Abstract

Peripartum cardiomyopathy (PPCM), heart failure from pregnancy-associated cardiomyopathy, entered the modern era in the USA in 2000, with the report from the Workshop on Peripartum Cardiomyopathy from the National Institutes of Health. Since then, there has been a great reduction in mortality in the USA (from a range of 18-56 % down to a range of 1-5 % ) and an increasing number of women who have experienced recovery of heart function in the USA (from less than one-third to over onehalf). PPCM may be the non-ischemic cardiomyopathy that has the greatest potential of all cardiomyopathies for full recovery. Despite these impressive changes, from one-third to one-half of PPCM patients still go on to chronic heart failure; and experience other life-threatening complications. An essential key to a better path is to make an earlier diagnosis. Time-of-diagnosis left ventricular systolic function (LVEF) greater than 30-35 % is associated with high survival and recovery rates. Increased mortality, chronic cardiomyopathy, thromboembolic complications, serious ventricular tachyarrhythmias, left ventricular assist devices and transplantation are more likely to be associated with diagnostic LVEF below 30-35 %. An earlier diagnosis may be associated with the more favorable diagnostic levels, while any delay in diagnosis is more likely to be associated with lower LVEF. Earlier diagnosis can be greatly facilitated when there is an awareness of the possibility of heart failure in a peripartum patient, who ordinarily would be expected to have a healthy heart. This awareness must importantly be present not only in the mother herself, but in all those health professionals with whom she comes in contact, including nurses, mid-wives, obstetricians, emergency room physicians, and primary care providers. A new tool has been developed to help distinguish heart failure signs and symptoms from those of normal pregnancy. There are 3 areas of newer investigations that may help both with earlier diagnosis and more effective treatment: Immune system activation, role of cardiotoxic prolactin metabolites, and soluble FLT1 with angiogenic imbalance.

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