Risk assessment for a high-altitude alpinist with coronary artery disease

Dear Editor, we report the case of a 60-year-old man, professional climber, who was attending a mountaineering expedition in Annapurna. At an altitude of about 5500 m the patient felt sudden onset of dyspnea, out of proportion to the effort he was making, for which he was trained. After coming back to Italy, the patient underwent cardiologic examination. A 12-lead electrocardiogram (ECG) was performed: no signs of ischemia were present but a significant increase of troponin I was reported. Transthoracic echocardiography showed no alterations in left ventricular regional kinetics and a normal ejection fraction. However, it was decided to carry out a coronary angiography, which documented a stenotic lesion in a single vessel occluding the mid anterior descending artery, treated by percutaneous coronary intervention and bare metal stenting. Thereafter, the patient performed regular cardiologic follow-ups (including ECG, echocardiography and exercise stress test), always resulting negative for inducible myocardial ischemia. 18 months later, the patient expressed the desire to continue performing high-altitude mountaineering, so he was directed to our centre for advice. In order to have an assessment as faithful as possible to the conditions that he would meet at high altitude, the patient underwent cardiopulmonary exercise testing with cycle ergometer breathing a hypoxic gas mixture (oxygen at 12%), simulating an altitude of 4800 m. The patient remained asymptomatic for the whole duration of the test. There were no ECG changes indicative of inducible myocardial ischemia. The oxygen consumption (VO2) at anaerobic threshold was 13.6 mL/kg/min, while the peak VO2 was 26.5 mL/kg/min (equal to 116% of the predicted maximum that is 22.8 mL/kg/min) and the indexes of cardio-respiratory functional capacity were greater than normal. Comparing the values of arterial oxygen saturation (SaO2) at baseline and during hypoxia, the difference in SaO2 (ΔSaO2%) at rest was 8.32% (normal value <21%), with a value of minimum SaO2 at rest in hypoxia of 85%, while the ΔSaO2% during exercise was 17.5% (normal value <33%), with a value of minimum SaO2 during exercise in hypoxia of 65%. Furthermore, the patient showed a good cardio-respiratory response to hypoxia (Figure 1). Considering these data,