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2026-07-11 PubMed

Swimming-induced pulmonary edema (SIPE) linked to transient cardiac dysfunction and elevated biomarkers in open water swimmers.

CARDIAC FINDINGS IN SWIMMING-INDUCED PULMONARY EDEMA - IMPLICATIONS FOR ACUTE ASSESSMENT.

Background

Swimming-induced pulmonary edema (SIPE) is a poorly understood condition affecting athletes, particularly in open water events. While previous case reports have hinted at cardiac involvement, a comprehensive characterization of acute cardiac changes in SIPE patients has been lacking. Understanding these cardiac findings is crucial for accurate diagnosis, differentiating SIPE from other acute cardiac events, and guiding appropriate clinical management. This study addresses the gap by systematically evaluating cardiac function and biomarkers in a cohort of SIPE patients.

Study Design

A prospective cohort study evaluated 45 patients with SIPE and 45 asymptomatic control swimmers participating in Sweden's largest open water swimming event, Vansbrosimningen, from 2022-2024. Participants underwent Transthoracic echocardiogram (TTE), electrocardiogram (ECG), and cardiac biomarker assessment (high-sensitivity cardiac troponin I, N-terminal pro-B-type natriuretic peptide) within two hours after swimming. A follow-up TTE was conducted within 12 months to assess the resolution of any observed cardiac pathology.

Results

Cardiac assessments revealed significant differences between SIPE patients and controls. Systolic ventricular function on TTE was mildly impaired after swimming in 43% of SIPE patients compared to only 10% of controls (p=0.003). Systolic pulmonary artery pressure was also increased in 30% of SIPE patients, while none of the controls showed this increase (p=0.005). Notably, TTE pathology had improved at follow-up in all but one SIPE patient, indicating the transient nature of these changes. ECG findings post-swim showed no significant difference between groups (p=0.746).

Key Findings

  • Systolic ventricular function was mildly impaired in 43% of SIPE patients vs. 10% of controls (p=0.003).
  • Systolic pulmonary artery pressure increased in 30% of SIPE patients vs. 0% of controls (p=0.005).
  • High-sensitivity cardiac troponin I was elevated in 67% of SIPE patients vs. 40% of controls (median 47 pg/ml vs. 14 pg/ml, p<0.001).
  • N-terminal pro-B-type natriuretic peptide was higher in SIPE patients (median 169 pg/ml vs. 65 pg/ml, p<001).
  • Cardiac TTE abnormalities largely resolved at 12-month follow-up in SIPE patients.

Why It Matters

This study provides a crucial reference for expected cardiac findings in patients presenting with SIPE, enabling clinicians to better interpret acute cardiac assessments. The transient nature of the observed cardiac dysfunction and biomarker elevations helps differentiate SIPE from more severe, persistent cardiac pathologies. Clinicians can now use these benchmarks to avoid over-investigation or misdiagnosis when evaluating athletes with suspected SIPE, particularly in the context of elevated troponin. This data is vital for developing standardized diagnostic protocols and improving acute management strategies for this increasingly recognized condition in athletic populations.


swimming-induced pulmonary edema sipe cardiac function biomarkers echocardiography open water swimming
Source: pubmed:42431395 · Ingested 2026-07-11 · Digest: gemini-2.5-flash