Therapeutic implications of circadian variations in myocardial ischemia and related physiologic functions.
Electrocardiographic (ECG) monitoring for long periods documents circadian patterns in myocardial ischemic episodes. The rise begins between 6 AM and 8 AM for patients with effort angina, the zenith of ischemic activity occurs at about noon. Similar peaks occur in the frequency of acute myocardial infarction and sudden death. Triggering mechanisms common to all of these events may include rises in catecholamine secretion, sympathetic nervous system activity, blood pressure, heart rate, cortisol secretion, and aggregability of platelets, as well as a trough in fibrinolytic activity. These coincident peaks and troughs would be expected to increase myocardial oxygen demand and decrease oxygen supply after a person arises in the morning. This vulnerable period merits recognition. Tailoring the dosing and choice of medication to prevent or reduce ischemia may be important if potential disease-activity triggering mechanisms are to be attenuated. By modifying triggering mechanisms, we may be able to modify the frequencies of adverse outcomes such as acute myocardial infarction and sudden death.
Division of Cardiology, University of Florida, Gainesville 32610-0277.
C J
CJ
Pepine
D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D001682:Biological Availability; D002121:Calcium Channel Blockers / Q000627:therapeutic use; D002940:Circadian Rhythm; D003327:Coronary Disease / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D005996:Nitroglycerin / Q000627:therapeutic use; D010100:Oxygen / Q000378:metabolism
D000319:Adrenergic beta-Antagonists; D002121:Calcium Channel Blockers; D005996:Nitroglycerin; D010100:Oxygen