An unexpected battle with peripartum cardiomyopathy: a case report

Figures

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  Figure 1.. Pathophysiology of PPCM. Prolactin, secreted by the anterior pituitary gets broken to a 16 kDa fragment which results in upregulation of microRNA-146a. Separately, DNA mutations in sarcomere genes, such as TTN encoding for titin, contribute to the pathogenesis. The other main contributing factor is from sFlt-1, an anti-angiogenic protein associated with pre-eclampsia. Beyond these three factors, there are still many other unclear factors which are still being investigated. sFlt-1, soluble fms-like tyrosine kinase-1.

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  Figure 2.. Parasternal long axis view in M mode echocardiogram. M mode displays movement of the heart over multiple cardiac cycles, as shown by the electrocardiogram in the figure. Here we can see a significant reduction in movement along the posterior wall of the left ventricle, which is consistent with the final interpretation of global hypokinesis when taken in context with the wall motion seen from different views. LVESD, left ventricular end systolic dimension; LVEDD left ventricular end diastolic dimension.

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  Figure 3.. Apical four chamber view echocardiogram. Here we can see global chamber enlargement with accompanying thinning of the myocardium. In addition, the utilization of color Doppler in this view showed both mitral and tricuspid regurgitation. These findings are often seen in dilated cardiomyopathies, which peripartum cardiomyopathy falls within. RV, right ventricle; RA, right atrium; LV, left ventricle; LA, left atrium.