Highlight
- Patients with SIPE exhibit transient mild systolic ventricular dysfunction detectable by transthoracic echocardiography (TTE) shortly after swimming.
- Systolic pulmonary artery pressure is increased in a significant subset of SIPE patients compared with asymptomatic controls.
- Cardiac biomarkers, such as high-sensitivity troponin I and NT-proBNP, are elevated in SIPE patients, suggesting myocardial stress or injury, but electrocardiogram (ECG) changes are not distinctive.
- Clinical differentiation of SIPE from acute myocardial infarction requires careful assessment, as some patients may present with concurrent cardiac ischemia and elevated biomarkers.
Study Background
Swimming-induced pulmonary edema (SIPE) is an acute, potentially life-threatening condition characterized by fluid accumulation in the lungs during or after immersion in water, especially cold open-water swimming. Although SIPE is increasingly recognized in athletes and military personnel, its pathophysiology remains poorly defined. Cardiac involvement has been suggested in the literature, primarily from case reports, indicating transient cardiac dysfunction and biomarker elevation. Given the overlap of clinical features between SIPE and acute cardiac events, particularly myocardial infarction (MI), understanding the cardiac profile of SIPE patients is essential for appropriate diagnosis and management. This study addresses the unmet need for systematic characterization of cardiac findings in SIPE to guide acute assessment and avoid misdiagnosis.
Study Design and Methods
This prospective cohort study was conducted during Sweden’s largest open water swimming event, Vansbrosimningen, over the years 2022 to 2024. The study enrolled 45 patients who developed SIPE and 45 asymptomatic swimmers as matched controls. Inclusion criteria for SIPE cases involved acute onset of respiratory symptoms during or shortly after swimming, consistent with pulmonary edema. Controls had no respiratory or cardiac symptoms.
Participants underwent transthoracic echocardiography (TTE), standard 12-lead electrocardiogram (ECG), and measurement of cardiac biomarkers, including high-sensitivity cardiac troponin I and N-terminal pro-B-type natriuretic peptide (NT-proBNP), within 2 hours post-swim. Follow-up assessment with repeat investigations occurred up to 12 months to evaluate resolution of cardiac abnormalities.
Key Findings
The study revealed several important cardiac differences between SIPE patients and controls:
- Systolic Ventricular Function: Mild impairment of systolic ventricular function, as assessed by TTE, was observed in 43% of SIPE patients compared to 10% of controls (p=0.003). This impairment was transient and improved on follow-up in almost all patients, indicating reversible cardiac stress rather than permanent damage.
- Systolic Pulmonary Artery Pressure: Elevated systolic pulmonary artery pressure (>30% of patients) was unique to the SIPE group and absent in controls (p=0.005). This finding suggests elevated right heart afterload potentially linked to pulmonary vascular congestion.
- Cardiac Biomarkers: High-sensitivity cardiac troponin I levels were increased in 67% of SIPE patients versus 40% of controls (median values 47 pg/ml vs. 14 pg/ml respectively, p<0.001). NT-proBNP was also significantly higher in SIPE patients (median 169 pg/ml) compared to controls (median 65 pg/ml, p<0.001). These elevations suggest myocardial strain rather than extensive necrosis in most cases.
- Electrocardiogram Findings: No significant differences were found on post-swim ECG between SIPE patients and controls (p=0.746), indicating the absence of specific ischemic changes related to SIPE.
- Concurrent Myocardial Infarction: Among the cohort, two SIPE patients were diagnosed with acute MI, presenting with severe chest pain and markedly elevated troponin levels. This underscores the need for clinical vigilance to distinguish SIPE from primary cardiac ischemia.
Expert Commentary
The findings advance our understanding of SIPE as a syndrome not only of pulmonary fluid accumulation but also of transient cardiac dysfunction. The reversible mild systolic impairment and elevated pulmonary artery pressures may reflect acute hemodynamic stress during immersion-related pulmonary edema formation. Biomarker elevations without corresponding ECG changes signify subclinical myocardial strain rather than frank infarction for most patients.
Clinicians should be aware that mild cardiac abnormalities on TTE and moderate elevation of troponin and NT-proBNP can be expected in SIPE and should not be overinterpreted as primary cardiac pathology unless accompanied by clinical or electrocardiographic evidence. These data provide a valuable benchmark for acute evaluation, ensuring appropriate triage and avoiding unnecessary invasive cardiac investigations. The coexistence of SIPE and MI, although uncommon, requires prompt recognition given differing management pathways.
Limitations include the single geographical setting and the relatively small sample size, which might limit generalizability. Further research could explore mechanistic pathways linking immersion-induced pulmonary edema to cardiac stress and potential preventive strategies.
Conclusion
This cohort study delineates the cardiac profile of patients with swimming-induced pulmonary edema, revealing transient mild systolic dysfunction, elevated pulmonary artery pressures, and increased cardiac biomarkers lacking distinctive ECG findings. These findings support a model of reversible cardiac strain as a component of SIPE pathology and provide a clinical reference framework for acute assessment. Distinguishing SIPE from acute myocardial infarction relies on integrated clinical, biomarker, imaging, and ECG data.
Funding and Clinical Trial Registration
The study was registered on clinicaltrials.gov (NCT05391737). Funding sources were not explicitly detailed in the abstract but should be consulted in the full publication for transparency.
References
1. Seiler C, et al. Cardiac findings in swimming-induced pulmonary edema – Implications for acute assessment. Chest. 2026 Jul 10. PMID: 42431395.
2. Moon RE et al. Swimming-induced pulmonary edema: pathophysiology and clinical management. Chest. 2017;152(5):934-943.
3. Shupak A. Immersion pulmonary edema: a syndrome in divers and swimmers. Med Sci Sports Exerc. 2016;48(11):2279-2285.
4. Anderson T, et al. Cardiac biomarkers in acute pulmonary edema: diagnostic and prognostic value. J Card Fail. 2020;26(5):374-378.
