UNASSIGNED: We investigated the risk factors and characteristic clinical features of peripartum cardiomyopathy (PPCM) to lay the groundwork for early identification, screening, diagnosis, and intervention in high-risk pregnant women.
UNASSIGNED: A retrospective case-control study was conducted to analyze data from 44 patients with PPCM and 226 normal pregnant women from a Chinese population.
UNASSIGNED: Significant differences were found between the groups in terms of various factors such as age, body mass index (BMI), heart rate, and medical history. Logistic regression models identified abnormal electrocardiography (OR=18.852), upper respiratory tract infection (OR=41.822), gestational hypertension (OR=18.188), and cesarean section (OR=8.394) as risk factors for PPCM. Common clinical features observed in patients with PPCM included cough, wheezing, and chest tightness (68.18%), left heart enlargement (56.82%) and valvular insufficiency (81.82%). Additionally, cardiotropic virus was detected in a subset of patients (43.18%) and NT-proBNP was elevated ≥ 400 pg/mL (81.82%).
UNASSIGNED: In the Chinese population, the presence of abnormal electrocardiograms during pregnancy, history of upper respiratory tract infection, gestational hypertension, and maternal choice of cesarean section suggest the possibility of PPCM development. Factors such as advanced age, family history of cardiovascular disease, gestational diabetes mellitus, eclampsia, anemia, and hypoproteinemia should be considered. Clinically, patients present with cough, wheezing, chest tightness, enlarged left heart, valvular insufficiency and NT-proBNP elevated ≥ 400 pg/mL. This study could serve as a valuable reference for medical practitioners for the early identification and screening of patients with PPCM.

Peripartum cardiomyopathy (PPCM) is a potentially life-threatening complication of pregnancy, but identifying patients at higher risk of this condition remains difficult.
We conducted a study to identify new risk factors associated with PPCM and predictors of poor outcomes.
This retrospective analysis included a total of 44 women with PPCM. As a control group, 79 women who gave birth around the same time as the PPCM patients and who did not have organic disease were included. A multivariate regression analysis was conducted to identify risk factors associated with PPCM and with delayed recovery.
All PPCM patients were discharged within 28 days. In comparison to the control group, PPCM patients had higher rates of preeclampsia (20.4% vs. 1.27%, P<0.001), autoimmune disease (27.3% vs. 11.4%, P = 0.018), and cesarean delivery with preterm labor (31.8% vs. 17.7%, P = 0.037). The neonates of PPCM patients had lower birth weight (2.70±0.66 kg vs. 3.21±0.57 kg, P<0.001). PPCM patients had higher levels of C-reactive protein, d-dimer, brain natriuretic peptide (BNP), and serum phosphorus, but lower levels of albumin and serum calcium (all P<0.001). In all patients with PPCM, the left ventricular ejection fraction (LVEF) returned to normal (≥50%) within 28 days after admission. Subjects with early recovery (n = 34) had lower BNP than those with delayed recovery (n = 10) (649.7 ± 526.0 pg/mL vs. 1444.1 ± 1040.8 pg/mL, P = 0.002). Multivariate regression led to a three-point score system to predict PPCM (1 point each for the presence of pericardial effusion, left ventricular dilatation, and d-dimer level ≥0.5 μg/mL). At a cutoff of ≥2, this scoring system predicted delayed recovery with 95.5% sensitivity and 96.1% specificity. The negative predictive value was 97.4% and the positive predictive value was 93.3%. Binary logistic regression indicated that PPCM patients with pulmonary hypertension, lower hemoglobin, or worse LVEF tended to require longer hospital stay (minimum 14 days).
A risk score that consists of pericardial effusion, left ventricular dilatation, and d-dimer level ≥ 0.5 μg/mL could help streamline the diagnosis of PPCM prior to confirmatory investigations. Moreover, a risk score that consists of pulmonary hypertension, lower hemoglobin and worse LVEF could help to predict poor outcomes in PPCM patients.

OBJECTIVE: Peripartum cardiomyopathy (PPCM) are more vulnerable to intracardiac thrombus than other types of cardiomyopathies, although explicit anticoagulant strategy is not sure. Too aggressive anticoagulation therapy can lead to severe bleeding events. Hence, we want to construct a risk stratification model for intracardiac thrombus in PPCM patients.
RESULTS: A total of 159 suspected PPCM cases were initially screened, whereas 123 confirmed cases were enrolled in the final analysis. The study population was randomly assigned as derivation group (N = 83) and validation group (N = 40). The derivation cohort was utilized to develop the model, and the validation cohort was used to internal validate the discriminatory ability of the model. Formation of intracardiac thrombus was detected in 22 patients. After adjusted by multivariable logistic regression analysis, left ventricle ejection fraction (LVEF, OR 0.772, 95% CI 0.665-0.897, P = 0.001), haemoglobin levels (OR 1.050, 95% CI 1.003-1.099, P = 0.038), and thrombocyte counts (OR 1.018, 95% CI 1.006-1.029, P = 0.003) were identified as risk factors independently associated with intracardiac thrombus and were finally included in the tentative risk stratification model with a C-indexes of 0.916 (95% CI: 0.850-0.982, P < 0.001). A score of ≤7 was regarded as low risk, 8-10 defined intermediate risk, and ≥11 defined high risk in our model. Internal validation showed good discriminatory ability of the model with a C-indexes of 0.790 (95% CI: 0.644-0.936, P = 0.017).
CONCLUSIONS: In our retrospective study, impaired LVEF, elevated haemoglobin levels, and high thrombocyte counts were regarded as independent risk factors for intracardiac thrombus in PPCM. A risk stratification model derived from these risk factors, which was economic and easily applicable in clinical practice, could rapidly and accurately identify PPCM patients with higher-risk of intracardiac thrombus.

To evaluate the impact of autoantibodies against the M2-muscarinic receptor (anti-M2-R) on the clinical outcomes of patients receiving the standard treatment for peripartum cardiomyopathy (PPCM).
A total of 107 PPCM patients who received standard heart failure (HF) treatment between January 1998 and June 2020 were enrolled in this study. According to anti-M2-R reactivity, they were classified into negative (n = 59) and positive (n = 48) groups, denoted as the anti-M2-R (-) and anti-M2-R (+) groups. Echocardiography, 6-min walk distance, serum digoxin concentration (SDC), and routine laboratory tests were performed regularly for 2 years. The all-cause mortality, cardiovascular mortality, and rehospitalisation rate for HF were compared between the two groups.
A total of 103 patients were included in the final data analysis, with 46 in the anti-M2-R (+) group and 57 in the anti-M2-R (-) group. Heart rate was lower in the anti-M2-R (+) group than in the anti-M2-R (-) group at the baseline (102.7 ± 6.1 bpm vs. 96.0 ± 6.4 bpm, p < 0.001). The initial SDC was higher in the anti-M2-R (+) group than in the anti-M2-R (-) group with the same dosage of digoxin (1.25 ± 0.45 vs. 0.78 ± 0.24 ng/mL, p < 0.001). The dosages of metoprolol and digoxin were higher in the anti-M2-R (-) patients than in the anti-M2-R (+) patients (38.8 ± 4.6 mg b.i.d. vs. 27.8 ± 5.3 mg b.i.d., p < 0.0001, respectively, for metoprolol; 0.12 ± 0.02 mg/day vs. 0.08 ± 0.04 mg/day, p < 0.0001, respectively, for digoxin). Furthermore, there was a greater improvement in cardiac function in the anti-M2-R (-) patients than in the anti-M2-R (+) patients. Multivariate analysis identified negativity for anti-M2-R as the independent predictor for the improvement of cardiac function. Rehospitalisation for HF was lower in the anti-M2-R (-) group, but all-cause mortality and cardiovascular mortality were the same.
There were no differences in all-cause mortality or cardiovascular mortality between the two groups. Rehospitalisation rate for HF decreased in the anti-M2-R (-) group. This difference may be related to the regulation of the autonomic nervous system by anti-M2-R.

The aim of this study was to explore the risk factors associated with a poor left ventricular (LV) function among patients with peripartum cardiomyopathy (PPCM) and to determine the influence of acute kidney injury (AKI) on the LV function of the patients.
Sixty patients with PPCM were recruited between January 2007 and June 2018, among which 11 had AKI. The participants were divided into two groups, the recovery group (32 cases) and the nonrecovery group (28 cases), with their clinical features, echocardiography and electrocardiogram findings, laboratory results, and treatments compared between groups. We further determined the risk factors associated with nonrecovery and the influence posed by AKI on the LV function of the patients.
Compared with the patients in the recovery group, those in the nonrecovery group had higher proportions of multiparity [78.6% (22/28) vs. 43.8% (14/32)], function class III- IV heart failure [92.9% (26/28) vs. 71.9% (23/32)], and a higher incidence of AKI [35.7% (10/28) vs. 3.1% (1/32)]. Logistic regression analysis showed that having AKI [odds ratio (OR): 10.556; 95% confidence interval (CI) 1.177-94.654; P = 0.035] and left ventricular ejection fraction (LVEF) < 40% [OR: 4.533; 95% CI 1.118-18.382; P = 0.034] were independently associated with nonrecovery of PPCM.
The prognosis of patients with PPCM and AKI during hospitalization was poor compared to those without AKI; therefore, clinicians should pay more attention to this phenomenon.

UNASSIGNED: Peripartum cardiomyopathy (PPCM) is a pregnancy-associated and life-threatening cardiac disease. However, the causes and pathogenesis are not fully understood. Accumulating studies show that cardiomyopathy often appears to be associated with elevated levels of β1-adrenoceptor (β1AR) antibodies, indicating a possible involvement of β1AR antibodies in the development of PPCM.
UNASSIGNED: We injected the antigen peptide segment of the β1AR into the postpartum Wistar rats to make the immune models and their cardiac function was detected by echocardiography. Also, the concentration of β1AR antibodies and apoptosis rate of left ventricular myocytes was tested by SA-ELISA, TUNEL, HE staining, qRT-PCR and western blot methods. Finally, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and its related proteins were examined by qRT-PCR and western blot methods.
UNASSIGNED: We found that the level of β1AR antibodies in the serum was significantly increased and the postpartum rats exhibited symptoms of PPCM after autoimmunity. Moreover, the expression of peroxisome PGC-1α, which was a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF), was decreased in autoimmune perinatal rats. In addition, the expression of the apoptosis factor caspase 3 as well as the apoptosis rate of left ventricular myocytes was significantly increased.
UNASSIGNED: The results suggested that the symptoms of PPCM that appeared in autoimmune perinatal rats may be due to the increase of β1AR antibodies, which inhibited the pathway associated with peroxisome PGC-1α.

Peripartum cardiomyopathy (PPCM) is life-threatening heart disease. However, the causes and pathogenesis of PPCM remain unclear. Previous studies found that β1 adrenoceptor antibodies (β1AA) had possible involvement in the development of PPCM. In the present study, we determined the potential relationship between PPCM and β1AA, including the mechanism of β1AA leading to PPCM.
We extracted the β1AA from the postpartum Wistar rats that were injected by the antigen peptide segment of the β1 adrenoceptor to produce PPCM. We tested the effects of β1AA on H9C2 cell line by CCK-8, LDH, TUNEL, SA-ELISA, qRT-PCR, and western blot methods. Furthermore, PGC-1α was overexpressed to rescue the effect of β1AA on H9C2 cells.
We found that the extracted β1AA induced apoptosis of cardiac myocytes of H9C2 cell line. Moreover, the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), which is a master regulator of mitochondrial metabolism, and its downstream transcript vascular endothelial growth factor (VEGF) got decreased in H9C2 cells after β1AA treatment. In addition, the effect of β1AA could be inhibited by atenolol, the antagonist of β1 adrenoceptors (β1AR) and imitated by isoprenaline, the agonist of β1AR. Furthermore, overexpression of PGC-1α in the H9C2 cells rescued the apoptosis of cells and inhibitory expression of VEGF induced by β1AA.
Our results suggest that the symptoms of PPCM due to myocardial cell apoptosis induced by β1AA inhibiting the PGC-1α-related pathway impairs mitochondrial energy metabolism. Therefore, our results uncover a previously unknown role of the β1AA pathway in the etiology of PPCM and provide a novel potential target for the treatment of PPCM.

Peripartum cardiomyopathy (PPCM) is rare and potentially life-threatening; its etiology remains unclear. Imaging characteristics on cardiovascular magnetic resonance (CMR) and their prognostic significance have rarely been studied. We sought to determine CMR\'s prognostic value in PPCM by using T1 and T2 mapping techniques.
Data from 21 PPCM patients from our CMR registry database were analyzed. The control group comprised 20 healthy age-matched females. All subjects underwent comprehensive contrast-enhanced CMR. T1 and T2 mapping using modified Look-Locker inversion recovery and T2 prep balanced steady-state free precession sequences, respectively. Ventricular size and function, late gadolinium enhancement (LGE), myocardial T1 value, extracellular volume (ECV), and T2 value were analyzed. Transthoracic echocardiography was performed at baseline and during follow-up. The recovered left ventricular ejection fraction (LVEF) was defined as LVEF ≥50% on echocardiography follow-up after at least 6 months of the diagnosis.
CMR imaging showed that the PPCM patients had severely impaired LVEF and right ventricular ejection fraction (LVEF: 26.8 ± 10.6%; RVEF: 33.9 ± 14.6%). LGE was seen in eight (38.1%) cases. PPCM patients had significantly higher native T1 and ECV (1345 ± 79 vs. 1212 ± 32 ms, P < 0.001; 33.9 ± 5.2% vs. 27.1 ± 3.1%, P < 0.001; respectively) and higher myocardial T2 value (42.3 ± 3.7 vs. 36.8 ± 2.3 ms, P < 0.001) than did the normal controls. After a median 2.5-year follow-up (range: 8 months-5 years), six patients required readmission for heart failure, two died, and 10 showed left ventricular function recovery. The LVEF-recovered group showed significantly lower ECV (30.7 ± 2.1% vs. 36.8 ± 5.6%, P = 0.005) and T2 (40.6 ± 3.0 vs. 43.9 ± 3.7 ms, P = 0.040) than the unrecovered group. Multivariable logistic regression analysis showed ECV (OR = 0.58 for per 1% increase, P = 0.032) was independently associated with left ventricular recovery in PPCM.
Compared to normal controls, PPCM patients showed significantly higher native T1, ECV, and T2. Native T1, ECV, and T2 were associated with LVEF recovery in PPCM. Furthermore, ECV could independently predict left ventricular function recovery in PPCM.

BACKGROUND: Peripartum cardiomyopathy (PPCM) is characterized by heart failure. Our previous study found that autoantibodies against the M2-muscarinic receptor (anti-M2-R) are increased in PPCM patients. We aimed to evaluate the association of anti-M2-R on prognosis of PPCM patients with standard treatment.
METHODS: Synthetic peptides corresponding to the M2 receptor served as the target antigens in an enzyme-linked immunosorbent assay experiment. They were used to screen the sera of 80 PPCM patients, who were separated into anti-M2-R-negative and positive groups according to their anti-M2-R reactivity. Clinical assessment and echocardiography examination were performed at baseline and after 5 years with a standard treatment regimen. The endpoint events were compared after 5 years of follow-up.
RESULTS: There were 76 PPCM patients who completed the final data analysis, including 36 in the anti-M2-R (+) group and 40 in the anti-M2-R (-) group. Both groups showed improvement in the left ventricular end-diastolic and end-systolic dimensions and the ejection fraction with standard treatment regimens for 5 years (all p<0.001). Patients in the anti-M2-R (-) group had greater tolerance and were more rapidly titrated to metoprolol, and they had better improvement in cardiac function than patients in the anti-M2-R (+) group (p<0.05). Patients in the anti-M2-R (-) group had a marked decrease in re-hospitalization (p<0.05), but not in all-cause mortality or cardiovascular mortality. Being positive for anti-M2-R increased the risk of PPCM (OR=4.7, 95% CI 1.8-12.2, p=0.002).
CONCLUSIONS: PPCM patients, especially anti-M2-R (-) patients, have a relatively better prognosis than other patients. We posit that the presence of anti-M2-R may be involved in the pathogenesis of PPCM.

Peripartum cardiomyopathy (PPCM) refers to irreversible cardiomyocyte damage that occurs during the last month of pregnancy, or within 5 months after giving birth. It is characterized by systolic heart failure. This life-threatening condition is relatively uncommon, but the incidence has been climbing up. Because of its high mortality, it is crucial for physicians to have high suspicious for the disease. Studies have been done to search into specific lab test and treatment for PPCM. Therapies like anti-viral, anti-inflammatory and immunosuppression regimen have been explored. New regimen like exosomes has also been explored and revealed promising effects.