Impact on the Elderly who visit high altitude regions

Benjamin D. Levine, MD; Julie H. Zuckerman, RN, RDMS; Christopher R. deFilippi, MD /circ.ahajournals.org

Abstract

Background More than 5 million people/year over age 60 visit high altitude, which may exacerbate underlying cardiac or pulmonary disease. We hypothesized that the elderly would exhibit an impaired functional capacity at altitude, with increased myocardial ischemia compared with sea level (SL).

Methods and Results Twenty veterans (68±3 years) were studied at (1) SL, (2) acute simulated altitude to 2500 m, and (3) after 5 days of acclimatization to 2500 m. With acute altitude, Pao2 and oxyhemoglobin saturation decreased and pulmonary artery pressure increased 43%, associated with sympathetic activation. V̇o2peak decreased 12% acutely but normalized after acclimatization. The best predictor of V̇o2peak with acute altitude was V̇o2peak at SL (r=.94). The double product that induced 1-mm ST depression during exercise with acute altitude was 5% less than SL but normalized after acclimatization. One patient with severe coronary disease sustained a myocardial infarction after an exercise test.

Conclusions Moderate altitude exposure in the elderly is associated with hypoxemia, sympathetic activation, and pulmonary hypertension resulting in a reduced exercise capacity that is predictable based on exercise performance at SL. Patients with coronary artery disease who are well compensated at SL do well at moderate altitude, although acutely ischemia may be provoked at modestly lower myocardial and systemic work rates. The elderly acclimatize well with normalization of SL performance after 5 days. A prudent policy would be for elderly individuals, particularly those with coronary artery disease, to limit their activity during the first few days at altitude to allow this acclimatization process to occur.

Risk of Moderate High-Altitude Exposure to the Patient With Coronary Artery Disease

For patients with coronary artery disease, the critical questions are whether high altitude (1) increases ischemia, (2) increases the risk of arrhythmias, or (3) provokes the transition to unstable syndromes such as unstable angina or acute myocardial infarction. Numerous anecdotal reports exist describing clinical exacerbation of underlying coronary disease by high altitude,26 but it is difficult to determine whether such instances are a direct consequence of high altitude or simply a variable manifestation of the coronary artery disease.

Myocardial ischemia may develop by alterations in either side of the myocardial oxygen supply/demand ratio. In the face of fixed coronary stenoses, the reduction in arterial oxygen content at high altitude would be expected to reduce oxygen supply and increase ischemia, depending on the degree of oxyhemoglobin desaturation and the severity of the coronary lesions. Thus, in this study, at rest and during submaximal exercise, heart rate was higher with acute altitude exposure, increasing myocardial oxygen demand and resulting in ischemia at lower systemic work rates.

In addition to the increased demand, the sympathetic activation associated with hypoxia39 may cause coronary vasoconstriction in regions with abnormal endothelial vasomotor control, further compromising myocardial oxygen delivery. Abnormal coronary vasomotion due to atherosclerosis has been reported during exercise40 or after infusion of acetylcholine,41 but not to our knowledge during hypoxia. It is likely that in the present study, one or both mechanisms (reduction in oxygen content and coronary vasoconstriction) were operational as we observed the induction of ischemia with acute altitude exposure at a lower myocardial oxygen demand than at sea level. This acute response is in contrast to that observed by Morgan et al37 in long-term acclimatized patients with coronary disease or in our patients after short-term acclimatization. We speculate that acclimatization may reduce abnormal coronary vasomotion in response to hypoxia, although this question requires further study.

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We are disturbed by the occurrence of a myocardial infarction in one of our patients after an exercise test at altitude. However, there is no evidence that altitude exposure results in hematological changes that would increase the risk of plaque rupture, vascular thrombosis, and myocardial infarction.42 Exercise is associated with a small but finite risk of myocardial infarction, particularly after heavy exertion.43 Although many high-altitude activities, such as hiking, require absolute work rates that are of low intensity, for elderly patients at high altitude, the present study suggests that these relative intensities may actually be extremely high. It is also possible that this patient was demonstrating the natural history of his disease and would have had a myocardial infarction at sea level. However, we cannot exclude an interaction between altitude and exercise in this individual patient. Moreover, our small numbers preclude our being able to quantify any clear risk of acute coronary syndromes associated with high-altitude exposure. We are reassured, however, by the results of the larger survey study, which did not identify any other elderly individuals with a myocardial infarction at this same altitude.12

In addition to the risk of ischemia, we were concerned with the possibility of altitude exacerbating ventricular arrhythmias because of the well-described association of such arrhythmias with sympathetic activation, particularly in patients with known coronary artery disease.44 In the present study, we were unable to identify any change in arrhythmic substrate, at least within the limits of the signal-averaged ECG to detect delays in ventricular activation and late potentials from the surface. The negative predictive value of the signal-averaged ECG for identifying patients who are not at risk for sustained ventricular arrhythmias is very high, identifying >95% of patients after a myocardial infarction who are at low risk for developing life-threatening ventricular arrhythmias.45 Moreover, although we could not perform 24-hour Holter monitoring to quantify ambient ectopy, we were able to use exercise testing, which provokes repetitive ventricular premature beats in the majority of patients with a history of sustained ventricular arrhythmias.21 Although single PVCs during exercise appeared to increase modestly with acute altitude exposure, there was no increase in repetitive forms, and the frequency of this inducible ectopy returned to baseline levels within 5 days of acclimatization. It is important to emphasize that there is substantial interindividual and intraindividual variability in the frequency of PVCs,46 which may reduce the sensitivity of this measure as a reliable index of the trigger for ventricular arrhythmias. We therefore must interpret the observation of a small, albeit statistically significant, increase in frequency of premature ventricular contractions during and after exercise with caution. However, we are reassured by the example of the one patient with known recurrent ventricular tachycardia who had his arrhythmia occur at altitude and who tolerated it as well as at sea level. The sum of evidence available suggests that although minor inducible ectopy may increase acutely, it appears unlikely that moderate high altitude substantially alters the risk for life-threatening arrhythmias in the elderly or patients with coronary artery disease.
Study Limitations

There are a number of limitations to the present study that must be acknowledged. First of all, the number of patients studied was small, and our methods for quantifying coronary artery disease were entirely noninvasive, making it difficult to provide true estimates of the risk associated with altitude exposure in this population or to clearly categorize the subjects into statistically meaningful groups according to the presence or absence of coronary artery disease. Nevertheless, the physiological response of the elderly to moderate high altitude appears to be predictable based on careful testing at sea level, thereby allowing the physician to individualize recommendations for specific patients. Second, the period of acclimatization was short, consisting of only 5 days, during which time acclimatization is certainly not complete, particularly with regard to the autonomic nervous system.28 However, most of the acute response to high altitude, namely, hyperventilation with metabolic compensation, is likely to be completed within the first few days at high altitude.47 In addition, this exposure pattern is typical of many travels for business or recreational purposes. Finally, we studied only one altitude of 2500 m, and our results may not be applicable to higher altitudes. Read Full Article