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Diurnal physiologic processes and circadian variation of acute myocardial infarction
1Institute for Prevention of Cardiovascular Disease, Boston, Massachusetts 02215, USA.
Insights
Cardiovascular events like heart attacks are more common in the morning due to increased sympathetic activity and platelet aggregation. These daily changes, especially with stress, can trigger plaque rupture, leading to myocardial infarction.
Area of Science:
- Cardiology
- Physiology
- Pathophysiology
Background:
- Acute myocardial infarction and sudden cardiac death exhibit a circadian pattern, with increased incidence in the morning.
- This suggests non-random onset and points towards underlying physiological mechanisms.
- Vulnerable atherosclerotic plaques may be susceptible to rupture due to morning physiological changes.
Purpose of the Study:
- To investigate the physiological mechanisms contributing to the circadian variation in cardiovascular events.
- To explore the role of sympathetic activation and platelet aggregability in morning myocardial infarction.
- To understand how transient hemodynamic and prothrombotic forces act as acute risk factors.
Main Methods:
- Observational analysis of cardiovascular event timing.
- Review of physiological factors influencing cardiovascular risk.
- Evaluation of the impact of beta-adrenergic blocking agents and aspirin on morning cardiac events.
Main Results:
- Morning hours show increased plasma catecholamines, sympathetic activity, heart rate, blood pressure, vascular tone, platelet aggregability, and blood viscosity.
- Vagal activity and fibrinolytic activity decrease in the morning.
- Beta-blockers and aspirin reduce morning myocardial infarction incidence, supporting the role of sympathetic activity and platelet aggregation.
Conclusions:
- The circadian pattern of cardiovascular events is influenced by daily physiological fluctuations.
- Stress, particularly in the morning, combined with increased sympathetic drive and platelet activity, can precipitate plaque rupture.
- Transient hemodynamic, vasoconstrictive, and prothrombotic forces act as acute risk factors for myocardial infarction.
Abstract:
The observation that acute myocardial infarction and sudden cardiac death are more frequent in the morning indicates that the onset of these cardiovascular events is not random, and provides a clue to mechanism. An atherosclerotic plaque is exposed to systemic physiologic processes that could increase the likelihood of plaque rupture and thrombosis in the presence of a vulnerable plaque. Many of these processes increase in intensity in the morning, including plasma catecholamine levels, sympathetic activity, heart rate, blood pressure, vascular tone, platelet aggregability and blood viscosity increase, whereas some protective factors such as vagal activity and fibrinolytic activity are decreased. Similar changes may also occur after stressful activities. The ability of beta-adrenergic blocking agents and aspirin preferentially to reduce the incidence of myocardial infarction in the morning supports the hypothesis that sympathetic activation and increased platelet aggregability contribute to the circadian pattern of acute cardiovascular disease. Although the extent of atherosclerosis changes slowly with time under the influence of chronic risk factors, it is proposed that stress, particularly in the morning, may produce a combination of transient hemodynamic, vasoconstrictive and prothrombotic forces that can be considered acute risk factors for plaque disruption and thrombosis, the final pathway of most myocardial infarctions.