| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
(Circulation. 2007;116:2944-2951.)
© 2007 American Heart Association, Inc.
Epidemiology |
From the Laboratory of Clinical Epidemiology of Cardiovascular Disease (M.G.S., R. Marfisi, G.L., R. Marchioli, G.T.), Consorzio Mario Negri Sud, Santa Maria Imbaro, Chieti, Italy; Ospedale San Giovanni (A.B.), Rome, Italy; Ospedale Civile, Caserta (C.C.), Italy; Department of Cardiovascular Research (M.F.), Istituto Mario Negri, Milan, Italy; Ospedale Cervello (E.G.), Palermo, Italy; Centro Studi ANMCO (A.P.M.), Florence, Italy; Ospedale Santa Maria degli Angeli (G.N.), Pordenone, Italy; Ospedale Civile, Presidio di Riabilitazione (C.S.), Passirana di Rho, Milan, Italy; and Fondazione IRCCS Policlinico San Matteo (L.T.), Pavia, Italy.
Reprint requests to Roberto Marchioli, MD, Consorzio Mario Negri Sud, Via Nazionale 8/A, 66030, Santa Maria Imbaro, Italy. E-mail marchioli{at}negrisud.it
Received May 9, 2007; accepted October 19, 2007.
| Abstract |
|---|
|
|
|---|
Methods and Results— Prospectively ascertained information among 11 231 Italian patients (9584 males and 1647 females) with recent (
3 months) myocardial infarction enrolled in the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nellInfarto miocardico)-Prevenzione trial was used. Usual dietary habits were assessed at baseline and updated at 0.5 and 1.5 years. Coffee consumption was categorized as never/almost never, <2 cups per day, 2 to 4 cups per day, and >4 cups per day. Medication use and fasting glucose were assessed at 0.5, 1, 1.5, 2.5, and 3.5 years. Risk was evaluated with Cox proportional hazards with time-varying covariates. The main outcome measure was the cumulative incidence of cardiovascular events (cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke). A total of 1167 cardiovascular events occurred during 36 961 person-years of follow-up. After multivariable adjustment for potential confounders in the time-dependent analysis, the relative risk of cardiovascular events across categories of coffee consumption was 1.02 (95% CI 0.87 to 1.20) for <2 cups per day, 0.91 (95% CI 0.75 to 1.09) for 2 to 4 cups per day, and 0.88 (95% CI 0.64 to 1.20) for >4 cups per day compared with abstainers (P for trend=0.18). Ultimately, coffee consumption did not change the risk of coronary heart disease events, stroke, and sudden death.
Conclusions— No association between moderate coffee intake and cardiovascular events was observed in post–myocardial infarction patients.
Key Words: coronary disease coffee diet lifestyle prevention
| Introduction |
|---|
|
|
|---|
Clinical Perspective p 2951
Case-control studies suggest a harmful effect of coffee drinking on the risk of coronary heart disease (CHD),1–3 whereas prospective cohort studies show either no association,2,4–6 an association with lower risk,7 or even a higher risk of CHD.8 Recent findings support the hypothesis that coffee consumption may lower the risk of type 2 diabetes mellitus, a major coronary risk factor.9–12
Overall, scarce evidence is available on the association between coffee consumption and cardiovascular events (CVEs) among patients with documented CHD. One case-control study found that heavy coffee consumption (ie, >10 cups daily) was associated with a significant increase in the risk of sudden cardiac arrest in patients with established CHD.13 A multicenter prospective study on patients who survived myocardial infarction (MI) found no association between coffee consumption and mortality, even in the heaviest consumers.14
To address the relationship of coffee consumption and cardiovascular disease after acute MI, we analyzed data from a large cohort of patients enrolled in the GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nellInfarto miocardico)-Prevenzione trial. We also evaluated the effect of gender, obesity, smoking status, and type 2 diabetes mellitus on the association between coffee consumption and risk of CVE.
| Methods |
|---|
|
|
|---|
In brief, 11 323 men and women with recent MI (
3 months, median 16 days) were enrolled from 172 Italian cardiology centers between October 1993 and September 1995. Patients were followed up for 3.5 years by means of clinical visits. In addition to randomly allocated treatments, each patient was treated with standard preventive intervention and was given lifestyle advice that included information on dietary habits so as to increase consumption of fish, fruit, raw and cooked vegetables, and olive oil. At baseline, information was collected on demographic characteristics, cardiovascular risk factors, prior events, medications, dietary habits, and results of transthoracic echocardiogram, exercise testing, and coronary angiography. Height, weight, heart rate, and blood pressure were measured, and fasting blood was drawn for assessment of serum glucose, lipids, and other measures, including complete blood count and fibrinogen. Follow-up visits were scheduled at 6, 12, 18, 30, and 42 months. During each visit, updated information was obtained on smoking habits, medications, and interim events. Weight was remeasured, and fasting blood was drawn for laboratory testing. For the present analyses, we excluded 92 patients with missing information on coffee intake at baseline.
Assessment of Coffee Consumption
The assessment of coffee consumption was made through a simple dietary questionnaire aimed at assessing Mediterranean dietary habit17 and recording the frequency of consumption of fish, fruit, raw vegetables, cooked vegetables, olive oils, other oils, butter, cheese, wine, and coffee. Specifically for the coffee item, each participant was asked to report its use as never/almost never, <2 cups per day, 2 to 4 cups per day, and >4 cups per day. The coffee preparation method was not recorded.
The dietary questionnaire was administered by cardiologists/nurses during clinical visits at the baseline examination and at the 6th, 18th, and 42nd month of follow-up. Baseline information described dietary habits at and before the index MI, whereas follow-up information recorded current habits.
Assessment of CVEs
The primary end point for the present analysis was the combined outcome measure of cardiovascular death, nonfatal MI, or nonfatal stroke that occurred during the course of the study. Additional analyses were performed with the cumulative rate of sudden death, nonfatal plus fatal stroke, and nonfatal plus fatal MI used as dependent variables. CVEs were validated by a committee of experts.15,16
Statistical Analysis
Participants were classified according to levels of coffee consumption. Person-years of exposure were calculated from the date of randomization to the date of first major nonfatal CVE, cardiovascular death, or last follow-up visit, whichever came first.
Cox regression models were used to investigate the association between coffee consumption and incidence of CVE. Hazard ratios were used to estimate relative risks. Relative risks were evaluated in an unadjusted model and then adjusted for age, gender, and smoking status. Furthermore, we adjusted for the most important potential confounding factors, such us dietary habits, cardiovascular risk factors, history of MI before the index MI, time from the index MI to enrollment, post-MI complications, and pharmacological therapies, with inclusion of the allocation treatments. Tests for interaction were performed by the addition of interaction terms between coffee intake and the variables of interest to the regression model. Tests for trend were calculated by the assignment to each category of its median value and by evaluation of the latter as a continuous variable. To account for both former dietary habits (before the index MI) and changing food consumption (during follow-up), we used the cumulative average update of coffee consumption and other dietary variables intake in the time-dependent analysis.18 Time-varying covariates were used to update information on dietary habits and other risk factors (body mass index, smoking, revascularization procedures, and medications) at 6 and 18 months. Indicator variables were used for missing data on baseline covariates; values were otherwise carried forward for missing time-varying covariates. Stratified analyses were conducted according to gender, smoking status, obesity, and history of diabetes mellitus. All analyses were performed with the SAS statistical package, version 9.1 (SAS Institute Inc, Cary, NC). All probability values were 2-sided.
The authors had full access to the data and take full responsibility for its integrity. All authors have read and agree to the manuscript as written.
| Results |
|---|
|
|
|---|
30 kg/m2), with a shorter period of time from enrollment in the study until the index event. Frequent coffee consumption was also associated with smoking habit, with 1 of 4 smokers drinking >4 cups per day. Patients who drank more coffee were less likely to have a history of hypertension, diabetes mellitus, prior MI, heart failure, low ejection fraction, and angina pectoris. Patients taking antiplatelet drugs and β-blockers were more likely to be heavy coffee drinkers, whereas no difference was observed for the distribution of treatment with n-3 polyunsaturated fatty acids according to coffee-drinking habit.
|
Table 2 shows dietary habits of the population according to level of coffee consumption. Overall, patients with better dietary habits were less likely to have a high intake of coffee. Subjects with a high intake of fish, vegetables, and fruits tended to drink less coffee than patients with worse dietary habits. The intake of butter and cheese was consistently high among those who drank >4 cups of coffee per day.
|
During 36 961 person-years of follow-up, we documented a total of 1167 CVEs (670 cardiovascular deaths, 456 nonfatal MIs, and 119 nonfatal strokes), with
70% of CVEs being registered among patients with a low intake of coffee (never/almost never to <2 cups per day; Table 3). The incidence rate of CVEs was 3.0 and 3.9 cases per 100 person-years in patients with the highest and lowest intake of coffee, respectively.
|
In the unadjusted time-dependent analysis, we found an inverse association between coffee consumption and risk of CVEs: The risk of CVE was 46% lower in the highest category of coffee intake compared with the reference category of subjects who did not drink coffee (test for trend P<0.0001). After adjustment for age and gender, the association between coffee consumption and risk of CVE was no longer statistically significant, and no relation between coffee consumption and incidence of CVE was found (Table 3). Further adjustment for smoking and dietary habits did not change the substance of the latter results, although the probability value for trend became significant (P for trend=0.05). No association between coffee intake and CVEs was found after further multivariable adjustment for other potential confounders.
We performed stratified analyses according to smoking status, gender, diabetes mellitus, and obesity (data not shown). Such analyses confirmed that the null association between coffee and CVEs was independent of gender (P for interaction=0.97), diabetes mellitus (P for interaction=0.20), obesity (P for interaction=0.97), and smoking status (P for interaction=0.67). We found no statistically significant relationship between coffee intake and risk of cerebrovascular events, MI, or sudden death in the multivariable-adjusted models (Table 4).
|
| Discussion |
|---|
|
|
|---|
In accordance with the study by Lopez-Garcia and colleagues,19 confounding due to smoking status was nonrelevant, although cigarette smoking was strongly correlated with coffee consumption and age. Similarly, no interaction between coffee intake and diabetes mellitus at baseline was found on the risk of CVEs.
In the present study, we also evaluated the effect of coffee consumption on cerebrovascular events. We did not find an association between coffee consumption and risk of stroke, in agreement with the scant previous evidence.20–23 Coffee appeared to be positively associated with an increased risk of thromboembolic stroke in nonsmoking, hypertensive middle-aged men enrolled in only 1 study, the Honolulu Heart Study.24
The effects of coffee consumption on the risk of cardiovascular disease have long been investigated and debated. The majority of prospective cohort studies have not found a significant association between coffee consumption and risk of CHD,2,4,5,19 with only 2 studies showing beneficial effects,7,25 whereas most case-control studies suggested a negative effect of coffee consumption on CHD.1–3,26,27
The present study is the first to evaluate the effects of coffee consumption on a large, prospective cohort of patients with established CHD. One case-control study, performed on 117 patients with CHD, found that only heavy coffee consumption (>10 cups per day) was associated with a significant increase in the risk of sudden cardiac arrest.13 However, we did not find any effect of coffee intake on the risk of sudden cardiac death. The findings for sudden death are of particular interest because of the concern that coffee consumption may increase fatal arrhythmias. Other studies did not show moderate coffee or caffeine intake (5 to 6 cups daily) to increase the frequency or severity of cardiac arrhythmias, ie, the leading cause of sudden death.28–31 In addition, a prospective study of 1902 patients who survived an MI found no association between coffee consumption and survival over the following 4 years.14
Two recent findings suggest a complex dose-response relationship between coffee intake and the risk of CHD. One study found a J-shaped association whereby moderate coffee intake (<300 mL/d) was associated with lower CHD risk, whereas heavy coffee consumption (>300 mL/d) was associated with increased risk.32 The other study suggested a U-shaped relationship that caused people with light or occasional coffee intake to have an increased risk of CHD events compared with drinkers of moderate amounts daily.8 In another study, the relative risk of MI was transiently increased 1.5-fold during the 1-hour period after intake of coffee compared with risk at other times.33
Can the discrepancies between the results from different studies be reconciled or explained? Selection and recall bias may explain the positive association suggested by case control-studies. An inadequate adjustment for confounding factors such as smoking, poor diet, and sedentary lifestyle (frequently associated with coffee consumption) could also affect the relationship between coffee consumption and health outcomes, especially in earlier studies. The limited number of published prospective studies on coffee intake (ie, a dietary habit that can be easily ascertained in epidemiological studies) also raises the possibility that publication bias could have spuriously decreased the appearance of studies that showed results pertaining to CHD and coffee intake that were not statistically significant. Variations in cup size, brewing methods for coffee preparation,26,34–38 and amount of caffeine contained in the coffee beans,39 as well as the multitude of biologically active substances that are contained in the coffee,40 all could contribute to misclassification of exposure and may in part explain some conflicting results. Furthermore, the development of complete41 or partial42 tolerance to the humoral and hemodynamic effects of caffeine among habitual drinkers41 adds to the complexity of the effects of coffee. This, in turn, may also render difficult the extrapolation of results from short-term metabolic studies to long-term use of coffee.
Genetic and lifestyle factors may also affect individual reactions to the bioactive compounds of coffee. For instance, the association between coffee and MI was only found among individuals with the slow CYP1A2*1F allele, which impairs caffeine metabolism.43 In addition, cigarette smoking increases caffeine clearance by inducing CYP1A2 activity.44,45
The present analysis had several strengths. Prospectively collected data on coffee intake, other risk factors, and events were available in >11 000 patients with recent MI who were followed up for 3.5 years. The patients were enrolled and monitored by general cardiology practitioners and represented a "real-life" cross section of post-MI patients. Dietary habits were assessed with a simple diet questionnaire designed to maximize the detection in clinical practice of dietary variation among Italian adults.16 Repeated measurements of coffee intake at baseline and at various time points during follow-up were performed, which strengthens the reliability of the results. This approach allowed us to describe long-term exposure after MI, to use the change in coffee intake habits in the years after MI in the analysis, and thus to reduce measurement errors due to intraindividual variation. Data on other dietary habits and risk factors were also updated during follow-up, which enabled us to perform time-varying multivariable adjustment.
The present study has some limitations. Because GISSI-Prevenzione was a pragmatic, population study conducted in a nationwide setting by hospital cardiologists, we adopted a simple questionnaire aimed at assessing macroscopic indicators of dietary habits, and therefore, the questionnaire was not validated. The diet questionnaire assessed the intake of coffee semiquantitatively according to predefined categories, and no information was collected for very high intake of coffee. We did not collect information on physical activity; however, we adjusted for both heart failure class and anginal symptoms, both of which predict tolerance for physical activity and for exercise tolerance during stress testing, a measure of physical fitness. Finally, because the vast majority of the patients in the present study drank mocha or espresso coffee, virtually the only method of coffee preparation used in Italy, the results may not be applicable to other populations that use different methods of coffee preparation.
In conclusion, our findings suggest that moderate coffee intake is neither a hazard nor a protective factor for cardiovascular health in patients who have had an MI.
| Acknowledgments |
|---|
Sources of Funding
The present study received no economic support. GISSI is endorsed by Associazione Nazionale Medici Cardiologi Ospedalieri (ANMCO), Firenze, Italy; by Istituto di Ricerche Farmacologiche Mario Negri, Milan; and by Consorzio Mario Negri Sud, Santa Maria Imbaro, Italy. The GISSI-Prevenzione group had full responsibility for the study design; the conduct, collection, management, analysis, and interpretation of data; and the preparation, review, and approval of the manuscript. The GISSI-Prevenzione trial was supported by grants from Bristol-Myers Squibb, Pharmacia-Upjohn, Societá Prodotti Antibiotici, and Pfizer.
Disclosures
None.
| References |
|---|
|
|
|---|
2. Kawachi I, Colditz GA, Stone CB. Does coffee drinking increase the risk of coronary heart disease? Results from a meta-analysis. Br Heart J. 1994; 72: 269–275.
3. Tavani A, Bertuzzi M, Negri E, Sorbara L, La Vecchia C. Alcohol, smoking, coffee and risk of non-fatal acute myocardial infarction in Italy. Eur J Epidemiol. 2001; 17: 1131–1137.[CrossRef][Medline] [Order article via Infotrieve]
4. Myers MG, Basinski A. Coffee and coronary heart disease. Arch Intern Med. 1992; 152: 1767–1772.
5. Willett WC, Stampfer MJ, Manson JE, Colditz GA, Rosner BA, Speizer FE, Hennekens CH. Coffee consumption and coronary heart disease in women: a ten-year follow-up. JAMA. 1996; 275: 458–462.
6. Rosner SA, Akesson A, Stampfer MJ, Wolk A. Coffee consumption and risk of myocardial infarction among older Swedish women. Am J Epidemiol. 2007; 165: 288–293.
7. 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 Commun Health. 1999; 53: 481–487.[Abstract]
8. Happonen P, Voutilainen S, Salonen JT. Coffee drinking is dose-dependently related to the risk of acute coronary events in middle-aged men. J Nutr. 2004; 134: 2381–2386.
9. van Dam RM, Feskens EJ. Coffee consumption and risk of type 2 diabetes mellitus. Lancet. 2002; 360: 1477–1478.[CrossRef][Medline] [Order article via Infotrieve]
10. Tuomilehto J, Hu G, Bidel S, Lindstrom J, Jousilahti P. Coffee consumption and risk of type 2 diabetes mellitus among middle-aged Finnish men and women. JAMA. 2004; 291: 1213–1219.
11. van Dam RM, Hu FB. Coffee consumption and risk of type 2 diabetes: a systematic review. JAMA. 2005; 294: 97–104.
12. van Dam RM. Coffee and type 2 diabetes: from beans to beta-cells. Nutr Metab Cardiovasc Dis. 2006; 16: 69–77.[CrossRef][Medline] [Order article via Infotrieve]
13. de Vreede-Swagemakers JJ, Gorgels AP, Weijenberg MP, Dubois-Arbouw WI, Golombeck B, van Ree JW, Knottnerus A, Wellens HJ. Risk indicators for out-of-hospital cardiac arrest in patients with coronary artery disease. J Clin Epidemiol. 1999; 52: 601–607.[CrossRef][Medline] [Order article via Infotrieve]
14. Mukamal KJ, Maclure M, Muller JE, Sherwood JB, Mittleman MA. Caffeinated coffee consumption and mortality after acute myocardial infarction. Am Heart J. 2004; 147: 999–1004.[CrossRef][Medline] [Order article via Infotrieve]
15. Gruppo Italiano per lo Studio della Sopravvivenza nellInfarto miocardico. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Lancet. 1999; 354: 447–455.[CrossRef][Medline] [Order article via Infotrieve]
16. Marchioli R, Barzi F, Bomba E, Chieffo C, Di Gregorio D, Di Mascio R, Franzosi MG, Geraci E, Levantesi G, Maggioni AP, Mantini L, Marfisi RM, Mastrogiuseppe G, Mininni N, Nicolosi GL, Santini M, Schweiger C, Tavazzi L, Tognoni G, Tucci C, Valagussa F. Early protection against sudden death by n-3 polyunsaturated fatty acids after myocardial infarction: time-course analysis of the results of the Gruppo Italiano per lo Studio della Sopravvivenza nellInfarto Miocardico (GISSI)-Prevenzione. Circulation. 2002; 105: 1897–1903.
17. Barzi F, Woodward M, Marfisi RM, Tavazzi L, Valagussa F, Marchioli R. Mediterranean diet and all-causes mortality after myocardial infarction: results from the GISSI-Prevenzione trial. Eur J Clin Nutr. 2003; 57: 604–611.[CrossRef][Medline] [Order article via Infotrieve]
18. Hu FB, Stampfer MJ, Rimm E, Ascherio A, Rosner BA, Spiegelman D, Willett WC. Dietary fat and coronary heart disease: a comparison of approaches for adjusting for total energy intake and modeling repeated dietary measurements. Am J Epidemiol. 1999; 149: 531–540.
19. Lopez-Garcia E, van Dam RM, Willett WC, Rimm EB, Manson JE, Stampfer MJ, Rexrode KM, Hu FB. Coffee consumption and coronary heart disease in men and women: a prospective cohort study. Circulation. 2006; 113: 2045–2053.
20. Adolfsson R, Svardsudd K, Tibblin G. 1913 Men study: a longitudinal study of the development of stroke in a population. Scand J Soc Med Suppl. 1977; 14: 122–127.[Medline] [Order article via Infotrieve]
21. Grobbee DE, Rimm EB, Giovannucci E, Colditz G, Stampfer M, Willett W. Coffee, caffeine, and cardiovascular disease in men. N Engl J Med. 1990; 323: 1026–1032.[Abstract]
22. Heyden S, Tyroler HA, Heiss G, Hames CG, Bartel A. Coffee consumption and mortality: total mortality, stroke mortality, and coronary heart disease mortality. Arch Intern Med. 1978; 138: 1472–1475.
23. Bidel S, Hu G, Qiao Q, Jousilahti P, Antikainen R, Tuomilehto J. Coffee consumption and risk of total and cardiovascular mortality among patients with type 2 diabetes. Diabetologia. 2006; 49: 2618–2626.[CrossRef][Medline] [Order article via Infotrieve]
24. Hakim AA, Ross GW, Curb JD, Rodriguez BL, Burchfiel CM, Sharp DS, Yano K, Abbott RD. Coffee consumption in hypertensive men in older middle-age and the risk of stroke: the Honolulu Heart Program. J Clin Epidemiol. 1998; 51: 487–494.[CrossRef][Medline] [Order article via Infotrieve]
25. Kleemola P, Jousilahti P, Pietinen P, Vartiainen E, Tuomilehto J. Coffee consumption and the risk of coronary heart disease and death. Arch Intern Med. 2000; 160: 3393–3400.
26. Hammar N, Andersson T, Alfredsson L, Reuterwall C, Nilsson T, Hallqvist J, Knutsson A, Ahlbom A. Association of boiled and filtered coffee with incidence of first nonfatal myocardial infarction: the SHEEP and the VHEEP study. J Intern Med. 2003; 253: 653–659.[CrossRef][Medline] [Order article via Infotrieve]
27. Palmer JR, Rosenberg L, Rao RS, Shapiro S. Coffee consumption and myocardial infarction in women. Am J Epidemiol. 1995; 141: 724–731.
28. Chelsky LB, Cutler JE, Griffith K, Kron J, McClelland JH, McAnulty JH. Caffeine and ventricular arrhythmias: an electrophysiological approach. JAMA. 1990; 264: 2236–2240.
29. Myers MG. Caffeine and cardiac arrhythmias. Ann Intern Med. 1991; 114: 147–150.
30. Frost L, Vestergaard P. Caffeine and risk of atrial fibrillation or flutter: the Danish Diet, Cancer, and Health Study. Am J Clin Nutr. 2005; 81: 578–582.
31. Wilhelmsen L, Rosengren A, Lappas G. Hospitalizations for atrial fibrillation in the general male population: morbidity and risk factors. J Intern Med. 2001; 250: 382–389.[CrossRef][Medline] [Order article via Infotrieve]
32. Panagiotakos DB, Pitsavos C, Chrysohoou C, Kokkinos P, Toutouzas P, Stefanadis C. The J-shaped effect of coffee consumption on the risk of developing acute coronary syndromes: the CARDIO2000 case-control study. J Nutr. 2003; 133: 3228–3232.
33. Baylin A, Hernandez-Diaz S, Kabagambe EK, Siles X, Campos H. Transient exposure to coffee as a trigger of a first nonfatal myocardial infarction. Epidemiology. 2006; 17: 506–511.[CrossRef][Medline] [Order article via Infotrieve]
34. Zock PL, Katan MB, Merkus MP, van Dusseldorp M, Harryvan JL. Effect of a lipid-rich fraction from boiled coffee on serum cholesterol. Lancet. 1990; 335: 1235–1237.[CrossRef][Medline] [Order article via Infotrieve]
35. Urgert R, Katan MB. The cholesterol-raising factor from coffee beans. Ann Rev Nutr. 1997; 17: 305–324.[CrossRef][Medline] [Order article via Infotrieve]
36. Jee SH, He J, Appel LJ, Whelton PK, Suh I, Klag MJ. Coffee consumption and serum lipids: a meta-analysis of randomized controlled clinical trials. Am J Epidemiol. 2001; 153: 353–362.
37. Urgert R, van der Weg G, Kosmeijer-Schuil TG, van de Bovenkamp P, Hovenier R, Katan MB. Levels of the cholesterol-elevating diterpenes cafestol and kahweol in various coffee brews. J Agric Food Chem. 1995; 43: 2167–2172.[CrossRef]
38. Gross G, Jaccaud E, Huggett AC. Analysis of the content of the diterpenes cafestol and kahweol in coffee brews. Food Chem Toxicol. 1997; 35: 547–554.[CrossRef][Medline] [Order article via Infotrieve]
39. McCusker RR, Goldberger BA, Cone EJ. Caffeine content of specialty coffees. J Anal Toxicol. 2003; 27: 520–522.[Medline] [Order article via Infotrieve]
40. Viani R. The composition of coffee. In: Caffeine, Coffee and Health. New York, NY: Raven; 1993: 17–41.
41. Robertson D, Wade D, Workman R, Woosley RL, Oates JA. Tolerance to the humoral and hemodynamic effects of caffeine in man. J Clin Invest. 1981; 67: 1111–1117.[Medline] [Order article via Infotrieve]
42. James JE. Is habitual caffeine use a preventable cardiovascular risk factor? Lancet. 1997; 349: 279–281.[CrossRef][Medline] [Order article via Infotrieve]
43. Cornelis MC, El-Sohemy A, Kabagambe EK, Campos H. Coffee, CYP1A2 genotype, and risk of myocardial infarction. JAMA. 2006; 295: 1135–1141.
44. Joeres R, Klinker H, Heusler H, Epping J, Zilly W, Richter E. Influence of smoking on caffeine elimination in healthy volunteers and in patients with alcoholic liver cirrhosis. Hepatology. 1988; 8: 575–579.[CrossRef][Medline] [Order article via Infotrieve]
45. Kalow W, Tang BK. Caffeine as a metabolic probe: exploration of the enzyme-inducing effect of cigarette smoking. Clin Pharmacol Ther. 1991; 49: 44–48.[Medline] [Order article via Infotrieve]
| Footnotes |
|---|
This article has been cited by other articles:
![]() |
T. Richardson, J. Baker, P.W. Thomas, C. Meckes, A. Rozkovec, and D. Kerr Randomized control trial investigating the influence of coffee on heart rate variability in patients with ST-segment elevation myocardial infarction QJM, August 1, 2009; 102(8): 555 - 561. [Abstract] [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2007 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |