Peripartum cardiomyopathy (PPCM) is a relatively uncommon but potentially life-threatening cause of cardiomyopathy occurring during late pregnancy or in the early postpartum period. PPCM is characterized by significant systolic dysfunction causing heart failure (HF) and accounts for over 60% of pregnancy-related cardiogenic shock cases in the United States.1 Despite significant therapeutic advances in HF management, specific evidence-based therapies for PPCM remain limited. Sodium glucose co-transporter 2 inhibitors (SGLT2i) constitute a mainstay of guideline-directed medical therapy (GDMT) for HF; however, data regarding their impact in patients with PPCM are limited.2 PPCM is traditionally managed with GDMT for HF with reduced ejection fraction (HFrEF), extrapolated from HFrEF clinical trials, which generally exclude PPCM.
What is the clinical question being addressed?
What is the effectiveness of the sodium glucose co-transporter 2 inhibitor among patients with peripartum cardiomyopathy?
What is the main finding?
The use of SGLT2i in peripartum cardiomyopathy is associated with a significant reduction in the risk of all-cause mortality, ischemic stroke, heart failure exacerbation, and all-cause rehospitalization.
We used the United States Collaborative Network of the TriNetX database (Cambridge, MA), which includes deidentified, aggregated data from >70 national health care organizations, complies with Health Insurance Portability and Accountability Act (HIPAA) Section §164.514, and has been exempted from the requirements of the Western Institutional Review Board. Using International Classification of Diseases-Tenth Revision codes, we identified adult patients (≥18 years) with PPCM (International Classification of Diseases-Tenth Revision: O90.3) from January 1, 2013, to December 31, 2025, and grouped them by postdiagnosis SGLT2i prescription. To minimize covariate confounding, 1:1 propensity score matching (PSM) was performed using greedy nearest-neighbor matching without replacement (0.1 pooled SD caliper). Covariates were deemed balanced if the standardized mean difference post-PSM was ≤0.1. Outcomes were assessed at 3 years and included all-cause mortality, acute myocardial infarction, ischemic stroke, HF exacerbation, atrial fibrillation, ventricular tachycardia/fibrillation, and all-cause rehospitalization. Survival analyses used Kaplan-Meier estimates, with comparisons via the log-rank test to calculate HRs and 95% CIs in matched cohorts. HRs and CIs were computed using the R Survival package (v3.2-3) within the TriNetX platform (parameter: robust = FALSE).
Between 2013 and 2025, a total of 10,907 patients with PPCM were identified (SGLT2i use: n = 1,313; no SGLT2i use: n = 9,594). Following PSM, each cohort included 680 matched pairs (n = 1,360). Following matching, the mean age was 37.4 ± 9.7 years, with more Black patients (46.7%) than White patients (39.2%). The cohorts were well balanced in demographics, comorbidities (HF: 74.4% vs 72.9%; diabetes mellitus: 25% vs 24%; chronic kidney disease: 11.5% vs 9%), medication usage, and laboratory parameters (Table 1). At a median follow-up of 1.6 years (IQR: 0.8-3.0), patients with PPCM treated with SGLT2i demonstrated a lower cumulative incidence of mortality (2.2% vs 3.8%), corresponding to a 52% lower hazard of death (HR: 0.48; 95% CI: 0.25-0.92; P = 0.02) compared to non-SGLT2i users. SGLT2i use was also associated with a significantly lower risk of ischemic stroke (3.5% vs 5.0%; HR: 0.76; 95% CI: 0.55-0.98; P = 0.04), HF exacerbation (36.7% vs 40.4%; HR: 0.83; 95% CI: 0.76-0.90; P = 0.01), and all-cause rehospitalization (57.2% vs 61%; HR: 0.81; 95% CI: 0.70-0.93; P = 0.006) compared to non-SGLT2i users. No differences in acute myocardial infarction, atrial fibrillation, and ventricular tachycardia/fibrillation were noted.
Table 1.
Baseline Characteristics of the Study Cohort Before and After Propensity Score Matching
| Before Propensity Score Matching |
After Propensity Score Matching |
|||||||
|---|---|---|---|---|---|---|---|---|
| SGLT2i (n = 1,313) | No SGLT2i (n = 9,594) | P Value | Std. Difference | SGLT2i (n = 680) | No SGLT2i (n = 680) | P Value | Std. Difference | |
| Current age, y | 40.1 ± 9.1 | 40.7 ± 9.3 | 0.04 | 0.061 | 40.3 ± 9.7 | 40.4 ± 10.1 | 0.97 | 0.002 |
| Age at index, y | 37.4 ± 9.0 | 34.2 ± 8.8 | <0.01 | 0.353 | 37.2 ± 9.4 | 37.5 ± 9.9 | 0.68 | 0.023 |
| Race | ||||||||
| White | 475 (36.2) | 4,431 (46.2) | <0.01 | 0.204 | 265 (39) | 267 (39.3) | 0.91 | 0.006 |
| Black | 648 (49.4) | 3,605 (37.6) | <0.01 | 0.239 | 318 (46.8) | 316 (46.5) | 0.91 | 0.006 |
| Asian | 39 (3) | 284 (3) | 0.98 | 0.001 | 20 (2.9) | 23 (3.4) | 0.64 | 0.025 |
| Others | 86 (6.5) | 733 (7.6) | 0.16 | 0.042 | 48 (7.1) | 45 (6.6) | 0.75 | 0.017 |
| Comorbidities | ||||||||
| Hypertension | 877 (66.8) | 2,415 (25.2) | <0.01 | 0.919 | 399 (58.7) | 408 (60) | 0.62 | 0.027 |
| Coronary artery disease | 404 (30.8) | 658 (6.9) | <0.01 | 0.643 | 157 (23.1) | 139 (20.4) | 0.24 | 0.064 |
| Acute myocardial infarction | 177 (13.5) | 196 (2) | <0.01 | 0.438 | 61 (9) | 49 (7.2) | 0.23 | 0.065 |
| Heart failure | 1,132 (86.2) | 2,206 (23) | <0.01 | 1.644 | 506 (74.4) | 496 (72.9) | 0.54 | 0.033 |
| Stroke | 123 (9.4) | 245 (2.6) | <0.01 | 0.291 | 44 (6.5) | 45 (6.6) | 0.91 | 0.006 |
| Diabetes mellitus | 390 (29.7) | 778 (8.1) | <0.01 | 0.574 | 170 (25) | 163 (24) | 0.66 | 0.024 |
| Cardiomyopathy | 955 (72.7) | 2,248 (23.4) | <0.01 | 1.134 | 404 (59.4) | 389 (57.2) | 0.41 | 0.045 |
| Paroxysmal tachycardia | 361 (27.5) | 511 (5.3) | <0.01 | 0.627 | 128 (18.8) | 118 (17.4) | 0.48 | 0.038 |
| Atrial fibrillation | 158 (12) | 277 (2.9) | <0.01 | 0.353 | 68 (10) | 65 (9.6) | 0.78 | 0.015 |
| Atrioventricular or left bundle-branch block | 160 (12.2) | 243 (2.5) | <0.01 | 0.376 | 59 (8.7) | 57 (8.4) | 0.85 | 0.011 |
| Nonrheumatic mitral valve disorders | 461 (35.1) | 704 (7.3) | <0.01 | 0.722 | 166 (24.4) | 161 (23.7) | 0.75 | 0.017 |
| Nonrheumatic tricuspid valve disorders | 178 (13.6) | 299 (3.1) | <0.01 | 0.385 | 71 (10.4) | 72 (10.6) | 0.93 | 0.005 |
| Nonrheumatic aortic valve disorders | 77 (5.9) | 143 (1.5) | <0.01 | 0.234 | 35 (5.1) | 36 (5.3) | 0.91 | 0.007 |
| Cardiac arrest | 43 (3.3) | 87 (0.9) | <0.01 | 0.166 | 18 (2.6) | 20 (2.9) | 0.74 | 0.018 |
| Pericardial effusion | 163 (12.4) | 162 (1.7) | <0.01 | 0.428 | 53 (7.8) | 50 (7.4) | 0.76 | 0.017 |
| Pulmonary embolism | 90 (6.9) | 197 (2.1) | <0.01 | 0.234 | 28 (4.1) | 34 (5) | 0.44 | 0.042 |
| Dyslipidemia | 391 (29.8) | 861 (9) | <0.01 | 0.546 | 163 (24) | 169 (24.9) | 0.71 | 0.021 |
| Thyroid disorders | 222 (16.9) | 858 (8.9) | <0.01 | 0.239 | 110 (16.2) | 122 (17.9) | 0.39 | 0.047 |
| Overweight/obesity | 736 (56.1) | 2,299 (24) | <0.01 | 0.693 | 337 (49.6) | 329 (48.4) | 0.66 | 0.024 |
| Chronic lower respiratory diseases | 385 (29.3) | 1,473 (15.4) | <0.01 | 0.340 | 176 (25.9) | 179 (26.3) | 0.85 | 0.010 |
| Respiratory failure | 279 (21.2) | 380 (4) | <0.01 | 0.539 | 99 (14.6) | 99 (14.6) | 1.00 | <0.001 |
| Chronic kidney disease | 142 (10.8) | 277 (2.9) | <0.01 | 0.318 | 78 (11.5) | 61 (9) | 0.13 | 0.083 |
| Gastro-esophageal reflux disease | 366 (27.9) | 1,211 (12.6) | <0.01 | 0.387 | 160 (23.5) | 156 (22.9) | 0.80 | 0.014 |
| Liver diseases | 214 (16.3) | 325 (3.4) | <0.01 | 0.444 | 76 (11.2) | 76 (11.2) | 1.00 | <0.001 |
| Iron deficiency anemia | 373 (28.4) | 852 (8.9) | <0.01 | 0.518 | 141 (20.7) | 150 (22.1) | 0.55 | 0.032 |
| Osteoarthritis | 118 (9) | 301 (3.1) | <0.01 | 0.247 | 52 (7.6) | 52 (7.6) | 1.00 | <0.001 |
| Sleep apnea | 283 (21.6) | 535 (5.6) | <0.01 | 0.480 | 116 (17.1) | 127 (18.7) | 0.44 | 0.042 |
| Neoplasms | 251 (19.1) | 1,105 (11.5) | <0.01 | 0.212 | 118 (17.4) | 128 (18.8) | 0.48 | 0.038 |
| Smoking | 295 (22.5) | 1,075 (11.2) | <0.01 | 0.304 | 121 (17.8) | 115 (16.9) | 0.67 | 0.023 |
| Cannabis-related disorders | 94 (7.2) | 340 (3.5) | <0.01 | 0.161 | 41 (6) | 39 (5.7) | 0.82 | 0.013 |
| Alcohol use disorders | 58 (4.4) | 202 (2.1) | <0.01 | 0.130 | 24 (3.5) | 29 (4.3) | 0.48 | 0.038 |
| Cocaine-related disorders | 32 (2.4) | 102 (1.1) | <0.01 | 0.105 | 10 (1.5) | 14 (2.1) | 0.41 | 0.045 |
| Opioid-related disorders | 45 (3.4) | 206 (2.1) | <0.01 | 0.078 | 18 (2.6) | 21 (3.1) | 0.63 | 0.026 |
| Inhalant-related disorders | 11 (0.8) | 61 (0.6) | 0.40 | 0.024 | 10 (1.5) | 10 (1.5) | 1.00 | <0.001 |
| Medications | ||||||||
| Beta-blockers | 1,132 (86.2) | 3,484 (36.3) | <0.01 | 1.193 | 530 (77.9) | 517 (76) | 0.40 | 0.045 |
| Statins | 372 (28.3) | 708 (7.4) | <0.01 | 0.569 | 160 (23.5) | 158 (23.2) | 0.90 | 0.007 |
| Diuretics | 1,137 (86.6) | 2,612 (27.2) | <0.01 | 1.498 | 513 (75.4) | 508 (74.7) | 0.75 | 0.017 |
| Spironolactone | 777 (59.2) | 833 (8.7) | <0.01 | 1.261 | 292 (42.9) | 263 (38.7) | 0.11 | 0.087 |
| Eplerenone | 21 (1.6) | 20 (0.2) | <0.01 | 0.147 | 11 (1.6) | 10 (1.5) | 0.83 | 0.012 |
| ARBs | 850 (64.7) | 769 (8) | <0.01 | 1.460 | 308 (45.3) | 304 (44.7) | 0.83 | 0.012 |
| ACE inhibitors | 643 (49) | 1,613 (16.8) | <0.01 | 0.728 | 279 (41) | 266 (39.1) | 0.47 | 0.039 |
| Sacubitril/ARNI | 603 (45.9) | 250 (2.6) | <0.01 | 1.171 | 184 (27.1) | 179 (26.3) | 0.76 | 0.017 |
| Calcium-channel blockers | 455 (34.7) | 1,257 (13.1) | <0.01 | 0.522 | 212 (31.2) | 218 (32.1) | 0.73 | 0.019 |
| Antiarrhythmics | 903 (68.8) | 3,565 (37.2) | <0.01 | 0.668 | 420 (61.8) | 414 (60.9) | 0.74 | 0.018 |
| Hydralazine | 510 (38.8) | 1,153 (12) | <0.01 | 0.647 | 224 (32.9) | 218 (32.1) | 0.73 | 0.019 |
| Antianginals | 479 (36.5) | 681 (7.1) | <0.01 | 0.762 | 190 (27.9) | 175 (25.7) | 0.36 | 0.050 |
| Epinephrine | 472 (35.9) | 1,733 (18.1) | <0.01 | 0.411 | 214 (31.5) | 212 (31.2) | 0.91 | 0.006 |
| Phenylephrine | 371 (28.3) | 1,224 (12.8) | <0.01 | 0.391 | 157 (23.1) | 154 (22.6) | 0.85 | 0.011 |
| Ephedrine | 216 (16.5) | 907 (9.5) | <0.01 | 0.210 | 96 (14.1) | 86 (12.6) | 0.43 | 0.043 |
| Terbutaline | 202 (15.4) | 998 (10.4) | <0.01 | 0.149 | 94 (13.8) | 93 (13.7) | 0.94 | 0.004 |
| Norepinephrine | 151 (11.5) | 146 (1.5) | <0.01 | 0.413 | 55 (8.1) | 47 (6.9) | 0.41 | 0.045 |
| Dobutamine | 119 (9.1) | 124 (1.3) | <0.01 | 0.356 | 35 (5.1) | 32 (4.7) | 0.71 | 0.020 |
| Insulin | 456 (34.7) | 960 (10) | <0.01 | 0.621 | 201 (29.6) | 178 (26.2) | 0.16 | 0.075 |
| Metformin | 261 (19.9) | 509 (5.3) | <0.01 | 0.450 | 113 (16.6) | 116 (17.1) | 0.83 | 0.012 |
| Anticoagulants | 917 (69.8) | 2,192 (22.8) | <0.01 | 1.068 | 404 (59.4) | 399 (58.7) | 0.78 | 0.015 |
| Antiplatelets | 637 (48.5) | 1,756 (18.3) | <0.01 | 0.676 | 299 (44) | 276 (40.6) | 0.21 | 0.069 |
| Aspirin | 633 (48.2) | 1,742 (18.2) | <0.01 | 0.673 | 297 (43.7) | 276 (40.6) | 0.25 | 0.063 |
| Bronchodilators | 899 (68.5) | 3,812 (39.7) | <0.01 | 0.602 | 417 (61.3) | 415 (61) | 0.91 | 0.006 |
| Glucocorticoids | 849 (64.7) | 3,703 (38.6) | <0.01 | 0.540 | 398 (58.5) | 392 (57.6) | 0.74 | 0.018 |
| Antidepressants | 547 (41.7) | 1,944 (20.3) | <0.01 | 0.476 | 257 (37.8) | 259 (38.1) | 0.91 | 0.006 |
| Antineoplastics | 98 (7.5) | 397 (4.1) | <0.01 | 0.143 | 53 (7.8) | 44 (6.5) | 0.34 | 0.051 |
| Hemoglobin, g/dL | 11.9 ± 1.9 | 11.2 ± 2.0 | <0.01 | 0.348 | 11.8 ± 1.9 | 11.4 ± 2.0 | <0.01 | 0.216 |
| CRP, mg/mL | 29.2 ± 44.2 | 31.2 ± 57.1 | 0.59 | 0.038 | 24.0 ± 37.5 | 35.8 ± 57.7 | 0.05 | 0.244 |
| ESR, mm/h | 33.9 ± 28.4 | 28.6 ± 26.4 | <0.01 | 0.196 | 34.0 ± 30.1 | 38.7 ± 30.6 | 0.21 | 0.154 |
| Total cholesterol, mg/dL | 168.8 ± 47.3 | 176.5 ± 44.4 | <0.01 | 0.167 | 173.3 ± 49.0 | 170.0 ± 45.5 | 0.36 | 0.071 |
| LDL-C, mg/dL | 98.7 ± 36.0 | 103.4 ± 35.2 | <0.01 | 0.133 | 102.7 ± 37.3 | 99.4 ± 37.2 | 0.26 | 0.088 |
| HDL-C, mg/dL | 39.8 ± 17.3 | 47.6 ± 19.2 | <0.01 | 0.429 | 42.2 ± 16.3 | 43.7 ± 19.9 | 0.28 | 0.083 |
| Triglyceride, mg/dL | 147.8 ± 128.3 | 126.4 ± 111.3 | <0.01 | 0.178 | 145.4 ± 81.3 | 139.8 ± 117.6 | 0.46 | 0.056 |
| PT, s | 14.3 ± 5.8 | 13.3 ± 4.7 | <0.01 | 0.197 | 13.6 ± 4.7 | 14.2 ± 5.4 | 0.12 | 0.122 |
| aPTT, s | 34.2 ± 16.8 | 31.2 ± 11.8 | <0.01 | 0.209 | 32.1 ± 14.5 | 35.0 ± 16.9 | 0.02 | 0.186 |
| INR | 1.3 ± 0.6 | 1.2 ± 0.5 | <0.01 | 0.201 | 1.2 ± 0.4 | 1.2 ± 0.6 | 0.23 | 0.093 |
| NT-proBNP, pg/mL | 1,817.6 ± 3,383.8 | 1,891.2 ± 5,055.3 | 0.76 | 0.017 | 1,842.7 ± 3,733.4 | 2,355.6 ± 5,536.8 | 0.27 | 0.109 |
| HbA1c, % | 6.3 ± 1.8 | 5.8 ± 1.5 | <0.01 | 0.304 | 6.4 ± 1.8 | 6.3 ± 1.9 | 0.46 | 0.055 |
| Creatinine, mg/dL | 1.0 ± 4.0 | 0.9 ± 3.0 | 0.22 | 0.036 | 0.9 ± 0.4 | 1.0 ± 1.1 | 0.05 | 0.117 |
| Troponin I, ng/mL | 0.4 ± 2.2 | 0.5 ± 4.5 | 0.62 | 0.043 | 0.1 ± 0.5 | 0.3 ± 1.7 | 0.37 | 0.122 |
| LVEF, (%) | 33.7 ± 14.3 | 49.5 ± 14.5 | <0.01 | 1.095 | 35.0 ± 14.7 | 45.0 ± 17.2 | <0.01 | 0.625 |
| BMI, kg/m2 | 35.9 ± 9.8 | 34.0 ± 9.2 | <0.01 | 0.193 | 35.7 ± 9.9 | 35.2 ± 10.0 | 0.43 | 0.048 |
Values are mean ± SD orn (%).
ACE = angiotensin-converting enzyme; aPTT = activated partial thromboplastin time; ARB = angiotensin-receptor blockers; ARNI = angiotensin-receptor neprilysin inhibitor; BMI = body mass index; CRP = C-reactive protein; ESR = erythrocyte sedimentation rate; HDL-C = high-density lipoprotein cholesterol; INR = international normalized ratio; LDL-C = low-density lipoprotein cholesterol; LVEF = left ventricular ejection fraction; NT-proBNP = N-terminal pro–B-type natriuretic peptide; PT = prothrombin time; SGLT2i = sodium glucose co-transporter 2 inhibitor.
This real-world contemporary analysis of nationwide data demonstrated that SGLT2i use in PPCM is associated with lower mortality, stroke, HF exacerbation, and all-cause readmission. These findings are notable given the limited evidence base for disease-modifying therapies in PPCM beyond extrapolated GDMT for HFrEF and underscore the role of SGLT2i in this high-risk population.
The observed mortality reduction aligns with the established mortality benefits of SGLT2i across a broad spectrum of HF phenotypes, including patients with reduced and preserved ejection fractions.3,4 In PPCM, where adverse outcomes are driven by persistent ventricular dysfunction, progressive congestion, and systemic complications, the lower associated rates of HF exacerbation and rehospitalization suggest longitudinal disease improvement stability rather than short-term symptomatic relief alone. Importantly, the absence of a signal for reduced acute myocardial infarction supports a mechanism of benefit that is not mediated by atherosclerotic risk modification, but instead suggests HF-centric pathways.
The association with lower ischemic stroke risk is clinically relevant in PPCM, a condition characterized by an elevated thromboembolic risk related to pregnancy-associated hypercoagulability, ventricular dysfunction, and arrhythmia burden. While causality cannot be inferred, less decompensated HF and improved hemodynamic profiles may indirectly mitigate embolic risk over time. These findings warrant cautious interpretation but are consistent with broader HF populations, in which SGLT2i therapy has been associated with reduced cerebrovascular events.5
From a cardio-obstetric perspective, these data support consideration of SGLT2i in appropriately selected PPCM patients beyond the immediate peripartum period, particularly those with persistent HF or recurrent hospitalizations. There are limited data on the transmission of SGLT2i in breastmilk, which is a crucial parameter for future investigations. The desire to breastfeed might limit the use of SGLT2i in patients, despite ejection fraction cutoffs for therapeutic qualification. However, given the retrospective design, potential residual confounding, and lack of granular data on left ventricular recovery, lactation status, patient adherence, and postpartum timing of initiation, these results should be viewed as hypothesis-generating. Furthermore, there have been significant improvements in PPCM management and SGLT2i pharmacotherapeutics over the study period; hence, the timing of treatment may influence risk estimation and bias toward SGLT2i therapy. Prospective studies with detailed phenotyping are needed to define the optimal role, timing, dosage, and safety profile of SGLT2i therapy in PPCM.
Funding support and author disclosures
Dr Goldsweig has done consulting for Philips, Abbott, Occlutech, and Conformal Medical; and speaking for Philips and Boston Scientific. Dr Mentz has received research support and honoraria from Abbott, American Reagent, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Boston Scientific, Cytokinetics, Fast BioMedical, Gilead, Innolife, Eli Lilly, Medtronic, Medable, Merck, Novartis, Novo Nordisk, Pfizer, Pharmacosmos, Relypsa, Respicardia, Roche, Rocket Pharmaceuticals, Sanofi, Verily, Vifor, Windtree Therapeutics, and Zoll. Dr Fonarow has done consulting for Abbott, Amgen, AstraZeneca, Bayer, Boehringer Ingelheim, Cytokinetics, Eli Lilly, Johnson & Johnson, Medtronic, Merck, Novartis, and Pfizer. Dr Sharma is supported by AHA979462 and the Martha Schar Endowment in Women’s CVH at Inova Schar Heart and Vascular. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
Footnotes
The authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the Author Center.
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