Little evidence of cardiac involvement in Mild and Moderate Swimming- Induced Pulmonary Oedema (SIPE).

OBJECTIVES

Swimming-induced pulmonary oedema (SIPE) is a potentially fatal condition associated with open-water swims. We sought to quantify the contribution of cardiac dysfunction to SIPE.

DESIGN

We aimed to assess the incidence of SIPE during an endurance cold water swim. We determined associations between SIPE and changes in cardiac function through a SIPE questionnaire, lung ultrasound (LUS), cardiac biomarkers (N-Terminal pro-B-type natriuretic peptide (NT proBNP) and cardiac troponin I (cTnI)) and transthoracic echocardiograms (TTE).

METHODS

Twenty open-water swimmers (10 males) underwent a TTE, LUS for pulmonary oedema and cardiac biomarkers before, 2-hours and 24-hours after an 8-hour swim. Swimmers had an additional LUS and rated their breathlessness upon leaving the water. Participants with breathlessness and 3 or more B-lines present in two or more LUS views were considered SIPE positive.

RESULTS

Five swimmers (25 % of cohort) presenting with post-event breathlessness and evidence of lung water were considered SIPE positive. SIPE had no demonstrable effect on left systolic function (LV ejection fraction, global longitudinal strain [GLS]), diastolic function (left atrial volume, E/e') and right ventricular (RV) function (RV fractional area change and RV free wall GLS). SIPE was associated with a small increase in troponin post-swim (at 2 hours SIPE+ 32.1 ng/L, SIPE- 12.6 ng/L, p = 0.004: at 24 hours SIPE+ 12.6 ng/L, SIPE- 4.8 ng/L, p = 0.04) but had no impact on NT proBNP.

CONCLUSIONS

SIPE is common in open-water swimmers following an endurance swim and is identified using LUS. Whilst SIPE was associated with a small increase in post-swim troponin levels, no further evidence of cardiac dysfunction was identified at two hours after the swim to explain the pulmonary oedema.