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Circadian variation of the total ischemic burden and influence by beta-blocking agents
1Department of Ambulatory Monitoring, National Heart Hospital, London, England.
Insights
Coronary artery disease patients experience most ischemic episodes during daytime hours. Atenolol treatment significantly reduced these episodes and altered their circadian pattern, notably eliminating the morning peak.
Area of Science:
- Cardiology
- Circadian Biology
- Pharmacology
Background:
- Coronary artery disease (CAD) is a leading cause of mortality.
- Ischemic episodes in CAD patients exhibit circadian patterns.
- Silent myocardial ischemia is common and often undertreated.
Purpose of the Study:
- To investigate the circadian pattern of ischemic episodes in patients with CAD.
- To evaluate the effect of atenolol on the frequency, duration, and circadian distribution of ischemic episodes.
Main Methods:
- 150 unselected patients with proven CAD were monitored off antianginal treatment.
- A subgroup of 41 patients underwent double-blind, placebo-controlled atenolol treatment.
- Continuous ECG monitoring was used to detect ischemic episodes.
Main Results:
- Ischemic episodes predominantly occurred during daytime (0730-1930 h), with a morning peak.
- Atenolol significantly reduced the frequency and total duration of ischemic episodes.
- Atenolol eliminated the morning peak and reduced the evening peak of ischemic episodes.
Conclusions:
- Ischemic episodes in CAD patients show a distinct circadian pattern, with a pronounced morning peak.
- Beta-blocker therapy, specifically atenolol, effectively modulates this circadian variation.
- The findings suggest a link between circadian patterns of ischemia and major adverse cardiac events, warranting further investigation.
Abstract:
We investigated 150 unselected patients with proven coronary artery disease. All patients were off all routine antianginal treatments and there were 598 ischemic episodes, of which 75% were silent. It was found that episodes of ischemia, both silent and painful, occurred predominantly during the daytime hours from 0730 to 1930 h. This pattern is similar to that described by others. There was a significant excess of episodes of ischemia in the morning hours (0730-1330 h), with a secondary peak occurring in the evening hours. We further investigated a subgroup of 41 patients who were monitored for 1,581 h while being treated with atenolol. These patients were investigated in a double-blind fashion, and during the off treatment phase the circadian pattern of ischemic episodes was similar to that described for the group as a whole. However, on treatment with atenolol, there was a significant reduction in the frequency and total duration of ischemic episodes throughout the day. Atenolol significantly altered the circadian distribution of ischemic episodes with elimination of the morning peak; there was some preservation of the evening peak although this was smaller than that described when the patients were off therapy. The circadian distribution of ischemic episodes and the observed changes with beta-blocking treatment resemble the reported circadian variation of acute myocardial infarction and sudden death. Although these studies do not in any way prove that myocardial ischemic episodes and their alteration by treatment are related to the development of acute myocardial infarction and death, the relationship between ischemic episodes and the end points of coronary disease require further investigation.