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Diurnal rhythms and clinical events in coronary artery disease
1Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Insights
Cardiovascular events like heart attack and sudden death peak in the morning due to increased sympathetic activity. Atherosclerosis impairs blood vessel response, raising risk upon waking.
Area of Science:
- Cardiovascular Medicine
- Physiology
Background:
- Coronary atherosclerosis causes angina, myocardial infarction, and sudden death.
- These cardiovascular events exhibit diurnal variation, peaking in the morning.
- Morning hours show increased sympathetic nervous system activity and catecholamine levels.
Purpose of the Study:
- To explore the mechanisms behind the diurnal variation of cardiovascular events.
- To investigate the role of sympathetic activity and endothelial dysfunction in morning cardiac events.
Main Methods:
- Review of experimental and clinical research on cardiovascular events and diurnal rhythms.
- Analysis of physiological parameters including heart rate, blood pressure, and catecholamine levels.
- Examination of endothelial function and vascular procoagulant status in atherosclerosis.
Main Results:
- Cardiovascular events, including angina and myocardial infarction, show a distinct morning peak.
- Increased sympathetic outflow and catecholamines post-waking elevate cardiac workload.
- Endothelial dysfunction in atherosclerosis limits vasoconstriction response to catecholamines.
Conclusions:
- The interaction between heightened sympathetic activity and atherosclerotic changes may lower the threshold for ischemia in the morning.
- Morning increases in angina, myocardial infarction, and sudden death are linked to sympathetic surges and vascular dysfunction.
- Understanding these diurnal patterns is crucial for optimizing cardiovascular therapies and guiding future research.
Abstract:
Patients with coronary atherosclerosis present with angina, myocardial infarction and sudden death, most often caused by atherosclerotic stenosis complicated by spasm and/or occlusive thrombosis. All of these events have been shown to exhibit similar diurnal rhythms, with a peak incidence in the morning after waking and rising. Other cardiovascular parameters also show a similar diurnal rhythm associated with increased sympathetic outflow and circulating catecholamines, producing increases in heart rate, blood pressure, myocardial contractility and oxygen demand soon after waking and rising. Experimental and clinical research has recently pointed to several possible mechanisms that might be responsible for these events. In patients with atherosclerosis, dysfunction of the endothelium in the epicardial coronary arteries results in a failure to limit the constrictor response to catecholamines. Catecholamines can also alter the procoagulant nature of vascular surfaces. We speculate that the interaction between increased sympathetic activity and the procoagulant and vasoconstrictor states of atherosclerotic coronary stenoses may lead to a lower threshold to ischaemia in the waking hours, with a corresponding increase in angina, myocardial infarction and sudden death. These factors may be important considerations for the selection of suitable therapies and for future research.