DOI: 10.1097/01.ede.0000231372.34197.2a
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PMID: 16906053
Issn Print: 1044-3983
Publication Date: 2006/09/01
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Excerpt
Where does this finding fit in the broader context of triggers of clinical coronary heart disease (CHD) and its prevention? CHD results from coronary atherosclerosis, a long-term process that begins early in life. Acute clinical events such as MI occur during the later stages of coronary atherosclerosis. Acute coronary events in turn lead to further damage to the heart, culminating in heart failure and life-threatening arrhythmia, the primary mechanisms of CHD death. There has been considerable progress in understanding coronary risk development, but the identification of triggers of acute events remains a challenge.
Using animal models, physiological studies have demonstrated the role of ischemia, exercise, and drug therapies as potential triggers of acute coronary events. Pathologic triggers include coronary atherosclerotic plaque rupture and erosions. Histologic characteristics of plaques such as inflammatory infiltrates and thin caps might also influence risk of rupture.2 Case series have raised concerns that drug therapies that activate the sympathetic nervous system might contribute to acute events. In addition, studies have considered factors that affect cardiac susceptibility to triggers, eg, prior MI, drug therapies, habitual physical activity, and dietary intake of long-chain n-3 polyunsaturated fatty acids.
Epidemiologic studies have suggested that the occurrence of MI and sudden cardiac arrest is not random in time; there is a peak of MI and cardiac arrest in the early morning hours, and beta-blocker therapy blunts this morning increase in risk.3,4 Epidemiologic studies also have identified several exposures associated with an acute, transient increase in the risk of MI and cardiac arrest, including acute bouts of exercise or physical exertion,5–7 sexual activity,8 marijuana use,9 anger,10 war,11 and air pollution.12 Taken together, these findings provide some support for the hypothesis that exposures that alter sympathetic activity have the potential to trigger acute CHD events.
Coffee consumption is another factor that alters sympathetic activity. Baylin et al test the hypothesis that coffee is associated with the onset of (nonfatal) MI, particularly in the presence of other factors that predispose to atherosclerotic coronary disease. Using a case–crossover design, the authors report that the risk of MI was transiently increased 1.5-fold during the 1-hour period after intake of coffee compared with risk at other times. When the hazard period was extended to 2 or 3 hours after a cup of coffee, there was no increase in risk, supporting 1 hour as the appropriate hazard period.
This report illustrates issues of design and analysis related to the identification of triggers. The authors focused on a common, transient exposure, namely the acute (recent) consumption of caffeinated coffee. The caffeine in coffee has acute physiological effects such as increases in sympathetic tone and the release of catecholamines,13 which have the potential to trigger an MI. The authors chose a hazard period based on the pharmacology (absorption and bioavailability in the blood) of caffeine.14 They estimated the time at risk from coffee and the time not at risk, using reports of habitual coffee consumption and assuming that relevant effects persist for 1 hour after a cup of coffee.
