| LinkExchange Member | Free Home Pages at GeoCities |
| LinkExchange Member | Free Home Pages at GeoCities |
Personally, I find these results alarming. It seems that any single apneic event could trigger off myocardial ischemia, potentially leading to myocardial infarction and death without warning signs during sleep. Even a patient using CPAP religiously may have an occasional apnea. Events seem to conspire against us: the apnea both reduces blood oxygen supply to the heart while increasing the heart’s need for blood oxygen due to the falling chest pressure of the struggle to breathe. When this happens during REM sleep, as it usually does, the heart is also beating faster, demanding more oxygen, in relation to the overall physiological activation of the dream state. Moreover, the occurrence of an ischemia during an apnea seems to make the apnea worse. Finally, being asleep may reduce awareness of the developing heart attack, and prevent possibly life-saving action. Remember that even clear-cut, waking heart attacks with the warning signs for itnervention kill one-third of all affected the first time they happen.
The authors studied 21 patients with OSA, defined by an apnea index of 10 or greater, for six consecutive nights in the sleep laboratory. In Group I, 14 patients had both OSA and CHD, the latter proven by coronary angiography (see Glossary) that showed the arteries of the heart to be narrowed by at least 50%. In Group II were 7 patients with OSA who had coronary angiography that proved negative. All patients had this test done because of a history of chest pain or abnormal findings in the electrocardiogram during an exercise test. The patients’ average age was 56 years (range 47 to 67) and their average weight was 179 lbs (range 158 to 283). Sleep architecture was similar in the two groups, with overall an excess of stages 1 and 2 (67%) and a deficit of stages 3 and 4 (15%), along with 18% REM. Their Apnea Indices averaged 33/hr (SD=+/-15/hr) with a minimum of 11/hr and a maximum of 80/hr. Minimum blood oxygen saturation averaged 73, ranging from 45 to 89.
Two days before the six nights of sleep testing, all patients were taken off medication for chest pain, calcium channel blockers (generally used for hypertension) and beta blockers (for hypertension and slowing heart rate). During the first two nights, they received no medication. During the remaining four nights, they received two consecutive nights of a slow-release form of nitrate, 100 mg of isorbide dinitrate, related to nitroglycerine, for suppression of myocardial ischemia. The other two nights they received a placebo (an inactive substance that looks like the active drug).
Six patients had episodes of myocardial ischemia during the sleep studies. Five of these six patients came from Group I; the sixth came from Group II. These six patients had a total of 144 episodes of myocardial ischemia during three nights (the second night under each of the conditions: no meds, nitrate, and placebo). This means an average of 8 episodes of myocardial ischemia per patient per night, but two patients had very few episodes (4 altogether in one, only one in another), whereas others had many more, up to 59 (about 20 per night). The episodes lasted from 10 seconds to 96 seconds. They occurred mainly (85%) during periods of high apnea activity and oxygen desaturation. Nitrate had no effect.
Just before apnea-associated ischemia, blood oxygen saturation averaged 91%; during the ischemia, it fell to 77%. Most (78%) of ischemic events occurred during REM sleep.
Note that 15% of ischemic events took place without associated apneas or oxygen desaturations. But these too occurred mainly in REM sleep.
During the 144 episodes of myocardial ischemia, there were a total of 175 EEG arousals, most (95%) of the ischemic episodes being associated with at least one arousal. Ischemia also was associated with more severe arousals, especially with greater drops in blood oxygen saturation. During the ischemic episodes not associated with apneas, there was also a high frequency (71%) of relatively severe arousals.
The authors mentioned a prior study which found similar signs of myocardial ischemia in 7 of 23 (30%) of patients with OSA not previously believed to have coronary heart disease. The supply of blood oxygen to the heart is decreased by hypoxemia; this may be one cause of myocardial ischemia. However, obstructive sleep apneas also increase the demand for oxygen to the heart because of the reduction of pressure within the chest as the obstructed patient attempts to breathe. During REM sleep, when ischemic and apneic events were most frequent, there is an increase in heart rate with increased demand for blood to the heart, related to the autonomic activation typical of REM sleep.
The authors noted that, in addition to the disruptive effects of the apneas themselves on sleep continuity, the ischemic episodes also provoked unusually severe arousals and disrupted sleep, potentially contributing to even greater daytime sleepiness.
If you have any reluctance to seek or continue treatment for your sleep apnea, this kind of finding should help convince you. Likewise, you may find it helpful in convincing a reluctant bed partner with obvious snoring and cessation of breathing to go for an evaluation.
Is there any basis for reassurance here? Small as it may be, I noted that the authors’ Apnea Index did not include hypopneas, so the numbers they cite are underestimates of OSA severity as we usually regard it. Our own AHIs are not equivalent. Furthermore, I suspect that the withdrawal of known coronary heart disease patients from possibly multiple cardiac medications two days prior to the sleep studies may have worsened their cardiac conditions. Furthermore, there followed on the medication withdrawal six nights essentially spent without effective cardiac medication. At the same time, these patients’ severe obstructive sleep apnea went untreated. One notes that this study was done in Germany, whereas such studies might not be possible in the United States.
The authors also remarked that the patients said to be free of coronary heart disease were not devoid of some signs of cardiac problems, as with exercise testing. On the other hand, medical lore is filled with stories of patients who go to the doctor for a routine physical with electrocardiogram, are declared in the best of health, and drop dead the next day! We sleep apneics, it seems, have special reason to fear the night.
WHAT DO YOU THINK ABOUT THIS
ARTICLE AND MY COMMENTS ON IT? CAN YOU RELATE IT TO ANY PERSONAL EXPERIENCES?
If you can add any thoughts or comments, please E-mail me (and mention the article you are commenting on) at
Get your own Free Home Page