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Circadian variation and triggers of cardiovascular disease
1Cardiology Division, Deaconess Hospital, Boston, MA 02215, USA.
Insights
Most heart attacks result from plaque rupture and clot formation, often occurring in the morning. Timing medication to protect vulnerable patients during these peak hours may reduce cardiovascular deaths.
Area of Science:
- Cardiology
- Vascular Biology
- Chronobiology
Background:
- Myocardial infarction (MI) and sudden cardiac death are frequently caused by coronary atherosclerotic plaque disruption and subsequent thrombus formation.
- A well-established circadian pattern shows increased MI incidence during morning hours.
Purpose of the Study:
- To explore the link between patient activities, vulnerable plaque rupture, and morning MI occurrence.
- To investigate the potential for chronotherapy in reducing cardiovascular events.
Main Methods:
- Review of existing literature on plaque rupture, thrombosis, and circadian rhythms in cardiovascular disease.
- Postulation of a synchronized trigger mechanism for morning MI onset.
Main Results:
- Approximately 90% of non-fatal MIs and many sudden cardiac deaths stem from plaque disruption and thrombus formation.
- Patient activities can trigger plaque disruption and thrombus formation.
- Morning MI onset may result from synchronized triggers.
Conclusions:
- Recognizing the circadian variation of MI allows for targeted pharmacologic protection during early waking hours.
- Long-acting anti-ischemic agents may offer superior protection against morning MIs compared to short-acting ones.
- Future research should aim to decouple triggering activities from MI development.
Abstract:
It has recently been shown that approximately 90% of cases of non-fatal myocardial infarction and many cases of sudden cardiac death are caused by disruption of a coronary atherosclerotic plaque, followed by occlusive thrombus formation. Secondly, the circadian pattern of myocardial infarction is well known to feature a prominent increase in the morning hours. Taken together, these factors may provide an opportunity to reduce deaths caused by cardiovascular disease. Findings indicate that, in many cases, plaque disruption and thrombus formation are triggered by the activities of the patient. It is postulated that onset occurs when a 'vulnerable' atherosclerotic plaque becomes disrupted and occlusive thrombus formation occurs. The occurrence of a myocardial infarction in the morning hours could result from the synchronization of a number of potential triggers. The importance of the recognition of the circadian variation of acute onset of myocardial infarction is that pharmacologic protection can be directed at the early waking hours. It would seem reasonable to propose that long-acting anti-ischemic agents would have an advantage over short-acting agents in providing protection against the morning occurrence of myocardial infarction. A future goal would be to design therapeutic regimens that would have the ability to sever the linkage between a potential triggering activity and the development of myocardial infarction.