Effects of high altitude on patients with cardiovascular disease

The physiologic effects of high altitude on patients with cardiovascular disease are qualitatively equal to those occurring in healthy individuals, but they may differ in magnitude or with regard to the clinical impact. In healthy individuals, altitudes above 2,500 m cause hypoxemia to a degree that it leads to a noticeable reduction in aerobic capacity and an increased activity of the sympathetic nervous system. Exercise exacerbates hypoxemia and sympathetic activity. Thanks to acclimatization, hypoxemia decreases within the first 2 weeks at a given altitude with a major increase of arterial PO2 and SaO2 occurring during the first few days already. Thus, for patients with impaired blood supply to any organ, the first days after a substantial gain in altitude are the most critical. In untrained people, the altitude-related decrease of maximum aerobic performance starts at an altitude of about 1,500 m and increases by approximately 1% per each 100 m above 1,500 m. Thus, the impact of an altitude-related decrease in performance for patients also depends on their aerobic capacity at sea level, i.e. how much reserve capacity they have above what is needed for daily activities. When advising patients with heart failure, it is important to know that the decrease of maximum aerobic performance is twofold greater with mild to moderate heart failure and fourfold greater with severe heart failure at any given altitude when compared to the loss of performance in healthy individuals. For a patient with coronary artery disease and stable angina pectoris reduction in performance at altitude means that angina will occur at a lower level of exercise. However, several studies demonstrate that the heart rate at this ischemic threshold will be similar at low and high altitude. In general, we can say that any cardiac patient with a stable disease and sufficient work capacity for a normal life at low altitude can tolerate comparable daily activities at altitudes up to 2,500 m without a significantly increased risk for his health. Exposures above 2,500 up to 3,500 m may be allowed, when cardiovascular evaluation with exercise testing and echocardiography yield a stable disease, an ejection fraction >40%, no significant arrhythmias and a symptom-free exercise capacity of 2 W/kg. This recommendation does not apply to patients with primary or secondary pulmonary hypertension or with unilateral absence of a pulmonary artery, who should not go above 2,000 m because these patients are at risk for developing high altitude pulmonary edema and/or right heart failure. In general, patients with significant cardiovascular disease should be advised not to go above altitudes of 3,500 m. Often, patients with cardiovascular disease have risk factors for this disease that may also be affected by high altitude. Increasing sympathetic stimulation over time raises blood pressure over 3 weeks at 4,300 m by 5–10 mm Hg in healthy individuals. With acute and with short term exposure to high altitude, blood pressure does not rise because hypoxia dilates systemic blood vessels and counteracts sympathetic vasoconstriction. It is not known whether changes of blood pressure at altitude are smaller or greater in patients with systemic hypertension compared to normotensive individuals. In a recent study in patients with metabolic syndrome at moderate altitudes of 1,700– 2,500 m blood pressure decreased during a 3 week training program indicating that the blood pressure lowering effect of regular exercise outweighs the effect of hypoxia at moderate altitude. Weight loss might be slightly favoured in obese patients at high altitude since hypoxia is associated with an increased basal metabolic rate which is, at an altitude of 4,300 m, in the order of 20% compared to sea level. Altitudes, which obese people can reach in the Alps,