Peripartum cardiomyopathy (PPCM) is a cause of pregnancy-associated heart failure. It typically develops during the last month of, and up to 6 months after, pregnancy in women without known cardiovascular disease. The present position statement offers a state-of-the-art summary of what is known about risk factors for potential pathophysiological mechanisms, clinical presentation of, and diagnosis and management of PPCM. A high index of suspicion is required for the diagnosis, as shortness of breath and ankle swelling are common in the peripartum period. Peripartum cardiomyopathy is a distinct form of cardiomyopathy, associated with a high morbidity and mortality, but also with the possibility of full recovery. Oxidative stress and the generation of a cardiotoxic subfragment of prolactin may play key roles in the pathophysiology of PPCM. In this regard, pharmacological blockade of prolactin offers the possibility of a disease-specific therapy.

/pdf/current-state-of-knowledge-on-aetiology-diagnosis-management-1xftx63vj4.pdf

Current state of knowledge on aetiology, diagnosis, management, and therapy of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Working Group on peripartum cardiomyopathy

Protein carbonylation, one of the most harmful irreversible oxidative protein modifications, is considered as a major hallmark of oxidative stress-related disorders. Protein carbonyl measurements are often performed to assess the extent of oxidative stress in the context of cellular damage, aging and several age-related disorders. A wide variety of analytical techniques are available to detect and quantify protein-bound carbonyls generated by metal-catalyzed oxidation, lipid peroxidation or glycation/glycoxidation. Here we review current analytical approaches for protein carbonyl detection with a special focus on mass spectrometry-based techniques. The utility of several carbonyl-derivatization reagents, enrichment protocols and especially advanced mass spectrometry techniques are compared and discussed in detail. Furthermore, the mechanisms and biology of protein carbonylation are summarized based on recent high-throughput proteomics data. © 2013 Wiley Periodicals, Inc. Mass Spec Rev 33: 79–97, 2014.

Protein carbonylation as a major hallmark of oxidative damage: update of analytical strategies.

A recent report of the EuroHeart project has shown that women are still underrepresented in many cardiovascular clinical trials, while important gender differences are present within most areas of heart disease. As the burden of cardiovascular disease is increasing in middle-aged women relative to men, a more profound understanding is needed of the fundamental biological differences that exist between men and women. In the current review, we aim to address the need for more explanatory sex-specific cardiovascular research to be able to adapt existing guidelines for a better heart health in women.

/pdf/red-alert-for-women-s-heart-the-urgent-need-for-more-2z0n288jdp.pdf

Red alert for women's heart: the urgent need for more research and knowledge on cardiovascular disease in women

Aims An anti-angiogenic cleaved prolactin fragment is considered causal for peripartum cardiomyopathy (PPCM). Experimental and first clinical observations suggested beneficial effects of the prolactin release inhibitor bromocriptine in PPCM. Methods and results In this multicentre trial, 63 PPCM patients with left ventricular ejection fraction (LVEF) ≤35% were randomly assigned to short-term (1W: bromocriptine, 2.5 mg, 7 days) or long-term bromocriptine treatment (8W: 5 mg for 2 weeks followed by 2.5 mg for 6 weeks) in addition to standard heart failure therapy. Primary end point was LVEF change (delta) from baseline to 6 months assessed by magnetic resonance imaging. Bromocriptine was well tolerated. Left ventricular ejection fraction increased from 28 ± 10% to 49 ± 12% with a delta-LVEF of + 21 ± 11% in the 1W-group, and from 27 ± 10% to 51 ± 10% with a delta-LVEF of + 24 ± 11% in the 8W-group (delta-LVEF: P = 0.381). Full-recovery (LVEF ≥ 50%) was present in 52% of the 1W- and in 68% of the 8W-group with no differences in secondary end points between both groups (hospitalizations for heart failure: 1W: 9.7% vs. 8W: 6.5%, P = 0.651). The risk within the 8W-group to fail full-recovery after 6 months tended to be lower. No patient in the study needed heart transplantation, LV assist device or died. Conclusion Bromocriptine treatment was associated with high rate of full LV-recovery and low morbidity and mortality in PPCM patients compared with other PPCM cohorts not treated with bromocriptine. No significant differences were observed between 1W and 8W treatment suggesting that 1-week addition of bromocriptine to standard heart failure treatment is already beneficial with a trend for better full-recovery in the 8W group. Clinical trial registration ClinicalTrials.gov, study number: NCT00998556.

/pdf/bromocriptine-for-the-treatment-of-peripartum-cardiomyopathy-3n70ixn1vk.pdf

Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study.

Prolactin and autoimmunity.

Peripartum cardiomyopathy (PPCM) is a serious, potentially life-threatening heart disease of unknown etiology in previously healthy women that develops between the last month of pregnancy and 5-6 months after delivery. PPCM is a distinct clinical entity in which echocardiography demonstrates the features of an idiopathic dilated cardiomyopathy with a high morbidity and mortality, but in addition, patients suffering with PPCM have a chance of reaching full recovery. A variety of potential risk factors related to PPCM have been suggested over the last decades, which may help to identify women at risk in the future. Recent advances in understanding the pathophysiology of PPCM assign a key role to unbalanced oxidative stress and the generation of a cardiotoxic prolactin subfragment. In this regard, pharmacological blockade of prolactin holds the promise of novel, more disease-specific therapy options. The present article provides an overview on the clinical appearance and management, risk factors and potential pathophysiological mechanisms of PPCM.

Reviewing peripartum cardiomyopathy: current state of knowledge.

Background Peripartum cardiomyopathy (PPCM) is a pregnancy-associated cardiomyopathy in previously healthy women. Mice with a cardiomyocyte-restricted deletion of signal transducer and activator of transcription-3 (STAT3, CKO) develop PPCM. PI3K-Akt signalling is thought to promote cardiac hypertrophy and protection during pregnancy. We evaluated the role of activated Akt signalling in the maternal heart postpartum.

Methods and results CKO mice were bred to mice harbouring an Akt transgene, specifically expressed in cardiomyocytes (CAkttg) generating CKO; CAkttg, CAkttg, CKO, and wild-type sibling mice. CAkttg and CKO;CAkttg female mice developed PPCM with systolic dysfunction. Both genotypes displayed cardiac hypertrophy and lower capillary density, showed increased phosphorylation of p66 Src homology 2 domain containing protein and FoxO3A, and reduced expression of manganese superoxide dismutase as well as increased cathepsin D activity and increased miR-146a levels [indicative for generation of the anti-angiogenic 16 kDa prolactin (PRL)]. Cardiac inflammation and fibrosis was accelerated in CKO;CAkttg and associated with high postpartum mortality. The PRL blocker, bromocriptine (BR), prevented heart failure and the decrease in capillary density in CKO;CAkttg and CAkttg mice. BR attenuated high mortality, up-regulation of CCL2, and cardiac inflammation as well as fibrosis in CKO;CAkttg. PRL infusion induced cardiac inflammation in CKO;CAkttg independent of pregnancy. In neonatal rat cardiomyocytes, PRL and interferon γ (IFNγ) induced the expression of CCL2 via activation of Akt.

Conclusion Postpartum Akt activation is detrimental for the peripartum heart as it lowers anti-oxidative defence and in combination with low STAT3 conditions, accelerate cardiac inflammation and fibrosis. PRL and its cleaved 16 kDa form are central for Akt-induced PPCM as indicated by the protection from the disease by PRL blockade.

Opposing roles of Akt and STAT3 in the protection of the maternal heart from peripartum stress.

Peripartum/postpartum cardiomyopathy (PPCM) is a potentially life-threatening disease of uncertain aetiology in previously healthy women. Clinical and experimental data suggested inflammation, autoimmune processes, apoptosis and endothelial dysfunction as typical pathophysiological features of PPCM. Recent data discovered that unbalanced peri/postpartum oxidative stress linked to proteolytic cleavage of the nursing hormone prolactin into a potent anti-angiogenic, pro-apoptotic and pro-inflammatory 16-kDa subform as a potential pathomechanism for the development of PPCM. Consistent with these idea, blockade of prolactin by bromocriptine, a dopamine D2 receptor agonist, prevented the onset of disease in an experimental model of PPCM and appeared successful in small pilot trials with respect to prevention or treatment of PPCM in patients. Here we highlight the current state of knowledge on diagnosis of PPCM, provide novel insights into the pathophysiology behind the disease and outline potential consequences for the clinical management and treatment options for patients at risk for or with PPCM.

https://heart.bmj.com/content/heartjnl/96/17/1352.full.pdf?96%2F17%2F1352=

Prolactin: a new therapeutic target in peripartum cardiomyopathy

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Reviewing peripartum cardiomyopathy: current state of knowledge.

Opposing roles of Akt and STAT3 in the protection of the maternal heart from peripartum stress.

Prolactin: a new therapeutic target in peripartum cardiomyopathy