Comment On: Peripartum Cardiomyopathy Treatment with Dopamine Agonist and Subsequent Pregnancy with a Satisfactory Outcome.
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ABSTRACT:
SUBMITTER: Triebel J
PROVIDER: S-EPMC10309486 | biostudies-literature | 2016 Nov
REPOSITORIES: biostudies-literature
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Comment On: Peripartum Cardiomyopathy Treatment with Dopamine Agonist and Subsequent Pregnancy with a Satisfactory Outcome.
Triebel Jakob J Clapp Carmen C Bertsch Thomas T
Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia 20161122 11
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Project description:Study objectiveTo evaluate patient-level differences and decision making surrounding subsequent pregnancies (SSP) after peripartum cardiomyopathy (PPCM).DesignMixed methods approach to evaluate quantitative demographic and clinical differences between patients with and without a SSP and to qualitatively describe the decision-making regarding a SSP with a survey component.Setting/participants220 PPCM cases within the University of Pennsylvania Health System.Main outcome measuresDemographic, clinical and obstetrical outcomes.Results73 patients (33 %) had a SSP, 37 with a live birth. Those with a SSP were more likely to self-identify as Black (70 % vs. 52 %; p = 0.04), be nulliparous in index pregnancy (68 % vs. 45 %, p = 0.02), were younger at diagnosis (24.3 vs. 30.5 years; p < 0.01), and a higher left ventricular ejection fraction (LVEF) at diagnosis (35 % vs. 27.5 %; p = 0.03) compared to patients without a SSP. There was no difference in recovery rates of LVEF (62 % vs. 50 %, p = 0.17), or need for LVAD, transplant, or death. 22 patients completed the survey (representing 44 SSPs): 41 % of SSPs (n = 18) resulted in termination, 18 % (n = 8) in a first/s trimester loss, and 41 % (n = 18) in a live-born delivery. All patients who elected termination indicated risk of recurrence/worsening heart failure to be a motivating factor.ConclusionsLess than 20 % of patients in this single-center, multi-racial cohort had a SSP and delivery after PPCM with fear of recurrence as a large driver in this decision. Patients with a SSP were younger with a higher EF at diagnosis but ultimately had similar cardiac outcomes as patients without a SSP.
| S-EPMC11541426 | biostudies-literature
Project description:ObjectiveThe aim of this study is to evaluate the contribution of pre-pregnancy obesity and overweight to peripartum cardiomyopathy.Study designThis population-based study used linked birth record and maternal hospital discharge data from live births in California during 2007 to 2012 (n = 2,548,380). All women who had a diagnosis of peripartum cardiomyopathy during the childbirth hospitalization or who were diagnosed with peripartum cardiomyopathy during a postpartum hospital readmission within 5 months of birth were identified as cases. Pre-pregnancy body mass index (BMI, kg/m2) was classified as normal weight (18.5-24.9), overweight (25.0-29.9), obesity class 1 (30.0-34.9), obesity class 2 (35.0-39.9), and obesity class 3 (≥40). Because of small numbers, we excluded women with underweight BMI, and in some analyses, we combined obesity classes into one group. Logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) expressing associations between BMI and peripartum cardiomyopathy, adjusted for maternal age, race/ethnicity, education, health care payer, parity, plurality, and comorbidities.ResultsThe overall prevalence of peripartum cardiomyopathy during hospital admissions was 1.3 per 10,000 live births (n = 320). Unadjusted ORs were 1.32 (95% CI: 1.01-1.74) for women with overweight BMI and 2.03 (95% CI: 1.57-2.62) for women with obesity, compared with women with normal pre-pregnancy BMI. Adjusted ORs were 1.26 (95% CI: 0.95-1.66) for overweight women and 1.38 (95% CI: 1.04-1.84) for women with obesity. The ORs suggested a dose-response relationship with increasing levels of obesity, but the 95% CIs for the specific classes of obesity included 1.00.ConclusionPre-pregnancy obesity was associated with an increased risk of peripartum cardiomyopathy. These findings underscore the importance of BMI during pregnancy. There is a need to recognize the increased risk of peripartum cardiomyopathy in women with high BMI, especially in the late postpartum period.Key points· Pre-pregnancy obesity affects maternal health.. · Effects may extend to peripartum cardiomyopathy.. · The risk includes peripartum cardiomyopathy that emerges postpartum..
| S-EPMC7722175 | biostudies-literature
Project description: Not available
| S-EPMC10332675 | biostudies-literature
Project description:AimsPeripartum cardiomyopathy (PPCM) is a rare heart disease, occurring in previously heart-healthy women during the last month of pregnancy or the first months after delivery due to left ventricular (LV) systolic dysfunction. A common pathomechanistic pathway of PPCM includes increased oxidative stress and the subsequent generation of a cleaved prolactin fragment (16 kDa PRL), which promotes the onset of heart failure (HF) in a microRNA (miR)-146a-dependent manner. Inhibition of prolactin secretion with the dopamine D2 receptor (D2R) agonist bromocriptine combined with standard HF therapy supports cardiac recovery. This study examined whether treatment with the more selective D2R agonist cabergoline prevents HF development in an experimental PPCM mouse model and might be used as an alternative treatment regime for PPCM.Methods and resultsPostpartum (PP) female PPCM-prone mice with a cardiomyocyte restricted STAT3-deficiency (αMHC-Cretg/+ ; Stat3fl/fl ; CKO) were treated over two consecutive nursing periods with cabergoline (CKO Cab, 0.5 mg/kg/day) and were compared with bromocriptine treated CKO (CKO Br) and postpartum-matched WT and CKO mice. Cabergoline treatment in CKO PP mice preserved cardiac function [fractional shortening (FS): CKO Cab: 34.5 ± 9.4% vs. CKO: 22.1 ± 9%, P < 0.05] and prevented the development of cardiac hypertrophy, fibrosis, and inflammation as effective as bromocriptine therapy (FS: CKO Br: 33.4 ± 5.6%). The myocardial up-regulation of the PPCM biomarkers plasminogen inhibitor activator 1 (PAI-1) and miR-146a were prevented by both cabergoline and bromocriptine therapy. A small cohort of three PPCM patients from the German PPCM Registry was treated with cabergoline (1 mg per week for 2 weeks, followed by 0.5 mg per week for another 6 weeks) due to a temporary unavailability of bromocriptine. All PPCM patients initially presented with a severely reduced LV ejection fraction (LVEF: 26 ± 2%). However, at 6 months of follow-up, LV function (LVEF: 56 ± 2%) fully recovered in all three PPCM patients, and no adverse events were detected.ConclusionsIn the experimental PPCM mouse model, the selective D2R agonist cabergoline prevents the onset of postpartum HF similar to bromocriptine. In PPCM patients, cabergoline treatment was safe and effective as all patients fully recovered. Cabergoline might serve as a promising alternative to bromocriptine. However, these findings are based on experimental data and a small case series and thus have to be interpreted with caution and should be validated in a larger clinical trial.
| S-EPMC9871652 | biostudies-literature
Project description:BackgroundPeripartum cardiomyopathy (PPCM) is a serious cardiac disorder occurring late in pregnancy or early in the postpartum period. We examined associations between hypertensive disorders of pregnancy (HDP: preeclampsia and gestational hypertension) and PPCM, accounting for other pregnancy-related risk factors for PPCM.MethodsUsing nationwide Danish register data, we constructed a cohort of all women with ≥1 live birth or stillbirth in Denmark between 1978 and 2012. Using log-linear binomial regression and generalized estimating equations, we estimated risk ratios (RRs) for PPCM associated with HDP of varying severity.ResultsIn a cohort of 1,088,063 women with 2,078,822 eligible pregnancies, 126 women developed PPCM (39 in connection with an HDP-complicated pregnancy). The risks of PPCM were significantly higher in women with HDP-complicated pregnancies than in women with normotensive pregnancies (severe preeclampsia, RR 21.2, 95% confidence interval [CI] 12.0-37.4; moderate preeclampsia, RR 10.2, 95% CI 6.18-16.9; gestational hypertension, RR 5.16, 95% CI 2.11-12.6). The RRs for moderate preeclampsia and gestational hypertension were not significantly different from one another (p = 0.18); the RR for severe preeclampsia was significantly different from the RR for moderate preeclampsia and gestational hypertension combined (p = 0.02).ConclusionsAlthough 70% of PPCM occurred in women with normotensive pregnancies, HDPs were associated with substantial increases in PPCM risk that depended on HDP severity. The heart's capacity to adapt to a normal pregnancy may be exceeded in some women already susceptible to cardiac insult, contributing to PPCM. HDPs, severe preeclampsia in particular, probably represent an additional cardiac stressor during pregnancy.
| S-EPMC6382119 | biostudies-literature
Project description:BackgroundPredictors, pregnancy and subsequent pregnancy outcomes in women with peripartum cardiomyopathy (PPCM) are poorly understood in our geographical region.MethodsWe retrospectively analysed 58 women with PPCM diagnosed using criteria by the European Society of Cardiology during 2015 to 2019. The main outcome measures were predictors of left ventricular (LV) recovery. LV recovery was defined as return of LV ejection fraction to over 50%.ResultsNearly 80% of women had LV recovery during 6 months follow up. Univariate logistic regression revealed LV end diastolic diameter (adjusted odds ratio (OR); 0.87; 95% CI, 0.78-0.98; p = 0.02), LV end systolic diameter (OR; 0.89; 95% CI, 0.8-0.98; p = 0.02) and inotrope use (OR; 0.2, 95% CI, 0.05-0.7; p = 0.01) as predictors of LV recovery. Relapse was not seen in any of the nine women who had a subsequent pregnancy.ConclusionLV recovery was higher than those reported in contemporary PPCM cohorts from other parts of the world.
| S-EPMC10150308 | biostudies-literature
Project description:Purpose of reviewPeripartum cardiomyopathy (PPCM) is an idiopathic disorder defined as heart failure occurring in women during the last month of pregnancy and up to 5 months postpartum. In this review, we outline recent reports about the disease pathogenesis and management and highlight the use of diagnosis and prognosis biomarkers.Recent findingsNovel data strengthen the implication of endothelial function in PPCM pathogenesis. The first international registry showed that patient presentations were similar globally, with heterogeneity in patient management and outcome. Despite large improvement in patient management and treatment, there is still a sub-group of women who die from PPCM or who will not recover their cardiac function. Remarkable advances in the comprehension of disease incidence, pathogenesis, and prognosis could be determined with multi-center and international registries.Clinical trialsClinicalTrials.gov Identifier: NCT02590601.
| S-EPMC6132730 | biostudies-literature
Project description:Peripartum cardiomyopathy (PPCM) is a severe cardiac disease occurring in the last month of pregnancy or in the first 5 months after delivery and shows many similar clinical characteristics as dilated cardiomyopathy (DCM) such as ventricle dilation and systolic dysfunction. While PPCM was believed to be DCM triggered by pregnancy, more and more studies show important differences between these diseases. While it is likely they share part of their pathogenesis such as increased oxidative stress and an impaired microvasculature, discrepancies seen in disease progression and outcome indicate there must be differences in pathogenesis as well. In this review, we compared studies in DCM and PPCM to search for overlapping and deviating disease etiology, pathogenesis and outcome in order to understand why these cardiomyopathies share similar clinical features but have different underlying pathologies.
| S-EPMC4295435 | biostudies-other
Project description:Peripartum cardiomyopathy is a rare and potentially fatal disease. Though approximately half of the patients recover, the clinical course is highly variable and some patients develop refractory heart failure and persistent left ventricular systolic dysfunction. It is diagnosed when women present with heart failure secondary to left ventricular systolic dysfunction towards the end of pregnancy or in the months following delivery, where no other cause of heart failure is found. Etiology remains unclear, and treatment is similar to other cardiomyopathies and includes evidence-based standard heart failure management strategies. Experimental strategies such as intravenous immunoglobulin and bromocriptine await further clinical validation.
| S-EPMC3600883 | biostudies-other
Project description:BackgroundPeripartum cardiomyopathy (PPCM) remains a major cause of maternal morbidity and mortality.ObjectivesThis study sought to prospectively evaluate recovery of the left ventricular ejection fraction (LVEF) and clinical outcomes in the multicenter IPAC (Investigations of Pregnancy Associated Cardiomyopathy) study.MethodsWe enrolled and followed 100 women with PPCM through 1 year post-partum. The LVEF was assessed by echocardiography at baseline and at 2, 6, and 12 months post-partum. Survival free from major cardiovascular events (death, transplantation, or left ventricular [LV] assist device) was determined. Predictors of outcome, particularly race, parameters of LV dysfunction (LVEF), and remodeling (left ventricular end-diastolic diameter [LVEDD]) at presentation, were assessed by univariate and multivariate analyses.ResultsThe cohort was 30% black, 65% white, 5% other; the mean patient age was 30 ± 6 years; and 88% were receiving beta-blockers and 81% angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. The LVEF at study entry was 0.35 ± 0.10, 0.51 ± 0.11 at 6 months, and 0.53 ± 0.10 at 12 months. By 1 year, 13% had experienced major events or had persistent severe cardiomyopathy with an LVEF <0.35, and 72% achieved an LVEF ≥0.50. An initial LVEF <0.30 (p = 0.001), an LVEDD ≥6.0 cm (p < 0.001), black race (p = 0.001), and presentation after 6 weeks post-partum (p = 0.02) were associated with a lower LVEF at 12 months. No subjects with both a baseline LVEF <0.30 and an LVEDD ≥6.0 cm recovered by 1 year post-partum, whereas 91% with both a baseline LVEF ≥0.30 and an LVEDD <6.0 cm recovered (p < 0.00001).ConclusionsIn a prospective cohort with PPCM, most women recovered; however, 13% had major events or persistent severe cardiomyopathy. Black women had more LV dysfunction at presentation and at 6 and 12 months post-partum. Severe LV dysfunction and greater remodeling at study entry were associated with less recovery. (Investigations of Pregnancy Associated Cardiomyopathy [IPAC]; NCT01085955).
| S-EPMC5645077 | biostudies-literature