Recent PPCM Articles for Patients

This study did genetic testing on 469 women with PPCM and tested for 62 genetic abnormalities associated with heart muscle weakness. It found that about 10% of women with PPCM had a genetic abnormality in protein that makes up heart muscle cells called Titin (compared with 1% of the general population). PPCM survivors with this genetic abnormality (truncating mutation of Titin) had lower left ventricular ejection fraction at the time of presentation than women without the genetic abnormality; however the women with a Titin abnormality did not differ significantly in timing of presentation after delivery, in prevalence of preeclampsia, or in rates of clinical recovery. This study supports the contribution of a genetic predisposition to the development of PPCM.

A retrospective study was conducted to determine whether first trimester N-terminal pro-B type natriuretic peptide (NT-proBNP) or high sensitivity cardiac troponin I (hs-cTnI) differed among women who developed PPCM versus those who did not. 

Four cases of women with available blood tests prior to PPCM onset were identified. The PPCM women were matched to samples from women by age, race, number of prior pregnancies, and gestational age at which the blood sample was taken (Control A). A second comparison group was matched for all of the initial characteristics in addition to systolic BP at first prenatal visit and pregnancy weight gain (Control B).

First trimester NT-proBNP were numerically higher among women who developed PPCM (116 pg/mL [83–177]) as compared with women in Control A (56.1 pg/mL [38.7–118.7], not statistically significant) and control B (37.6 [23.3 − 53.8], p <0.05). A higher proportion of women who subsequently developed PPCM (50%) had detectable levels of hs-cTnI as compared with control A (0%, p = 0.03) or control B (18.8%, p = 0.52). Among both cases and controls, hs-cTnI values were low and often below the limit of detection.