Case Series of Triathletes with Takotsubo Cardiomyopathy Presenting with Swimming-Induced Pulmonary Edema

Abstract

Objectives: To report three cases of triathletes who presented with swimming-induced pulmonary edema (SIPE) following water immersion. They were subsequently diagnosed with Takotsubo cardiomyopathy (TCM).

Design: Retrospective case series.

Method: All cases were recreational athletes competing in mass participation triathlons between June 2018 and 2019. They were initially managed by the event medical team and subsequently at the local tertiary level hospital. Written consent was gained from all the subjects.

Results: The three triathletes were aged between 50 and 60 years, two were females, and all presented with acute dyspnoea on exiting the water. Two also presented with chest pain and haemoptysis. A diagnosis of SIPE was suspected by the medical event team on initial presentation of low oxygen saturations and clinical signs of pulmonary oedema. All were transferred to the local emergency department and had signs of pulmonary oedema on chest radiographs. Further investigations led to a diagnosis of TCM with findings of T wave inversion in anterolateral electrocardiogram leads and apical hypokinesia on transthoracic echocardiogram and unobstructed coronary arteries.

Conclusions: This case series presents triathletes diagnosed with SIPE and TCM following the open water swim phase. It is unclear whether the myocardial dysfunction contributed to causation of SIPE or was the result of SIPE. Mass participation race organizers must be prepared that both SIPE and TCM can present in this population. Those presenting with an episode of SIPE require prompt evaluation of their cardiac and pulmonary physiology. Further research is required to ascertain the exact nature of the relationship between TCM and SIPE.

Figure 1

CXR. (a) Case 1 displaying bilateral pulmonary oedema in the hilar region; (b) Case 2 displaying pulmonary oedema with upper zone diversion; (c) Case 3 showing bilateral perihilar interstitial oedema in keeping with evidence of pulmonary oedema.

Figure 2

Cardiovascular Magnetic Resonance imaging (CMR) of case 3 performed just prior to the coronary angiogram showed classical features of TCM. There was severe hypokinesia ((a)) and evidence of myocardial oedema on T1 map ((b) and (c)) of mid to apical regions of the left ventricle. The LV ejection fraction was moderately impaired at 43% and the mean global T1 time was elevated at 1311ms. Normal T1 time for a female in 3 Tesla scanner is 1151-1251ms. Late Gadolinium Enhancement (LGE) imaging confirmed the absence of myocardial infarction or fibrosis ((d)). CMR at 6 months shows complete resolution of the regional wall motion abnormalities ((e)) and myocardial oedema ((f) and (g)). The LVEF was much improved to 56% and the mean global T1 time became normalised to 1192 ms with no significant regional differences. Once again, there was no evidence of any myocardial infarction nor fibrosis on LGE imaging ((h)).