Pharmacological Research 196 (2023) 106936

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Pharmacological Research
journal homepage: www.elsevier.com/locate/yphrs

European guidelines for the treatment of dyslipidaemias: New concepts and

future challenges
Angela Pirillo a, 1, Manuela Casula b, c, 2, Alberico L. Catapano b, c, *, 3
a
Center for the Study of Atherosclerosis, E. Bassini Hospital, Cinisello Balsamo, Milan, Italy
b
Epidemiology and Preventive Pharmacology Service (SEFAP), Department of Pharmacological and Biomolecular Sciences, University of Milan, Milan, Italy
c
IRCCS MultiMedica, Sesto S. Giovanni, Milan, Italy

A R T I C L E I N F O A B S T R A C T

Keywords: Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality and morbidity worldwide. Low-
Guidelines density lipoprotein cholesterol (LDL-C) is one of the most important causal factors for ASCVD. Based on the
Dyslipidaemias evidence of the clinical benefits of lowering LDL-C, the current 2019 European Society of Cardiology (ESC) and
Lipid-lowering therapy
European Atherosclerosis Society (EAS) guidelines provide guidance for optimal management of people with
Low-density lipoprotein cholesterol
Cardiovascular risk
dyslipidaemia. These guidelines include new and revised concepts, with a general tightening of LDL-C goals to be
achieved, especially for patients at high and very high cardiovascular risk, based on the results of clinical trials of
the recently approved drugs for the treatment of hypercholesterolaemia. However, some issues are still open for
discussion. Among others, the concept of lifetime exposure to elevated LDL-C levels will probably drive the
pharmacological approach and future guidelines. In addition, other factors such as non-HDL-C, apolipoprotein B,
and lipoprotein(a) are becoming increasingly important in determining cardiovascular risk. Finally, there is the
question of whether combination therapy should be used as the first step to maximise the effectiveness of the
pharmacological approach, avoiding the stepwise approach, which is likely to have a detrimental effect on
adherence. Given the ever-changing landscape and the availability of new drugs targeting other important lipids,
future guidelines will need to consider all these issues.

1. Introduction duration of exposure to elevated LDL-C also plays an important role.

Atherosclerotic cardiovascular disease (ASCVD) is the leading cause
of mortality and morbidity worldwide. Among the risk factors for
ASCVD, low-density lipoproteins (LDL) or more generally apolipopro­
tein (apoB)-containing lipoproteins play a causative role, as shown by
genetic, epidemiological and clinical data [1,2]. Individuals who carry
variants in genes that cause lifelong elevated LDL-cholesterol (LDL-C)
levels have a significantly increased risk of premature ASCVD, if left
untreated [3,4]. Conversely, individuals who carry variants in genes
associated with lower LDL-C have a lower risk of ASCVD [5–8]; genetic
studies have shown a 54% reduction in coronary heart disease risk for
every 1 mmol/L of lower LDL-C [1]. The clear clinical benefit of
lipid-lowering therapies in relation to ASCVD events is proportionally
related to the extent of LDL-C-lowering. In addition to the level, the
Based on this strong evidence, the current 2019 European Society of
Cardiology (ESC) and European Atherosclerosis Society (EAS) guidelines
for the management of dyslipidaemias have been produced to provide
guidance for optimal management of people with dyslipidaemia [9].
Compared to the previous 2016 version, the current guidelines have
introduced new LDL-C goals, updated the CV risk stratification, and
provided new advice for patient management [9].
In this review, we discuss the novelties in the current 2019 ESC/EAS
guidelines on dyslipidaemias and report the increasing relevance of
some aspects that should be taken into account when designing the next
guidelines.

* Correspondence to: IRCCS MultiMedica, Milan, Italy.

E-mail addresses: alberico.catapano@multimedica.it, alberico.catapano@unimi.it (A.L. Catapano).
1
https://orcid.org/0000–0002-2948–6257
2
https://orcid.org/0000–0002-5124–5361
3
https://orcid.org/0000–0002-7593–2094

https://doi.org/10.1016/j.phrs.2023.106936
Received 27 July 2023; Received in revised form 20 September 2023; Accepted 20 September 2023
Available online 20 September 2023
1043-6618/© 2023 The Authors. Published by Elsevier Ltd. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-
nc-nd/4.0/).
A. Pirillo et al.
2. Main principles in LDL-C-lowering therapy
The 2019 ESC/EAS guidelines for the management of dyslipidaemias
were released to provide updated recommendations based on new evi­
dence [9]. These guidelines are inspired by four main principles (Fig. 1):
1) genetic, epidemiological and clinical studies suggest that LDL-C plays
a causal role in atherosclerotic vascular disease; 2) clinical trials of
LDL-C-lowering drugs show that relative risk reduction is proportional
to absolute LDL-C reduction; 3) the greater the LDL-C reduction ach­
ieved, the greater the clinical benefit; this appears to be largely inde­
pendent of the type of drug used to lower LDL-C (statins, ezetimibe or
PCSK9 inhibitors, alone or in combination) but rather related to the
extent of LDL-C lowering; 4) the intensity of LDL-C reduction should be
based on individual risk, regardless of the determinant(s) of the risk (e.g.
primary or secondary prevention, diabetes or chronic kidney disease).
In addition to LDL-C levels, the concept of duration of exposure to
elevated LDL-C levels is also receiving more attention than in the past: a
reduction in LDL-C levels of 1 mmol/L results in a benefit proportional
to the duration of exposure, with reductions of approximately 23%
observed in randomised trials (with an average follow-up of 5 years),
33% in prospective studies (with an average follow-up of 12 years) and
53% in Mendelian randomised studies (with an average follow-up of 52
years) [1]. This is of particular importance as it is well consistent with
the concept that the development of coronary atherosclerosis is a life­
long process that becomes apparent in early adulthood, and that
elevated LDL-C levels in young adulthood can lead to an increased risk of
ASCVD later in life. As a consequence, even a relatively small reduction
achieved earlier in life may lead to greater clinical benefit than a large
reduction achieved later in life. For example, a diet and lifestyle-based
approach may result in a modest reduction in LDL-C levels
(0.2–0.3 mmol/L), but sufficient to produce a substantial benefits
(15–20% reduction) if maintained throughout life [1]. Accordingly,
expanding statin therapy or intensive lifestyle intervention in young
adults could lead to improved population health [10–12]. However,
because young adults have a low 10-year ASCVD risk - the most common
approach to global risk assessment - only a small proportion of them are
eligible for lipid-lowering treatment.
There are several important aspects that should be considered. First,
the clinical benefit observed per 1 mmol/L reduction in LDL-C level is
comparable across different patient groups, with no differences in sub­
groups by sex, age, current therapy, or baseline LDL-C level [9].
Although LDL-C lowering can be achieved within a few weeks, the
clinical benefit is not immediate: in fact, the benefit in the first year of
lipid-lowering therapy is only about half that in subsequent years of
2019 ESC/EAS Guidelines on Dyslipidaemias
Main principles
 LDL-C plays a causal role in ASCVD
 The relative risk reduction is proportional to
the absolute reduction in LDL-C
 The greater the LDL-C reduction, the
greater the clinical benefit
 The intensity of LDL-C-lowering should be
based on individual risk
Fig. 1. Main principles driving current 2019 ESC/EAS Guidelines for the
management of dyslipidaemias.
2
Pharmacological Research 196 (2023) 106936
treatment. Therefore, in a clinical trial of short duration, a moderate
benefit in the first year should be considered, as it averages out over the
following years. For example, the two outcome trials of monoclonal
antibodies (mAbs) targeting PCSK9 showed a substantial reduction in
LDL-C (≥1 mmol/L), but resulted in (only) a 15% relative risk reduction
[13,14]. This discrepancy with the expected reduction can be explained
by the relatively short duration of these two trials (2.2 years in the
FOURIER and 2.8 years in the ODYSSEY OUTCOMES) [15]. Finally, it is
important to consider the overall risk of the individual: for the same
overall risk, a greater reduction in LDL-C leads to a greater CV benefit,
but the same reduction in LDL-C levels in subjects with different abso­
lute risk leads to a different absolute risk reduction.
3. Novelties introduced in the 2019 ESC/EAS Guidelines
Compared with the 2016 guidelines, the current guidelines have
introduced more demanding LDL-C goals for the categories of very high-
and high-risk patients (Fig. 2) [9,16]. For people at high and very high
risk, both an LDL-C goal of < 1.8 mmol/L and < 1.4 mmol/L
(<70 mg/dL and <55 mg/dL, respectively) and an LDL-C reduction of
≥ 50% from baseline are now recommended, regardless of baseline
LDL-C. This is a particularly important aspect: on the one hand, this
ensures a large reduction in LDL-C levels (≥50%), and on the other
hand, a reduction of about 1 mmol/L (~39 mg/dL) can be achieved in
patients with lower baseline levels (<100 mg/dL). These recommen­
dations apply to patients in both secondary prevention and primary
prevention, although for the latter the level of evidence is lower due to
the smaller number of available clinical trials. In addition, for patients
with ASCVD who experience a second ischaemic event within two years
of the first event, an LDL-C < 40 mg/dL goal may be considered. The
LDL-C goal has also been lowered for moderate-risk individuals (LDL-C
goal < 100 mg/dL), whereas for low-risk individuals the LDL-C goal is
unchanged (LDL-C <116 mg/dL).
As statins represent the class of lipid-lowering drugs for which the
largest number of clinical trials are available, these drugs are recom­
mended as the first therapeutic approach, whether in combination or not
is discussed later in this paper. The current guidelines suggest that if the
LDL-C goal is not achieved, ezetimibe and possibly a PCSK9 inhibitor
(PCSK9i) can be added to a statin (sequential approach) (Fig. 2). It is
worth noting that the addition of a PCSK9i in secondary prevention or in
patients with familial hypercholesterolaemia (FH) has a higher class of
recommendation thanks to recent clinical trials conducted precisely in
these patient groups [9,13,14]. In patients who cannot tolerate statins,
ezetimibe, PCSK9i or a bile acid sequestrant may be considered. For
Fig. 2. Novelties introduced in 2019 ESC/EAS guidelines.
A. Pirillo et al.
patients with hypertriglyceridaemia, the recommendations are less
stringent as the evidence from clinical trials is far from being compel­
ling. For this reason, the guidelines only provide guidance on triglyc­
eride levels above which intervention is appropriate once the LDL-C goal
has been achieved. It should be emphasised that the only triglyceride
(TG)-lowering drug that effectively reduces CV risk when added to a
statin is icosapent ethyl [17]. Other TG-lowering approaches (such as
the omega-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid
in the STRENGTH trial and pemafibrate in the PROMINENT trial) failed
to lower CV risk [18,19].
In addition to the recommendations for the treatment of hyper­
cholesterolaemia according to the individual risk category, the guide­
lines also include recommendations for specific patient groups (Fig. 2):
1) patients with FH, 2) women, 3) older people (>75 years), 4) diabetics
and 5) patients with an acute coronary syndrome. For other patient
groups, such as patients with chronic kidney disease, heart failure,
stroke or percutaneous coronary intervention (PCI), the recommenda­
tions are based on the risk category.
1) For patients with FH, LDL-C goals have been lowered to < 55 mg/dL
if at very high-risk or < 70 mg/dL if no other risk factors are present.
Not surprisingly, LDL-C goals for children with FH are less stringent
(in children >10 years, an LDL-C <3.5 mmol/L [<135 mg/dL] and
at younger ages, a ≥50% LDL-C reduction) in the absence of ad hoc
studies. Drugs used in children are limited to atorvastatin and pra­
vastatin. Data are now available on the safety and efficacy of PCSK9i
in paediatric patients [20–22]. There is also a recommendation for
screening of family members if a FH person is identified.
2) For women, the same recommendations apply as for men, with the
note to suspend therapy during pregnancy/breastfeeding or if preg­
nancy is planned.
3) In elderly patients (>75 years old), the benefit of statin therapy
seems to be similar to that in younger patients. However, potentially
impaired renal and hepatic function must be considered and therapy
should be started at a low dose.
4) Patients with diabetes are classified as very high risk or high risk
depending on the presence or absence of organ damage and the
duration of the disease, whereas young people (<50 years) with
diabetes duration of < 10 years, no other risk factors and a calculated
10-year risk of fatal CVD ≥ 1% and < 5% fall into the moderate risk
category [9]. Therefore, LDL-C goals for diabetics depend on their
risk category. However, some secondary goals have also been
established for these patients, related to the role of apoB-containing
lipoproteins in diabetes and metabolic syndrome. These patients
have abnormalities in other atherogenic lipoproteins (beyond LDL)
and the determination of non-HDL-cholesterol (non-HDL-C) and
apoB levels (with goals always depending on the risk category) is a
useful approach.
5) Patients with acute coronary syndromes are considered high-risk. In
these patients, the addition of a PCSK9i to the maximally tolerated
dose of statin and ezetimibe should be considered. This is based on
evidence from clinical trials that report significant reductions in LDL-
C levels and allow the recommended goals to be easily achieved [14,
23].
4. What are the future challenges?
Several aspects deserve attention in future guidelines on dyslipi­
daemia, as they could help improve the treatment of hyper­
cholesterolaemia (and thus also of ischaemic-related CV diseases) based
on the latest evidence, and can be summarised as follows (Fig. 3).
1) Lifetime risk. Current 2019 ESC/EAS guidelines on dyslipidaemia
recommend to assess CV risk by the use of the SCORE (Systematic
Coronary Risk Estimation) system [9]. The SCORE system provides
the 10-year risk of fatal CVD, with the risk being highest in older
3
Pharmacological Research 196 (2023) 106936
2019 ESC/EAS Guidelines on Dyslipidaemias
Open questions
 Lifetime risk
 HDL-C: still protective?
 Non-HDL-C and/or apoB for all?
 How to define the role of Lp(a)-lowering in ASCVD prevention?
 Should we be satisfied with LDL-C goals or should we push for a
percentage reduction?
 How to define the right target population during trial design?
 Is the stepwise approach always useful to achieve goals?
Fig. 3. Main open questions.
people, as age is the dominant factor. Of note, recently the SCORE
system has been recalibrated and updated to reflect actual CVD rates
in Europe: the SCORE2 model provides estimates of the 10-year risk
of fatal and non-fatal CVD events in individuals aged 40–69 years
[24] and the SCORE2-OP (Older Persons) has been specifically
developed for people aged ≥ 70 years [25], both included in the
latest ESC guidelines on CVD prevention in clinical practice [26]. In
addition, the SCORE2-Diabetes model has been developed for the
specific use in individuals with diabetes but without previous CVD
[27]. Despite these improvements, age is still the main determinant
of risk, which may lead to an underestimation of future risk espe­
cially in young people. To overcome this issue, definitions based on
genetics and the concept of cholesterol burden are now gaining
importance [28]. The integration of these concepts will allow us to
calculate a lifetime risk that is independent of age and to define the
CV benefit based only on LDL-C lowering (thus moving from a
non-modifiable factor - age - to a modifiable and causal factor -
LDL-C). This concept is supported by both Mendelian randomisation
studies, prospective cohort studies, and randomised controlled trials,
which show that the effect of LDL-C on the risk of ASCVD increases
with increasing duration of exposure and that, for the same LDL-C
lowering, earlier lowering leads to greater benefit (from 22% in
randomised clinical trials to 54% in Mendelian randomisation
studies for every 1 mmol/L lower LDL-C) [1]. Further support is
provided by the observations that in FH patients, in whom the cu­
mulative LDL-C burden is much higher at a young age compared with
unaffected individuals, early pharmacological intervention can shift
the curve of CV events so that the threshold for CHD is reached later
in life [3].
2) HDL-C. Although observational studies have shown that HDL-C
levels are inversely associated with CVD risk, suggesting that
increasing HDL-C levels may confer clinical benefits, randomised
clinical trials testing different approaches to increasing HDL-C levels
have not shown a reduction in the incidence of CV events [29–31].
The observation that genetic variants associated exclusively with
higher HDL-C levels are not associated with a reduced risk of
myocardial infarction has reinforced the notion that high HDL-C
levels are not necessarily associated with clinical benefit [32]. In
addition, U-shaped associations have been found between HDL-C
levels and CV and mortality risk, suggesting that either low or very
high HDL-C levels are associated with increased CV risk [33]. Several
observations suggest that increasing HDL particle quality rather than
cholesterol content should be the goal. In light of these findings, it is
debated whether we should continue to consider HDL as a protective
factor [34].
3) Non-HDL-C and apoB. Although LDL-C levels are the primary treat­
ment goal, it is now clear that an overall assessment of a person’s
lipid profile should not be ignored. This includes determining the
A. Pirillo et al.
levels of non-HDL-C and apoB, which provide a more comprehensive
picture of atherogenic lipoproteins. Non-HDL-C measures cholesterol
content in all atherogenic particles including but not limited to LDL
particles. Since apoB is present in a single copy in each apoB-
containing lipoprotein, apoB determination provides the number of
all atherogenic particles, including remnant lipoproteins and lipo­
protein(a). Both parameters are excellent markers and are associated
with CV risk [35–39]. A Mendelian randomisation analysis has
shown that apoB remains significantly associated with CV risk, even
after adjustment for several parameters such as LDL-C cholesterol
and plasma TG. This suggests that changes in cholesterol or tri­
glycerides (and consequently non-HDL-C) that are not accompanied
by corresponding changes in apoB may not lead to a reduction in CV
risk [40], as evidenced by the REDUCE-IT trial with icosapent ethyl
(which reduced TG and apoB as well as CV risk) and the STRENGTH
trial with eicosapentaenoic acid+docosahexaenoic acid and the
PROMINENT trial with pemafibrate (both of which reduced TG but
not apoB and did not reduce CV risk) [17,19]
4) Lipoprotein(a) [Lp(a)]. Lp(a) is an LDL-like lipoprotein with an
additional apoprotein, apolipoprotein(a), covalently bound to apoB
on the particle surface. Lp(a) levels are genetically determined and
are not related to lifestyle. Therefore, Lp(a) levels do not change
significantly throughout life [41]. Elevated Lp(a) levels are an in­
dependent cardiovascular risk factor [41]. Current European guide­
lines recommend that Lp(a) levels should be measured at least once
in life to identify individuals who are at increased cardiovascular risk
due to high Lp(a) levels despite normal LDL-C levels [9]. Mendelian
randomisation studies have shown that the same clinical benefit
obtained by lowering LDL-C by 1 mmol/L (~40 mg/dL) requires
lowering Lp(a) levels by 65–100 mg/dL [42,43]. The drugs
commonly used to treat hypercholesterolaemia do not significantly
lower Lp(a) levels. Ongoing clinical trials are investigating the effi­
cacy of drugs that can substantially and specifically lower Lp(a)
levels. Nucleic acid-based approaches have led to the development of
an antisense oligonucleotide (ASO, pelacarsen) and a small inter­
fering ribonucleic acid (siRNA, olpasiran) that enable selective gene
silencing and prevent the production of apo(a). These approaches
can reduce Lp(a) levels by up to 80–90% [44,45]; ongoing trials will
show whether this reduction translates into clinical benefit.
Recently, the EAS published a consensus statement on Lp(a) [41].
This consensus includes the latest evidence on the role of Lp(a) in
ASCVD and aortic valve stenosis, as well as recommendations for Lp
(a) measurements and treatment of high Lp(a) levels [41]. Inclusion
of Lp(a) levels in risk algorithms has been shown to improve CV risk
prediction [46–48]. However, while waiting for drugs that specif­
ically target Lp(a), the best approach to reducing CV risk in people
with high Lp(a) levels is to lower other risk factors, such as LDL-C
levels [41].
5) Percent LDL-C reduction versus LDL-C goal. Setting LDL-C level goals is
of utmost importance, especially for patients at high or very high
risk. However, the introduction of mandatory percentage LDL-C
reduction in addition to the goals ensures a reduction in CV risk
even in patients starting from lower baseline LDL-C levels [9]. For
example, a high-risk patient with a baseline LDL-C level of 80 mg/dL
will achieve an LDL-C level of 40 mg/dL if treated to achieve a 50%
reduction, which provides a greater risk reduction than "simply"
achieving the recommended goal of 70 mg/dL for this risk category.
In fact, lowering LDL-C continuously reduces the risk of CV events
even at lower LDL-C levels (although the absolute risk decreases
less). Although this concept has been included in recent guidelines, it
should be emphasised that physicians are often satisfied with
achieving only one of the two goals. It is of utmost importance to
understand how important achieving both goals can be for reducing
cardiovascular risk in high- and very high-risk patients.
6) Trial design. Careful design of a clinical trial increases the chance of
evaluating the true efficacy of a therapeutic approach. Two
4
Pharmacological Research 196 (2023) 106936
parameters seem to be crucial for the success of a trial: the duration
of the study and the definition of the right patient population. The
study duration has to take into account that the clinical benefit of
LDL-C lowering is lower in the first year than in the following years;
thus, the longer the study duration, the lower the weight of the first-
year results [49]. Furthermore, the selection of the target population
is another crucial step in clinical trial design: no matter how effective
an LDL-C-lowering drug is, if it is given to patients with the same
global CV risk but with lower baseline LDL-C levels, it will inevitably
lead to a lower absolute risk reduction.
7) Stepwise approach. The treatment algorithm included in the current
ESC/EAS guidelines provides for a stepwise approach. If there is an
indication for drug therapy, the first approach is a high-potency
statin at the highest recommended/tolerated dose to achieve the
goal. If the goal is not achieved, ezetimibe should be added and, if
this is not sufficient to reach the goal, a PCSK9i can be added [9]. A
stepwise approach for the treatment of dyslipidaemia may be locally
relevant to ensure reimbursement for more expensive therapies (such
as monoclonal antibodies against PCSK9 or siRNAs). While this
approach is based on a reasonable sequence, it may not be appro­
priate when treating high-/very high-risk patients who need effective
interventions to rapidly lower their LDL-C levels to achieve faster
clinical benefit and possibly better adherence to therapy [50].
Indeed, a cautious start of therapy in subjects requiring large re­
ductions in LDL-cholesterol levels could result in a feeling of
dissatisfaction by the patient with a therapy that does not achieve the
desired results [51]. In these patients, is combination therapy indi­
cated as the first approach to achieve goals faster and reduce risk
[52]? The fundamental aspect to consider when choosing the
appropriate drug therapy should be the baseline LDL-C level (i.e.
before starting an intervention): if the baseline LDL-C level is high,
combination therapy is likely to lead to earlier goal attainment. We
should also consider that a greater reduction in LDL-C is associated
with greater clinical benefit. The observational study DA VINCI
showed that in patients with established ASCVD, the percentage of
those who achieved the LDL-C goal recommended in the 2016
ESC/EAS guidelines (i.e. the guidelines that were in place when this
study was conducted) was higher if they were taking a high-intensity
statin, combination therapy with ezetimibe or a PCSK9i [53].
Meanwhile, when the updated 2019 ESC/EAS guidelines were pub­
lished, analysis of the data from the DA VINCI study showed that
fewer patients were able to achieve the goals and that the highest
goal achievement was in those taking combination therapy with a
PCSK9i [53], which was also confirmed by several other observa­
tional studies, including the EUROASPIRE V [54], the ACS EuroPath
[55] and the recently published SANTORINI [56,57]. It is note­
worthy that the SANTORINI trial assessed LDL-C goal attainment
exclusively according to the 2019 ESC /EAS guidelines and
confirmed that only a minority of patients at high or very high CV
risk receive combination therapy [56,57]; the planned 1-year
follow-up analysis will shed light on whether more adequate use of
available lipid-lowering combinations can contribute to LDL-C goal
attainment.
8) Adherence to therapy. Adherence has important implications for CV
benefits, and low treatment adherence inevitably increases an in­
dividual’s CV risk. Too many patients with established atheroscle­
rotic disease are still inadequately treated: a high proportion of
patients receive moderate-dose statin therapy, few receive the statin
in combination with ezetimibe, and an even lower proportion are
treated with PCSK9i. Inadequate therapy leading to suboptimal LDL-
C levels increases the likelihood of low adherence or even discon­
tinuation of therapy and thus the risk of CV events. A meta-analysis
of 44 prospective studies with 1978,919 participants has shown that
a relevant proportion of patients have inadequate treatment adher­
ence to therapy and that a substantial proportion of CVD events can
be attributed to poor treatment adherence [58].
A. Pirillo et al.
5. Conclusion
Scientific guidelines, based on the assessment of the most relevant
evidence in the field and updated over time as much as possible, are a
valuable tool to guide clinical practice. The two main challenges are the
need for continuous updating and the importance of training health
professionals.
The first point is particularly important in the context of cholesterol
management and cardiovascular prevention, an area that is constantly
evolving, especially due to the availability of new and innovative ther­
apies. The timely incorporation of current evidence into guidelines is
crucial for further improving the management of cardiovascular disease
and personalising therapeutic approaches.
The second aspect is crucial to ensure that the potential benefits of
the recommendations can be translated into an effective strategy. Sci­
entific societies and policy makers should work together to educate an
up-to-date class of health professionals and enable the implementation
of the recommendations in daily clinical practice.
Author statement
All authors have participated in Conceptualization, Writing – Orig­
inal Draft, and Writing – Review & Editing.
CRediT authorship contribution statement
AP Writing - original draft, Writing – review & editing; MC and ALC
Writing – review & editing.
Declaration of Competing Interest
The authors declare that they have no known competing financial
interests or personal relationships that could have appeared to influence
the work reported in this paper.
Acknowledgements
The work of ALC is supported in part by Ministero della Salute
Ricerca Corrente to MultiMedica.
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