Commercial flights usually fly at an altitude of 25,000 to 35,000 ft. However, flight cabins are pressurised to an equivalent altitude of 5000–8000 ft., which equates to an inspired oxygen fraction of 0.17–0.15 at sea level [4]. Alveolar oxygen tension is known to decrease to 65 mmHg at 8000 ft., with a resultant reduction in arterial oxygen tension to 60 mmHg in healthy individuals [5]. Hypoxaemia augments the sympathetic nervous system and has many physiological effects. There is an increase in ventilatory effort in response to hypoxic conditions and the cardiovascular system responds by elevation of the heart rate, with subsequent reduction of stroke volume and an increased risk of angina and dysrhythmias in coronary patients [6]. The oxygen dissociation curves in healthy adults show that even at 65 mm. Hg the haemoglobin is still 80% saturated with oxygen [7]. The healthy adult is therefore hardly affected at the highest altitude that an aircraft cabin may reach in ordinary conditions, but an individual with impairment to the respiratory or cardiovascular system, may be distressed by this degree of hypoxia [8].

In one study, moderate altitude exposure in the elderly was associated with hypoxemia, sympathetic activation, and pulmonary hypertension resulting in a reduced exercise capacity that is predictable based on exercise performance at sea level. Patients with coronary artery disease who are well compensated at sea level do well at moderate altitude, although acute ischemia may be provoked at modestly lower myocardial and systemic work rates [9].

Cardiac output characteristically increases initially with hypoxia in a dose-dependent fashion, primarily due to tachycardia. The cardiac response slowly decreases over time despite continued hypoxia for unclear reasons [10, 11].

In our case described above, there was a critical right coronary artery stenosis, and a long segment of LAD disease, the severity of which was confirmed using fractional flow reserve. After coronary revascularisation, he made another journey from UK to Australia, and his symptoms did not recur. Therefore, we believe that the chest tightness which he had developed in-flight during his index journey was indeed due to cardiac ischaemia. The hypoxia during the flight would have led to an increased sympathetic response which brought on symptoms of ischaemia at rest. It remains unclear why he did not have any anginal symptoms on exertion prior to his flight. He led a rather sedentary lifestyle which may explain his lack of day-to-day symptoms.

A working group publication by the British Cardiovascular Society relating to fitness to fly for passengers with cardiovascular disease, was published in 2010 [12]. In patients with CCS class I-II angina, flight was unrestricted. Patients with class III angina are suggested to have airport assistance and in flight oxygen available. Delay of travel is recommended in patients with class IV angina. If there is no alternative to flight, a medical escort and in flight oxygen is advised. In the case of elective PCI with no complications, a rest period of 2 days is suggested.

In patients who have recently suffered an Non-ST segment elevation myocardial infarction (NSTEMI), or ST segment elevation myocardial infarction (STEMI), guidelines are based on age, whether reperfusion was successful, and ejection fraction after the event. Those aged less than 65 was successful reperfusion and an ejection fraction > 45% are deemed low risk, and can fly after 3 days. An ejection fraction > 40% with no symptoms of heart failure, and no urgently planned treatment or investigations are deemed medium risk, and are advised it is safe to fly after 10 days. Patients with an ejection < 40% with symptoms of heart failure and incomplete treatment or investigations are high risk, and advised to defer travel completely.