Current Hypertension Reports

, Volume 12, Issue 4, pp 282–289

Antihypertensive Effects of Aspirin: What is the Evidence?


    • Population Health SciencesUniversity of Wisconsin Medical School
  • Lina M. Vera
    • Population Health SciencesUniversity of Wisconsin Medical School
    • Departamento de Salud Publica, Universidad Industrial de Santander, Escuela de Medicina

DOI: 10.1007/s11906-010-0115-5

Cite this article as:
Bautista, L.E. & Vera, L.M. Curr Hypertens Rep (2010) 12: 282. doi:10.1007/s11906-010-0115-5


Nonsteroidal anti-inflammatory drugs are known to increase blood pressure and blunt the effect of antihypertensive drugs. Surprisingly, it has been suggested recently that aspirin lowers blood pressure and could be used for preventing hypertension. This review summarizes published data on the effects of aspirin on blood pressure. Trials suggesting that aspirin administered at bedtime lowers blood pressure are uncontrolled, unmasked, and potentially biased. They also conflict with cohort studies showing an 18% increase in the risk of hypertension among aspirin users. Fortunately, short-term use of aspirin does not seem to interfere with antihypertensive drugs. Regardless of its effect on blood pressure, low-dose aspirin effectively prevents cardiovascular events in patients with and without hypertension, but its benefits should be carefully weighed against a potential increase in the risk of adverse effects such as gastric bleeding and hemorrhagic stroke, as well as a small increase in the risk of hypertension.


Nonsteroidal anti-inflammatory agentsAspirinBlood pressureHypertensionAntihypertensive treatmentMeta-analysisDrug chronotherapy


Nonsteroidal anti-inflammatory drugs (NSAIDs) such as acetylsalicylic acid (aspirin) exert their pharmacologic effects by inhibiting the synthesis of prostanoids involved in pain signaling, smooth muscle cell relaxation and contraction, and inflammation modulation. Aspirin irreversibly acetylates a serine residue in the active site of prostaglandin H synthase (PGHS), also known as cyclooxygenase (COX), thereby blocking the entrance of arachidonic acid to the active site of the enzyme and inhibiting the synthesis of prostaglandins and thromboxane [1]. The COX-1 isoform, a constitutive enzyme found in most cells, is responsible for the synthesis of prostanoids required for homeostasis functions such as gastric protection, maintenance of renal blood flow, and regulation of platelet activation and aggregation [2]. COX-2, on the contrary, is undetectable in most cells and is induced by inflammatory stimuli. However, low levels of COX-2 are constitutively expressed in the macula densa and renal medulla and are important physiologic regulators of kidney function [3].

Aspirin is a commonly used drug. About 36% of adults in the United States who are 35 years of age or older (54 million) use aspirin daily or every other day, including 83% (13.8 million) of those with a history of cardiovascular disease [4] and 52% (24.6 million) of those with a diagnosis of hypertension [5]. Between 1999 and 2003, the use of aspirin increased 20% in the whole population and 12% in those with a history of cardiovascular disease [4].

The efficacy of aspirin in primary and secondary prevention of cardiovascular events has been well documented [6, 7]. However, short-term trials suggest that NSAIDs use could increase blood pressure (BP) and blunt the effect of antihypertensive drugs [8, 9]. It is uncertain whether similar increases occur in individuals taking aspirin. Because of the widespread use of aspirin and the strong association between BP and cardiovascular risk [10], even small aspirin-related increases in BP could result in a large disease burden. This review summarizes and discusses the published data on the potential effects of aspirin on BP in normotensive individuals, in nontreated hypertensive patients, in patients receiving antihypertensive drugs, and on the incidence of hypertension.

Search Strategy

A literature search was conducted in MEDLINE and the Cochrane Database, using the keywords “Blood Pressure” or “Hypertension” combined with “aspirin” or “NSAIDs.” The search was restricted to English-language articles reporting results of studies on adult humans (≥18 years of age). Studies in pregnant women were excluded. We identified additional studies by hand-searching references of original and review articles on this topic. When multiple reports were based on overlapping samples of participants, only the one with the largest sample size was included. We deliberately excluded those studies of NSAIDs that were included in two meta-analyses conducted in the early 1990s [8, 9].

The primary outcome measures were the difference in the change in systolic and diastolic BP in individuals receiving aspirin as compared with placebo and the relative risk of incident hypertension in users of aspirin versus nonusers. We abstracted data on the participant characteristics, dose and duration of aspirin use, control group, treatment assignment, and outcome. Whenever needed, depending on the data available, we estimated the average effect of aspirin on systolic and diastolic BP and on incident hypertension using a random-effect model [11].

Effect of Aspirin on BP in Normotensive Individuals

Hermida et al. [12, 13] assessed the effect of aspirin on BP in two studies of healthy individuals. In the first study [12], participants were randomly assigned to take 500 mg/day of aspirin at awakening (n = 18), during the afternoon (n = 26), or at bedtime (n = 11). After 1 week of treatment, no significant changes were observed in diastolic BP; systolic BP decreased significantly (−2.3 mm Hg; P = 0.006), but only in subjects receiving aspirin during the afternoon. Results from this study are hard to interpret because baseline BP levels were not reported and it is unlikely that they were comparable among treatment arms, considering the small sample size. More important, before-after changes in BP cannot be interpreted as aspirin effects unless they are compared with before-after changes in a control group.

In the second study [13], a group of 73 normotensive individuals and 18 participants with mild hypertension (clinic diastolic BP ≥ 90 and <110 mm Hg) received a 1-week course of placebo and a 1-week course of aspirin. Between 11 and 13 normotensive participants were randomly assigned to one of six groups defined by two doses of aspirin/placebo (500 and 100 mg/day) and three times of administration (awakening, afternoon, and bedtime). Four to eight mild-hypertensive individuals were assigned to 100 mg/day of aspirin or placebo at the same three times. Authors made no use of the control treatment in the analysis and reported only before-after changes in BP. To measure the effect of aspirin (100 mg/day) while accounting for its placebo effect, we conducted a meta-analysis of 24-hour-average BP data shown in figures in this article [13]. Overall, aspirin decreased systolic BP by 1.86 mm Hg (95% CI, −3.04 to −0.67) and seemed to have a stronger effect in those with mild hypertension than in those with normal BP (−3.56 vs −1.17 mm Hg; P = 0.06). Similarly, the reduction in systolic BP was larger when aspirin was administered in the afternoon (−1.78 mm Hg) or at night (−2.42 mm Hg), rather than on awakening (−1.09 mm Hg), but the trend failed to reach statistical significance (P = 0.20). On the other hand, aspirin lowered diastolic BP by 1.0 mm Hg (95% CI, −1.46 to −0.55; P = 0.001) and the effect was similar in normotensive and mild-hypertensive participants (−0.98 and −1.96 mm Hg, respectively; P = 0.43). Also, the decrease in diastolic BP was larger (but not significantly so) when aspirin was administered in the afternoon or at bedtime (−0.97 and −1.55 mm Hg, respectively) compared with on awakening (−0.49 mm Hg; P = 0.19). Unfortunately, a separate analysis for the group receiving 500 mg per day of aspirin was not possible because this dose was used only in normotensive individuals, resulting in only six treatment groups. Moreover, we decided against pooling the results for 500 and 100 mg per day because when administered at bedtime, the higher dose increased BP whereas the lower dose decreased BP. In summary, a placebo-controlled analysis of this study suggests that aspirin at 100 mg/day administered for 1 week decreases systolic BP by about 2 mm Hg and diastolic BP by about 1 mm Hg. The effect seemed to increase with higher BP, but it did not vary significantly with time of administration of aspirin.

Effect of Aspirin in Nontreated Hypertensive Individuals

Several recent trials from a single group of investigators suggest that low doses of aspirin administered at bedtime could significantly lower systolic and diastolic BP in patients with mild hypertension and prehypertension who are not taking antihypertensive medication [14, 15, 16•].

Hermida et al. [14] conducted a parallel trial in 328 untreated patients with mild hypertension (SBP 140–159 and DBP 90–99 mm Hg), who were randomly assigned to receive hygienic and dietary recommendations (HDR, n = 169), HDR plus 100 mg/day of aspirin on awakening (n = 77), or HDR plus 100 mg/day of aspirin at bedtime (n = 82). Investigators obtaining the BP measurements were blinded to the treatment assignments, but the patients were not. Six clinic BP measures were taken with validated automatic devices and ambulatory BP monitoring (ABPM) was performed with an oscillometric device (Spacelabs 90207; Spacelabs Healthcare, Issaquah, WA) at baseline and after 3 months of treatment. Mean baseline BPs (systolic/diastolic) were very similar in the three treatment groups: HDR alone, 146.8/85.1; aspirin on awakening, 146.2/84.4; and aspirin at bedtime, 147.2/85.9 mm Hg. The authors estimated the before-after change in BP means and concluded that aspirin administered at bedtime significantly reduced systolic and diastolic BP (6.8 and 4.6 mm Hg, respectively). However, before-after contrasts provide a valid measure of the effect of aspirin only under the questionable assumption that without treatment, BP would not have changed in these patients during the follow-up period.

To address the limitation of before-after comparisons, we used data shown on their Table 1 to compare the average clinic BP after intervention among treatment groups using a two-sample t-test [14]. Because the baseline BPs were almost identical in all the treatment groups, this approach provides a valid estimate of the effect of aspirin. Systolic BP increased 1.1 mm Hg (P = 0.29) and DBP increased 0.2 mm Hg (P = 0.44) when aspirin on awakening was compared with HDR. Also, systolic BP decreased 0.9 mm Hg and diastolic BP decreased 0.4 mm Hg (P = 0.67 and 0.62, respectively) when aspirin at bedtime was compared with HDR. When aspirin at bedtime was compared with aspirin on awakening, systolic and diastolic BP decreased 2.0 mm Hg (P = 0.83) and 0.6 mm Hg (P = 0.72), respectively. Therefore, the data on clinic BP do not support a BP-lowering effect of aspirin administered on awakening or at bedtime. Unfortunately, ABPM data were presented as separate figures that do not allow between-treatment formal comparisons. Nevertheless, the average 24-hour BP from these figures indicate that aspirin at bedtime decreased systolic and diastolic BP by 9.3 and 6.2 mm Hg, compared with aspirin on awakening. These rather large changes, which were partly due to an increase in BP in the group taking aspirin on awakening, contradict the lack of an aspirin effect in clinic BP.

The effect of the time of administration of aspirin was further studied by Hermida et al. [15] in a group of 257 patients with mild hypertension (systolic BP, 140–159 mm Hg; diastolic BP, 90–99 mm Hg), who were randomized to receive a 100 mg/day of aspirin on awakening (n = 126) or at bedtime (n = 131) for 3 months [15]. Results from this trial closely mimic those of the trial discussed above [14], and it is unclear whether the samples of the two trials overlap. Basically, clinic systolic BP (−2.9 mm Hg, P = 0.07) and diastolic BP (−0.3 mm Hg, P = 0.761) decreased with aspirin at bedtime, but not significantly. On the contrary, aspirin at bedtime lowered 24-hour average systolic and diastolic BP by 7.6 mm Hg (P < 0.001) and 5.5 mm Hg (P < 0.001), respectively. Unfortunately, BP changes in the group receiving aspirin at bedtime were not compared with BP changes in the group receiving aspirin on awakening.

In a more recent trial, Hermida et al. [16•] studied a sample of prehypertensive individuals (systolic BP, 120–139, and diastolic BP, 80–89 mm Hg), following the same methodology as in the previous studies [14]. A total of 124 patients were allocated to HDR, 61 to aspirin on awakening, and 59 to aspirin at bedtime. Baseline characteristics were similar among the treatment groups. After the intervention, clinic systolic BP was 6 mm Hg lower in patients receiving aspirin at bedtime than in those given aspirin on awakening (P < 0.001), whereas diastolic BP was only 1 mm Hg lower (P = 0.048). Corresponding reductions for 24-hour systolic and diastolic BP were 7 mm Hg (P < 0.001) and 5 mm Hg (P < 0.001). The inconsistency between the effect of aspirin at bedtime on clinic and ABPM diastolic BP in this and previous trials [14, 15] was not addressed by the authors. It is worth noticing that this discrepancy cannot be explained by differences in the methods used to measure clinic and ambulatory BP. First, plots presented by the authors clearly show a constant before-after reduction in systolic and diastolic BP through the awake period [14, 15, 16•]. Therefore, this reduction should have been apparent in clinic BP. Second, the discrepancy cannot be attributed to a lower precision in clinic measures, because the standard deviation of clinic-systolic BP was only 50% larger than that of diurnal ambulatory systolic BP (11.4 vs 7.3, respectively), and the corresponding standard deviations for diastolic BP were virtually identical (7.4 and 7.6). Of note, clinic BP in these studies was measured with validated automatic devices known to reduce observer error [14, 15, 16•].

The BP-lowering effect of aspirin reported by Hermida et al. [14, 15, 16•] is not only unexpected but also has important potential implications in the management of hypertension. Unfortunately, this finding is questionable, considering that it comes from short-term, uncontrolled, open-label trials [14, 15, 16•]. As stated above, estimates of before-after changes in BP do not provide a measure of the effect of aspirin beyond its placebo effect and rely on the unverifiable assumption that changes in BP are due only to treatment. Hermida et al. [15, 17] have argued against the need for a placebo arm in trials with ABPM. However, this argument is debatable [18]. Some studies suggest a lack of placebo effect on ABPM [19, 20], but others do not [21, 22]. For instance, Staessen et al. [21] have shown that 20–24% of the long-term changes in BP observed during active treatment could be attributed to placebo effects. Moreover, an 8-week trial in patients with mild to moderate hypertension showed a placebo effect of −6.4 and −3.5 mm Hg in 24-hour average systolic and diastolic BP [22]. In view of the uncertainty regarding this issue, rigorous testing of the effect of aspirin should have included a placebo control group.

Hermida et al. [17] also argued against the need for double blinding, as prospective, randomized, open-label, blinded end point (PROBE) trials [23] produce valid results [24]. However, PROBE trials emphasize the need for strictly defined, blinded measures of end points as a mean to minimize information bias [23]. In fact, successful PROBE trials, such as the Hypertension Optimal Treatment (HOT) trial [25], have included a placebo arm and robust methods to preserve the masking of the treatments. Although a recent meta-analysis of PROBE trials suggests that double blinding may not be needed in trials of antihypertensive drugs based on ABPM [24], it is worth noting that investigators involved in decisions about ABPM data quality and analysis in those trials were blinded to treatment assignment and (contrary to the trials of Hermida et al. [14, 15, 16•]) had no easy way to discover the assignment. Moreover, ABPM removes observer bias and expectation but not regression to the mean and participant-related factors that contribute to the placebo effect [26]. Briefly, the trials by Hermida et al. [14, 15, 16•] do not fulfill the strict requirement of blinding outcome evaluators, which characterizes successful PROBE trials.

The lack of a placebo control group in these trials [14, 15, 16•] made it almost impossible to mask the treatments and opened the opportunity for observer and participant biases. Treatment assignment was known to the patients and could have easily been discovered by investigators, intentionally or unintentionally, because patients were either receiving no drug treatment or aspirin at different times of day. Moreover, patients could have revealed information indicating treatment received even if instructed not to. Knowledge of treatment assignment could have led investigators to consciously or unconsciously introduce systematic differences in the way participants were informed, instructed, and evaluated. For instance, the effort expended in HDR instructions, as well as participants’ efforts in following these instructions, could have differed by treatment.

Also, without strict blinding, one cannot rule out that study participants may have inadvertently been induced to believe that taking aspirin at bedtime lowers BP. This effect could have occurred during the administration of consent, when participants should have been informed of the study objectives and hypothesis. Moreover, participants could have accessed scientific reports by themselves and learned about the presumed benefits of aspirin administered at bedtime. Of particular concern is that the device used for ABPM in these studies displays BP readings on a small screen. If the screen was not turned off, it could have altered the patient’s behavior and BP.

In summary, without a placebo group and effective masking of treatments, one cannot discard the idea that the BP-lowering effect of aspirin at bedtime in mildly hypertensive patients not receiving antihypertensive medication may be partly or fully a consequence of the participant’s and the investigator’s beliefs, behaviors, and hopes about the treatment [27•].

Effect of Aspirin on Blood Pressure in Patients Treated with Antihypertensive Drugs

Two meta-analyses of short-term randomized trials and one observational study have shown that NSAIDs can increase BP and antagonize the BP-lowering effect of antihypertensive drugs [8, 9, 28]. The most likely mechanism by which NSAIDs increase BP is the inhibition of the synthesis of vasodilator prostaglandins (PGI2 and PGE2) via inactivation of COX-1 and COX-2, which results in increased renal sodium and water retention [29]. The potential blunting of the effect of angiotensin-converting enzyme (ACE) inhibitors by NSAIDs has been of particular concern, because the BP-lowering effect of ACE inhibitors is partly mediated by an increase in the synthesis of vasodilator prostaglandins that results from decreased inactivation of bradykinin [30].

Similar to NSAIDs, aspirin could increase BP and blunt the effect of antihypertensive drugs by inactivating COX-1 and COX-2. This hypothesis has been tested in several short trials among patients with essential hypertension (Table 1) [3140]. None of these trials has shown a significant difference in the effect of antihypertensive drugs, including ACE inhibitors, in the context of treatment with varying doses of aspirin.
Table 1

Trials evaluating the effect of aspirin on blood pressure among patients receiving antihypertensive medication




Antihypertensive drug

Aspirin dosage

Change in effect of antihypertensive drug

Moore et al. [37]



Captopril 25–100 mg once

600 mg every 6 h


Smith et al. [34]

Crossover trial


Captopril for 2 wk

75 mg/d for 2 wk


Magagna et al. [31]

Crossover trial


Captopril/atenolol for 4 wk

100 mg/d for 4 wk


Tison et al. [38]

Parallel trial


Isradipine (n = 20) or nitrendipine (n = 19)

100 mg/d for 8 wk


Polónia et al. [35]

Crossover trial


Enalapril/nifedipine-GITS for 4 wk

100 mg/d for 2 wk


Boger et al. [40]

Crossover trial



100 mg/d for 7 days


Guazzi et al. [36]

Parallel trial


Enalapril/nifedipine-GITS for 5 d

100/300 mg/d


Nawarskas et al. [33]

Crossover trial


Enalapril/losartan for 2 wk

81/325 mg/d for 2 wk


Avanzini et al. [32]

Parallel trial



100 mg/d for 12 wk


Fisman et al. [39]



ACE inhibitors

100 mg/d and 500 mg/d for 1 wk each


aNormotensive women

GITS gastrointestinal therapeutic system.

Although they suggest that aspirin does not modify the effect of antihypertensive drugs, most of the trials in Table 1 had important methodologic limitations. First, all were based on small samples and were probably underpowered to detect small but clinically significant effects. Second, only short-term effects of such drug interactions could be measured in these trials, as the longest duration of treatment was 4 weeks. Third, the statistical analysis of these trials is questionable because within-subject effects were not disentangled from between-subjects effects and a valid causal contrast (aspirin vs placebo) was not estimated. More important, these short-term trials could provide important information on biologic mechanisms, but they should not be used for therapeutic decisions, as they provide no information on clinical outcomes.

The only trial that has evaluated the long-term effects of aspirin on BP in patients receiving antihypertensive medication is the HOT trial (N = 18,790) [25]. In a reanalysis of the HOT trial, Zanchetti et al. [41] found that 75 mg per day of aspirin for an average of 3.8 years resulted in minimal, nonsignificant increases in systolic and diastolic BP (0.6 and 0.3 mm Hg). Unfortunately, the HOT trial was not well suited to measure a potential effect of aspirin on BP because patients were randomized to achieving a predefined target diastolic BP. In this context, any aspirin effect should have been minimized, even if antihypertensive therapy were similar in the treatment and control groups.

In summary, short-term use of low doses of aspirin does not seem to modify the effect of antihypertensive drugs. These results are consistent with those from Pope et al. [9], who found a nonsignificant decrease of 1.76 mm Hg in mean arterial pressure (P = 0.80) in a meta-analysis of four studies with 39 hypertensive patients receiving more than 1.5 mg per day of aspirin for at least 6 weeks. Similarly, results from another meta-analysis (105 participants from 8 trials) showed that aspirin did not interact with antihypertensive drugs [8].

Effect of Aspirin on the Incidence of Hypertension

Evidence of a significant association between use of aspirin and the development of hypertension has come from several large, prospective cohort studies [4246, 47•, 48]. Dubach et al. [42] measured salicylate concentrations in three urine samples taken within a week in 1244 women 30–49 years old who were observed for 20 years. They found that women with salicylate in their urine were 1.3 times more likely to develop hypertension, but the increase was not statistically significant (P = 0.11) and was not adjusted for other risk factors. More recent studies have been based on self-reported use of aspirin and self-reported diagnosis of hypertension. Three of these studies have been conducted in women from the Nurse’s Health Study I and II cohorts [4345]; two others were in men from the Physician’s Health Study Cohort [46] and from the Health Professionals Follow-up Study cohort [47•]. Additionally, the effect of aspirin has been reported as part of a study on the effects of a selective COX-2 inhibitor on the incidence of hypertension [48]. The latter study (N = 51,444) used a database of electronic medical records of patients cared for by clinicians in a national network of outpatient practices to ascertain aspirin use and incident hypertension. We obtained a pooled average of the relative risks from these studies using a random-effects model and found that they were homogeneous (P = 0.18 for heterogeneity test) and that the use of aspirin at any dose or frequency increased the risk of hypertension by 18% (95% CI, 11–24%) (Fig. 1). Although we could not formally test it, there was a consistent dose-response relationship in all studies.
Fig. 1

Relative risk (RR) of incident hypertension related to aspirin use, from cohort studies. NHS—Nurses’ Health Study. For each study, the frequency of use of aspirin increases from bottom to top

Potential sources of bias should be carefully considered in interpreting cohort studies of the aspirin-hypertension association. First, the distribution of known and unknown risk factors could be different in aspirin users and nonusers and partly or fully explain the increase in risk of hypertension among aspirin users. However, these studies [4246, 47•, 48] adjusted for known risk factors for hypertension, excepting C-reactive protein level, a marker of mild, chronic inflammation that could also be associated with use of aspirin [49, 50]. A higher probability of detection of new cases of hypertension among users of aspirin could also explain the observed increased in risk, but this is unlikely, as an effect was not observed for other analgesic drugs or in subjects with comparable levels of physician contacts. Moreover, errors in self-reported diagnosis are unlikely to be related to the use of aspirin. Similarly, it is unlikely that errors in exposure measurement could explain the observed effect, because aspirin use was ascertained before occurrence of the outcome.

In summary, cohort studies suggest that regular use of aspirin results in a small increase in the risk of hypertension. However, there is considerable uncertainty regarding a dose-response relationship, threshold levels, minimum duration of exposure, time at risk of exposure effects, and whether exposure effects are reversible.


Currently available evidence regarding the effect of aspirin on BP in normotensive individuals is very limited. One small controlled trial suggests that low-dose aspirin (100 mg/day) administered for 1 week slightly decreases BP (2 mm Hg systolic and 1 mm Hg diastolic) [13]. In this study, the BP-lowering effect of aspirin seemed to increase with higher BP, but did not vary significantly with the time of administration of aspirin. Unfortunately, these findings have not been independently corroborated in other studies. More important, there seem to be no data on the long-term effects of aspirin on BP among normotensive individuals.

Several trials in patients with prehypertension and mild hypertension who were not receiving antihypertensive medication have shown significant before-after reductions in BP when 100 mg per day of aspirin were administered at bedtime [14, 15, 16•]. However, these were uncontrolled, open-label, short-term trials, and the BP-lowering effect of aspirin at bedtime could be partly or fully a consequence of participants’ and investigators’ beliefs, behaviors, and hopes about the treatment [27•]. Although the authors postulate that the decrease in BP related to aspirin at bedtime could be attributed to a reduction in the nocturnal peak of plasma renin activity and an enhancement in the bioavailability of nitric oxide [16•], these mechanisms cannot explain the increase in BP observed when aspirin was administered on awakening.

Multiple short-term trials also show that low doses of aspirin do not seem to modify the effect of antihypertensive drugs, including ACE inhibitors. These results are consistent with those from two previous meta-analyses [8, 9]. Although a large, long-term trial suggests that aspirin does not interfere with the effect of antihypertensive drugs, antihypertensive treatment was tailored to reach a predefined target BP, compromising the ability to detect significant interactions between aspirin and antihypertensive drugs [41]. Therefore, whether high doses or long-term use of aspirin could blunt the effect of antihypertensive drugs is still uncertain.

Prospective cohort studies consistently suggest that regular use of aspirin results in a small increase in the risk of hypertension (about 20%) [4246, 47•, 48]. Residual confounding due to unknown or unmeasured risk factors could explain the higher risk of hypertension among regular users of aspirin, but other sources of bias have been reasonably ruled out. However, there is considerable uncertainty regarding a dose-response relationship, whether there is a dose-threshold level or minimum duration of exposure, time at risk of exposure effects, and whether exposure effects are reversible.

Regardless of a potential effect on BP, low-dose aspirin (75–100 mg/day) is effective in preventing cardiovascular events in patients with and without a previous history of cardiovascular disease [6, 7]. The benefits of aspirin should be carefully weighed against a potential increase in the risk of undesirable effects such as gastric bleeding and hemorrhagic stroke, as well as a potential increase of 11–24% in the risk of hypertension. In contrast, a recent suggestion that aspirin administered at bedtime could be used to prevent the development of hypertension is unwarranted, as it is supported only by studies of questionable validity [16•]. Finally, there seems to be little reason for concern about the use of aspirin in treated hypertensive patients with normal kidney and cardiac function. In fact, short-term use of low-dose aspirin appears not to blunt the BP-lowering effect of antihypertensive drugs. More importantly, the results from the HOT trial strongly suggest that the relative benefit of aspirin therapy in preventing cardiovascular events is of similar magnitude in hypertensive and nonhypertensive patients [41].


No potential conflicts of interest relevant to this article were reported.

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