Pregnancy Induced Heart Failure

Peripartum Cardiomyopathy (PPCM)


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.[1][2][3][4][5]

PPCM is a diagnosis of exclusion, wherein patients have no prior history of heart disease and have no other known possible causes of heart failure. Echocardiogram is used to diagnose and monitor the effectiveness of treatment for Peripartum Cardiomyopathy.


The cause of PPCM is unknown. Currently, researchers are investigating cardiotropic viruses, autoimmunity or immune systemdysfunction, 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]



  1. Pearson GD, Veille JC, Rahimtoola S, et al. (March 2000). "Peripartum cardiomyopathy: National Heart, Lung, and Blood Institute and Office of Rare Diseases (National Institutes of Health) workshop recommendations and review". JAMA. 283 (9): 1183–8. doi:10.1001/jama.283.9.1183. PMID 10703781.
  2. Elkayam U, Akhter MW, Singh H, et al. (April 2005). "Pregnancy-associated cardiomyopathy: clinical characteristics and a comparison between early and late presentation". Circulation. 111 (16): 2050–5. doi:10.1161/01.CIR.0000162478.36652.7E. PMID 15851613.
  3. Sliwa K, Fett J, Elkayam U (August 2006). "Peripartum cardiomyopathy". Lancet. 368 (9536): 687–93. doi:10.1016/S0140-6736(06)69253-2. PMID 16920474.
  4. Murali S, Baldisseri MR (October 2005). "Peripartum cardiomyopathy". Crit. Care Med. 33 (10 Suppl): S340–6. doi:10.1097/01.CCM.0000183500.47273.8E. PMID 16215357.
  5. Phillips SD, Warnes CA (2004). "Peripartum Cardiomyopathy: Current Therapeutic Perspectives". Curr Treat Options Cardiovasc Med. 6 (6): 481–488. doi:10.1007/s11936-004-0005-8. PMID 15496265.
  6. Ansari AA, Fett JD, Carraway RE, Mayne AE, Onlamoon N, Sundstrom JB (December 2002). "Autoimmune mechanisms as the basis for human peripartum cardiomyopathy". Clin Rev Allergy Immunol. 23 (3): 301–24. doi:10.1385/CRIAI:23:3:301. PMID 12402414.
  7. Fett JD (October 2008). "Understanding peripartum cardiomyopathy, 2008". Int. J. Cardiol. 130 (1): 1–2. doi:10.1016/j.ijcard.2008.03.076. PMID 18590935.