Peripartum cardiomyopathy (PPCM) is a form of dilated cardiomyopathy that is defined as a deterioration in cardiac function presenting typically between the last month of pregnancy and up to six 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.
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.
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 deficiencies, and genetics as possible components that contribute to or cause the development of PPCM.
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.
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