Altitude and atrial fibrillation.
The patient lived at an altitude of 1,008 m (3,300 feet) until 2 1/2 years ago, at which time he moved to an altitude of 2,750 m (9,000 feet). The recurrent episodes of palpitations disappeared after the move. No episodes were noted until a 7-week stay at an altitude of 763 m (2,500 feet), which occurred 10 months after the move to the higher altitude. The palpitations then returned and were confirmed to be atrial fibrillation. After the 7-week stay, the patient returned to live at 2,750 m and the palpitations again went away completely. Ten months later, after no evidence of recurrent atrial fibrillation, the patient again returned to an altitude of 763 m. The recurrent episodes of palpitations returned and were again confirmed to be atrial fibrillation. After a 3-month stay, he returned to the 2,750-m elevation and the recurrent palpitations resolved completely. The initial testing was done at an altitude of 1,008 m.
The fact that the recurrent atrial fibrillation resolved specifically when the resident altitude increased and reappeared when resident altitude returned to a lower level, on several occasions without any other variables, suggests an association with resident altitude. Lone atrial fibrillation describes atrial fibrillation in the absence of demonstrable underlying cardiac disease or history of hypertension. (1) This patient had no obvious preexisting or coexisting medical conditions that could be associated with atrial fibrillation, which placed him into a category of lone atrial fibrillation. To approach this situation, it seems appropriate to examine the effect of altitude on the cardiovascular system.
Pulmonary hypertension is usual on ascent to higher altitude in the normal cardiovascular system. The cause of pulmonary hypertension is hypoxic pulmonary vasoconstriction. Studies involving inhabitants of high altitude locations have revealed an increased prevalence of right ventricular hypertrophy and pulmonary hypertension. The following conclusion was made concerning the study of natives at high altitude in the Himalayan region. Echocardiographic examination showed normal left ventricular function in all, whereas 27% of the natives at an altitude of 4,500 to 5,000 m had evidence of pulmonary hypertension and rise of normalized right ventricular pre-ejection period. (2)
A study made the following observations at high altitude. Stroke volume falls and pre-ejection period to left ventricular ejection time ratio rises at 3,100 m because of diminished venous return despite preservation of left ventricular systolic performance. (3)
Also noted is a decrease in plasma volume reflected by a rise in hematocrit, which in part explains the finding of a decreased venous return.
Considering the above facts, it is possible to propose the following mechanism for the above-described case. Hypoxic pulmonary artery vasoconstriction secondary to increased resident altitude would contribute to a decrease in venous return, along with altitude-associated decreased plasma volume. This would reduce left atrial size by decreasing atrial wall tension, thereby eliminating a trigger for atrial fibrillation.
The above deduction is proposed from the facts listed. More studies would be needed to further examine mechanisms for this association.
1. Falk RH. Atrial fibrillation. N Engl J Med 2001;344:1067-1076.
2. Sharma S. Clinical, biochemical, electrocardiographic and noninvasive hemodynamic assessment of cardiovascular status in natives at high to extreme altitudes (3000m-5500m) of the Himalayan region. Indian Heart J 1990;42:375-379.
3. Alexander JK, Grover RF. Mechanism of reduced cardiac stroke volume at high altitude. Clin Cardiol 1983;6:301-303.
V. Taylor Smith, MD
Lake City, CO
Retired, Department of Internal Medicine
Covenant Medical Group
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|Author:||Smith, V. Taylor|
|Publication:||Southern Medical Journal|
|Article Type:||Letter to the Editor|
|Date:||Jan 1, 2005|
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