Biomarkers and Personalized Medicine in Cardiovascular Disease Symposium

Beyond Acute Coronary Syndrome: Troponin Kinetics and Assay Concordance Reveal ICI-Associated Myocarditis

Haley Kempf¹, Nilesh Vora²

University of California Irvine, CA, USA

Long Beach Memorial Hospital, CA, USA

Background: High-sensitivity cardiac troponin has evolved from a diagnostic marker for acute coronary syndrome (ACS) to a central tool in cardio-oncology for detecting subclinical myocardial injury, risk stratification, and treatment-related toxicity. However, interpretation remains challenging in cancer patients, where elevations may reflect overlapping processes including immune-mediated inflammation, microvascular dysfunction, and extracardiac sources. Emerging evidence highlights the importance of troponin kinetics, assay-specific differences (hs-cTnI vs hs-cTnT), and integration with multimodal imaging, yet clinical frameworks remain limited—particularly in patients with persistently rising troponin despite non-obstructive coronary arteries.

Case Presentation: A 73-year-old female with metastatic renal cell carcinoma on lenvatinib and pembrolizumab presented with acute chest pain. Electrocardiogram showed lateral ST-segment elevations and T-wave inversions. High-sensitivity (hs) troponin I was elevated at 13,600 ng/L, rising to >125,000 ng/L within 12 hours. Hs-troponin T was 2430 ng/L. Creatine phosphokinase was 354 U/L. She was treated for suspected ACS and underwent emergent coronary angiography, which revealed non-obstructive disease. Recurrent chest pain prompted repeat angiography with unchanged findings. Persistent biomarker elevation prompted evaluation for non-ischemic etiologies. Cardiac MRI demonstrated mildly reduced left ventricular systolic function (LVEF 44%) with extensive non-ischemic late gadolinium enhancement and elevated T2 signal, consistent with immune checkpoint inhibitor (ICI)–associated myocarditis. Inflammatory markers were elevated, and BNP rose from 53 to 645 pg/mL. High-dose intravenous corticosteroids were initiated; however, troponin continued to rise, prompting escalation to abatacept therapy, after which biomarkers stabilized. Subsequent testing demonstrated normalization of troponin I. Following resolution of heart failure, imaging revealed profound tumor response to ICI, allowing the patient to become a surgical candidate.

Discussion: This case highlights the diagnostic value of troponin kinetics, as a persistent rise despite two negative angiograms raised suspicion for a non-ischemic process. Cardiac MRI confirmed myocarditis, emphasizing biomarker–imaging concordance. Concordance between hs-cTnT and hs-cTnI, with elevated creatine phosphokinase, underscores the complexity of biomarker interpretation in cardio-oncology. In immune checkpoint inhibitor therapy, re-expression of fetal troponin T in skeletal muscle may occur; when myocarditis coexists with myositis, elevated troponin T may originate from skeletal muscle while cardiac-specific troponin I remains normal.

Conclusion: Persistent troponin elevation in oncology patients without obstructive coronary disease represents a high-risk, under-defined entity. Early integration of advanced imaging and nuanced biomarker interpretation may reduce unnecessary invasive procedures and improve diagnostic accuracy.

Key words: High-sensitivity troponin, Immune Checkpoint Inhibitor, Myocarditis

Disclosure: We do not have any financial or non-financial interest that has arisen directly from application of this research. There is no competing interest to declare.

Breast arterial calcification and cardiovascular risk prediction in women with and without standard modifiable risk factors

Authors: Sophia Y. Xiao MD, MS¹; Richard Mantey²; Quan M. Bui, MD³; Lori B. Daniels, MD, MAS⁴

¹Department of Medicine, UC San Diego Health, San Diego, CA, USA

²Department of Applied AI and Clinical Research, CureMetrix

³Advanced Heart Failure/Transplant Cardiology, Division of Cardiology, UC San Diego Health, San Diego, CA, USA

⁴Divison of Cardiology, UC San Diego Health, San Diego, CA, USA

Background: Risk identification among women, particularly those without standard modifiable risk factors (SMuRFs) for cardiovascular disease (CVD), remains suboptimal. Breast arterial calcification (BAC), found incidentally on mammography, is a promising biomarker associated with CVD. We evaluated BAC’s utility for predicting CVD and mortality between SMuRFless and SMuRF+ women. Among SMuRF+ women, we examined whether treatment of hypertension or hyperlipidemia modifies the relationship between BAC and CVD.

Methods: This single-center retrospective cohort study included 19,718 women aged 40–90 years who underwent screening digital mammography from 2006-2016. BAC was quantified using validated deep-learning software (cmAngio®, CureMetrix). SMuRFless women had no hypertension, hyperlipidemia, diabetes, smoking history, chronic kidney disease, prevalent CVD, or related preventive pharmacotherapy. The primary composite outcome included acute myocardial infarction, heart failure, stroke, and death; the secondary outcome was all-cause mortality.

Results: Mean age was 56.8±11.5 years. Prevalent risk factors (RFs) included hypertension (24%), hyperlipidemia (27%), and diabetes (7%). 8,813 women (42%) were SMuRFless; 18% of SMuRFless and 31% of SMuRF+ women were BAC-positive. Over a mean follow-up of 5.9±3.2 years, a composite event occurred in 4.8% of BAC-negative and 14% of BAC-positive women (p<0.001). Among SMuRF+ women, BAC was associated with a 50% higher adjusted risk of the composite outcome (aHR 1.50 [95% CI 1.30–1.73], p<0.001) and 51% higher mortality risk (aHR 1.51 [95% CI 1.25–1.82], p<0.001). Among SMuRFless women ≤60 years, there was a similar association between BAC and the composite outcome (aHR 1.51 [95% CI 0.96–2.36], p=0.07). Among women on lipid-lowering therapy (LLT), BAC was independently associated with a 44% increased risk of the composite outcome (aHR 1.44 [95% CI 1.18–1.76], p<0.001) and a 42% increased mortality risk (aHR 1.42 [95% CI 1.08–1.87], p<0.001). Among women on antihypertensive therapy, BAC was independently associated with a 45% increased risk of the composite outcome (aHR 1.45 [95% CI 1.19–1.76], p<0.001) and a 24% increased mortality risk (aHR 1.24 [95% CI 1.10–1.38], p=0.006). Women with RFs and BAC not receiving LLT or antihypertensive medication had highest risk across all subgroups.

Conclusion: Among women undergoing routine mammography, BAC identifies women at higher-risk for incident CVD and mortality. BAC provides incremental prognostic information in SMuRF+ women  and may improve risk stratification in younger women without traditional RFs.

Keywords: coronary artery disease, risk stratification, breast arterial calcification, sex-specific biomarkers

Disclosure statement: The authors have no conflicts of interest to disclose relevant to the contents of this abstract.

Corresponding Author contact information:

Sophia Xiao, MD, MS

soxiao@health.ucsd.edu

RILONACEPT REDUCES PERICARDITIS RECURRENCE RISK, HOSPITALIZATIONS, AND ED VISITS: OUTCOMES FROM THE RESONANCE PATIENT REGISTRY

Paul C. Cremer, MD¹, Michael S. Garshick, MD^2,3, Sushil A. Luis, MBBS, PhD⁴,  Ajit Raisinghani, MD⁵, Brittany Weber, MD, PhD⁶,  MohamedAl-Kazaz, MD¹, Tracy Hagerty, MD⁷, John J. Ryan, MD⁸, Jonathan R. Salik, MD⁹, Taylor Corey¹⁰, Vidhya Parameswaran, MPH¹⁰, Allan L. Klein, MD¹¹, John F. Paolini, MD, PhD¹⁰, on behalf of the RESONANCE Study Group.

Presenter: Corina Grancorvitz¹⁰

*Corresponding author:

Vidhya Parameswaran, MPH

Kiniksa Pharmaceuticals

100 Hayden Ave. Lexington, MA 02421

+1 7814319100

vparameswaran@kiniksa.com

¹Bluhm Cardiovascular Institute, Northwestern University Feinberg School of Medicine, Chicago, IL, USA

²Cardio-Rheumatology Program, Center for the Prevention of Cardiovascular Disease, NYU Langone Health, New York, NY, USA

³Leon H. Charney Division of Cardiology, Department of Medicine, New York University School of Medicine, New York, NY, USA

⁴Department of Cardiovascular Medicine, Mayo Clinic, Rochester, MN, USA

⁵Division of Cardiology, Department of Medicine, Sulpizio Cardiovascular Center, University of California San Diego, San Diego, California, USA

⁶Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women‘s Hospital, Harvard Medical School, Boston, MA, USA

⁷University of Vermont Medical Center, Burlington, Vermont, USA

⁸University of Utah Hospital, Salt Lake City, Utah, USA

⁹Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA

¹⁰Kiniksa Pharmaceuticals Corp., Lexington, Massachusetts, USA

¹¹Department of Cardiovascular Imaging, Center for the Diagnosis and Treatment of Pericardial Diseases, Heart and Vascular Institute, Cleveland Clinic, Cleveland, Ohio, USA 

Word count: (245/375) words (NO FIGURES)

Background: Recurrent pericarditis (RP) is an IL-1-mediated chronic autoinflammatory disease. Based on clinical trial evidence, the 2025 ACC Concise Clinical Guidance (ACC CCG) on RP management elevated IL-1 pathway inhibition to 2^nd line as the preferred option over corticosteroids (CS) after NSAIDs/colchicine.

Methods: Annualized recurrence rate (ARR) and healthcare resource utilization (HCRU) data were extracted by chart review from pts who had 1 yr minimum follow-up in RESONANCE, a multicenter US RP pt registry, and were compared by RP treatment regimen.

Results: As of 15 Aug 2025, of the 154 pts (77% idiopathic; median disease duration: 5.2 yrs; median [IQR] observation: 3.8 [1.4] yrs) analyzed, 59.7% (92/154) intensified treatment from NSAIDs ± colchicine to 2^nd line therapy. 2^nd line rilonacept significantly reduced ARR (0.086) versus prior NSAIDs ± colchicine (1.26), P<0.001, whereas 2^nd line CS significantly increased ARR (3.04) versus prior NSAIDs ± colchicine (1.38), P=0.012; almost all recurrences on CS (94.1%) occurred while tapering. Outcomes from 2^nd line rilonacept were significantly superior to 2^nd line CS in both recurrence risk and HCRU (ARR: 0.086 vs. 3.04, P<0.001; hospitalizations: 0 vs. 14.5, P<0.001; ED visits: 0 vs. 43.4, P<0.001).

Conclusion: Real-world data from RESONANCE demonstrate that second-line IL-1 pathway inhibition with rilonacept provides superior clinical outcomes and reduced hospitalizations/ED visits versus corticosteroid-based management strategies. In pts failing NSAIDs/Colchicine, 2^nd line rilonacept provided superior recurrence rate and disease burden reductions versus 2^nd line CS, affirming the evidence-based corticosteroid-sparing paradigm shift recommended by the 2025 ACC CCG.

Keywords: autoinflammatory disease; interleukin‐1; recurrent pericarditis; rilonacept

Disclosures:P.C. Cremer: grants and consultant fees from Kiniksa Pharmaceuticals, grants and personal fees from Sobi; M. S. Garshick: consultant fees from BMS, Agepha, Kiniksa Pharmaceuticals; S.A. Luis: consultant fees from Kiniksa Pharmaceuticals, Cardiol Therapeutics, and Medtronic; A. Raisinghani: consultant fees from Kiniksa Pharmaceuticals; B. Weber: consultant fees from Kiniksa Pharmaceuticals, Novo Nordisk, Horizon Therapeutics, and BMS; M. Al-Kazaz: research grant support from Kiniksa Pharmaceuticals, Ventyx, and Cardiol Therapeutics; speaking honoraria from Kiniksa Pharmaceuticals, and consulting fees from Edwards Lifesciences; T. Hagerty: no relationships to disclose; J.R. Salik: no relationships to disclose; J.J. Ryan: research funding from Merck, Bayer, Liquidia, Janssen PH, Kiniksa, and served as a consultant for Merck, Liquidia, Janssen PH, United Therapeutics, and Kiniksa; T. Corey: no relationships to disclose; C. Grancorvitz, V. Parameswaran and J.F. Paolini: shareholders and employees of Kiniksa Pharmaceuticals; A.L. Klein: grants and consultant fees from Kiniksa Pharmaceuticals, Cardiol Therapeutics, Ventyx, and Pfizer.

Threshold and Kinetic Differences Between Fifth- and Sixth-Generation High-Sensitivity Cardiac Troponin T in Routine Clinical Care Testing

Megan Palacio^1*, Lori B. Daniels^2, Nolan R. Martin², Spencer Seely¹, Ronald W. McLawhon¹, Robert L. Fitzgerald¹, Raymond T. Suhandynata^1,3

¹Department of Pathology, University of California San Diego, San Diego, CA, USA

²Division of Cardiovascular Medicine, University of California San Diego, San Diego, CA, USA

³Skaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego, San Diego, CA, USA

*Author for correspondence

Center for Advanced Laboratory Medicine

University of California San Diego

10300 Campus Point Dr.

San Diego, CA 92121

mepalacio@health.ucsd.edu

Background: High-sensitivity cardiac troponin T (hs-cTnT) assays are central to the evaluation of myocardial injury, with clinical interpretation directed by the assay-specific 99^th percentile upper reference limit (URL). Transition from the fifth-generation (Gen5) to sixth-generation (Gen6) hs-cTnT assays may introduce analytical differences that impact threshold-based interpretation, particularly near the 99^th percentile URL where small concentrations changes may alter classification. Data describing the real-world clinical implications of this assay transition remain limited.

Methods: Residual clinical specimens from patients undergoing routine hs-cTnT testing were analyzed in parallel using Roche Gen5 and Gen6 assays in a retrospective paired study design. Longitudinal paired measurements (n=3,617) from 1,847 encounters representing 1,737 unique patients were evaluated. Comparative analyses included time to first elevation above the assay-specific 99^th percentile URL, peak hs-cTnT values, simulated 0/1/3-hour clinical pathway categorization, and temporal kinetic characteristics.

Results: Gen5 and Gen6 assays demonstrated strong concordance overall for paired measurements and encounter-level peak classification. Observed differences were concentrated near the 99^th percentile URL rather than across the full analytical measurement range. Gen6 crossed the 99^th percentile URL earlier than Gen5 more frequently than the reverse scenario (2.6% vs 0.1%; p=0.0001). Simulated application of a 0/1/3-hour clinical pathway showed high overall agreement between assays, though select encounters were reassigned among rule-out, indeterminate, and abnormal categories. Compared with Gen5, Gen6 exhibited larger relative changes during early rising phase and more rapid decline following peak concentration, with decay characteristics more closely approximating CK-MB kinetics.

Conclusion: Gen5 and Gen6 hs-cTnT assays show high overall analytical concordance yet modest differences near clinical decision thresholds can alter timing of 99^th percentile URL crossing and downstream modeled pathway classification. These findings underscore the need for careful assay-specific validation and interpretation when adopting newer hs-cTnT assay generations.

Keywords: high-sensitivity cardiac troponin T, myocardial injury, assay comparison

Disclosure Statement: This investigator-initiated study was supported by Roche Diagnostics, which supplied all study reagents. MP, NRM, SS, RWM, RLF, and RTS received no salary support related to this work. LBD has served as a consultant for QuidelOrtho, Roche Diagnostics, and Siemens; has participated on clinical endpoint adjudication committees for Abbott Laboratories, Pfizer, QuidelOrtho, and Tosoh Corporation; and has received research funding and/or served as an investigator for clinical studies sponsored by Cardiosense, DalCor Pharmaceuticals, and Roche Diagnostics.

Association between Triglyceride- Glucose Index and Heart Failure Risk by Body Mass  Index in a Multi-Ethnic Cohort

Nandan Thakkar, MD, MSc¹; Kimberly Hong, MD, MHSA²; Michael D. Shapiro, DO, MCR³; Alain G. Bertoni, MD, MPH⁴; Harpreet S. Bhatia, MD, MAS, FACC²¹ Department of Medicine, University of California San Diego, La Jolla, CA² Division of Cardiovascular Medicine, Department of Medicine, University of California San Diego, La Jolla, CA³ Center for Preventive Cardiology, Wake Forest University School of Medicine, Winston-Salem, NC⁴ Department of Internal Medicine and Public Health Sciences, Wake Forest University School of Medicine, Winston-Salem, NCBackground: Insulin resistance contributes to heart failure (HF) through metabolic dysregulation, systemic inflammation, and adverse myocardial remodeling. However, commonly used measures of cardiometabolic risk, such as body-mass-index (BMI), may not capture underlying metabolic dysfunction in all populations. The triglyceride-glucose index (TyG) is a validated surrogate marker of insulin resistance that may better reflect pathophysiologic processes associated withHF, particularly in non-obese individuals.

Methods: We analyzed 6,683 participants from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort who were free of baseline HF. TyG was calculated as ln(fasting triglycerides × fasting glucose/2). Multivariable cox proportional hazards models were used to evaluate the association between TyG (per 1-unit increase) and incident HF, adjusting for age, sex, race, systolic blood pressure, total and HDL cholesterol, eGFR, diabetes, C-reactive protein, antihypertensive and lipid-lowering medication use, and smoking status. Analyses were stratified by BMI (obese ≥30 kg/m² vs. non-obese <30 kg/m²) and HF subtype (HFpEF ≥50%, HFrEF <50%).

Results: Over a median follow-up of 15.2 years, 502 HF events occurred. In fully adjusted models, higher TyG was associated with increased HF risk (HR 1.24, 95% CI 1.02–1.50, p=0.032). This association was significantly modified by BMI, with a BMI-by-TyG interaction (p = 0.010), andrestricted to non-obese participants (n=4,544; 302 events; HR 1.35, 95% CI 1.05–1.74, p=0.018), with no significant association among obese individuals (n=2,139; 200 events; HR 1.09, 95% CI 0.80–1.48, p=0.60). In HF subtype analyses, TyG demonstrated a trend towardassociation with HFpEF (HR 1.32, 95% CI 0.96–1.82, p=0.085) but not HFrEF (HR 1.03, 95% CI 0.78–1.37, p=0.81).

Conclusions: The TyG index is associated with incident HF independent of traditional risk factors – a relationship that appears to be modified by BMI and most pronounced in non-obese individuals. These findings suggest that insulin resistance—reflecting underlying metabolic dysfunction even in the absence of elevated BMI—may be a key contributor to HF risk. Incorporating markers of metabolic dysregulation such as TyG might improve identification of at-risk individuals not captured by conventional anthropometric measures.

Nocturnal Respiratory Rate: a Stable, Heritable Trait that Predicts All-Cause Mortality

Raimon Padrós-Valls, MS1,2, Mijia Ma, MS3, Keshav Gupta, MBBS, MS1, Nicholas Harrington, PhD1, Jeremy E. Orr, MD4, Robert L. Owens, MD4, Rany Salem, PhD5, Kevin R. King, MD, PhD1,6

1.Department of Bioengineering, Jacobs School of Engineering, UC San Diego; 2.Bioinformatics and Systems Biology Graduate Program, UC San Diego; 3.Department of Biostatistics, Harvard T.H. Chan School of Public Health; 4.Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, UC San Diego; 5.Herbert Wertheim School of Public Health and Longevity Science, UC San Diego; 6.Department of Medicine, Division of Cardiovascular Medicine, UC San Diego.

Abstract:

Respiratory rate is a fundamental vital sign controlled by brainstem circuits, yet its determinants and prognostic potential remain poorly defined. Because activity and conscious modulation confound waking measurements, we hypothesized that nocturnal respiratory rate (NRR) could serve as a stable, passively measurable trait suitable for longitudinal monitoring and population-scale study. Using non-contact home bed sensors, we found that NRR was highly consistent within and between nights for a given individual but varied substantially across individuals, consistent with a subject-specific set point. In a survival analysis of 5,679 older adults from the Sleep Heart Health Study, individuals in the high NRR group exhibited nearly 5-fold higher all-cause mortality, with an adjusted hazard ratio of 2.15 (95% CI 1.30–3.55) after controlling for major clinical covariates. To investigate genetic determinants, we combined polysomnography from the National Sleep Research Resource with dbGaP genotyping data from four cohorts to perform the first genome-wide association study of respiratory rate (N=14,277). We identified significant loci implicating ion-channel (DPP10), neuronal (PIRT), structural (TNR, DACH1), and immune/cardiac (NFATC1) genes, with SNP-based heritability of 0.247 (SE 0.035). Together, these results establish NRR as a stable, heritable, and prognostic biomarker with inherited and acquired determinants.

Title: Association of Lipoprotein(a) with ASCVD Risk in Women by Menopausal Status: the UK Biobank

Author names: Mikaila P. Reyes¹, Alexander C. Razavi², Harpreet S. Bhatia³

Affiliations:

¹University of California San Diego School of Medicine, San Diego, CA, USA; mpr006@health.ucsd.edu

²Division of Cardiology, Emory University School of Medicine, Atlanta, GA, USA; alexander.c.razavi@emory.edu

³Division of Cardiovascular Medicine, University of California San Diego, CA, USA; hsbhatia@health.ucsd.edu 

ABSTRACT

Introduction: Lipoprotein(a) [Lp(a)] is a predominantly genetically determined risk factor for atherosclerotic cardiovascular disease (ASCVD); however, menopause is one of the few conditions that can lead to an increase in Lp(a). We aimed to investigate whether menopause status modifies the association between Lp(a) and ASCVD risk.

Methods: A total of 153,890 pre- and post-menopausal women free of prior ASCVD were studied using data from the UK Biobank. Menopause status was based on self-report while ASCVD was a composite outcome based on ICD10-coded myocardial infarction, stroke or cardiovascular death. Multivariable Cox proportional hazards models evaluated the association between Lp(a) and incident ASCVD events stratified by menopause status.

Results: The median age was 56.1 years, with 60% of women post-menopausal. Median Lp(a) was 22.5 [10.1, 62.1] nmol/L, 21% had Lp(a) >75 nmol/L, and 12% had Lp(a) ≥125 nmol/L. There were 5,160 (3.4%) incident ASCVD events during a median follow up of 13.7 years. Standard deviation increases in Lp(a) were associated with higher risk of ASCVD events among pre-menopausal (HR 1.06, 95% CI 1.00-1.12, p = 0.041) and post-menopausal women (HR 1.06, 95% CI 1.03 - 1.09, p <0.001). Among post-menopausal women, Lp(a) between 75-125 nmol/L (HR 1.13, 95% CI 1.01, 1.25, p = 0.03) and >125 nmol/L (HR 1.15, 95% CI 1.05, 1.26, p = 0.003) were associated with increased ASCVD risk when compared to Lp(a) < 75 nmol/L. The association between Lp(a) and ASCVD risk did not vary with menopause status (p-interactions >0.05).

Conclusion: Lp(a) is an independent risk factor for ASCVD events for both pre- and post-menopausal women.

Cardiac Testing and Return-to-Exercise Guidance in Non-Fulminant Myocarditis: A Mixed-Methods Study

Oscar P. Levine, MD¹; Mark Wendle, MD¹; David Torres Barba, MD, PhD²; Ori Ben-Yehuda, MD²

Affiliations:

¹ Division of General Internal Medicine, Department of Medicine, University of California San Diego

402 Dickinson St, Ste 380

San Diego, CA 92103, USA

² Division of Cardiovascular Medicine, Department of Medicine, University of California San Diego

9434 Medical Center Drive

San Diego, CA 92037, USA

Background: Cardiac testing, including cardiac troponin levels, transthoracic echocardiography (TTE), and cardiac magnetic resonance (CMR), is central to risk stratification and guides return-to-exercise recommendations following myocarditis. However, contemporary guidelines show limited uniformity regarding the optimal selection and use of cardiac testing modalities to guide patients through the recovery phase. Furthermore, real-world practice patterns and patient experiences remain poorly characterized.

Methods: We conducted a single-center mixed-methods study of adults aged ≤50 years hospitalized with non-fulminant myocarditis between July 1, 2014 and June 30, 2024. Quantitative data including cardiac troponin, TTE, CMR, ambulatory rhythm monitoring, and exercise stress testing were abstracted from the electronic medical record. Exercise recommendations were obtained from patient discharge instructions and stratified by ejection fraction (EF) at presentation. Semi-structured interviews were conducted with a subset of patients to explore experiences with myocarditis follow-up and were analyzed using reflexive thematic analysis.

Results: The cohort included 57 patients (mean age 27.6 ± 7.7 years). Documented discharge instructions showed no evidence of a trend toward longer restriction among patients with EF <50% versus EF ≥50% at presentation when analyzed ordinally (no restriction, <3 months, ≥3 months; p = 0.43). Among 37 (64.9%) patients with documented outpatient follow-up, repeat troponin testing was performed in 22 (59.5%) patients, of whom 18 (81.8%) demonstrated normalized levels. Follow-up TTE was obtained in 26 (70.3%) patients; all 8 patients with EF <50% at presentation who underwent follow-up TTE demonstrated recovery of EF to ≥50% at follow-up. Use of other assessments was infrequent, including CMR (18.9%), ambulatory rhythm monitoring (16.2%), and exercise stress testing (10.8%). Qualitative interviews (n=16) identified two major themes related to return-to-exercise guidance and cardiac testing: (1) inconsistent and nonspecific exercise guidance; and (2) additional testing as a source of reassurance during recovery.

Conclusions: In this mixed-methods study of patients hospitalized with non-fulminant myocarditis, discharge exercise recommendations were not consistently aligned with disease severity, and patients often interpreted them as non-specific. Additionally, basic follow-up cardiac testing consisting of repeat cardiac troponin and TTE was performed in the majority of patients with documented follow-up and showed favorable recovery trajectories. However, more advanced evaluations, including CMR, ambulatory rhythm monitoring, and stress testing, were infrequently implemented despite being valued by patients as a source of reassurance and selectively recommended by contemporary guidelines.

Keywords: Myocarditis, troponin, transthoracic echocardiography, cardiac magnetic resonance, risk stratification, return-to-exercise, mixed-methods

Disclosures: The authors report there are no competing interests to declare.