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Circadian variation and triggering of acute coronary events
1Gill Heart Institute, University of Kentucky Medical Center, Lexington, KY 40502, USA.
Insights
Cardiovascular events like heart attacks and strokes show a daily rhythm, peaking in the morning due to stress and body changes. Understanding these triggers can improve prevention strategies for coronary artery disease.
Area of Science:
- Cardiology
- Chronobiology
- Pathophysiology
Background:
- Cardiovascular events exhibit circadian periodicity, with morning peaks observed for myocardial infarction, sudden cardiac death, and ischemic stroke.
- Onset is often triggered by physical or mental stress, sympathetic nervous system activation upon assuming an upright posture, and activities like heavy exertion or anger.
Purpose of the Study:
- To explore the circadian patterns and triggers of cardiovascular events.
- To propose a hypothesis for the mechanism of coronary thrombosis onset.
- To identify potential avenues for improved preventive therapies.
Main Methods:
- Review of existing literature on circadian rhythms and cardiovascular events.
- Quantification of trigger risks through studies like the Determinants of Myocardial Infarction Onset Study.
- Formulation of a general hypothesis for coronary thrombosis triggering.
Main Results:
- Morning hours represent a period of increased risk for acute cardiovascular events.
- Vulnerable atherosclerotic plaque disruption, influenced by hemodynamic and vasoconstrictive changes, initiates thrombosis.
- Coagulability and vasoconstriction are key factors in occlusive thrombus formation.
Conclusions:
- Findings support the clinical use of long-acting anti-ischemic agents for morning protection.
- Understanding event triggers offers insights into mechanisms for more effective preventive therapies.
- Further research is warranted due to the high mortality from coronary artery disease before acute treatment can be administered.
Abstract:
The recognition that the onset of cardiovascular events follows a circadian periodicity and is frequently triggered by physical or mental stresses has created new possibilities for disease prevention. Morning peaks in occurrence are now well-documented for acute myocardial infarction, sudden cardiac death, transient myocardial ischemia, and ischemic stroke. The morning increase in events begins after subjects assume an upright posture and start the day's activities, during a time of sympathetic nervous system activation. Additional triggers of onset include heavy physical exertion, sexual activity, and anger, the risks of which have been quantified in the Determinants of Myocardial Infarction Onset Study. A general hypothesis of the triggering of coronary thrombosis has been proposed. The process begins with the development of a vulnerable atherosclerotic plaque, which may become disrupted by internal forces or by external hemodynamic or vasoconstrictive changes. Once disrupted, the plaque becomes a thrombogenic focus. An occlusive thrombus is more likely to form if other factors come into play to increase coagulability and vasoconstriction. From a clinical standpoint these findings provide theoretical support for the use of long-acting agents to provide adequate anti-ischemic protection during the higher risk morning hours in patients already taking anti-ischemic medications. From a research standpoint this new information on triggering provides clues to a mechanism of onset that might lead to more effective preventive therapy. Because most deaths from coronary artery disease occur before any type of acute therapy can be given, further efforts to explore this new field are warranted.