Comments and Opinions

Statin Treatment in Patients With Intracerebral Hemorrhage

Matthias Endres, MD; Christian H. Nolte, MD; Jan F. Scheitz, MD

E ver since the publication of the SPARCL trial (Stroke

Prevention by Aggressive Reduction in Cholesterol
Levels) in 2006, neurologists became aware of the fact that
statins may increase the risk for future intracerebral hem-
orrhage (ICH) in patients with previous ischemic stroke or
ICH.1,2 At the same time, observational studies reported an
increased risk for hemorrhagic transformation or even symp-
tomatic bleeding in ischemic stroke patients undergoing
thrombolysis who were pretreated with statins.3,4 As a con-
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(sudden) discontinuation is associated with increased mortal-
ity. In addition, even though statins may be associated with
a (modest) increased risk for future ICH, these effects may
have been overestimated and also must be weighed against the
well-known beneficial effects on vascular events and vascu-
lar mortality in individual patients. Late, PCSK9 (proprotein
convertase subtilisin/kexin type 9) inhibitors have been tested
in randomized clinical trials in patients at high vascular risk
including stroke patients and may evolve as an alternative cho-

sequence, many physicians were very careful to administer
statins in patients with ICH and often stopped statin medi-
cation immediately after hospital admission in those who
had been taking the medication before the event. In 2011,
Westover et al5 provided a Markov decision model that came
to the conclusion that statins should be avoided in patients
with a history of ICH, particularly in those cases with a lobar
location. In clinical practice, this often results in the some-
what counterintuitive situation that after an ICH, statins are
often permanently discontinued, whereas platelet inhibitors
or even oral anticoagulants are resumed depending on the
underlying comorbidity.6
Statins exert many pleiotropic effects in addition to choles-
terol lowering. These properties may contribute to both its pro-
tective effects and also some unwanted side effects, including
an increased risk for bleeding.7,8 On the other hand, however,
sudden discontinuation of statins may lead to rebound effects
which may impair vascular function and induce adverse clini-
cal effects in patients with acute vascular events.9–12 Some years
ago, we formulated the recommendation that statins should not
be paused and acutely discontinued in ischemic stroke patients
undergoing thrombolysis and inferred—based on only sparse
clinical data—that this probably also applies for patients after
acute ICH.13 In the meantime, a relevant number of research
articles including 2 systematic reviews have been published
and have addressed the issue of statin use after ICH.14–19 Most
of these data were not derived from randomized controlled
trials but rather from clinical cohorts, observations, or case–
control studies and must therefore be interpreted with caution.
The wealth of data, however, suggests that statin treatment may
in fact have a favorable impact on outcome after ICH, whereas
lesterol-lowering treatment in patients after ICH.20
Pleiotropic Effects of HMG CoA-Reductase
Inhibitors (Statins) and Mechanisms After
Sudden Discontinuation
Statins exert many cholesterol-independent, pleiotropic effects
that contribute to the beneficial effects but are also respon-
sible for some of the unwanted side effects (which include
myopathy, incidence of diabetes mellitus, but also increased
propensity for ICH). Most of the pleiotropic effects are medi-
ated via the main mechanism of action, that is, inhibition
of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA)
reductase activity.8 In particular, it has been demonstrated
that statins inhibit platelet activity21 and also interact with
the coagulation cascade, for example, by upregulating PAI-1
(plasminogen activator inhibitor-1) leading to a mild antico-
agulatory effect.22,23 On the other hand, there is good preclini-
cal evidence that the acute discontinuation of statin treatment
may lead to a pharmacological rebound effect which results
in increased oxidative stress and impaired vascular function.9
Through HMG CoA-reductase inhibition, statin treatment
leads to the accumulation of small G proteins, such as rho and
rac, in a nonisoprenylated, inactivated form in the cytosol. At
the same time, because of a negative feedback regulation, they
become upregulated and accumulate in the cytoplasm. At the
moment when statin treatment is discontinued, isoprenoids
such as geranylgeranylation or farnesylate become available,
bind, and activate small G proteins. In turn, these small G pro-
teins switch to an active and membrane-bound state leading to
overshoot activation of NADPH oxidase or downregulation of
endothelial nitric oxide synthase.9,10

Received September 5, 2017; final revision received October 23, 2017; accepted October 27, 2017.
From the Klinik für Neurologie mit Experimenteller Neurologie and Center for Stroke Research Berlin, Charité-Universitätsmedizin Berlin, Germany
(M.E., C.H.N., J.F.S.); DZHK (German Center for Cardiovascular Research), Berlin Site, Germany (M.E., C.H.N., J.F.S.); DZNE (German Center for
Neurodegenerative Disease), Berlin Site, Germany (M.E.); and Berlin Institute of Health, Germany (M.E., C.H.N.).
The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.
Correspondence to Matthias Endres, MD, Department of Neurology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117 Berlin, Germany. E-mail
matthias.endres@charite.de
(Stroke. 2018;49:00-00. DOI: 10.1161/STROKEAHA.117.019322.)
© 2017 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org DOI: 10.1161/STROKEAHA.117.019322

1
 2  Stroke  January 2018

There are many clinical studies to support the relevance
of these preclinical finding in patients with acute (cerebro)
vascular events.11,24 One randomized clinical trial reported an
increased likelihood of early neurological deterioration and
worse outcome in acute ischemic stroke patients in whom
statin medication was discontinued.12 Unfortunately, there
are no similar data from randomized studies in patients with
ICH. However, several observational studies demonstrated
an association between statin discontinuation and poor func-
tional outcomes in patients with acute ICH (summarized in
Table 1).18,25–27
Do Statins Increase the Risk for ICH or ICH
Recurrence?
Increased cholesterol and in particular low-density lipopro-
tein (LDL) cholesterol emerge only as modest risk factors
for ischemic stroke. This association only becomes more
robust when the subgroup of atherothrombotic/macroan-
giopathic ischemic stroke is analyzed.28,29 In any case, the
attributable risk of cholesterol/LDL cholesterol for ischemic
stroke is much lower than for myocardial infarction.29 Vice
versa, it has been demonstrated that low cholesterol levels
correlate with an increased risk for hemorrhagic stroke.28,30
However, it has been argued that some of this correlation
may be explained by other factors such as alcohol consump-
tion, liver disease, but also hypertension as comorbidities
in individuals with low cholesterol levels.30 Recently, in
a single-center, retrospective analysis, Phuah et al31 dem-
onstrated in 212 ICH cases versus 301 control individuals
that triglyceride and LDL cholesterol levels declined in
serum during 6 months immediately preceding ICH. On the
basis of this correlation, increased risk for ICH would be a

Table 1.  Summary of Studies on Statin Discontinuation, Inpatient Statin Use, and Outcome After ICH
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First Author, Duration

Reference Setting, Design ICH Patients (n) Statin Use (n) of FU Finding Miscellaneous
Discontinuation of statins and outcome after ICH
 Dowlatshahi Discontinuation
et al25 higher rate of poor
537 with prior
outcome: (mRS No longer significant after
Canadian Stroke Retrospective, statins, 29.4%
2466 6 mo score of >3): 2.4 excluding patients with
Network multicenter discontinued
(1.1–4.6) and palliative strategy
statins
mortality: aOR, 1.7
(1.1–2.6)
 Flint et  al18 Discontinuation
1160 with Maintained after
Kaiser Permanente Retrospective, reduced survival:
3481 cessation of statin 30 d correcting for DNR status
Northern California multicenter aOR, 0.16 (0.12–
use instituted within 24 h
0.21)
 Tapia-Perez 18/63 Discontinuation
Hypertensive or Retrospective,
et al26 447 discontinued; 30 d higher risk of death:
OAC-related ICH single center
45/63 continued aHR, 6.9 (2.1–23.1)
 Siddiqui Ethnic/Racial
Not significant after
et al27 Variations of Continuation lower
Prospective, 268 discontinued; propensity score
Intracerebral 2457 3 mo mortality: aOR, 0.11
multicenter 423 continued corrected for confounding
Hemorrhage (ERICH) (0.03–0.44)
by indication bias
Study
In-hospital use of statins and outcome after ICH
 Flint et  al18 Results remained
1194 patients with In-hospital use:
Kaiser Permanente Retrospective, significant after
3481 in-hospital statin 30 d aOR for survival 4.3
Northern California multicenter controlling for severity/
use (3.5–5.2)
DNR status (P=0.12)
 Pan et  al19 Inpatient use: aOR
Results maintained
220 patients with for good outcome
Nationwide Chinese Retrospective, after 1 y (aOR for good
3218 in-hospital statin 3 mo /1 y (mRS score of
registry multicenter outcome 2.0), lower
use 0–2 at 3 mo) 2.3
mortality at 3 mo and 1 y
(1.5–3.4)
 Jung et  al14 In-hospital use
5 studies on in- associated with Includes Flint et al18 and
Meta-analysis 6952
hospital use lower mortality: OR, Pan et al19
0.34 (0.26–0.44)
 Chen et  al16 Not significant after
Taiwan National 749 patients with Lower all-cause
Retrospective, propensity score
Health Insurance 8332 statin use within 3 24 mo mortality: aHR, 0.74
multicenter matching: aHR, 0.87
Research Database mo after ICH (0.60–0.92)
(0.65–1.16)
aHR indicates adjusted hazard ratio; aOR, adjusted odds ratio; DNR, do not resuscitate; FU, follow-up; ICH, intracerebral hemorrhage; and OAC, oral anticoagulation.

potential side effect of any lipid-lowering therapy and statin
treatment in particular.
To some surprise and reassurance, however, the vast
majority of statin trials have failed to show any effect of
statin treatment (and associated LDL cholesterol lowering)
on hemorrhagic stroke risk. In fact, 2 recent large meta-
analyses including as many as 31 randomized controlled tri-
als including >90 000 patients unanimously failed to show
any association of statin treatment or low LDL cholesterol
levels with future risk for hemorrhagic stroke, although at
the same time, risk of total stroke and also mortality were
significantly reduced.32,33 These studies included different
patient populations at risk for vascular events but only few
patients with prior ischemic or hemorrhagic stroke (includ-
ing those enrolled in the SPARCL trial). Surprisingly, in a
matched case–control study including 7696 first-ever ICH
patients compared with 14 570 ICH-free controls, statin
therapy was associated with a decreased risk of incident
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ICH.34 Similarly, in a recent population-based cohort study
from the National Health Insurance Research Database of
Taiwan, patients receiving a higher dose of statin had a
reduced and not elevated risk of incident ICH compared
with patients using lower doses.17 It is not clear whether the
effect of statins on ICH risk correlates with statin dose or
class. In fact, a high-dose statin regimen (ie, atorvastatin 80
mg) was tested in SPARCL, and the relative risk of ICH was
shown to increase with decreasing total cholesterol levels.1,30
This could serve as an argument for a dose-dependent or
LDL-dependent association of statins on ICH risk. Indeed,
a dose-related increase of symptomatic ICH was demon-
strated in ischemic stroke patients undergoing thrombolysis
with the highest risk in patients using simvastatin 80 mg or
equivalent.35 However, this may also be explained by indica-
tion bias with unfavorable ICH-promoting characteristics of
high-dose statin users. Importantly, in a meta-analysis of the
Cholesterol Trialists Collaboration, there was no increased
risk of incident hemorrhagic stroke in high-intensity statin
regimens compared with standard statin regimens used for
prevention of cardiovascular events.36 Thus, the benefit of
high-dose versus low-dose statin treatment for ischemic
stroke prevention is not offset by an augmented risk of ICH.
In 726 patients who were prescribed statins after ICH from
the National Health Insurance Research Database in Taiwan,
intensity of statin use did not alter risk of recurrent ICH.15
Interestingly, ICH patients using hydrophilic statins had
a lower risk of recurrent ICH in this study. Theoretically,
hydrophilic statins have a lower ability to cross the blood–
brain barrier.8 In contrast to this finding, risk of ICH was
not different among 2766 elderly patients treated with lipo-
philic statins compared with hydrophilic statins 1 year after
ischemic stroke.37 Overall, there are no convincing data that
lipophilicity of statins should be considered clinically rel-
evant about ICH risk.
In fact, it seems that if statins increased ICH risk after
all this would be limited to those patients with prior isch-
emic or hemorrhagic stroke. Such a trend for higher ICH
risk was observed in the subgroup of patients in the HPS
(Heart Protection Study) who were included with a history
of stroke (while it failed to achieve statistical significance)38
Endres et al   Statin Treatment in ICH Patients   3
and was clearly demonstrated in the SPARCL trial.1,2 On
the basis of the relative risk of ICH in statin-exposed com-
pared with unexposed individuals from the SPARCL trial, a
Markov decision model found that avoiding statins should
be considered in patients with ICH, especially in patients
with lobar ICH. The model assumed a high risk of ICH
recurrence of ≈11.4% in patients with lobar ICH.5 In fact,
when the meta-analysis by Hackam et al32 was restricted
to 11 (mostly observational) studies including popula-
tions with history of cerebrovascular disease, no signifi-
cant association between statin exposure and occurrence of
ICH was observed (risk ratio, 1.03; 95% confidence inter-
val, 0.82–1.30). Recently, Scheitz et al39 analyzed use of
statins and risk for poststroke hemorrhagic complications in
8335 patients from the VISTA (Virtual International Stroke
Trials Archive), an international repository of clinical tri-
als data. Statin use before index ischemic stroke was not
associated with ICH during the acute phase, irrespective of
whether or not patients received thrombolysis. New initia-
tion of statins within 3 days after ischemic stroke did not
affect risk of subacute ICH within 6 months but might be
associated with improved functional outcome and lower
mortality.39 Interestingly, in SPARCL, hemorrhagic stroke
risk was particularly increased in statin-treated patients with
lacunar stroke (2.8% versus 0.6%; hazard ratio, 5.0; 95%
confidence interval, 1.7–14.6), although an overall reduc-
tion of ischemic stroke events by 3.4% was observed.2 This
increased ICH risk was not present in statin-treated patients
with large-artery atheroembolic stroke (2.0% versus 1.8%;
hazard ratio, 1.2; 95% confidence interval, 0.4–3.2).2 This
suggests that cerebral small-vessel disease might affect the
individual susceptibility for hemorrhagic complications
attributable to statin use. Woo et al40 observed that statin
use confers a higher risk for lobar ICH in patients carrying
ApoE4/E4 genotype, a genotype associated with cerebral
amyloid angiopathy. Having the latter in mind, an impor-
tant caveat is a small study by Haussen et al,41 who stud-
ied 163 consecutive ICH patients who underwent magnetic
resonance imaging within 30 days and demonstrated that
prior statin use was associated with higher number of coin-
cident cerebral microbleeds. These included particularly
corticosubcortical microbleeds, which are frequently seen
in patients with cerebral amyloid angiopathy. However, at
present, it is unclear whether these microbleeds serve as
surrogate markers for future ICH risk in statin users.
There is limited evidence analyzing future ICH risk
related to statin treatment in patients with prior hemor-
rhagic stroke/ICH (summarized in Table 2).1,2,16,32,33,42,43 In
the SPARCL trial, patients with previous ICH deemed to be
at risk for ischemic stroke or coronary heart disease were
also eligible for inclusion. This subgroup (which comprised
only 2% of the entire study population) markedly contrib-
uted to the effect of increased ICH risk by atorvastatin
treatment.2 In fact, having an ICH as the entry event was
associated with a >5.5-fold increased risk of hemorrhagic
stroke during follow-up (ICH rate 7/45 in atorvastatin group
versus 2/48 in placebo group). Overall, the number needed
to treat to prevent 1 ischemic stroke in SPARCL was 42 per
year, whereas the number needed to harm to cause 1 ICH
 4  Stroke  January 2018

Table 2.  Summary of Studies on Statin Use and Risk of ICH Recurrence
First Author, Follow-
Reference Setting, Design Sample Size (n) Up Finding Miscellaneous
Statin use and ICH recurrence
 Amarenco et  al1 55/2365 vs 33/2366 Significant reduction in
SPARCL trial RCT 4731 4.9 y hemorrhagic strokes: aHR, total stroke/ischemic
1.68 (1.09–2.59) stroke
 Goldstein et  al2 93 with hemorrhagic 7/45 vs 2/48; aHR 4.06
4.9 y
Post hoc analysis stroke as entry event (0.84–19.57)
SPARCL trial
of RCT 1409 with lacunar 20/708 vs 4/701; aHR, Absolute ischemic stroke
4.9 y
stroke as entry event 4.99 (1.71–14.61) risk reduction by 3.4%
 Hackam et  al32 absolute risk increase
23 RCTs patients 0.03%, significant
at vascular risk; Meta-Analysis 3.9 y RR, 1.10 (0.86–1.41)
reductions in total stroke/
11 studies with ischemic stroke
cerebrovascular
disease populations mostly observational
Meta-Analysis RR, 1.03 (0.82–1.30)
studies, except SPARCL
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 McKinney and Both: significant

14 RCTs—primary
Kostis33 Meta-Analysis 0.96 (0.75–1.23) reductions in total stroke/
prevention
ischemic stroke
16 RCTs—secondary
1.06 (0.87–1.29)
prevention
 FitzMaurice Prospective, 79/229 (35%) with ICH recurrence 11%, no
et al42 ICH survivors single-center statin use after 1.9 y aOR, 0.82 (0.34–1.99) association or pre-ICH
registry discharge statin use and outcomes
 Chen et  al16 Taiwan National 749 early statin use
9.2% vs 8.9%; HR, 1.04
Health Insurance Case–control vs 7583 no early 2y Table 1
(0.81–1.34)
Research Database statin
 Schmidt et  al43 15 270 patients with 1-y cumulative recurrence Definition of statin use
Danish National Health
Case–control ICH, 2258 statin >1 y 8.2% vs 9.0%; aRR, 1.01 (pre- or post-ICH) not
Register
users (0.86–1.17) specified
aHR indicates adjusted hazard ratio; aOR, adjusted odds ratio; aRR, adjusted risk ratio; HR, hazard ratio; ICH, intracerebral hemorrhage; RCT, randomized controlled
trial; RR, risk ratio; and SPARCL, Stroke Prevention by Aggressive Reduction in Cholesterol Levels.

was 111 per year.2 One study by FitzMaurice et al42 showed
that ICH survivors treated with statins after discharge did not
have a higher rate of ICH recurrence. Using Taiwan National
Health Insurance Research Database, Chen et al16 followed
749 ICH patients in whom statins were initiated during hos-
pitalization or within 3 months for as long as 24 months and
compared them to 7538 ICH patients without statin treat-
ment. Early statin use did not increase the risk of recurrent
ICH in this cohort.
Taken together, there is a correlation of low cholesterol
with increased ICH risk (at least in part explained by other
comorbidities), although statin treatment as such does not
increase ICH risk in patients at vascular risk in general.
Only in the subgroup of patients with prior (lacunar) isch-
emic stroke, and especially ICH, this association becomes
evident. Observational studies, however, failed to confirm
the finding of an increased risk of ICH recurrence among
statin users.
Does Statin Treatment Affect Outcome
After ICH?
Experimental evidence suggests that statin treatment may
reduce perihematomal cell death and improve recovery after
brain hemorrhage, even when statins are administered after the
event.44–46 There is growing evidence from clinical studies cor-
roborating these preclinical observations (Table 1).14,16,18,19,26,47
Flint et al18 conducted a retrospective cohort study and retrieved
data from 3481 ICH patients from 20 hospitals in Kaiser
Permanente Northern California. Inpatient statin use was
clearly associated with lower mortality and higher likelihood
of being discharged to home or rehabilitation facility compared
with patients with no inpatient statin use. Patients who received
statin therapy as outpatients before ICH were at particularly
high risk of dying in hospital if statins were discontinued.18
Similarly, retrospective data from the Chinese National Stroke
Registry demonstrated that functional outcome at 3 months and
at 1 year was better, and mortality was lower in ICH patients
who received statins during hospitalization (ie, 220 patients
on statins out of 3218 consecutive ICH patients).19 Likewise,
Winkler et al47 in a single center prospectively collected data-
base demonstrated in 190 ICH patients exposed to statins
versus 236 unexposed patients that statin use was associated
with improved long-term outcome at 12 months after ICH. In
addition to showing that ICH recurrence was not increased in
749 ICH patients with new statin therapy after the event com-
pared with 7538 ICH patients without statin treatment (vide

supra), Chen et al16 demonstrate that all-cause mortality was
significantly reduced (12% versus 20% at 24 months). On the
basis od this finding, the authors even conclude that initiation
of statin may be beneficial for patients with ICH.16
A recent meta-analysis by Jung et al14 identified 16 studies
that addressed the question of ICH outcome and statin use (as
of 2015). Pre-ICH statin use was associated with improved
outcome but not reduced mortality (total of 26 757 patients
from 12 studies). In-hospital statin use was associated with
reduced risk of mortality (6952 patients). This is corrobo-
rated by a second meta-analysis analyzing 17 studies: statins
improved short-term and (less evident) long-term outcome,
and continuation was associated with improved outcome.48
An important caveat is the fact that data suggesting a potential
benefit of statin use during the acute phase after ICH were all
derived from observational studies, mostly using a retrospective
case–control design. The lack of rigorous randomization entails
the possibility of confounding by indication bias. This means
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that patients conceived to have a better prognosis were more
likely to receive continuous or new statin treatment. Siddiqui
et al27 observed that ICH patients in whom statins were acutely
discontinued were older, more likely to have intraventricular
hemorrhage and lobar hemorrhage, had larger ICH volumes and
higher premorbid modified Rankin Scale. After correcting for a
propensity score including factors that could influence the deci-
sion to give statins, continuation or initiation of statins was no
longer associated with good outcome.27 It is important to point
out, however, that even if observational studies carry the risk of
confounding by indication bias, there seems to be no signal that
statin use during the acute phase after ICH worsens outcomes
or that statin use increases short-term risk of ICH recurrence.
PSCK9 Inhibitors
Recently, PCSK9 inhibitors have been introduced as novel
therapeutic option for lowering LDL cholesterol and decreas-
ing cardiovascular disease risk.49 Large trials such as the
OSLER trial (Open-Label Study of Long-Term Evaluation
Against LDL Cholesterol) with evolocumab or the ODYSSEY
LONG TERM trial (Long-Term Safety and Tolerability
of Alirocumab in High Cardiovascular Risk Patients With
Hypercholesterolemia Not Adequately Controlled With Their
Lipid Modifying Therapy) with alirocumab have demonstrated
that PCSK9 inhibitors can consistently lower LDL cholesterol
levels to 40 to 50 mg/dL in patients at high vascular risk who
do not achieve target LDL cholesterol levels with statins or
other lipid-lowering approaches.50,51 Clearly, safety of PCSK9
inhibitors is a concern in particular on a potential risk for ICH.
In this respect, recent results from the FOURIER trial (Further
Cardiovascular Outcomes Research With PCSK9 Inhibition in
Subjects With Elevated Risk) which assessed clinical outcomes
in 27 564 patients with cardiovascular risk are reassuring.20
Treatment with the PCSK9 inhibitor evolocumab on a back-
ground of statin therapy lowered LDL cholesterol levels as low
as 30 mg/dL and significantly reduced the risk of cardiovas-
cular events including ischemic stroke. Importantly, there was
no signal toward an increased risk of ICH, even though ≈20%
of the study population had a history of ischemic (nonhem-
orrhagic) stroke. More precisely, there were 29 hemorrhagic
Endres et al   Statin Treatment in ICH Patients   5
strokes in the evolocumab group (13 784 patients) versus 25 in
the placebo group (13 780 patients), resulting in a nonsignifi-
cant hazard ratio of 1.16 (95% confidence interval, 0.68–1.98).
Conclusions
On the basis of the above evidence we would recommend the
following: preexisting statin medication should not be discon-
tinued in the acute phase in patients admitted with ICH. After
the acute phase, when the rehabilitation potential and long-term
prognosis of an individual patient can be estimated, a decision
should be made whether to continue or discontinue statin treat-
ment. Arguments for statin continuation are high global athero-
sclerotic vascular risk, whereas arguments for discontinuation
are lobar localization of ICH, multiple bleeds, or severe small-
vessel disease as indicated by (multiple) microbleeds. On the
basis of the available evidence, however, we would not gener-
ally recommend to initiate statins in statin-naive ICH patients
either in the acute phase (as to improve outcome) or chronic
phase (unless there is a high—and previously unrecognized—
thromboembolic/atherosclerotic vascular risk). Randomized tri-
als assessing this topic would be very welcome but are unlikely
to be performed. Although additional data are always desirable,
a randomized trial on statin resumption after ICH will probably
not yield meaningful results, given the small estimated effect size
and arguments made before. If the finding that PCSK9 inhibitors
do not increase ICH risk can be confirmed in additional trials
and in particular in the subgroup of patients with ischemic (or
even hemorrhagic) stroke, these drugs could emerge as alterna-
tive therapy to lower LDL cholesterol in ICH patients.
Sources of Funding
Dr Endres receives funding from the Deutsche Forschungsgemeinschaft,
Bundesministerium für Bildung und Forschung, European Union,
Fondation Leducq, and Corona Foundation.
Disclosures
Dr Endres reports fees paid to the Charité by Amgen. The other
authors report no conflicts.
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KEY WORDS: cerebral hemorrhage ◼ comorbidity ◼ hydroxymethylglutaryl-
CoA reductase inhibitors ◼ risk ◼ stroke ◼ treatment outcome
 Statin Treatment in Patients With Intracerebral Hemorrhage
Matthias Endres, Christian H. Nolte and Jan F. Scheitz

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