Peripartum cardiomyopathy (PPCM) is a rare form of dilated cardiomyopathy occurring in women during the last month of pregnancy or within five months postpartum. It is characterized by left ventricular systolic dysfunction with a reduced ejection fraction (LVEF < 45%) and presents as heart failure(HF) without any cardiac abnormality. PPCM leads to weakening and  enlargement of the heart, reducing its ability to pump blood effectively, causing symptoms such as fatigue, shortness of breath, palpitations and swollen legs. Diagnosis is primarily clinical and confirmed by ECHO  showing reduced LV function. The cause is idiopathic but may involve inflammatory, autoimmune, viral, or hormonal factors, including a harmful prolactin fragment. Management requires multidisciplinary care and HF treatment, with outcomes ranging from full recovery to persistent systolic dysfunction or severe complications. Close monitoring in late pregnancy and postpartum period is essential for patient safety. PPCM is a diagnosis of exclusion with no prior heart disease and no other cause for Heart Failure (HF).1   Clinical and ECHO predictors of outcomes in patients with PPCM have been studied to guide prognosis and treatment strategies. Key clinical predictors include severity of HF symptoms at presentation, need for inotropic support, and presence of comorbidities such as gestational diabetes and preeclampsia. Echocardiographic predictors that strongly correlate with outcomes are left ventricular ejection fraction (LVEF), left atrial volume index (LAVi), right ventricular fractional area change (RVFAC), and left ventricular end-diastolic diameter (LVEDD).2,3 

Several studies have shown that a lower RVFAC (<31.4%) and a larger LAVi (>29.6 ml/m²) at presentation are indicators of poor outcomes, such as increased mortality and rehospitalization rates.4-6 While baseline LVEF reduction is a hallmark of PPCM, it is less predictive on its own for long-term prognosis compared with RV and atrial parameters. Larger LV cavity size and lower LVEF are associated with lower likelihood of recovery of cardiac function. Clinically, higher body mass index (BMI), presence of gestational diabetes, and prolonged QRS duration on ECG also portend worse recovery. Recovery of LVEF within the first year strongly correlates with better survival and fewer adverse events.4-6 Thus, poor outcomes in PPCM patients are predicted by echocardiographic markers like low RVFAC, high LAVi, and large LV dimensions, in addition to clinical factors such as severe heart failure at presentation and metabolic comorbidities. Timely diagnosis and heart failure management based on these predictors are crucial for improving prognosis and functional recovery in PPCM. 

Therefore, in our study we have decided to assess the predictors for outcome in PPCM patients. 

A single-center prospective cohort study was conducted on 88 patients aged 19–35 years diagnosed with PPCM within 5 months postpartum. During hospitalization, patients received anticoagulation therapy using heparin, followed by vitamin K antagonists during follow-up. Oral bromocriptine (2.5 mg twice daily for 2 weeks) was administered. Those with LVEF < 45% were included. Hemodynamic stabilization involved inotropic therapy (dobutamine) and vasodilators (nitroglycerin). Dobutamine infusion began at 5 µg/kg/min, then increased up to 20 µg/kg/min for 24 hours if tolerated. After discharge, patients were called for follow-up at 15 days, 1 month, 3 months and 6 months. Each visit included clinical evaluation, medication compliance, and therapy adjustments. ECHO at 6 months assessed recovery, defined as partial left ventricular recovery for LVEF 45–55% and full recovery for LVEF > 55%. Inclusion Criteria HF secondary to LV systolic Dysfunction with LVEF<45% Onset between last month of pregnancy and 5 months following delivery. Exclusion Criteria Pre-exisiting cardiac or thyroid disease Drug abuse Any therapy for systemic illness Hb <8gm/dl at the time of study initiation Congenital heart disease Statistical Analysis Continuous variables were expressed as means, while categorical variables were presented as frequencies. Multivariate logistic regression analysis was conducted to identify independent predictors, and receiver operating characteristic (ROC) curves, along with Mann–Whitney 95% confidence intervals, were evaluated to determine the optimal cut-off value corresponding to the maximum Youden index. Event-free survival was assessed using Kaplan–Meier curves with the log-rank (Mantel–Haenszel) test. All statistical analyses were performed using EZR® (version 3.5.2; R Foundation for Statistical Computing). A p-value of less than 0.05 was considered statistically significant.

Table 1: Clinical, Investigatory And Management Outcome Data

According to our study we have found that, mean age was 28.6±4.8 years. Diagnosis of PPCM after delivery was in 78 patients out of 88 patients, of  who 31 received inotropes. Further, risk factors such as hypertension, tocolysis and other were seen in 18%, 5% and 14 % patients respectively. In addition to above, mean Hb was 10.8±1.5 g/dl, mean serum creatinine was 0.9 ±0.3mg/dl and mean serum bilirubin was 1.2±0.4mg/dl and dobutamine infusion rate was 10±0.5 mg/kg/min among patients. Other than this, all patients received standard HF therapies, and oral bromocriptine was prescribed (2.5 mg twice daily for 2 weeks followed by once daily for 4 weeks). Anticoagulation with heparin (in-hospital) and vitamin K antagonists (follow‑up) were administered as indicated in patients with LV thrombus. Inotropic and vasodilator (dobutamine, dopamine, noradrenaline, nitroglycerin) were used for hemodynamic stabilization in selected cases. 

TABLE 2: ECHO COMPARASION 

In our study we have found that, there was a statistically significant difference found from baseline to 6^th month follow up analysis as the p value was <0.001 and <0.01 for each respectively. Thus, there was marked enhancement in LVEF and regression of LV and LA volumes confirming significant myocardial recovery with standard and adjunctive therapies. 

TABLE 3: ECHO LV AT 6^th MONTH 

Through our study we have found that  

1. For LV-EDVi (mL/m²): Larger EDVi predicts slower recovery and persistent dilation
2. For LV-ESVi (mL/m²): Elevated ESVi correlates with reduced chance of LVEF ≥ 50%
3. For LVEF (%) baseline LVEF < 35% is strongly associated with non-recovery
4. For mitral E/A diastolic dysfunction: It is not an independent predictor of recovery of LV Function.
5. For LAVi (mL/m²): LAVi > 29.6 mL/m² independently predicts non-recovery and rehospitalization and
6. For RVFAC(%): RVFAC < 31.4% independently predicts poor 6-month LV recovery

  TABLE 4 : OUTCOME  

Through our research we have found that, death was recorded in 6 patients due to LVEF <25%, high LV-EDVi, and poor hemodynamic response, poor LV recovery was reported in 18 patients, partial LV recovery was seen in 36 patients due to predictive improvement with higher Mitral E/A and lower LAVi, full LV recovery was noticed in 36 patients who had LVEF ≥35% at baseline, optimal bromocriptine adherence, lower LV volumes, and re-hospitalization was recorded for 10 patients due to persistent LV dilation and higher LVEDVi and finally, composite adverse outcome was seen 28 patients due to strong predictive link to baseline LVEF <35%, elevated LAVi, and RVFAC <35%. 

In our study, we tried to assess the impact of LAV in PPCM, along with bromocriptine & inotropic therapy outcomes. During the course of our research, no patient was absent.  In univariate regression we found that, LV-EDVi and LV-ESVi showed higher baseline LV volumes (EDVi, ESVi) , thus are significantly associated with non-recovery. For LVEF(%), lower LVEF at 6 months, thus strongly predicts non-recovery, with a significant relationship.  Patients achieving full recovery (EF ≥50-55%) tend to have higher LVEF at baseline and follow-up. For mitral E/A ratio we found that, there was higher baseline mitral E/A, consistent with restrictive LV filling, predicts adverse outcomes (OR ~1.44), but incremental analysis shows that LVEF remains strong single predictor. For LAVi, an increased LAVi (≥29.6 ml/m2)  was associated with worse outcomes and delayed recovery of LV function in univariate analysis and for RVFAC (%) we found that, RVFAC <31.4% was a significant independent predictor of poor outcomes, and lower RV function impedes LV recovery.   For multivariate regression, our research showed that, baseline LVEF and LV volumes (EDVi, ESVi) remain as main independent predictors for LV recovery after adjusting for confounders like age, hypertension, treatment, and severity indices. Mitral E/A and LAVi showed no statistical significance for multivariate models after including LV volumes and LVEF, but still contribute to risk stratification, and  RV dysfunction (impaired RVFAC) remains independently associated with non-recovery, even after adjustment for LV indices. Thus, there were 6 patient deaths , poor recovery in 18 patients, partial recovery in 36 patients, full recovery in 28 patients , re-hospitalization in 10 patients and composite adverse effects in 28 patients reported after 6 month follow up. Thus, positive predictors of LV recovery showed reduced LV-EDVi and LVESVi, preserved RVFAC and negative predictors / adverse outcomes showed higher LV volumes, lower LVEF, and elevated LAVi respectively. 

In a randomized clinical study which evaluated whether varying durations of bromocriptine therapy could impact recovery outcomes in women with PPCM, where 2 treatment groups were compared: a 1-week group (1W) and an 8-week group (8W) of bromocriptine and baseline left ventricular ejection fraction (LVEF) values were similar between groups. They found that, 

LVEF showed improvement as at 1W group increased from 28 ± 10% to 49 ± 12%  (ΔLVEF = 21 ± 11%) and at 8W group: increased from 27 ± 10% to 51 ± 10% (ΔLVEF = 24 ± 11%). Therefore, the difference in ΔLVEF between groups was not statistically significant (P = 0.381). Secondary outcome was that hospitalizations for HF was seen in 9.7% (1W) vs. 6.5% (8W), P = 0.651, full recovery (LVEF > 50%): 52% (1W) vs. 68% (8W) while non-recovery at 6 months was less frequent in the 8W group. Thus, no heart transplantation, left ventricular assist device implantation, or deaths occurred among participants. Therefore, they concluded that, bromocriptine therapy in patients with peripartum cardiomyopathy (PPCM) significantly improved outcomes, showing a higher rate of full left ventricular recovery and reduced morbidity and mortality compared with PPCM patients who did not receive bromocriptine.  Both 1-week and 8-week treatment durations were effective, though a slight trend toward better recovery was noted with the 8-week regimen.7 

Another study highlighted the therapeutic potential of bromocriptine in PPCM, particularly among patients with right ventricular (RV) involvement. Patients with reduced right ventricular ejection fraction (RVEF) at presentation had a significantly lower rate of full cardiac recovery at 6 months (58% vs. 81%). Bromocriptine treatment improved both RVEF and left ventricular ejection fraction (LVEF) in 1-week and 8-week groups, with greater absolute improvements observed in the 8-week group. Full LV recovery occurred in 50% of the 1-week group and 64% of the 8-week group, while full RV recovery was achieved in 40% and 79%, respectively, indicating an overall trend toward better recovery with prolonged bromocriptine therapy. Thus, they concluded that, bromocriptine treatment in PPCM patients with RV Dysfunction led to high rates of both RV and LV recovery, despite their initial worse prognosis. There were no significant differences in recovery rates between short-term and long-term bromocriptine regimens. These results indicate that adding bromocriptine to standard HF therapy may benefit PPCM patients with biventricular involvement.8 A meta-analysis of 177 randomized trials involving 28,280 patients evaluated the impact of inotropes and vasopressors on mortality over the past 20 years. The pooled data revealed no significant difference in overall mortality between treated patients and controls (31.7% vs. 31.8%; risk ratio = 0.98, P = 0.23). However, mortality reduction was observed in specific settings such as vasoplegic syndromes, sepsis, and cardiac surgery. No subgroup exhibited increased mortality with inotrope/vasopressor use, leading to the conclusion that these therapies generally do not affect mortality in most clinical contexts.9  

Limitation Of Study 

1.       The study was conducted at a single center, limiting the generalizability of the finding. 

2.       The sample size was small, reducing the statistical validity and reliability of the results. 

3.       The follow-up duration was short (6 months), preventing assessment of long-term outcomes and disease progression. 

4.       There was no proper control group to evaluate the independent effects of bromocriptine and inotropes. 

5.       Prognostic significance of blood biomarkers such as BNP and CRP was not assessed. 

6.       The impact of bromocriptine-induced lactation suppression on newborn outcomes, especially in resource-limited settings, was not explored. 

The study identifies baseline LV volumes (EDVi, ESVi) and LVEF as the strongest independent predictors of LV functional recovery in PPCM. Lower baseline LVEF and higher LV volumes were significantly associated with non-recovery, while preserved LV function at diagnosis strongly predicted favorable outcomes. Although higher mitral E/A ratio and increased LAVi correlated with poor

recovery in univariate analysis, they lost significance in multivariate models but still aid in risk stratification. Notably, impaired right ventricular function (RVFAC < 31.4%) independently predicted adverse outcomes irrespective of LV indices. Clinically, patients with preserved RV function, smaller LV volumes, and higher baseline LVEF demonstrated better recovery trajectories. Overall, these ECHO parameters serve as crucial predictors for early identification of patients at risk for poor recovery and adverse events during follow-up. 

1.       Honigberg MC, Givertz MM. Peripartum cardiomyopathy. Bmj. 2019 Jan 30;364. 

2.       Kiran GR, RajKumar C, Chandrasekhar P. Clinical and echocardiographic predictors of outcomes in patients with peripartum cardiomyopathy: A single centre, six month followup study. Indian Heart Journal. 2021 May 1;73(3):319-24. 

3.       Shakya S, Gajurel RM, Poudel CM, Shrestha H, Devkota S, Thapa S, Manandhar B, Khanal R, Shrestha S, Sharma M. Outcome of Patients Presenting with Peripartum Cardiomyopathy in a Tertiary Care Center of Nepal. Journal of Cardiology and Cardiovascular Medicine. 2024 May 29;9(1):081-6. 

4.       Bak M, Youn JC, Bae DH, Lee JH, Lee S, Cho DH, Choi JO, PPCM registry investigators. Temporal Trends in Clinical Characteristics and Outcomes for Peripartum Cardiomyopathy: The Nationwide Multicenter Registry Over 20 Years. Journal of the American Heart Association. 2024 Jul 2;13(13):e034055. 

5.       Viljoen C, Hoevelmann J, Sliwa K. Peripartum cardiomyopathy: risk factors and predictors of outcome. Current Opinion in Cardiology. 2023 May 1;38(3):223-32.\ 

6.       Kiran GR, RajKumar C, Chandrasekhar P. Clinical and echocardiographic predictors of outcomes in patients with peripartum cardiomyopathy: A single centre, six month followup study. Indian Heart Journal. 2021 May 1;73(3):319-24. 

7.       Hilfiker-Kleiner D, Haghikia A, Berliner D, Vogel-Claussen J, Schwab J, Franke A, 

8.       Schwarzkopf M, Ehlermann P, Pfister R, Michels G, Westenfeld R. Bromocriptine for the treatment of peripartum cardiomyopathy: a multicentre randomized study. European heart

9.       journal. 2017 Sep 14;38(35):2671-9. 

10.    Haghikia A, Schwab J, Vogel-Claussen J, Berliner D, Pfeffer T, König T, Zwadlo C, Moulig VA, Franke A, Schwarzkopf M, Ehlermann P. Bromocriptine treatment in patients with peripartum cardiomyopathy and right ventricular dysfunction. Clinical Research in Cardiology. 2019 Mar 1;108(3):290-7. 

11.    Belletti A, Castro ML, Silvetti S, Greco T, Biondi-Zoccai G, Pasin L, Zangrillo A, Landoni G. The Effect of inotropes and vasopressors on mortality: a meta-analysis of randomized clinical trials. BJA: British Journal of Anaesthesia. 2015 Nov 1;115(5):656-75.