Peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is a potentially devastating disease that affects women during the last months of pregnancy or the first months after delivery. The aetiology and pathogenesis of this disease remain unclear, but oxidative stress and the generation of a cardiotoxic fragment of prolactin may play key roles. Diagnosing PPCM remains a challenge, as symptoms may mimic those women experience during normal pregnancy and the peripartum period. A high index of suspicion is thus necessary to make the diagnosis. Patients with PPCM have a varied clinical course, as some patients achieve full recovery while others progress to end-stage heart failure and even death. Standard heart failure treatment is indicated, although special provisions are necessary in pregnant and lactating women. Additional research into the pathophysiology of this disease, including possible genetic contributions, may lead to novel treatment strategies that can improve outcomes.

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Peripartum Cardiomyopathy

10.1093/med/9780190226459.003.0045 ◽

2017 ◽

Author(s):

Emily J. Baird

Keyword(s):

Heart Failure ◽

Treatment Strategies ◽

The United States ◽

Current Treatment ◽

Peripartum Cardiomyopathy ◽

Clinical Suspicion ◽

Maternal Deaths ◽

Pregnancy And Lactation ◽

Peripartum Period ◽

Pathophysiologic Mechanisms

Peripartum cardiomyopathy (PPCM) is an idiopathic form of heart failure that manifests during the last month of pregnancy or the first 5 months postpartum. Although the incidence is relatively low, the maternal impact is high, with up to 12% of maternal deaths in the United States resulting from sequelae of PPCM. Risk factors are poorly understood at the present time, as are the pathophysiologic mechanisms. Timely diagnosis continues to be a challenge, since many of the symptoms of PPCM mimic those commonly encountered during the normal peripartum period. Management of PPCM parallels current heart failure guidelines, with special consideration to the safety of medications and interventions during pregnancy and lactation. This chapter discusses proper clinical suspicion, processes for diagnosis, and current treatment strategies as well as the overall prognosis.

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Localization of endothelial nitric oxide synthase in the normal and failing human atrial myocardium

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100166397 ◽

1996 ◽

Vol 54 ◽

pp. 786-787

Author(s):

Chi-Ming Wei ◽

Margarita Bracamonte ◽

Shi-Wen Jiang ◽

Richard C. Daly ◽

Christopher G.A. McGregor ◽

...

Keyword(s):

Nitric Oxide ◽

Heart Failure ◽

Nitric Oxide Synthase ◽

Endothelial Nitric Oxide Synthase ◽

Cardiac Tissues ◽

Mammalian Tissues ◽

End Stage Heart Failure ◽

End Stage ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Nitric oxide (NO) is a potent endothelium-derived relaxing factor which also may modulate cardiomyocyte inotropism and growth via increasing cGMP. While endothelial nitric oxide synthase (eNOS) isoforms have been detected in non-human mammalian tissues, expression and localization of eNOS in the normal and failing human myocardium are poorly defined. Therefore, the present study was designed to investigate eNOS in human cardiac tissues in the presence and absence of congestive heart failure (CHF).Normal and failing atrial tissue were obtained from six cardiac donors and six end-stage heart failure patients undergoing primary cardiac transplantation. ENOS protein expression and localization was investigated utilizing Western blot analysis and immunohistochemical staining with the polyclonal rabbit antibody to eNOS (Transduction Laboratories, Lexington, Kentucky).

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