Cardiovascular effects of caffeine
on
Death by Coffee?
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· Score: 1
From utdol.com
Arrhythmias -- There is a widespread belief that caffeine, particularly at high doses, is associated with palpitations and a number of arrhythmias, including atrial fibrillation and supraventricular and ventricular ectopy [14]. However, despite the theoretical relationship between caffeine and arrhythmogenesis, there is no evidence in humans that caffeine can provoke any spontaneous arrhythmia or enhance the ability to induce an arrhythmia in the electrophysiologic laboratory [10,16-18]. Furthermore, among patients with arrhythmia, caffeine restriction has not been of benefit [19] and the administration of a modest dose of caffeine is not arrhythmogenic, even among patients with known life-threatening ventricular arrhythmia [20].
Although the relationship between caffeine and arrhythmia is uncertain, electrophysiologic studies have shown effects of caffeine that might promote arrhythmogenesis. High concentrations of caffeine can directly increase the transmembrane calcium current that is responsible for the oscillatory afterpotential (ie, triggered activity) [21,22,15]. In experimental models, even low concentrations of caffeine can increase triggered activity due to release of calcium from the sarcoplasmic reticulum [12,23].
Hemodynamic effects -- Caffeine can, in patients who are infrequently exposed, acutely raise the blood pressure (BP) by as much as 10 mmHg [24-27]. There is little or no effect of acute caffeine ingestion in habitual coffee drinkers [26,27]. Caffeine can also potentiate (by about 5 mmHg) the rise in blood pressure induced by stress, such as that occurring in the workplace [28]. The increase in vascular resistance associated with these changes also involves the cerebral and coronary circulations [7,29].
The acute effect of caffeine is more pronounced in hypertensive patients. In a study of 182 patients, caffeine raised the systolic and diastolic blood pressure in all patients [30]. However, the greatest response was observed in patients with diagnosed hypertension; compared to subjects with optimal blood pressure, those with hypertension had a >1.5 fold greater increase in blood pressure and 89 percent had a value that was in the hypertensive range, which occurred in less than 20 percent of normotensive subjects. The hypertensive effect may be more prominent in elderly patients with hypertension [31].
The effect of chronic caffeine ingestion is less clear. It does not appear to be associated with an increased incidence of hypertension due to attenuation of the pressor response [32-34]. However, there is some evidence that chronic caffeine use can cause a small elevation in blood pressure. A meta-analysis of eleven controlled clinical trials found that coffee ingestion (median dose of five cups per day) increased systolic and diastolic blood pressure by 2.4 and 1.2 mmHg, respectively [35]. Similar reductions in blood pressure may be seen when habitual coffee drinkers either abstain from coffee or switch to decaffeinated coffee [33,36,37].
The effect of coffee may not be solely explained by caffeine. In a study of 15 volunteers (six habitual and nine nonhabitual coffee drinkers), intravenous caffeine increased muscle sympathetic nerve activity and blood pressure to a similar degree in both groups [27]. Caffeinated coffee raised the blood pressure only in nonhabitual drinkers, despite similar plasma caffeine concentrations and a similar increase in muscle sympathetic nerve activity. Furthermore, nonhabitual drinkers had similar elevations in blood pressure and muscle sympathetic nerve activity with caffeinated and decaffeinated coffee.
TI - Caffeine and cardiac arrhythmias. An experimental study in dogs with review of literature.
AU - Mehta A; Jain AC; Mehta MC; Billie M
SO - Acta Cardiol 1997;52(3):273-83
TI - Coffee, catecholamines and cardiac arrhythmia.
AU - Wennmalm A; Wennmalm M
SO - Clin Physiol 1989 Jun;9(3):201-6.
TI - Caffeine and ventricular arrhythmias. An electrophysiological approach.
AU - Chelsky LB; Cutler JE; Griffith K; Kron J; McClelland JH; McAnulty JH
SO -
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From utdol.com Arrhythmias -- There is a widespread belief that caffeine, particularly at high doses, is associated with palpitations and a number of arrhythmias, including atrial fibrillation and supraventricular and ventricular ectopy [14]. However, despite the theoretical relationship between caffeine and arrhythmogenesis, there is no evidence in humans that caffeine can provoke any spontaneous arrhythmia or enhance the ability to induce an arrhythmia in the electrophysiologic laboratory [10,16-18]. Furthermore, among patients with arrhythmia, caffeine restriction has not been of benefit [19] and the administration of a modest dose of caffeine is not arrhythmogenic, even among patients with known life-threatening ventricular arrhythmia [20]. Although the relationship between caffeine and arrhythmia is uncertain, electrophysiologic studies have shown effects of caffeine that might promote arrhythmogenesis. High concentrations of caffeine can directly increase the transmembrane calcium current that is responsible for the oscillatory afterpotential (ie, triggered activity) [21,22,15]. In experimental models, even low concentrations of caffeine can increase triggered activity due to release of calcium from the sarcoplasmic reticulum [12,23]. Hemodynamic effects -- Caffeine can, in patients who are infrequently exposed, acutely raise the blood pressure (BP) by as much as 10 mmHg [24-27]. There is little or no effect of acute caffeine ingestion in habitual coffee drinkers [26,27]. Caffeine can also potentiate (by about 5 mmHg) the rise in blood pressure induced by stress, such as that occurring in the workplace [28]. The increase in vascular resistance associated with these changes also involves the cerebral and coronary circulations [7,29]. The acute effect of caffeine is more pronounced in hypertensive patients. In a study of 182 patients, caffeine raised the systolic and diastolic blood pressure in all patients [30]. However, the greatest response was observed in patients with diagnosed hypertension; compared to subjects with optimal blood pressure, those with hypertension had a >1.5 fold greater increase in blood pressure and 89 percent had a value that was in the hypertensive range, which occurred in less than 20 percent of normotensive subjects. The hypertensive effect may be more prominent in elderly patients with hypertension [31]. The effect of chronic caffeine ingestion is less clear. It does not appear to be associated with an increased incidence of hypertension due to attenuation of the pressor response [32-34]. However, there is some evidence that chronic caffeine use can cause a small elevation in blood pressure. A meta-analysis of eleven controlled clinical trials found that coffee ingestion (median dose of five cups per day) increased systolic and diastolic blood pressure by 2.4 and 1.2 mmHg, respectively [35]. Similar reductions in blood pressure may be seen when habitual coffee drinkers either abstain from coffee or switch to decaffeinated coffee [33,36,37]. The effect of coffee may not be solely explained by caffeine. In a study of 15 volunteers (six habitual and nine nonhabitual coffee drinkers), intravenous caffeine increased muscle sympathetic nerve activity and blood pressure to a similar degree in both groups [27]. Caffeinated coffee raised the blood pressure only in nonhabitual drinkers, despite similar plasma caffeine concentrations and a similar increase in muscle sympathetic nerve activity. Furthermore, nonhabitual drinkers had similar elevations in blood pressure and muscle sympathetic nerve activity with caffeinated and decaffeinated coffee. TI - Caffeine and cardiac arrhythmias. An experimental study in dogs with review of literature. AU - Mehta A; Jain AC; Mehta MC; Billie M SO - Acta Cardiol 1997;52(3):273-83 TI - Coffee, catecholamines and cardiac arrhythmia. AU - Wennmalm A; Wennmalm M SO - Clin Physiol 1989 Jun;9(3):201-6. TI - Caffeine and ventricular arrhythmias. An electrophysiological approach. AU - Chelsky LB; Cutler JE; Griffith K; Kron J; McClelland JH; McAnulty JH SO -