood vessel by a blood clot), and even sudden cardiac death. In essence, the heart muscle cannot contract forcefully enough to pump adequate amounts of blood for the needs of the body’s vital organs.[1][2][3][4][5]

PPCM is a diagnosis of exclusion, wherein patients have no prior history of heart disease and there are no other known possible causes of heart failure. Echocardiogram is used to both diagnose and monitor the effectiveness of treatment for PPCM.[1][2][3][4][5]

The cause of PPCM is unknown. Currently, researchers are investigating cardiotropic viruses, autoimmunity or immune system dysfunction, other toxins that serve as triggers to immune system dysfunction, micronutrient or trace mineral definciencies, and genetics as possible components that contribute to or cause the development of PPCM.[1][3][6]

The process of PPCM begins with an unknown trigger (possibly a cardiotropic virus or other yet unidentified catalyst) that initiates an inflammatory process in the heart. Consequently, heart muscle cells are damaged; some die or become scar tissue. Scar tissue has no ability to contract; therefore, the effectiveness of the pumping action of the heart is decreased. Also, damage to the cytoskeletal framework of the heart causes the heart to enlarge, stretch or alter in shape, also decreasing the heart’s systolic function or output. The initial inflammatory process appears to cause an autoimmune or immune dysfunctional process, which in turn fuels the initial inflammatory process. Progressive loss of heart muscle cells leads to eventual heart failure.[7]

It is estimated that the incidence of PPCM in the United States is between 1 in 1300 to 4000 live births.[1][8][9] While it can affect women of all races, it is more prevalent in some countries; for example, estimates suggest that PPCM occurs at rates of one in 1000 live births in South African Bantus, and as high as one in 300 in Haiti.[9][10]

Some studies assert that PPCM may be slightly more prevalent among older women who have had higher numbers of liveborn children and among women of older and younger extremes of childbearing age.[8][10] However, a quarter to a third of PPCM patients are young women who have given birth for the first time.[2][3][9][10][11][12]

While the use of tocolytic agents or the development of preeclampsia (toxemia of pregnancy) and pregnancy-induced hypertension (PIH) may contribute to the worsening of heart failure, they do not cause PPCM; the majority of women have developed PPCM who neither received tocolytics nor had preeclampsia nor PIH.[9][11]

In short, PPCM can occur in any woman of any racial background, at any age during reproductive years, and in any pregnancy.[13]

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