Peripаrtal Cardiomyopathy

Abstract

The purpose of the study is to describe a clinical case of peripartal cardiomyopathy (CM) and conduct literature analysis. Peripartal CM is defined as reduced ejection fraction of the left ventricle <45%, reduced fractional shortening <30%, as well as increased end-diastolic size of the left ventricle > 2.7 cm/m2. At the same time, there should be no detectable causes of heart failure, as well as development of heart failure in the last month of pregnancy or within 5 months after childbirth. The review presents data on possible causes of peripartal CM. Risk factors for peripartal CM are: age younger than 20 years and older than 30 years, preeclampsia, hypertension, multiple pregnancy, prolonged duration of viral infection, macro- and micronutrient insufficiency, etc. Prolactin and its 16 kDa fragment, as well as excessive activity of cathepsin D, play a leading role in pathogenesis of peripartal CM. A step-by-step algorithm for diagnosis of peripartal CM in real clinical conditions is described. Material and methods. The patient is K., 18 years old, in anamnesis: no prior history of cardiovascular diseases, according to the patient, she had pneumonia a year ago. The patient has not registered increased blood pressure. Physiological pregnancy proceeded satisfactorily; natural delivery was on time. On the 56th day after childbirth, the patient was admitted to the intensive care unit with complaints: shortness of breath, muscle weakness, palpitations, lower leg edema. From anamnesis: 1 month after childbirth, the next day after psychoemotional overstrain, the patient began to notice shortness of breath, lack of sleep, muscle weakness, decreased lactation. The examination revealed an increase in the sedimentation rate of erythrocytes, C-reactive blood protein, proteinuria, hematuria, as well as a decrease in the ejection fraction of the left ventricle. Results. Together with standard therapy, addition of prolactin secretion inhibitors and dopamine receptor stimulators led to significant improvement of the patient’s condition: proteinuria significantly decreased, edematous syndrome was gone, and LV contractile function significantly recovered. Conclusion. The clinical case demonstrates the development of a rare variant of peripartal CM, debuting with proteinuria and preserved kidney function, as well as normal serum prolactin levels. Apparently, there are different phenotypes of peripartal CM.