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J Am Coll Cardiol, 1999; 34:1744-1749 © 1999 by the American College of Cardiology Foundation |
* Sleep Laboratory, Technion-Israel Institute of Technology, Haifa, Israel
Heart Institute, ‘Bnei-Zion’ Medical Center, Haifa, Israel
Manuscript received August 24, 1998; revised manuscript received June 15, 1999, accepted August 6, 1999.
Reprint requests and correspondence: P. Lavie, Sleep Laboratory, Gutwirth Building, Technion-Israel Institute of Technology, Haifa, Israel 32000
plavie{at}techunixtechnion.ac.il
OBJECTIVES
To investigate the occurrence of nocturnal ischemic events in patients with obstructive sleep apnea syndrome (OSAS) and ischemic heart disease (IHD).
BACKGROUND
Although previous reports documented nocturnal cardiac ischemic events among OSAS patients, the exact association between obstructive apneas and ischemia is not yet clear. It is also not known what differentiates between patients showing nocturnal ischemia and those that do not.
METHODS
Fifty-one sleep apnea patients (age 61.3 ± 8.3) with IHD participated in the study (after withdrawal of beta-adrenergic blocking agents and anti-anginotic treatment). All patients underwent whole-night polysomnography including ambulatory blood pressure recordings (30 min interval) and continuous Holter monitoring during sleep. A control group of 17 OSAS patients free from IHD were also similarly studied. Fifteen of the 51 patients were also recorded under continuous positive airway pressure (CPAP).
RESULTS
Nocturnal ST segment depression occurred in 10 patients (a total of 15 events, 182 min), of whom six also had morning ischemia (06–08 am). Five additional patients had only morning ischemia. No ischemic events occurred in the control group. Age, sleep efficiency, oxygen desaturation, IHD severity and nocturnal-double product (DP) values were the main variables that significantly differentiated between patients who had ischemic events during sleep and those who did not. Nocturnal ischemia predominantly occurred during the rebreathing phase of the obstructive apneas, and it is characterized by increased heart rate (HR) and DP values. Treatment with continuous positive airway pressure significantly ameliorated the nocturnal ST depression time from 78 min to 33 min (p < 0.001) as well as the maximal DP values (14,137 ± 2,827 vs. 12,083 ± 2,933, p < 0.001).
CONCLUSIONS
Exacerbation of ischemic events during sleep in OSAS may be explained by the combination of increased myocardial oxygen consumption as indicated by increased DP values and decreased oxygen supply due to oxygen desaturation with peak hemodynamic changes during the rebreathing phase of the obstructive apnea. Treatment with CPAP ameliorated the nocturnal ischemia.
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