Coffee and Myocardial Infarction

Abstract

The authors respond: Flammer et al1 provides important physiological explanations for our epidemiological findings2 as well as relevant information that should be taken into account in future studies. They also mention the potential effect of decaffeinated coffee, which would support the role of substances other than caffeine in the cardiovascular effects attributed to coffee drinking. Unfortunately, the small number of decaf coffee drinkers in our Costa Rican population prevented us from evaluating its effects. Čulić3 suggests a series of other potential triggers that could have confounded the temporal association found between coffee intake and myocardial infarction in our study. In our analysis, we carefully evaluated potential confounders such as smoking, heavy physical exertion, sexual intercourse, and anger. Other plausible confounders will remain as alternative explanations to the findings since we do not have the data to either prove or refute their effect. Further studies are needed to understand the important effects of these other triggers. We agree with Čulić in that other issues related to chronobiological patterns need to be studied in more detail in the context of trigger research. Ana Baylin Department of Community Health Brown University Providence, RI [email protected] Sonia Hernandez-Diaz Department of Epidemiology Harvard School of Public Health Boston, MA Edmond K. Kabagambe Department of Epidemiology School of Public Health University of Alabama at Birmingham Birmingham, AL Xinia Siles Centro Centroamericano de Población Universidad de Costa Rica San Pedro, Costa Rica Hannia Campos Department of Nutrition Harvard School of Public Health Boston, MA Centro Centroamericano de Población Universidad de Costa Rica San Pedro, Costa Rica