围生期心肌病并重度妊娠期高血压的护理体会

围生期心肌病并重度妊娠期高血压严重威胁孕妇及胎儿生命安全,愈来愈受到医护人员的高度重视。1999年1月-2009年2月,我院收治该病患者21例,现将护理体会总结如下。     

围产期心肌病病因学研究进展

围产期心肌病是一种特发性心肌病,发病率低,但可以导致患者死亡。目前该病病因及发病机制尚不明确。本文就近年对围产期心肌病的病因学研究进行综述,为临床诊断治疗提供帮助。     

妊娠期心血管药物的应用

妊娠期最常见的心脏病有高血压、风湿性心脏病并发心力衰竭或心律失常,其次为先天性心脏病、原发性肺动脉高压、心肌病等。因此,妊娠期使用心血管药物,应考虑药物在妊娠早期对胎儿有否畸形的威胁,妊娠晚期是否会引起分娩功能的障碍,以及在正常妊娠过程中药物对母体和胎儿的影响。本文对各种     

围产期心肌病（PPCM）的回顾与展望

围产期心肌病是指在妊娠最后３个月或产后６个月内发生的以累及心肌为主的一种心脏病。临床上以充血性心衰为主要表现。近年来有关围产期心肌病的研究日渐增多，本文重点就该病病因，病理、临床特点、治疗及预后做一综述。     

围产期心肌病危险因素研究进展

围产期心肌病是一种特发性心肌病。该疾病相对少见,但发病率正在上升,目前对围产期心肌病危险因素的理解是有限的。本文结合最新的研究进展,从生活方式、人口学特点、合并症及分娩因素对围产期心肌病的危险因素进行综述,旨在进行预防和早期干预,降低围产期心肌病发病率及改善患者预后。     

围产期保健与优生

围产期保健与优生,就是要通过围产期保健达到优生(出生健康无损的新生儿)的目的。一、从围产期保健谈优生(一) 围产医学(Perinaual medicine):为近20多年来从产科学和新生儿学中形成的一门新兴科学。其主要研究为胚胎发育、遗传,胎儿生理与病理,胎儿疾病诊断及妊娠期、分娩期、产后期     

药物治疗妊娠期糖尿病的研究进展

妊娠期糖尿病(GDM)是指在妊娠阶段首次发生或发现的任何程度的糖耐量异常,GDM可导致母体及婴儿一系列产前、产时和产后并发症。早期诊断及正确治疗对孕母及胎儿的预后有重要意义。GDM的治疗主要包括饮食、运动和药物治疗,药物治疗首选人胰岛素治疗,慎用胰岛素类似物和口服降糖药。治疗的关键在于严格控制GDM患者血糖,减少围产期并发症的发生。本文就GDM药物治疗的进展予以综述。     

妊娠期哮喘处理的现代概念

据报道妊娠期哮喘的发生率为0.4～1.3%,为妊娠期最常见的阻塞性肺部疾病。虽则控制满意的皮质类固醇-依赖性哮喘的妇女,其妊娠的结果与普通妇女几乎一样良好,喘鸣发作若未能控制则与母亲围产期死亡率有关。哮喘的药物疗法对胎儿必须没有致畸形性,也不应危害母体。【妊娠期肺的生理性改变】     

应重视妊娠期高血压对女性远期心血管健康的影响

<正>妊娠期高血压疾病(妊娠期高血压)是女性孕期常见的并发症之一。过去医生们多关注妊娠期高血压对围产期的影响,如增加早产、胎儿宫内窘迫及胎儿成年后患心血管病等慢性疾病的风险("胎源性"假说),却忽略了其对女性自身远期健康的影响。直到近期研究发现,妊娠期高血压与传统心血管危险因素一样,是女性远期心血管疾病的独立危险因素。1妊娠期高血压与女性远期心血管疾病的关系:循证医学证据1.1对高血压的影响妊娠期间血压升高的女性,尽     

肝内胆汁淤积症孕妇的围产期管理(附172例报告)

妊娠期肝内胆汁淤积症(ICP)，最早可发生于妊娠10周，但多发生于妊娠晚期。因其可导致早产、胎儿宫内窘迫及胎儿猝死、产后出血，故其围产期管理越来越受到产科临床的重视。1998年1月～2003年8月，我院收治ICP患者172例，现对其围产期管理进行讨论。     

Pathophysiology,diagnosis and management of peripartum cardiomyopathy: a position statement from the Heart Failure Association of the European Society of Cardiology Study Group on peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is a potentially life‐threatening condition typically presenting as heart failure with reduced ejection fraction (HFrEF) in the last month of pregnancy or in the months following delivery in women without another known cause of heart failure. This updated position statement summarizes the knowledge about pathophysiological mechanisms, risk factors, clinical presentation, diagnosis and management of PPCM. As shortness of breath, fatigue and leg oedema are common in the peripartum period, a high index of suspicion is required to not miss the diagnosis. Measurement of natriuretic peptides, electrocardiography and echocardiography are recommended to promptly diagnose or exclude heart failure/PPCM. Important differential diagnoses include pulmonary embolism, myocardial infarction, hypertensive heart disease during pregnancy, and pre‐existing heart disease. A genetic contribution is present in up to 20% of PPCM, in particular titin truncating variant. PPCM is associated with high morbidity and mortality, but also with a high probability of partial and often full recovery. Use of guideline‐directed pharmacological therapy for HFrEF is recommended in all patients respecting contraindications during pregnancy/lactation. The oxidative stress‐mediated cleavage of the hormone prolactin into a cardiotoxic fragment has been identified as a driver of PPCM pathophysiology. Pharmacological blockade of prolactin release using bromocriptine as a disease‐specific therapy in addition to standard therapy for heart failure treatment has shown promising results in two clinical trials. Thresholds for devices (implantable cardioverter‐defibrillators, cardiac resynchronization therapy and implanted long‐term ventricular assist devices) are higher in PPCM than in other conditions because of the high rate of recovery. The important role of education and counselling around contraception and future pregnancies is emphasised.     

Peripartale Kardiomyopathie

Peripartum cardiomyopathy (PPCM) is a rare and potentially life-threatening heart disease of unknown etiology that is restricted to the last month of pregnancy and up to 6 months postpartum. The morphology similates that of idiopathic dilated cardiomyopathy with a rapid progression to end-stage heart failure and is associated with a high morbidity and mortality rate. PPCM is treated with standard therapy for heart failure in accordance with the current guidelines. New findings suggest that elevated oxidative stress in the postpartum phase promotes cleavage of the nursing hormone prolactin into a toxic 16-kDa fragment that affects microcirculation and cardiomyocyte metabolism. Thus prolactin blocking using bromocriptine as a more specific therapy option showed promising early clinical results and is currently being tested in larger randomized trials. Frequent symptoms such as general fatigue, dyspnea and dry cough are often misinterpreted as pregnancy-related disturbances, and diagnosis is therefore often late. Interdisciplinary management, early diagnosis and more disease-specific therapy options appear to promote cardiac recovery in PPCM patients.     

Recovery from peripartum cardiomyopathy after treatment with bromocriptine

Peripartum cardiomyopathy (PPCM) is a potentially devastating cause of heart failure that affects women late in pregnancy or in early puerperium. Recent findings showed that a 16 kDa fragment of prolactin may induce myocardial damage, and this offered a new option of treating PPCM by blocking prolactin with bromocriptine. We report on a 35-year-old woman with a twin gravidity who gave birth to two healthy boys at day 36/6 and developed a potentially fatal PPCM. Within 3 days since delivery she suffered from severe symptoms of heart failure (orthopnoea, pleural and pericardial effusion, reduced systolic function LVEF 15%). Bromocriptine 2.5 mg bid was added to standard heart failure therapy at day 6 after delivery, and within a week the patient recovered to NYHA functional class II. 2 months later she presented in a good state, NYHA class I, and MRI confirmed an LVEF of 60%. Balancing the potential side effects of bromocriptine against the very poor prognosis in severe PPCM our case supports the use of bromocriptine as a specific novel therapy.     

Peripartum cardiomyopathy

Peripartum cardiomyopathy is now increasingly recognized as a cause of heart failure in the later months of pregnancy and early postpartum period. Clinical diagnosis may be challenging as it closely resembles several common medical and obstetric complications. Complex pathogenesis, unpredictable onset, staggered recovery, and unanticipated fetomaternal risks pose unique challenge to clinicians. Prevalence seems to vary with race, geographic location, and diagnostic criteria. The presence of multiple risk factors substantially elevates the risk of PPCM. Transthoracic echocardiographic examination can exclude the majority of the mimickers. Symptomatic presentation is initially limited to, varying grades of low cardiac output syndrome. Rarely, PPCM begins with decompensated heart failure and cardiovascular collapse. Guideline-directed medical therapy involves graded initiation and titration of heart failure medications while ensuring the fetal and neonatal safety. Anesthetic and obstetric management should be individualized to improve fetomaternal outcomes. However, emergent cesarean delivery may be required in women with decompensated heart failure and cardiovascular collapse. An early institution of mechanical circulatory support has shown to improve outcome. Bromocriptine and other experimental drugs designed to target pathogenic pathway have yielded mixed results. A further change in approach to management requires a comprehensive understanding of pathophysiology and fetomaternal safety profiles of heart failure medications.

     

Reversal of IFN-gamma, oxLDL and prolactin serum levels correlate with clinical improvement in patients with peripartum cardiomyopathy

AIM: Peripartum cardiomyopathy (PPCM) is characterized by acute onset of heart failure of unknown aetiology. We aimed to identify mechanisms involved in initiation and progression of the disease. METHODS AND RESULTS: Serum markers related to cardiac function, apoptosis, oxidative stress, remodelling, inflammation and the nursing hormone prolactin were analyzed in PPCM patients and healthy controls. The kinetics of these markers were compared between patients who improved cardiac function (IMP) and those patients who did not improve (NIMP), over 6 months follow-up. All patients received ACE-inhibitors, beta-blockers and diuretics. Baseline levels of TGF-beta-1 were significantly lower, MMP-9 and VEGF were not different; all other markers were significantly higher in PPCM compared with controls. Only baseline NT-proBNP levels were higher in NIMP compared with IMP. After 6 months, NT-proBNP, oxLDL and IFN-gamma were significantly lower in IMP and the decrease in oxLDL, IFN-gamma and prolactin was significant in IMP but not in NIMP. Significant correlations were observed between the kinetics of NT-proBNP, oxLDL, prolactin and IFN-gamma in PPCM patients. CONCLUSION: Baseline NT-proBNP and the failure to decrease oxLDL, IFN-gamma and prolactin are associated with poor outcome in PPCM, suggesting a potential role of these factors in the pathophysiology of PPCM and for risk stratification of PPCM patients.     

Bromocriptine as a new therapeutic agent for peripartum cardiomyopathy

Peripartum cardiomyopathy (PPCM) is a poorly understood, rare disorder in which left ventricular systolic dysfunction and symptoms of heart failure occur between the last month of pregnancy and the first 5 months postpartum. Recent data suggest that uncontrolled oxidative stress leads to the activation of the prolactin cleaving enzyme cathepsin D that in turn leads to an increase in a cleaved 16 kDa prolactin. This cleaved form that has an angiostatic and proapoptotic role appears to drive the disease by adversely impacting the endothelium and cardiomyocyte. Bromocriptine that reduces the prolactin production by dopamine agonist actions may improve outcomes in patients with peripartum cardiomyopathy by eliminating the cleaved form of prolactin despite the activation of the cleaving enzyme. In limited case reports and proof of concept studies use of bromocriptine in the early stages has been shown to improve outcomes in patients with peripartum cardiomyopathy. However, larger randomized control study is still awaited.     

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

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.     

Peripartum Cardiomyopathy: a Review for the Clinician

Purpose of review

This review summarizes the pathophysiology, diagnosis, and treatment of peripartum cardiomyopathy (PPCM), with a focus on recent discoveries of clinical relevance.

Recent findings

An increase in oxidative stress and anti-angiogenic activity play key roles in the pathophysiology of peripartum cardiomyopathy. Therapies that target this dysregulation may have a future role in treatment. Suppression of prolactin release using bromocriptine, a dopamine-receptor antagonist, has been associated with more favorable outcomes in small studies but more research is needed. Similarly, VEGF agonists may prove to be a novel therapy by upregulating angiogenesis.

Summary

Peripartum cardimyopathy typically presents in the third trimester or in first few months postpartum. Both genetic and clinical risk factors for PPCM have been identified. Women with PPCM should be managed by a multidisciplinary team with experience in high risk pregnancy and the treatment of heart failure. These women benefit from the use of standard treatments for heart failure therapy with the exception of avoiding ACE inhibitors and ARBs while pregnant. While the rate of recovery of ventricular function in PPCM is higher than in other forms of dilated cardiomyopathy, mechanical circulatory support and/or cardiac transplantation are required in some cases.

     

Peripartum cardiomyopathy: recent insights in its pathophysiology

Peripartum/Postpartum cardiomyopathy (PPCM) is a serious, potentially life-threatening heart disease of uncertain etiology in previously healthy women. Previous clinical and experimental data have identified inflammation, autoimmune processes, apoptosis, and impaired cardiac (systemic) microvasculature as typical features in the pathophysiology of PPCM. However, recent data have shown that unbalanced peri/postpartum oxidative stress is linked to proteolytic cleavage of the nursing hormone prolactin into a potent antiangiogenic, proapoptotic, and pro-inflammatory factor. These observations strongly suggest that prolactin cleavage can operate as a specific pathomechanism for the development of PPCM. Consistent with these findings, inhibition of prolactin secretion by bromocriptine, a dopamine D2 receptor agonist, prevented the development of PPCM in an animal model of PPCM, and first clinical experience are promising in this respect. Thus, inhibition of prolactin release may represent a novel specific therapeutic approach to either prevent or treat patients with acute PPCM. In this review, we are highlighting the current knowledge on risk factors, potential pathomechanisms, and treatment options for PPCM.     

Peripartum cardiomyopathy: a comprehensive review

Peripartum cardiomyopathy (PPCM) is a rare disorder in which left ventricular dysfunction and symptoms of heart failure occur in the peripartum period in previously healthy women. Incidence of PPCM ranges from 1 in 1300 to 1 in 15,000 pregnancies. The etiology of PPCM is unknown, but viral, autoimmune, and idiopathic causes may contribute. The diagnostic criteria are onset of heart failure in the last month of pregnancy or in first 5 months postpartum, absence of determinable cause for cardiac failure, and absence of a demonstrable heart disease before the last month of pregnancy. Risk factors for PPCM include advanced maternal age, multiparity, African race, twinning, gestational hypertension, and long-term tocolysis. The clinical presentation of patients with PPCM is similar to that of patients with dilated cardiomyopathy. Early diagnosis and initiation of treatment are essential to optimize pregnancy outcome. Treatment is similar to medical therapy for other forms of dilated cardiomyopathy. About half the patients of PPCM recover without complications. The prognosis is poor in patients with persistent cardiomyopathy. Persistence of disease after 6 months indicates irreversible cardiomyopathy and portends worse survival.