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The Journal of Clinical Hypertension logoLink to The Journal of Clinical Hypertension
. 2007 May 17;9(6):460–467. doi: 10.1111/j.1524-6175.2007.06625.x

Statins and Blood Pressure: Is There an Effect or Not?

Pantelis A Sarafidis 1, Angeliki I Kanaki 1, Anastasios N Lasaridis 1
PMCID: PMC8109905  PMID: 17541332

Abstract

In addition to the lipid‐lowering effects of statins, several basic and clinical studies in recent years have examined the effects of these agents on other cardiovascular parameters. Some of these studies investigated the general impact of a statin on blood pressure (BP) among various other factors, while others were specifically designed to determine this effect. Data from animal studies are conflicting but the majority of human studies in the field report a beneficial effect, and most available statin compounds are reported to lower BP levels. Recent clinical studies using ambulatory BP measurements support these findings. Although the exact actions of statins involved in this effect are unknown, several possible mechanisms can be hypothesized. This review summarizes existing data on the effect of statins on BP, aiming to give an overview of the current knowledge and to provide perspectives for future research in the field.

3‐Hydroxy‐3‐methylglutaryl coenzyme A (HMG‐CoA) reductase inhibitors or statins are oral hypolipidemic agents used in the treatment of elevated total cholesterol and low‐density lipoprotein (LDL) cholesterol levels. Statins act through inhibition of HMG‐CoA reductase, a rate‐limiting enzyme that catalyzes the conversion of HMG‐CoA to mevalonate, which is a precursor of sterols, including cholesterol. 1 In addition to inhibiting cholesterol synthesis, statins also increase the number of LDL receptors on the hepatic cell surface. 2 These actions result in the decrease of intermediate‐density lipoprotein and very‐LDL cholesterol levels. 3 Variable increases in high‐density lipoprotein cholesterol and apolipoprotein A‐I levels are also observed with statin therapy. 4

Several clinical trials have demonstrated that statins are helpful in the primary and secondary prevention of adverse cardiovascular events. 5 , 6 , 7 This beneficial effect may not only be related to their lipid‐lowering effects but to additional actions, such as reduction of vascular inflammation, 8 decrease of arterial stiffness, 9 improvement of endothelial function 10 and insulin sensitivity, 11 reduction of oxidant stress, 12 inhibition of vascular smooth muscle cell (VSMC) migration and proliferation, 13 and inhibition of platelet adhesion. 14 Several animal and human studies have also evaluated the effect of statins on blood pressure (BP). Data from animal studies are conflicting; several studies have been positive but others have reported the absence of any effect of statins on BP. 15 , 16 The majority of human studies examined changes in BP levels along with other parameters; only a few were specifically designed to determine the effect of statins on BP, most of which had positive results. The aim of this review was to summarize the existing clinical data on the effect of statins on BP.

SEARCH STRATEGY

A systematic literature search of MEDLINE/PubMed and EMBASE databases was performed to identify English‐language original articles in humans published from 1966 until November 2006 that reported data on the effects of statins on BP. Search terms used were “statin,”“statins,”“HMG‐CoA enzyme inhibitor,”“lovastatin,”“pravastatin,”“simvastatin,”“atorvastatin,”“fluvastatin,”“cerivastatin,” and “rosuvastatin,” with “blood pressure” and “hypertension.” Reference lists of identified articles were also evaluated for additional relevant papers and information. Original studies using the above statins that either examine BP levels among other parameters or aim specifically to determine the effect of a statin on BP and provide information about this effect were included.

EFFECTS OF STATINS ON BP LEVELS

Data from Human Studies Using Office BP Measurements

Lovastatin. The first study to report the effects of lovastatin on BP in humans was part of a multicenter open‐label study on the efficacy and tolerability of lovastatin in patients with nonfamilial primary hypercholesterolemia published 14 years ago. 17 As shown in Table I, in a subgroup of 213 hypertensive participants in the original study population, no significant effect on office diastolic BP (DBP) was noted after 6 months of lovastatin treatment in dosages from 20 to 80 mg/d. In a subsequent study, Sung and colleagues 18 examined the effects of 6 weeks of lovastatin treatment on BP and BP reactivity to stress in 37 normotensive and hypercholesterolemic patients and 33 normolipidemic controls. All participants were given a standard mental arithmetic test, which was repeated in 26 of the hypercholesterolemic patients at the study's end. Lovastatin was associated with a nonsignificant decrease in resting BP but with a significant decrease in systolic BP (SBP) during the mental arithmetic test.

Table I.

Studies on the Effects of Statins on BP Levels Using Office Measurements

Study Patient Condition No. of Participants Regimens Compared Duration Mean Effect on SBP/DBP vs Baseline in the Statin Groups, mm Hg
D'Agostino et al 17 Hypercholesterolemia, hypertension 213 20–80 mg Lo 6 mo NA
Sung et al 18 Normotension, hypercholesterolemia, or normolipidemia 70 20 mg Lo 6 wk −3/−2a−8b/−3c
O'Callaghan et al 19 Hypercholesterolemia, hypertension 25 20–80 mg Pra vs placebo 12 wk NA
Glorioso et al 20 Hypertension 30 20–40 mg Pra vs placebo 32 wk −8b/−5b
Ikeda et al 21 Hypertension 52 10 mg Pra vs 500 mg Prob 12 mo −4.7b/−0.7
Kawano and Yano 22 Hypercholesterolemia, hypertension, or normotension 82 10 mg Pra 3 mo −4b/−1d−1/−1e
Morgan et al 23 Hypercholesterolemia, hypertension 49 40 mg Sim vs placebo 3 mo −5.2/−3.5
Antonicelli et al 24 Hypercholesterolemia, normotension 20 10 mg Sim 12 mo NA
Sartor et al 25 Hypercholesterolemia, normotension, type 1 diabetes mellitus 25 10–20 mg Sim vs placebo 16 wk NA
Tonolo et al 26 Hypertension, type 2 diabetes mellitus 26 20 mg Sim vs Chol 20 mo −5/−7b
Danaoglu et al 27 Normolipidemia, hypertension 56 Lis + 20 mg Sim vs Lis 12 wk −38b/−23b,f−32b/−22b,g
Borghi et al 28 Hypercholesterolemia 1356 20–40 mg Sim vs 4–24 g Chol vs 400–800 mg Gem vs diet 5 y NA
Leibovitz et al 29 Hypercholesterolemia, normotension 17 10 mg Ator 20 wk −6b/−3b
Ferrier et al 30 Normolipidemia, hypertension 22 80 mg Ator vs placebo 6 mo −6b/−2b
Velussi 31 Type 2 diabetes mellitus, ≥1 cardiovascular risk factor 165 10–40 mg Ator 18 mo −2/−4b
Raison et al 32 Hypercholesterolemia, hypertension 23 10 mg Ator 12 wk −2.6/−0.1
Shinohara et al 33 Hypercholesterolemia, type 2 diabetes mellitus 22 10 mg Ator 6 mo −4/−2
Jarai et al 34 Hypercholesterolemia, hypertension 49 20 mg Flu 12 wk −5.0b/−2.0b
Derosa et al 35 Hypercholesterolemia, obesity 99 80 mg Flu vs Orl vs 80 mg Flu+Orl vs placebo 12 mo −6b/−4b,h−9b/−6b,i
Sposito et al 36 Hypercholesterolemia, hypertension 70 ACEI + 10 mg Pra or 20 mg Lo vs ACEI 16 wk −23b/−19b,f−12b/−15b,g
Borghi et al 37 Hypercholesterolemia, hypertension 41 10–40 mg Pra or 10–40 mg Sim vs diet 3 mo −18.2b/−10.5b
Ichihara et al 9 Hypercholesterolemia, hypertension 85 10 mg Pra vs 5 mg Sim vs 20 mg Flu vs no statin 12 mo −2/+2j−3/−2k−1/+1h
Abbreviations: BP, blood pressure; SBP, systolic BP; DBP, diastolic BP; Lo, lovastatin; NA, not applicable; Pra, pravastatin; Prob, probucol; Sim, simvastatin; Chol, cholestyramine; Lis, lisinopril; Gem, gemfibrozil; Ator, atorvastatin; Flu, fluvastatin; Orl, orlistat; ACEI, angiotensin‐converting enzyme inhibitor. aResting blood pressure change. bSignificant change vs baseline levels or the other group compared. cBP change during mental arithmetic test. dBP change in hypertensive subjects. eBP change in normotensive subjects. fBP change in the statin + ACEI group. gBP change in the ACEI group. hBP change in the Flu group. iBP change in the Flu + Orl group. jBP change in the Pra group vs baseline. kBP change in the Sim group vs baseline.
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Pravastatin. In a study specifically designed to determine the short‐term effects of pravastatin on BP, O'Callaghan and associates 19 randomized 25 hypertensive patients with hypercholesterolemia who received background antihypertensive therapy of 20 to 80 mg pravastatin or placebo for 12 weeks. Pravastatin treatment reduced total and LDL cholesterol but did not affect office SBP or DBP. In a double‐blind crossover study, Glorioso and colleagues 20 randomized 30 participants with moderate hypercholesterolemia and untreated hypertension to pravastatin 20 to 40 mg/d or placebo. In the 25 participants who completed the 32‐week trial, pravastatin was associated with significant reductions of SBP (−8 mm Hg), DBP (−5 mm Hg), and pulse pressure (−3 mm Hg) compared with placebo. Pravastatin also blunted the BP increase induced by the cold pressor test and reduced the level of circulating endothelin 1. In another crossover study, 52 hypertensive patients who underwent long‐term treatment with antihypertensive drugs were randomly treated with pravastatin 10 mg/d or probucol for 6 months and vice versa for another 6 months. 21 Pravastatin treatment produced a significant reduction of about 5 mm Hg in SBP levels, whereas probucol did not affect BP. A recent report retrospectively analyzed data from a non‐placebo‐controlled study of 38 normotensive and 44 hypertensive hypercholesterolemic patients treated with pravastatin (10 mg/d) for 3 months. 22 Compared with baseline, statin treatment significantly decreased SBP (4 mm Hg) in hypertensive but not in normotensive subjects, without affecting DBP.

Simvastatin. Several trials in humans have reported data on the effect of simvastatin on BP. One study randomly allocated 49 hypercholesterolemic and hypertensive patients to simvastatin up to 40 mg/d or placebo. 23 After 3 months of treatment, simvastatin was associated with nonsignificant reductions in BP (5.2/3.5 mm Hg) compared with placebo. In another study, simvastatin 10 mg was added in 20 elderly normotensive hypercholesterolemic patients for 12 months and had no effect on BP. 24 Similarly, in 25 normotensive hypercholesterolemic patients with insulin‐dependent diabetes who received either simvastatin 10 to 20 mg/d or placebo, simvastatin did not affect BP after 16 weeks of treatment. 25

In a crossover study aiming to evaluate the effects of simvastatin on BP and urinary albumin excretion (UAE), Tonolo and colleagues 26 randomized 26 hypertensive patients with type 2 diabetes and microalbuminuria to simvastatin (20 mg/d) or cholestyramine (6 g every 8 hours) for 20 months. Although both drugs produced similar reductions in lipid parameters, only simvastatin significantly reduced DBP as well as UAE. Another study evaluated the effects of the angiotensin‐converting enzyme (ACE) inhibitor lisinopril, alone and in combination with simvastatin, on BP and endothelial function in 56 hypertensive normolipidemic patients. 27 After 12 weeks of treatment, the lisinopril/simvastatin combination reduced BP by 38/23 mm Hg; the reduction was 32/22 mm Hg in lisinopril‐treated participants. However, no between‐group comparison was reported. Borghi and colleagues 28 evaluated the effect of different lipid‐lowering strategies on BP in patients with hypercholesterolemia who were enrolled in the Brisighella Heart Study. In that study, 1356 subjects were randomly treated for 5 years with one of the following lipid‐lowering regimens: low‐fat diet, cholestyramine, gemfibrozil, or simvastatin. For patients receiving antihypertensive medication, the dosage was maintained unchanged for the whole duration of the study in 93%, whereas in the remaining 7% it was adjusted according to the extent of BP control. Patients were divided into quartiles according to baseline SBP. A significant decrease in BP was observed in the 2 upper quartiles of SBP with all the above‐mentioned lipid‐lowering regimens; this was greater in simvastatin‐treated patients compared with patients treated with nonstatin drugs.

Atorvastatin. The first relevant study aimed at determining the effects of atorvastatin on arterial compliance included 17 normotensive hypercholesterolemic patients. 29 All patients received atorvastatin at a starting dose of 10 mg/d, subsequently adjusted to achieve LDL cholesterol levels <100 mg/dL. After 20 weeks of treatment, atorvastatin reduced office BP by 6/3 mm Hg, in addition to improving lipid profile and small artery compliance. This study was not placebo‐controlled. Ferrier and colleagues 30 investigated the effects of intensive cholesterol reduction with atorvastatin on large artery stiffness and BP in 22 normolipidemic patients with isolated systolic hypertension. Following a crossover design, patients were assigned to atorvastatin 80 mg/d or placebo and vice versa for 6 months. Atorvastatin improved lipid levels and systemic arterial compliance and significantly reduced SBP by 6 mm Hg and DBP by 2 mm Hg compared with placebo.

Velussi 31 assigned 165 patients with type 2 diabetes and at least 1 other major cardiovascular risk factor to atorvastatin ranging from 10 mg to 40 mg/d for 18 months. At the study's end, atorvastatin had improved lipid parameters, DBP, UAE, and fibrinogen levels. The beneficial effects of atorvastatin on BP were not apparent in a placebo‐controlled study in 23 hypertensive patients with hypercholesterolemia, which aimed primarily to evaluate the effect of this drug on aortic stiffness. 32 After 12 weeks of treatment, 10 mg of atorvastatin did not lower BP. This was also the case in a study investigating the effect of atorvastatin on regional arterial stiffness. 33 Twenty‐two patients with hypercholesterolemia and type 2 diabetes were treated with atorvastatin 10 mg/d. After 6 months, small but nonsignificant reductions in BP were observed, although arterial stiffness of leg arteries was improved.

Fluvastatin. The effect of fluvastatin on BP was evaluated in a study conducted in 49 hypertensive hypercholesterolemic patients. Participants were originally placed on a lipid‐lowering diet for 8 weeks and then treated with fluvastatin 20 mg/d for another 12 weeks (without placebo control). At the end of this period, fluvastatin was associated with significant decreases in both SBP and DBP (−5/−2 mm Hg). 34 Another study assigned 99 obese patients with hypercholesterolemia to treatment with orlistat, 120 mg tid, 80 mg fluvastatin, a combination of the 2 drugs, or placebo for 12 months. Similar significant reductions in BP of 6/4 mm Hg compared with baseline were observed in fluvastatin‐ and orlistat‐treated patients, while in the fluvastatin/orlistat group the BP reduction was 9/6 mm Hg. 35

Different Statins. In one study investigating the BP‐lowering effects of an ACE inhibitor (enalapril or lisinopril) alone and in combination with a statin (pravastatin or lovastatin), 36 combination treatment resulted in greater reductions in BP compared with the ACE inhibitor alone; however, only the difference in DBP was statistically significant. In another study from Borghi and colleagues, 37 41 hypertensive hypercholesterolemic patients receiving antihypertensive treatment were assigned to pravastatin or simvastatin for 3 months and were compared with controls undergoing antihypertensive treatment combined with a low‐fat diet. Significantly greater reductions were observed in statin‐treated patients for both SBP (−18.2 mm Hg) and DBP (−10.5 mm Hg). More recently, Ichihara and colleagues 9 randomized 85 hyperlipidemic hypertensive patients receiving background antihypertensive therapy to either 10 mg of pravastatin, 5 mg of simvastatin, 20 mg of fluvastatin, or nonstatin hypolipidemic treatment. After a 12‐month treatment period, none of these 4 regimens significantly affected BP compared with baseline.

Data from Human Studies Using Ambulatory BP Measurements

Most studies have used office BP measurements to examine the effect of statins on BP; however, since ambulatory BP monitoring (ABPM) has many advantages over office BP monitoring (eg, higher accuracy and reproducibility, independence of the white coat effect, determination of BP during everyday activities, sleep), 38 , 39 ambulatory BP data may provide more reliable information to determine small changes in BP after a drug treatment, as in the case of statins.

In the first of the studies using ABPM, 23 hypertensive hypercholesterolemic patients were given open‐label treatment with fluvastatin 40 mg/d for 12 weeks (Table II). 40 At the end of treatment, significant reductions in SBP/DBP of 6.2/5.3 mm Hg were noted. This study did not involve a comparison group, however, and was unblinded. Subsequently, Magen and associates 41 randomized 48 hyperlipidemic patients whose BP was inadequately controlled on maximal doses of 3 antihypertensive drugs to atorvastatin 20 mg/d, vitamin C, or placebo. After 8 weeks of treatment, atorvastatin not only improved lipid profiles but was also associated with reductions in SBP (−13.7 mm Hg) and DBP (−7.8 mm Hg) compared with baseline and an improvement in flow‐mediated dilatation in the brachial artery. In another study, 50 hypertensive dyslipidemic 42 participants were assigned to open‐label treatment with atorvastatin 20 mg/d or diet alone for 8 weeks; at the study's end, significant reductions in BP (−5.1/−5.2 mm Hg) were observed in statin‐treated patients, which were sustained in both daytime and nighttime periods.

Table II.

Studies on the Effects of Statins on BP Level Using Ambulatory Measurements

Study Patient Condition No. of Patients Regimens Compared Duration Mean Effect on SBP/DBP vs Baseline in the Statin Groups, mm Hg
Abetel et al 40 Hypercholesterolemia, hypertension 23 40 mg Flu 12 wk −6.0a/−5.0a
Magen et al 41 Hypercholesterolemia, hypertension 48 20 mg Ator vs vitamin C vs placebo 8 wk −13.7a/−7.8a
Kanbay et al 42 Hypercholesterolemia, hypertension 50 20 mg Ator vs diet 8 wk −5.1a/‐5.2a
Terzoli et al 43 Hypercholesterolemia, hypertension, or normotension 74 10–20 mg Pra or 10–20 mg Sim or 5–10 mg Ator vs Lec 8 wk −5.7a/−3.5a,b−0.7/−1c Abbreviations: BP, blood pressure; SBP, systolic BP; DBP, diastolic BP; Flu, fluvastatin; Ator, atorvastatin; Pra, pravastatin; Sim, simvastatin; Lec, soy lecithin. aSignificant change vs baseline levels or the other group compared. bBP change in the group of hypertensives. cBP change in the group of normotensives.
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In a recent study, 74 hypertensive or normotensive hypercholesterolemic patients were assigned to statin therapy or control treatment for 8 weeks. 43 Statin therapy consisted of 10 mg to 20 mg simvastatin or pravastatin, or 5 mg to 10 mg atorvastatin, while control treatment consisted of 20 g of soy lecithin. At the end of treatment, statin therapy was associated with significant BP reductions of −5.7/−3.5 mm Hg compared with baseline in hypertensive subjects. In contrast to the aforementioned study, this change in 24‐hour BP was entirely the result of reduced daytime BP levels; no change in nighttime BP was noted. Further, no change in BP was observed in statin‐treated normotensive subjects or in lecithin‐treated patients.

Of note, all studies using ambulatory BP measurements have indicated a significant effect of statins on BP in hypertensive patients, although some were open‐label and not controlled. This suggests that statin treatment may be associated with reductions in 24‐hour BP of about 5 to 6 mm Hg, at least in patients with elevated BP. It should be emphasized, however, that these studies have limitations, the most important of which is the short follow‐up period, as well as the small number of patients and inadequate design. Thus, based only on these data, no definite conclusions should be made.

Meta‐Analyses With Statins

A recently published meta‐analysis on the effect of statins on BP provides additional information. In this analysis, Strazzullo and colleagues 44 included 20 randomized controlled trials in which concomitant antihypertensive treatment (if any) remained unchanged through follow‐up. Statin treatment was associated with a mean reduction in SBP of −1.9 mm Hg (95% confidence interval, −3.8 to −0.1) compared with placebo or control drug, along with a nonsignificant minor reduction in DBP of −0.9 mm Hg (95− confidence interval, −2.0 to 0.2). When the analysis was restricted to studies with higher BP levels at baseline and during follow‐up, there was a larger effect of statin treatment. Studies included in this meta‐analysis were heterogeneous, with different inclusion criteria and primary outcomes, as well as different design and comparators. In addition, the final sample size was limited, given that large outcome trials could not be used to this end because of reasons discussed below. Hence, these findings need to be carefully interpreted. The fact that they appear to indicate a small effect of statins on BP, however, should be considered.

Large Outcome Trials With Statins

Several multicenter clinical trials on the effects of statin treatment on cardiovascular morbidity and mortality have been published, some of which have included patients with hypertension. 5 , 6 , 7 , 45 , 46 , 47 , 48 These studies unfortunately cannot help to answer the question of whether there is a potential effect of statins on BP because they were not designed to this end. As a result, antihypertensive treatment did not remain unchanged throughout the long follow‐up periods. In particular, either antihypertensive medication was added or altered to achieve BP control during follow‐up 5 , 6 , 7 , 45 , 46 or the study followed a 2×2 design and the patients were also randomized to different antihypertensive regimens, which were titrated upward according to a specific protocol. 47 , 48 Overall, in all of these studies, BP changes resulting from alterations in antihypertensive agents would have masked a possible effect of statins on BP.

A recent post hoc subgroup analysis of the Cholesterol and Recurrent Events (CARE) trial, 49 examined whether pravastatin treatment affected office BP. At 3, 6, and 24 months after randomization to 40 mg of pravastatin or placebo, or at last follow‐up visit (median duration, 57.8 months), pravastatin was not associated with significant reductions in BP and did not reduce the adjusted risk of new‐onset systolic or diastolic hypertension. 50 The analysis was limited, however, by the post hoc nature and the highly selected population (patients who survived a myocardial infarction), 50 and its findings should be carefully interpreted.

POSSIBLE MECHANISMS OF BP LOWERING WITH STATINS

Although the pathophysiologic pathways through which statins might lower BP levels are generally unknown, several possible mechanisms can be hypothesized. Statins have been shown to contribute to the restoration of endothelial function by increasing nitric oxide production. This effect is evident even before significant reductions in serum cholesterol levels are observed. 51 , 52 It has been suggested that statins improve endothelial dysfunction not only by lowering LDL cholesterol levels but also through actions unrelated to their lipid‐lowering effects. These actions include up‐regulation of endothelial nitric oxide synthase expression, 53 reduction of plasma caveolin levels, 54 and decreased production of reactive oxygen species. 12 This improvement in endothelial function could be translated into an increase in arterial vasodilatation and, thus, might be related to decrease in BP levels. 15

In addition to the above, lipid lowering with statin compounds can beneficially affect the elastic properties of the arteries, because these agents have been shown to improve both small and large artery compliance. 9 , 29 , 30 This can be largely attributed to inhibition of VSMC migration and proliferation from statins, 13 , 55 which can attenuate the atherosclerotic and arteriosclerotic processes in the vascular wall. This improvement in arterial elasticity might contribute to BP reduction over time.

Other possible mechanisms through which these agents might influence BP levels include the decrease of endothelin 1, a potent vasoconstrictor; statins have been shown to inhibit the production of endothelin 1 from endothelial cells in vitro 56 and reduce plasma endothelin 1 levels in vivo. 20 Interference with actions of the renin‐angiotensin system can also be speculated on, as statins have been reported to down‐regulate angiotensin II type 1 receptor expression in VSMCs. 15 , 57

CONCLUSIONS

The effect of statins on various parameters of the cardiovascular system beyond plasma lipids has been a field of intensive research. BP is one of the less well studied among these cardiovascular factors. As quoted in the present review, the slight majority of human studies—including all the studies using ambulatory BP monitoring—show a favorable impact on BP, and the only meta‐analysis of the field indicates a small effect. Almost all of the statins used today in clinical practice have been shown to lower BP to some degree; several pathophysiologic mechanisms might be involved in this action.

A number of issues, however, do not allow for definite conclusions. A positive effect was not apparent in many of the studies described. Most did not evaluate the effect of a statin on BP as a primary end point; some were of short duration, small, open‐label, or not controlled, and only 4 used ambulatory BP measurements. Although most of the studies reported did not include BP changes as a primary end point and thus the decision on their publication was less related to BP changes, one should always take into consideration the possibility of publication bias; studies that show large and significant effects of statins on BP are more often published than others with smaller or insignificant effects. Further, post hoc findings of outcome trials with statins, although with some inherent limitations, question the beneficial effect on BP.

Overall, current evidence indicates that statins may have a small BP‐lowering effect. Few would possibly argue that even if this is true, it is not of clinical relevance since BP reductions of about 2 to 4 mm Hg are not clinically significant. Epidemiologic evidence in large numbers of people suggests, however, that even minor decreases in BP are associated with cardiovascular benefit in the long run (ie, a 2‐mm Hg decrease in SBP in midlife might result in a 7% reduction in coronary artery disease mortality and a 10% reduction in stroke mortality). 58 Thus, the small effect of statins might help to reduce cardiovascular risk. Future research in the field is needed, consisting of long‐term, controlled, randomized trials to elucidate the exact magnitude of the effect of statins on BP and background studies to clarify the mechanisms involved.

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