Taking a Deep Dive Into MINOCA

A 48-year-old male professional diver presented at the emergency department with acute chest pain during diving. He did not report any other symptoms compatible with arterial gas embolism (AGE) or decompression sickness (DCS). The patient was a smoker with unremarkable past medical history and no reported use of illicit drugs. He reported a weekly diving schedule of 2 40-minute repetitive dives per day at a maximum depth of 10 metres using simple air. Although he did not use a diving computer, the reported diving profile did not exceed the safety limits for nondecompression diving. Furthermore, the patient did not report any recent history of diving distress or other diving accidents. Electrocardiogram (ECG) and transthoracic echocardiogram (TTE) results were normal. High-sensitivity troponin levels were 34 ng/L at baseline, whereas peak value reached 805 ng/L (normal value, < 0.29 ng/L). Coronary angiogram did not reveal angiographically significant stenotic lesions; thus, the working diagnosis of myocardial infarction with nonobstructive coronary arteries (MINOCA) emerged (Video 1 and Video 2 , view videos online). Intracoronary imaging modalities, such as intravascular ultrasound or optical coherence tomography, were not available, and intracoronary acetylcholine provoking test (ACH-test) is not performed in our centre. Cardiac magnetic resonance (CMR) within 2 weeks of the episode showed mild hypokinesia of the mid- inferolateral segment of the left ventricle (Video 3 , view Video online) and myocardial edema at the mid-inferolateral segment of left ventricle as well as at the posteromedial papillary muscle (Fig. 1D). Late gadolinium enhancement (LGE) sequence demonstrated almost transmural lesions at mid- and apical-inferolateral segments, as well as the posteromedial papillary muscle (Fig. 1, A and C). Furthermore, another focal subendocardial lesion was noted at basal anteroseptal segment of the left ventricle (Fig. 1B). The subendocardial pattern of the lesions indicated ischemia and thus excluded the diagnosis of myocarditis or Takotsubo syndrome. Given the multifocal nature of the ischemic lesions, our diagnostic approach was focused on potential embolic sources. Bubble test results, performed during TTE, proved negative for patent foramen ovale (PFO). The patient refused a transesophageal echocardiogram (TEE) and was therefore referred for a transcranial Doppler (TCD) study, the results of which also proved negative. A 24-hour ECG Holter monitoring showed no events of atrial fibrillation. Thrombophilia test revealed only heterozygotic MTHFR 677 mutation. A brain magnetic resonance was prescribed for potential brain lesions in case of AGE, the results of which were negative. The patient was discharged asymptomatic with cardioprotective drugs and a single antiplatelet. After 6 months he underwent an exercise stress test, and he was allowed by his diving physician to continue the diving activities, using a validated diving computer and following a more conservative schedule.