Effects on the Cardiovascular System

Caffeine produces a direct stimulation of myocardial tissue leading to an increase in the rate and force of contraction. This direct cardiac effect can be inhibited by a depressant effect on the heart via medullary vagal stimulation. These opposing effects may explain why bradycardia, tachycardia, or no change can be observed in individuals receiving similar doses of caffeine. The traditional clinical view that caffeine induces arrhythmias in humans has not been confirmed by controlled experimental studies.

Caffeine decreases peripheral resistance by direct vasodilatation and increases blood flow to a small extent. This effect results from the relaxation of smooth muscle of blood vessels. For coronary arteries, vasodilatation is also observed in vitro, but the effects of caffeine in human coronary arteries in vivo are unknown. Different effects of caffeine on circulation can be observed in different vascular beds and, for example, the treatment of migraine headaches by caffeine is mediated through the vasoconstriction of cerebral arteries. It has also been shown that caffeine is capable of attenuating postprandial hypotension in patients with auto-nomic failure.

The observed cardiovascular effects consist of a 5-10% increase in both mean systolic and diastolic blood pressure for 1-3 h. A significant association was found between caffeine-related increase in systolic blood pressure and caffeine-related increase in pain tolerance. However, in contrast to the acute pressor effect reported, several epidemiological studies showed that habitual caffeine intake lowers blood pressure. Heart rate is decreased by 5-10% during the first hour, followed by an increase above baseline during the next 2 h. These effects are not detectable in regular coffee drinkers, suggesting that a complete tolerance can be developed. The tolerance to chronic caffeine intake can explain contradictory results reported in the literature. A few studies suggest that caffeine is partly responsible for the homocysteine-raising effect of coffee. This effect is associated with increased risk of cardiovascular disease, but it is uncertain whether this relation is causal.

Epidemiological studies designed to establish a relationship between caffeine intake and the incidences of myocardial infarction, mortality from ischaemic heart disease, or cerebrovascular accidents have provided conflicting results and have failed to establish a significant correlation.

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