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Epidemiology:
doi: 10.1097/01.ede.0000254657.56340.f0
Letters to the Editor

Coffee and Myocardial Infarction

Flammer, Andreas J.; Sudano, Isabella; Corti, Roberto

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Cardiology, Department of Internal; Medicine; University Hospital Zürich; Zurich, Switzerland

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To the Editor:

In the very nice and well-done study, Baylin et al1 found that transient exposure to coffee may trigger myocardial infarction (MI), especially in patients with occasional intake of coffee (≤1 cup/d). Interestingly, they found no risk elevation in heavy coffee drinkers. This is remarkable, as most studies until now examined the effect of coffee on cardiovascular function in patients without considering the amount of coffee consumed. In our opinion, this aspect should be taken into consideration and highlighted. There is a lot of speculation about how coffee may trigger MI but not why heavy coffee drinkers are protected.

We2 recently showed that coffee and caffeine similarly increase sympathetic activity as measured directly by microneurography. We found that while coffee increased blood pressure in nonhabitual drinkers, the effect was blunted in habitual drinkers, despite the same sympathetic activation. Caffeine infusion similarly increased sympathetic nervous activity and blood pressure in habitual and nonhabitual coffee drinkers. The lack of blood pressure response after coffee in habitual drinkers may explain why, in the study of Baylin et al, heavy drinkers are less likely to develop MI. Moreover, we were able to demonstrate that coffee blunts cardiovascular response to mental stress in habitual coffee drinkers, whereas nonhabitual drinkers showed a stress-induced response of systolic blood pressure.3

The case–control study by Baylin et al adds important information to the hypothesis that habitual coffee drinkers are somehow protected against the cardiovascular effects of coffee (and its main component, caffeine). These findings support not only our data, but also a previous epidemiologic study not mentioned in the article.4 When interpreting data on coffee, the amount of coffee drinking should always be taken into account.

Baylin et al hypothesized that the increase in MI risk is mainly attributed to the serum–caffeine concentration. Since decaffeinated coffee also increases blood pressure in nonhabitual coffee drinkers, it has to be stressed that substances other than caffeine may be responsible for blood pressure elevation and increased risk of MI in nonhabitual coffee drinkers.

Our above-mentioned studies showed that both decaffeinated coffee and caffeine resulted in a similar time-by-condition interaction for total sympathetic nerve activity in nonhabitual coffee drinkers. Thus, substances other than caffeine are likely to be responsible for the stimulating effect seen in this subset of individuals.

Andreas J. Flammer

Isabella Sudano

Roberto Corti

Cardiology, Department of Internal

Medicine

University Hospital Zürich

Zurich, Switzerland

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REFERENCES

1. Baylin A, Hernandez-Diaz S, Kabagambe EK, et al. Transient exposure to coffee as a trigger of a first nonfatal myocardial infarction. Epidemiology. 2006;17:506–511.

2. Corti R, Binggeli C, Sudano I, et al. Coffee acutely increases sympathetic nerve activity and blood pressure independently of caffeine content: role of habitual versus nonhabitual drinking. Circulation. 2002;106:2935–2940.

3. Sudano I, Spieker L, Binggeli C, et al. Coffee blunts mental stress-induced blood pressure increase in habitual but not in nonhabitual coffee drinkers. Hypertension. 2005;46:521–526.

4. Woodward M, Tunstall-Pedoe H. Coffee and tea consumption in the Scottish Heart Health Study follow up: conflicting relations with coronary risk factors, coronary disease, and all cause mortality. J Epidemiol Community Health. 1999;53:481–487.

© 2007 Lippincott Williams & Wilkins, Inc.

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