Despite robust evidence that quadruple guideline-directed medical therapy (GDMT), comprising angiotensin receptor-neprilysin inhibitors (ARNIs), evidence-based beta-blockers, mineralocorticoid receptor antagonists (MRAs), and sodium-glucose cotransporter 2 (SGLT2) inhibitors, reduces mortality and hospitalizations in heart failure with reduced ejection fraction (HFrEF), implementation in clinical practice remains markedly incomplete. This study aimed to provide updated national estimates of the eligible untreated HFrEF population and to quantify deaths and hospitalizations preventable with optimal implementation of quadruple GDMT in the United States. The authors performed a population-level decision analytic modeling study using contemporary U.S. epidemiologic data. National HFrEF prevalence estimates were derived from the American Heart Association Heart Disease and Stroke Statistics 2026 report, and annual HFrEF hospitalization counts were derived from the National Inpatient Sample 2022-2023. Eligible untreated populations were estimated after sequential exclusions and therapy-specific contraindication adjustments using primary treatment rates from Epic Cosmos 2023-2025, with sensitivity analyses using alternative treatment-rate sources. Trial-derived numbers needed to treat and relative risk reductions were applied to estimate deaths preventable over 12 months and annual heart failure (HF) hospitalizations prevented. An estimated 2.76 million U.S. adults with chronic symptomatic HFrEF were eligible for quadruple GDMT, yet only 18.2% received it. Eligible untreated populations included 733,891 for beta-blockers, 1,856,531 for ARNIs, 1,543,967 for MRAs, and 1,717,444 for SGLT2 inhibitors. Class-specific projected deaths preventable over 12 months were 26,210 for beta-blockers, 34,495 for ARNIs, 26,620 for MRAs, and 26,422 for SGLT2 inhibitors; the aggregate estimate across treatment gaps was 113,747 (95% uncertainty interval [UI]: 90,173-149,875). Optimal implementation was also projected to prevent 357,332 HF hospitalizations annually (95% UI: 297,493-425,674). Incomplete implementation of quadruple GDMT in HFrEF remains a major modifiable opportunity to reduce preventable deaths and HF hospitalizations in the United States.
Prediabetes is common among adults with hypertension, but its contribution to heart failure (HF) risk, particularly in the presence of subclinical myocardial abnormalities, remains uncertain. The objective of the study was to assess whether prediabetes combined with malignant left ventricular hypertrophy (LVH)-defined as LVH accompanied by subclinical myocardial injury or stress-is associated with increased HF risk in hypertensive adults without diabetes. This prospective cohort analysis included 8,131 hypertensive adults without diabetes or prior HF from the SPRINT (Systolic Blood Pressure Intervention Trial). LVH was defined using the Cornell voltage product. Subclinical myocardial injury was defined as high-sensitivity cardiac troponin I ≥6 ng/L (men) or ≥4 ng/L (women), and subclinical myocardial stress as N-terminal pro-B-type natriuretic peptide ≥125 pg/mL. Cox proportional hazards models estimated adjusted HRs and 95% CIs for HF. During a median 3.3-year follow-up, 115 HF events occurred. Compared with normoglycemic adults without malignant LVH, those with both prediabetes and malignant LVH had higher HF risk (adjusted HR: 3.55; 95% CI: 1.98-6.36). Similar patterns were observed for prediabetes with LVH plus myocardial injury (HR: 4.02; 95% CI: 2.21-7.30) or stress (HR: 4.04; 95% CI: 2.22-7.34). Prediabetes alone was not associated with HF (adjusted HR: 1.24; 95% CI: 0.80-1.91). Among hypertensive adults, the coexistence of prediabetes and malignant LVH identifies a subgroup at substantially elevated HF risk. Integrating glycemic status, ECG findings, and cardiac biomarkers may enhance HF risk stratification and inform preventive strategies.
Metabolic and musculoskeletal abnormalities in patients with heart failure (HF) may not be fully captured by body mass index. Body composition was studied in participants with HF and matched control subjects in the UK Biobank Imaging Study, and findings were compared among those with HF with reduced ejection fraction, HF with mildly reduced ejection fraction, and HF with preserved ejection fraction. Participants with HF and available ejection fraction (n = 185) were matched 1:5 to age-, sex-, and body mass index-matched control subjects (n = 925). Whole-body magnetic resonance-quantified visceral adipose tissue (VAT), abdominal subcutaneous adipose tissue, liver fat, thigh fat-free muscle volume (MV), and muscle fat infiltration (MFI) were assessed. Personalized z-scores adjusted for sex and body size were derived. Adverse muscle composition (AMC) was defined as low MV z-score and high MFI. Dual-energy x-ray absorptiometry was used to measure total fat and appendicular lean mass. Compared with control subjects, HF participants had higher VAT (z-score = 0.46 ± 1.1 vs 0.07 ± 1.0; P < 0.001), MFI (8.4 ± 2.3% vs 7.6 ± 2.0%; P < 0.001), and AMC (36% vs 17%; P < 0.001) and lower MV (z-score = -0.7 ± 1.0 vs -0.1 ± 0.9; P < 0.001). Despite the muscle derangements identified by magnetic resonance imaging assessment, the prevalence of sarcopenia diagnosed using combined grip strength and dual-energy x-ray absorptiometry-derived lean mass parameters varied considerably depending on the criteria applied. Among HF subtypes, HF with mildly reduced ejection fraction showed the highest VAT and lowest MV, HF with preserved ejection fraction had greater fat and MFI, and HF with reduced ejection fraction had the greatest prevalence of AMC and the weakest grip strength. Participants with HF showed higher VAT and adverse muscle changes, with weaker grip strength. Sarcopenia prevalence varied substantially across definitions, reflecting substantial variability and discrepancies among current sarcopenia definitions and criteria. Traditional anthropometric indexes underestimate the burden of body composition derangements in HF.
Tricuspid regurgitation (TR) is crucial for recurrent cardiac decompensation. Heterotopic transcatheter approaches enable symptomatic treatment of TR in patients who are ineligible for surgery or transcatheter edge-to-edge repair. The TRICENTO G2 prosthesis is a transcatheter bicaval valved stent graft, not yet approved for the market. To the best of our knowledge, this is the first published case of successful TRICENTO G2 transcatheter heart valve implantation, performed as compassionate use in an 81-year-old man with symptomatic TR following multiple interventions. No major complications occurred during the procedure, and a short-term functional improvement in right ventricular function resulted. Given intermittent third-degree atrioventricular block, leadless pacemaker implantation was conducted subsequently. The TRICENTO G2 represents a promising treatment option for symptomatic TR. However, wise patient selection and vigilant postprocedural observation are essential. The implementation of the TRICENTO G2 may expand our interventional armamentarium for treating TR. The TRICENTO G2 may improve tailored treatment of patients with symptomatic TR and right ventricular dysfunction who are ineligible for approved interventions.
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Following the 2018 U.S. heart allocation policy change, transplant centers became less likely to use a bridge-to-transplant (BTT) durable left ventricular assist device (LVAD) strategy. Previous work has shown that patients with BTT LVADs are less likely to be transplanted under this current allocation policy. Candidates from vulnerable communities also have lower transplant rates after listing. The authors sought to determine if listing with BTT-LVADs disproportionately changed in vulnerable communities after the 2018 policy change. This study used data from the SRTR (Scientific Registry of Transplant Recipients). The study cohort included adult heart transplant candidates initially listed between 2014 and 2024, divided into prepolicy and postpolicy cohorts (before or after October 18, 2018). The primary exposure was neighborhood deprivation, measured by the national ADI (Area Deprivation Index) of the candidate's place of residence. The association of the interaction of ADI and policy period and the odds of a candidate being listed with a BTT-LVAD were estimated using a mixed-effects logistic regression model with a random intercept based on the listing center, adjusted for center characteristics and candidate characteristics. The final study cohort included 43,342 candidates (17,655 prepolicy candidates and 25,687 postpolicy candidates). During the prepolicy period, 4,440 (25%) candidates were listed with a BTT-LVAD, compared to 4,658 (18%) under the current policy (P < 0.001). In our fully adjusted model, the impact of the candidate ADI on the likelihood of a candidate being listed with a BTT-LVAD differed significantly between policy periods (P < 0.001). In the prepolicy period, the ADI was not associated with odds of listing with a BTT-LVAD (prepolicy OR: 1.00 [95% CI: 0.98-1.02]; P > 0.9). In the postpolicy period, candidates in the 10th ADI decile (most disadvantage) had 59% higher odds of listing with a BTT-LVAD than first-decile candidates (postpolicy OR: 1.05 [95% CI: 1.03-1.08]; P < 0.001). After the 2018 heart allocation policy change, candidates from more vulnerable communities became more likely to be listed with a BTT-LVAD. This change in practice may exacerbate place-based disparities in heart transplant access. Policy changes are needed to ensure greater equity among candidates being listed with a BTT-LVAD and heart allocation.
Stereotactic arrhythmia radioablation (STAR) has been proposed to treat refractory ventricular tachycardia (VT) in patients with structural heart disease (SHD). The aim of the STAR-VT-2020 (Stereotactic Ablative Radiosurgery of Recurrent Ventricular Tachycardia in Structural Heart Disease) randomized trial was to compare the efficacy of STAR and catheter ablation (CA) after a failure of previous CA. Patients with VT recurrences were randomized at 2 centers (June 2020 to January 2024) to the STAR or CA group in a 1:1 fashion using a covariate-adaptive algorithm. In the STAR group, the arrhythmogenic substrate was irradiated by a single dose of 25 Gy delivered by a robotic system (CyberKnife). The planning target volume was delineated by coregistering the electroanatomical substrate map (CARTO 3) with the planning computed tomographic scan. In the CA group, CA was performed using substrate modification strategies. The primary endpoint was VT recurrence, while repeated CA was one of the secondary endpoints. A total of 22 patients (68% men, mean age 67 ± 11 years, 27% with ischemic cardiomyopathy, mean left ventricular ejection fraction 31% ± 9%, 3.0 ± 1.3 previous CAs) were enrolled (11 in each group) and followed for 28 ± 17 months. The STAR patients exhibited a nonsignificantly higher risk for VT recurrence (HR: 2.5; 95% CI: 0.97-6.6) than those who underwent CA, and a significantly higher risk of repeated CA for VT (HR: 4.0; 95% CI: 1.2-13.8). Throughout the trial, 13 patients died, 3 underwent heart transplantation, and 3 received left ventricular assist devices, with no significant differences between the 2 groups. The STAR-VT-2020 trial suggests a potential clinical benefit of repeated CA over STAR in patients with SHD, despite prior failed CA at specialized centers. Because of the small study cohort of highly selected patients and several methodological limitations, the results of the prematurely terminated trial should be considered exploratory and interpreted strictly as hypothesis generating. Larger trials with optimized design are warranted. (Stereotactic Ablative Radiosurgery of Recurrent Ventricular Tachycardia in Structural Heart Disease; NCT04612140).
p.(V142I)-associated variant transthyretin amyloid cardiomyopathy (ATTRv-CM) is biologically aggressive and predominantly affects individuals of African ancestry. A 51-year-old Nigerian man was diagnosed with double outlet right ventricle by the adult congenital heart disease service, although challenging social circumstances hindered adherence to clinic appointments. He re-established regular contact after 3 years and underwent workup for corrective surgery. Cardiac amyloidosis was suspected on repeat echocardiogram and confirmed on cardiac magnetic resonance and bone scintigraphy. Genetic sequencing later identified homozygosity for the p.(V142I) transthyretin variant. He was referred for emergency transplant assessment after developing cardiogenic shock. Unfortunately, he died despite receiving supportive therapies. Homozygous p.(V142I)-ATTRv-CM presents earlier and advances more aggressively than its heterozygous counterpart. This unusual case highlights the diagnostic pitfalls when genetics, adult congenital heart disease, and advanced heart failure intersect. In patients of African ancestry, a high index of suspicion for p.(V142I)-ATTRv-CM is needed to prompt early diagnosis and initiation of disease-modifying therapies.
Ankyrin-B (AnkB), encoded by ANK2, is essential for ion channel localization in the heart. We investigated its role in regulating sinoatrial node (SAN) responses to autonomic input. AnkB-haploinsufficient (AnkB+/-) mice showed baseline bradycardia, heightened SAN response to β-adrenergic stimulation, and increased heart rate variability. These mice exhibited reduced ICa,L and SAN sarcoplasmic reticulum Ca2+ content, unchanged IK,ACh density, but impaired IK,ACh desensitization. AnkB interacts with GIRK1/4 subunits, and its loss in cardiomyocyte-specific knockout mice reduced GIRK1 membrane localization. Our findings support that AnkB deficiency disrupts autonomic regulation of SAN function through downregulation of ICa,L and the reduction in IK,ACh desensitization.
Donor-derived hypertrophic cardiomyopathy (HCM) is an exceptionally rare posttransplant complication, traditionally diagnosed years after transplant. A 55-year-old woman received a heart from a 30-year-old man donor who suffered sudden cardiac death. On postoperative day 1, she developed severe dynamic left ventricular outflow tract obstruction (peak gradient, 110 mm Hg). Despite calcium channel blocker therapy and later beta-blockade, she remained in NYHA functional class III with persistent gradients. Cardiac magnetic resonance imaging 5 months posttransplant confirmed donor-derived HCM. Mavacamten (Camzyos; Bristol Myers Squibb) was initiated at 11 months, inducing gradient reduction to 11 mm Hg at rest and 25 mm Hg post-Valsalva, without adverse interactions with tacrolimus. At 50 months posttransplant, she demonstrated sustained intracavitary gradient reduction and functional recovery. This is the first report of early donor-derived HCM treated with mavacamten within 1 year of transplant. Targeted myosin inhibitor therapy appears promising, and CYP3A4-mediated pharmacokinetic interactions may be lower than previously believed. Mavacamten may be safe and effective for donor-derived HCM in the early posttransplant period. Utilization of carefully selected donors with HCM or left ventricular hypertrophy could increase the donor pool.
Body mass index (BMI) is commonly used to assess total adiposity, yet does not provide insight into overall body composition, potentially obscuring meaningful heterogeneity in cardiovascular disease (CVD) risk. Waist circumference (WC) and waist-to-hip ratio (WHR) are surrogate measures of central adiposity that are commonly discordant with BMI and may provide additional prognostic information. The purpose of this study was to quantify the reclassification and misclassification of traditional normal weight/overweight/obesity categories using central adiposity and to evaluate the prognostic implications for CVD risk using the CCC (Cross-Cohort Collaboration). We included 259,388 participants from 15 cohorts of the CCC with harmonized data on either WC or WHR data and at least 1 of 9 outcomes: time to first fatal and nonfatal myocardial infarction, fatal and nonfatal stroke, heart failure, atrial fibrillation, total coronary heart disease, total CVD, coronary heart disease mortality, CVD mortality, and all-cause mortality. Multivariable Cox proportional hazards models were used to estimate the HR of higher WC and WHR for each outcome across BMI categories. Our sample included 259,351 individuals with WC data and 218,984 with WHR data, with a median follow-up of 20.0 years (95% CI: 12.7-23.5 years). Among individuals with normal weight, 5% had high WC and 18% had high WHR; among those with overweight, 39% had high WC and 40% had high WHR. Among those with obesity, 9% had low WC and 45% had low WHR. Among individuals with normal weight or overweight, clinically defined high WC or WHR was associated with 15% to 50% greater risk for most outcomes. Among those with obesity, low WC was not associated with a significantly different risk compared with normal weight and low WC, except for all-cause mortality, for which risk was significantly lower. In contrast to men, women with obesity but low WHR retained significantly higher risk for all outcomes compared with normal weight and low WHR; however, the HRs were smaller compared with those with obesity and high WHR. Among individuals with obesity, the population attributable risk associated with elevated WC or WHR ranged from 13% to 49%, with the highest estimates observed for elevated WC in heart failure and atrial fibrillation. WC and WHR identifies misclassification of conventional BMI categories and reclassifies CVD risk across normal weight, overweight, and obesity, adding diagnostic and prognostic value.
To evaluate the reasons underlying the translational failure of cardioprotection in reperfused ST-elevation myocardial infarction (STEMI) and propose a framework for designing future clinical cardioprotection trials. The 2024 JACC Scientific Statement on reperfusion injury reframed the field as a network of interrelated injury pathways but stopped short of providing a clinically actionable framework. Contemporary cardioprotection trials in enriched patient STEMI cohorts have produced largely neutral results: STEMI-DTU, PiCSO-AMI-I, EURO-ICE, and COOL AMI EU failed to demonstrate cardioprotection on cardiovascular magnetic resonance (CMR) infarct size. Although the PITRI trial showed reduced periprocedural platelet reactivity with cangrelor there was no reduction in infarct size or microvascular obstruction (MVO), exemplifying proximal target engagement without affecting imaging surrogates. In contrast, the supersaturated oxygen (SSO₂) programme arc - AMIHOT → AMIHOT-II → IC-HOT → IC-HOT-MICRO - showed progressive patient enrichment yielding a progressive mechanistic signal, particularly in patients with severe coronary microvascular dysfunction. The Collaborative Registry on CMR in STEMI confirmed MVO ≥ 2.6% of left ventricular mass as an independent predictor of heart failure hospitalisation and all-cause death. The EU-CARDIOPROTECTION IMPACT criteria provide a preclinical standard for clinical translation. Translational failure of cardioprotection reflects misalignment between heterogeneous biology and trial design, not biological irrelevance. A biological ceiling cannot be excluded but is unlikely to be the dominant barrier. The path forward is to align patient selection, phenotype-specific endpoints, and adaptive trial architecture, and to test mechanical interventions together with pharmacological adjuncts rather than in isolation. When these elements are aligned - as the SSO₂ programme arc suggests - cardioprotection in STEMI may yet deliver clinically meaningful benefit.
Nicorandil, an adenosine triphosphate-sensitive potassium-channel opener with nitrate-like properties, may reduce reperfusion injury and microvascular obstruction in ST-segment elevation myocardial infarction (STEMI), but large-scale randomized evidence on long-term clinical outcomes is inconclusive. The CLEAN trial aimed to assess whether adjunctive intravenous nicorandil improves 12-month clinical outcomes in patients with STEMI undergoing primary percutaneous coronary intervention. In this multicenter, randomized, double-blind, placebo-controlled trial conducted at 49 hospitals in China, patients aged 18 to 80 years with STEMI within 12 hours of symptom onset were randomly assigned (1:1) to receive intravenous nicorandil (6 mg bolus before reperfusion followed by 6 mg/h infusion for 48 h) or matching placebo. Oral nicorandil was prohibited during follow-up. The primary outcome was a composite of cardiovascular death, nonfatal myocardial infarction, target vessel revascularization, or unplanned hospitalization for heart failure within 12 months. Between January 2021 and December 2023, 1,503 patients were enrolled and randomly assigned to nicorandil (n = 748) or placebo (n = 755). The primary composite outcome occurred in 98 patients (13.1%) in the nicorandil group (113 events over 717.2 person-years) and 99 (13.1%) in the placebo group (136 events over 710.3 person-years), with no significant difference between groups (rate ratio: 0.869; 95% CI: 0.650-1.162; P = 0.3429). Among secondary outcomes, nominal reductions were observed in cardiovascular death (1.9% vs 3.6%; HR: 0.515; 95% CI: 0.269-0.983) and target-vessel revascularization (1.1% vs 3.0%; HR: 0.322; 95% CI: 0.143-0.727), whereas rates of nonfatal myocardial infarction and unplanned hospitalization for heart failure were similar between groups. Adverse events did not differ between groups. In patients with STEMI undergoing primary percutaneous coronary intervention, adjunctive intravenous nicorandil did not significantly reduce the 12-month primary composite outcome. These findings do not support routine use of intravenous nicorandil in unselected patients with STEMI. (Clinical Efficacy and sAfety of Intravenous Nicorandil; NCT04665648).
Heart failure with functional mitral regurgitation (FMR) has poor prognosis, and mitral transcatheter edge-to-edge repair (M-TEER) is an effective treatment. However, patient responses are variable, highlighting the need for early markers of treatment success. Left atrial reservoir strain (LARS) reflects atrial compliance and chronic hemodynamic burden and may identify patients with reversible atrial dysfunction. We retrospectively analyzed 128 patients with FMR (median age 80 years, 37% female; 31% atrial subtype) undergoing M-TEER at Hiroshima University Hospital. LARS was measured at baseline and 1 month postprocedure, with improvement defined as ≥15% relative increase. Procedural success was high (98%), and LARS assessment showed excellent reproducibility. LARS improved in 33% of patients. Key predictors of early improvement were absence of persistent atrial fibrillation, lower baseline LARS, and better renal function. Procedural factors such as residual mitral regurgitation or transmitral gradient were not associated. Patients with LARS improvement showed greater reductions in pulmonary arterial wedge pressure, improved biventricular function, lower residual tricuspid regurgitation, and enhanced exercise capacity. During a median follow-up of 14 months, early LARS improvement was associated with significantly higher event-free survival. Multivariable analysis confirmed that LARS improvement independently predicted lower risk of all-cause death and heart failure hospitalization, beyond baseline LARS and conventional post-M-TEER risk factors. Continuous analysis of %ΔLARS further supported a dose-response relationship with outcomes. In summary, early LARS improvement reflects integrated atrial and cardiopulmonary reverse remodeling and is a strong independent predictor of short-term prognosis after M-TEER. Serial assessment of LARS shortly after M-TEER may serve as a practical tool for early risk stratification and therapeutic optimization across all FMR subtypes.
Severe tricuspid regurgitation (TR) is associated with morbidity and mortality and linked to intravascular venous congestion. Venous ultrasound of the hepatic, portal, and intrarenal veins-often integrated via the Venous Excess Ultrasound (VExUS) score-offers prognostic insight in heart failure, but its utility in transcatheter tricuspid valve intervention (TTVI) remains undefined. The aim of this study was to evaluate changes in hepatic, portal, and intrarenal venous flow before vs after TTVI, assess their durability, and explore associations with prognosis and functional status. In this prospective multicenter cohort patients undergoing TTVI (2022-2024) were included. Venous ultrasound was performed 24 hours pre- and postprocedure. Functional status, frailty, biomarkers, venous ultrasound and echocardiography were assessed at baseline and at 1, 6, and 12 months. All-cause mortality and heart failure hospitalization were recorded. Survival was analyzed by Kaplan-Meier and Cox regression. A total of 64 patients were included; mean age was 76.7 ± 8.1 years; 76.6% were women. Procedures included edge-to-edge repair (60.9%), percutaneous annuloplasty (18.7%), orthotopic replacement (14.1%), and heterotopic replacement (6.3%). At baseline, 70% had VExUS grade 3. Within 24 hours hepatic vein, portal pulsatility, and intrarenal venous flows improved, reclassifying 66% to VExUS ≤1, despite no change in diuretic dose or weight. Venous ultrasound improvements persisted during follow-up. Postprocedure VExUS grade 3 at 24 hours was a strong predictor of mortality (HR: 5.55; 95% CI: 1.60-19.21; P = 0.007). TTVI improved hepatic, portal, and intrarenal venous flow within 24 hours, with sustained effects at 1 year. Postprocedure VExUS score was associated with mortality and may serve as a procedural success indicator.
Midmyocardial and subepicardial late gadolinium enhancement (LGE) are typical in inherited arrhythmogenic cardiomyopathy (ACM) and dilated cardiomyopathy (DCM). Transmural LGE, usually considered ischemic and excluded from ACM criteria, may also occur, but its clinical relevance is unclear. The objective of this study was to assess the prevalence, genetic associations, and prognostic significance of transmural LGE in patients with genotype-positive, nonischemic ACM/DCM. We retrospectively analyzed 1,379 genotype-positive patients with ACM/DCM, identifying 711 with cardiac magnetic resonance imaging and no significant coronary artery disease. Patients were stratified by LGE pattern (transmural, nontransmural, or absent). Major ventricular arrhythmic (MVA) and advanced heart failure (AHF) events were evaluated using Kaplan-Meier and age-adjusted Cox regression analyses. Transmural LGE was present in 5% (33/711) of patients and was enriched in LMNA and DSP variant carriers. Compared with nontransmural or absent LGE, transmural LGE was associated with higher rates of thromboembolic events, atrial fibrillation, and implantable cardioverter-defibrillator implantation (all P ≤ 0.003). It also conferred increased rates of MVA events (45% vs 27% vs 14%) and AHF therapies (18% vs 12% vs 6%) (P < 0.05). In age-adjusted models, transmural LGE independently predicted the composite endpoint of MVA/AHF compared with nontransmural LGE (HR: 1.9; P = 0.03) and no LGE (HR: 2.9; P = 0.0005). Transmural LGE identifies a small but high-risk subset of genotype-positive ACM/DCM, particularly among patients with LMNA and DSP variants, with significantly increased arrhythmic and heart failure risk.
Myocarditis is an inflammatory cardiomyopathy with broad clinical spectrum. Pregnancy outcomes in women with a history of myocarditis are not well described. The aim of this study is to determine maternal and fetal outcomes in pregnant women with history of myocarditis/perimyocarditis. This was a retrospective study of pregnancy outcomes in patients with prior history of myocarditis/perimyocarditis followed in a CardioObstetrics Program (1998-2025). Adverse maternal cardiac outcomes included: maternal death, heart failure, and sustained arrhythmia. Echocardiographic changes during pregnancy were examined. Fetal adverse events: fetal death, prematurity, small for gestational age (<10th percentile). Thirty-six pregnancies in women (n=27) with a history of myocarditis were included [mean age 33±4.9 years, median interval between myocarditis and pregnancy 5.0 years]. In 50% of cases, there was moderate/severe left ventricular (LV) systolic dysfunction at time of myocarditis presentation. In most (83%,15/18) pregnancies, with significant LV dysfunction at time of myocarditis presentation, there was full recovery of LV systolic function prior to pregnancy. No adverse maternal cardiac events were reported in 97% (35/36) of pregnancies. One patient with moderately reduced LV systolic function during myocarditis, with recovery prior to pregnancy, developed heart failure. Two patients had reduction in LV systolic function in pregnancy, from mild/normal to moderate/severely reduced. There were no maternal or fetal deaths. Thirteen percent of pregnancies had premature delivery (31-36 weeks). Most women with prior myocarditis do not develop adverse cardiac events. However, echocardiographic surveillance during pregnancy may still be helpful to identify decreases in LV systolic function.