ARTICLE
Auteur(s) : Charalambos Vlachopoulos, Nikolaos
Alexopoulos, Christodoulos Stefanadis
Hypertension and Peripheral Vessels Units, 1 st Department
of Cardiology, Athens Medical School, Hippokration Hospital,
Athens, Greece
Nutrition has a significant impact on cardiovascular risk and its
effect on arterial stiffness and wave reflections has been an
appealing goal of investigation during the last decades for two
particular reasons. First, although arterial elastic properties are
genetically determined, they are also impaired in the presence of
risk factors, and they are influenced by pharmacological and
non-pharmacological interventions, such as nutritional habits [1,
2]. Second, arterial stiffness and wave reflections are important
determinants of cardiovascular function and arterial-heart
coupling. It has been repeatedly demonstrated that they are
implicated in the pathogenesis of hypertension and that they are
independent predictors of cardiovascular morbidity and mortality.
Research has focused especially on caffeine and coffee, tea, cocoa,
wine and other flavonoid-containing foods and beverages,
antioxidant vitamins, and sodium. In this review, the main findings
on the effect of these dietary/nutritional components on arterial
stiffness and wave reflections are summarized (table 1). Obesity and weight reduction are also
included in this review, since they are influenced by diet and
nutritional habits.
Coffee-caffeine
Several studies have examined the effect of coffee consumption on
cardiovascular risk with various results. Relationships vary from a
positive to a neutral one, while some studies have shown a J- or
U-shape association, denoting that low consumption may be
beneficial, while high consumption is clearly detrimental. Genetic
predisposition for rapid caffeine metabolism may account for
discrepancies seen in these studies.
Caffeine, the main vasoactive substance in coffee, exerts an
acute detrimental effect -lasting at least for 3 hours- on aortic
stiffness and wave reflections both in healthy subjects and in
hypertensives [3-7]. As far as coffee is concerned, we have shown
that habitual coffee consumption is associated with increased
aortic stiffness and wave reflections in healthy subjects [8]. In
hypertensive patients, coffee consumption was associated with
increased wave reflections but not with aortic stiffness [9]. This
finding denotes that coffee leads to vasoconstriction of medium and
small-sized arteries ; however, regarding large arteries,
hypertension “exhausts” any stiffening effect, rendering the aorta
of hypertensive patients unaffected by coffee. There are
substances, other than caffeine, in coffee that could have an
effect on vascular function. In preliminary studies we have shown
that coffee increases arterial stiffness more than its contained
caffeine and that de-caffeinated coffee increase also arterial
stiffness to a certain extent (Vlachopoulos C, et al, unpublished
data). In line with this, there are studies that have shown that
de-caffeinated coffee augments blood pressure and muscle
sympathetic nervous activity [10].
In contemporary lifestyle, smoking is very frequently combined
with coffee drinking and studies have shown that smoking and
caffeine have an unfavorable interaction on blood pressure and
cardiovascular risk. The effect of smoking on arterial stiffness
and wave reflections is not only additive to that of caffeine, but
also synergistic. The combined detrimental effect of these habits
is greater than the sum of the effect of each of them alone, both
on an acute, and a chronic basis (figure 1) [5].
Caffeine exerts its main cardiovascular effects through the
antagonism of adenosine and the release of catecholamines, both
resulting in vasoconstriction. Furthermore, chronic coffee
consumption is associated with increased inflammatory markers,
another possible way by which coffee may induce vascular
dysfunction [11].
Table I Summary of available data on nutrition and
arterial function
|
Nutritional element
|
Main Findings
|
Areas for further investigation
|
|
ARRAY(0x21bf14)
|
|
Coffee-Caffeine
|
- Increase in AS and WR both acutely and chronically
- Synergistic effect with smoking
|
Need clarification : cut-offs of consumption, effect of other
coffee ingredients
|
|
ARRAY(0x237a8c)
|
|
Tea
|
Only acute studies. Increase in WR both with black and green tea.
Neutral effect on AS (green), short-lasting increase in AS
(black)
|
- Chronic effect to be investigated.
- Mechanisms to be elucidated (caffeine vs. flavonoids)
|
|
ARRAY(0x23963c)
|
|
Cocoa/Chocolate
|
Decrease in AS (chronically) and in WR (chronically, acutely)
|
- Ideal dose not known
- Effect of milk chocolate?
- Although effects are flavonoid-related, exact mechanisms to be
elucidated
|
|
ARRAY(0x239ae0)
|
|
Alcohol
|
Decrease in AS and WR
|
- Most cross-sectional studies do not discriminate between
drinks
- Need investigation : alcohol or flavonoids
responsible?
- Differential effect of red wine not established
- Mechanisms to be elucidated
|
|
ARRAY(0x23c450)
|
|
Salt
|
- Positive association with AS in cross-sectional studies
- Beneficial effect of sodium restriction (intervention
studies)
|
Mechanisms to be elucidated
|
|
ARRAY(0x23cd28)
|
|
- In most studies obesity is associated with increased AS,
whereas in some with decreased
- Central obesity most likely detrimental
- Weight loss improves AS (independently of the type of
diet)
|
- Discrepant results of studies to be reconciled
- Mechanisms to be elucidated
- Pressure-dependent, or -independent effect?
|
Tea
Although not all studies agree, tea consumption has been associated
with decreased cardiovascular risk. The possible beneficial effect
is mainly attributed to its high flavonoid content. Indeed, tea is
rich is flavanols called catechins, found in monomers in green tea,
and in dimers or polymers in black tea. This difference between the
two types of tea is due to fermentation processes that result in
partial oxidation of catechins in black tea.
Tea consumption has an acute and short-term (i.e. one month)
beneficial effect on endothelial function. As is the case with
cardiovascular risk, the beneficial effect of tea on endothelial
function is attributed to its flavonoid content. To date, only
acute studies on arterial stiffness and wave reflections are
available. The effect of tea on aortic stiffness and wave
reflections appears to be complex. As we have shown, both black and
green tea increase acutely wave reflections in normal subjects
[12]. This effect becomes evident promptly after tea consumption
(30 minutes), which is actually the time that it takes caffeine to
absorb. On the other hand, the effect of tea on aortic stiffness is
less straightforward. Green tea has no significant effect, whereas
black tea increases aortic stiffness for less than 2 hours. For
comparison, the same amount of caffeine contained in black tea,
when ingested alone, has a pronounced effect on aortic stiffness
and wave reflections that lasts for 3 hours (figure 2). A unifying
explanation is that caffeine contained in tea increases arterial
stiffness. Flavonoids, which notably take more time than caffeine
to absorb (90-120 min) have a counterbalancing beneficial
effect resulting in a total neutral effect in arterial stiffness
with green tea (high concentration in flavonoids) and a delayed
neutral effect with black tea (lower concentration in
flavonoids).
Cocoa and chocolate
Cocoa and chocolate, and especially dark chocolate, are rich in
flavonoids, mainly proanthocyanidins. Habitual chocolate
consumption is inversely associated with blood pressure, an effect
observed both in prehypertensive or stage I hypertensive subjects
[13] and in the elderly [14]. It has also been associated with
decreased cardiovascular risk [14]. Its blood-lowering effect was
first noted in Kuna Indians who live in isolation, drink large
amounts of cocoa, and have very low prevalence of hypertension.
When they migrate to an urban area their blood pressure rises,
denoting a protective effect of environmental/nutritional factors
(most likely cocoa) in their island of origin.
As regards chronic consumption, we showed in a cross-sectional
study that chocolate consumption is inversely associated with
aortic pulse wave velocity and wave reflections in healthy
subjects. Consumption of as little as 5 grams of cocoa (i.e. the
cocoa content of approximately 12 grams of chocolate) per day was
associated with a significant decrease in carotid-femoral pulse
wave velocity and in augmentation index. Furthermore, increasing
intake of chocolate is associated with a decrease of central
(aortic) systolic pressure and of central pulse pressure, but not
of peripheral (brachial) pressure, denoting that its beneficial
effect is not always evident when only peripheral pressures are
measured (figure
3) [15].
While milk chocolate is the type most widely consumed, most
intervention studies on the effect of cocoa on vascular function
have used cocoa and dark chocolate due to the high flavonoid
content. Both exert a beneficial acute and short-term effect on
endothelial function, as it has been shown both in healthy subjects
and in subjects with cardiovascular risk factors, or cardiovascular
disease. Dark chocolate results acutely in a decrease in wave
reflections in normal individuals [16]. Aortic stiffness is not
largely affected by acute chocolate consumption, while a tendency
to decrease at a later stage (3 hours or more) begins to show [16].
These taken together, imply that cocoa exerts a vasodilatory effect
on small and medium size arteries possibly due to increased
flavonoid-related NO bioavailability and/or increased prostacyclin
production. The effect of milk chocolate is not known. Milk
chocolate contains much less flavonoids than dark chocolate, and
furthermore, flavonoids are absorbed to a lesser degree when milk
is present. Accordingly, effects are anticipated to be similar,
although not necessarily identical.
Alcohol and alcoholic drinks
Moderate alcohol consumption is associated with decreased
cardiovascular risk. The effect is not clearly related to specific
alcoholic beverages, although it is supported that wine, and
especially red, is more beneficial. This argument has been used to
explain the French paradox, according to which France suffers
relatively low incidence of coronary heart disease, despite the
adoption of a diet relatively rich in saturated fats.
A J- or U-shaped curve has been demonstrated between alcohol
consumption and aortic stiffness and wave reflections both in men
and in women [17-20]. Most cross-sectional studies on the effect on
arterial function do not discriminate between alcoholic drinks.
Possible mechanisms involved include increase in high density
lipoprotein cholesterol, while, interestingly enough, the
inflammatory effect of alcohol shows a U-shaped behaviour. The
effect of alcohol on endothelial function is not so clear.
Experimental data suggest that moderate alcohol consumption
increases NO production, while heavy alcohol drinkers have impaired
endothelial function. We have shown that the acute effect of pure
alcohol is neutral ; the vasodilation induced both in resting
and hyperemic diameter of the brachial artery results in a
non-significant change in flow-mediated dilatation [21].
The high flavonoid content of red wine is due to the
fermentation process which allows the red grape juice to remain in
contact with the seeds and skins. Red wine decreases aortic
stiffness and wave reflections acutely. Studies with de-alcoholized
wine have shown that part of the effect is due to alcohol-induced
vasodilation (figure
4) [19], and part to the high flavonoid content [22]. The
short-term (6 weeks) effect of red wine has been recently studied
in postmenopausal women. Neither red wine, nor de-alcoholized red
wine induced any changes in wave reflections and central
hemodynamics [23]. As regards endothelial function, in-vitro
studies have shown that red wine may enhance nitric oxide (NO)
production and inhibit endothelin-1 synthesis through an
antioxidant effect. In addition, in-vivo studies have indicated a
significant vasodilation, possibly through increased production of
NO after regular or de-alcoholized red wine consumption [22].
Other foods and vitamins
The effect of soy, rich in isoflavones, on blood pressure is
controversial. There are several reports demonstrating diverse
results, from a small pressor effect to a lowering effect in
various population groups. Isoflavones, found not only in soy but
also in red clover and other plants, have been shown to reduce
systemic arterial compliance and aortic pulse wave velocity when
given for a period of 5-10 weeks in men and in postmenopausal women
[24-26]. On the other hand, soy protein with isoflavones has been
found to have a neutral effect on aortic stiffness in hypertensives
[27].
The n-3 fatty acids eicosapentaenoic acid and docosahexaenoic
acid found in fish, beyond the beneficial effect they exert on
blood pressure, they also exert a beneficial effect on arterial
stiffness [28].
Garlic consumption has been associated with lower blood
pressure, although there is no consistency in the results of all
studies. Chronic garlic powder intake attenuated age-related
increases in aortic stiffness in one study [29]. Finally, vitamin C
(ascorbic acid) and vitamin E seem to favourably affect arterial
elastic properties [30].
Salt
Salt-sensitive hypertensives have increased arterial stiffness
compared to salt-resistant subjects with the same blood pressure
levels [31]. High salt intake has been associated with increased
aortic stiffness in the general population [32] and in normotensive
adults [33]. High salt diet results in a decrease in femoral
distensibility in diabetic subjects compared to non-diabetics,
which is reversed with angiotensin converting enzyme inhibition
[34].
Sodium restriction reduces blood pressure and it was recently
demonstrated in prospective randomized trials that sodium
restriction reduces cardiovascular events in prehypertensive
subjects [35]. A relatively brief period of sodium restriction
decreases arterial stiffness. The same effect has been observed
promptly, just one week after sodium restriction, in older adults
with systolic hypertension [36].
It has been suggested that salt intake has a
pressure-independent effect on arteriolar tone and arterial wall
properties. The detrimental effect of high sodium consumption on
arterial stiffness may be attributed, at least partly, to
endothelial impairment. Furthermore, and probably as an additional
consequence of the endothelial dysfunction, structural changes in
the arterial wall occur, that further deteriorate elastic
properties.
Obesity-weight loss
Obesity, and especially central (abdominal), is associated with
increased aortic stiffness, whereas the effect on other vascular
beds may differ [37, 38]. The effect on wave reflections is not
well-defined. The negative impact of obesity on arterial stiffness
has been observed even in children [39] and adolescents.
Importantly, in a cross-sectional study with prospective analysis
it was found that truncus subcutaneous fat accumulation during
adolescence was associated with increased central arterial
stiffness at the end of the follow-up (age 36) [40]. An important
pathophysiological mechanism linking central obesity and vascular
dysfunction is the production of adipocytokines, with detrimental
metabolic effects and an inflammatory stimulation.
Changes in weight affect arterial stiffness. While weight gain
increased large-artery stiffness, weight loss had the opposite
effect in a 2-year follow-up [41]. An improvement in aortic
distensibility was observed with weight reduction after bariatric
surgery (gastric bypass) in morbidly obese individuals [42]. The
beneficial effect of weight loss has been demonstrated to be
independent of the diet (meat- or plant-based) [43]. The
improvement in arterial elastic properties observed with weight
loss are largely explained by the concomitant reduction in blood
pressure [43] ; however, the reduction in aortic pulse wave
velocity observed with weight loss was independent of blood
pressure changes in one study [41].
In conclusion, the effect of nutrition or arterial function has
a varying but significant taste. Given the important
pathophysiological and risk-predictive role of arterial stiffness
and wave reflections, part of the cardiovascular benefits of
healthy nutritional habits could be mediated by an improvement of
arterial function. Accumulating evidence of this sort, further
enhance the scientific basis for advocating the adoption of a
healthy lifestyle, an important component of which is
nutrition.
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