The Impact of Nurse-led Programme With and Without Carotid Ultrasound on Addressing Cardiovascular Risk in Patients With Arthritis: a Prospective, Multicentre, Randomised, Controlled Trial
Phase: NA
Conditions: Arthritis, Rheumatoid, Arthritis, Psoriatic
Sponsor: Chinese University of Hong Kong

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The impact of nurse-led programme with and without statin treatment base on traditional 
cardiovascular risk score or carotid ultrasound on addressing cardiovascular risk in patients with 
arthritis: a prospective, multicentre, randomised, controlled trial 
 
 
Introduction:  
Cardiovascular disease (CVD) risk is elevated in patients with rheumatoid arthritis (RA) and psoriatic 
arthritis (PsA) compared with the general population, and is a major source of morbidity and mortality (1, 
2).  New evidence strengthens the notion that the excess risk of CVD morbidity and mortality in patients 
with RA is related to both traditional and novel CVD risk factors. In RA, novel risk factors include 
inflammation, presence of carotid plaques, anticitrullinated protein antibody (ACPA) and rheumatoid factor 
(RF) positivity (3). In PsA, the prevalence of traditional risk factors is elevated compared with the general 
population , probably because of the shared inflammatory pathway (4).  
 
CVD risk assessment is recommended for all patients with RA and PsA at least once every 5 years, so that 
lifestyle advice and CVD preventive treatment can be initiated when indicated (5). Current CVD risk 
prediction models, for example, Framingham Risk Score (FRS) or the Systematic COronary Risk Evaluation 
(SCORE) algorithm have been developed for use in the general population. Their performance in patients 
with RA appears to be suboptimal (6). Therefore, it has been suggested that CVD risk algorithms based 
solely on traditional risk factors may not be suited for use in the RA population. As a first step towards more 
accurate CVD risk prediction, it was proposed in the European League Against Rheumatism (EULAR) 
recommendations for CVD risk management in RA to apply a multiplication factor of 1.5 to the calculated 
CVD risk by SCORE (modified SCORE [mSCORE])  in selected patients to enhance the risk estimates (7). 
Nonetheless, a recent study showed that mSCORE do not provide sufficient improvement in risk prediction 
of future CVD in RA to serve as an appropriate alternative to the original SCORE (8).  
 
Using coronary computer tomography angiogram (CCTA), we and others have found that all types of 
coronary plaque were more common in RA and PsA patients compared with controls, highlighted the fact 
that most of these subjects with plaques are having silent ischemia, supporting the notion that more 
aggressive CV evaluation strategy should be considered in these patients (9, 10). Nonetheless, there are 
concerns regarding costs and radiation exposure using CCTA or even coronary artery calcium (CAC) as a 
screening tool. Carotid ultrasound is a noninvasive imaging technique which can identify the presence of 
carotid plaque and increased intima-media thickness (IMT), representing an unequivocal manifestation of 
atherosclerosis and serving as a surrogate for CV disease. Other than carotid ultrasound, non-invasive 
pulse tonometry examination by measuring pulse wave velocity (PWV) and augmentation index (Alx) could 
evaluate overall aortic stiffness, which is an independent predictor of cardiovascular risk (11). Subclinical 
carotid atherosclerosis been shown to be more prevalent in RA (12) and PSA (13) then controls, even 
without classic CV risk factors. Increased IMT significantly correlated with traditional risk factors and 
disease-related parameters (12, 13).  
 
Screening for asymptomatic atherosclerotic plaques by use of carotid ultrasound has been recommended 
as part of the CVD risk evaluation in patients with RA (5) as the presence of carotid plaques is associated 
with poor CVD-free survival and is strongly linked to future acute coronary syndrome (ACS)(14). The 
presence of bilateral plaque quadrupled the incidence of new ACS independently of any other risk factors 
compared with patients without carotid plaque (15). Incorporation of carotid ultrasound for patients at 
intermediate risk for CV disease has been used to further enhance CV risk stratification in the general 
population (16). Studies have supported the role of carotid ultrasound in re-stratification of CV risk. In RA, 
severe carotid ultrasound abnormalities were observed in 13% and 63% of patients with low and moderate 
mSCORE respectively (17). In PSA, our previous study showed that 35% of patients had subclinical 
atherosclerosis despite having a FRS-based low to moderate CV risk (13). Another study from Toronto also 
showed that 55.9% of the PsA patients from the FRS-based intermediate risk category were reclassified 
into an ultrasound-based high-risk category, while 47.1% of the patients in the FRS-based low-risk category 
were reclassified into a higher US-based risk group (18). Screening this population may help to identify 
those patients who are optimal candidates for intensive medical treatment. Prior studies suggest that 
incorporation of carotid ultrasound into treatment algorithms can impact progression of plaque and CV 
outcomes (19). However, the general applicability of these findings in rheumatology or primary care clinic 

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settings is not clear. Furthermore, guidelines on the management of patients with identified carotid plaque 
in RA and PsA have not been formulated.  
 
Despite demonstration of high CV risk by the presence of carotid plaque, implementation of preventive CV 
services and rates of statin and antiplatelet use in PsA remained low in a recent study (20). “Best practice” 
electronic referrals were not an effective strategy to increase rates of specialty CV screening, even with a 
preventive cardiology clinic available in the same institution. It is possible that demonstration of carotid 
plaque can improve risk stratification but will only be impactful if incorporated into treatment plans by the 
treating rheumatologists as recommended by EULAR (5).  
 
In RA patients, comorbidities are more common, more severe and less well-managed than in the general 
population (21).  The usefulness of a nurse-led programme for decreasing CV risk has already been shown 
in a recent study. A single visit with a nurse might facilitate the management of risk factors of CVD by the 
general practitioner and/or the rheumatologist and demonstrated short-term benefit of a nurse-led 
programme on RA comorbidity management (22). However, whether the program resulted in changes of 
surrogate marker of CV endpoint (eg, glycaemia for diabetes, blood pressure for hypertension) remained 
uncertain because of its short study duration. 
 
In addition to clinical screening, recent studies showed that various biomarker like calprotectin might play 
a role in detecting subclinical atherosclerosis, which calprotectin was associated with aortic PWV and 
presence of carotid plaque (23, 24). Our previous study also revealed that miRNA targeting IL-33 gene was 
associated with presence and progression of subclinical atherosclerosis . 
 
Aim and hypothesis: We hypothesize that CV risk stratification and management in RA and PsA may be 
improved by incorporation of carotid ultrasound to assess for carotid plaque. This study investigates the 
impact of a nurse-led programme  and initiation of statin treatment decided base on  result of traditional CV 
risk score or carotid ultrasound on CV risk factor control in asymptomatic RA and PsA patients. 
 
Patients and Methods 
Subjects 
Inclusion criteria 
One hundred and forty consecutive patients with RA fulfilled the 2010 ACR/EULAR classification criteria or 
PsA fulfilled the Classification of Psoriatic Arthritis (CASPAR) criteria attending the outpatient clinics of the 
Prince of Wales Hospital who are aged between 18 and 75 will be recruited.  
 
Exclusion criteria 
Patients will be excluded if they have any one of the followings: a history of overt CVD (ie, symptomatic 
coronary artery disease [CAD] or ischemic stroke or transient ischemic attack or peripheral vascular 
disease), had significant co-morbidities including severe renal impairment or severe deranged liver function, 
female of childbearing potential who are unwilling to use adequate contraception, pregnant or breastfeeding 
women, and patients who are already taking lipid lowering therapy. 
 
Nurses 
Rheumatology nurses will conduct the nurse-led clinic in Prince of Wales Hospital. 
 
Treating rheumatologists 
Treating rheumatologists will invite their patients to participate in the study and will be responsible for 
managing patients with specific instructions given as listed below. Referred patients will then undergo 
formal screening by the research assistant for interest in the project and eligibility. 
 
Trial design 
This is a 1-year prospective, hospital-based, open-label, randomized, controlled trial.  The trial comprised 
two arms. Both group will participate in the nurse-led programme on CV risk screening and carotid 
ultrasound for carotid plaque assessment. Subjects in group 1 will initiate statin treatment if their 
Franminham Risk Score >10%; while subjects in group 2 will initiate statin treatment if they had carotid 
plaque upon carotid ultrasound findings..  (Appendix 1). The method of concealed random allocation will 

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be used. Simple randomization will be conducted by a computer-generated random list. Randomisation will 
be centralized for all centres. Information on each patient’s allocated treatment will be recorded in the 
clinical report form (CRF) and also entered into the patient’s computerized medical record (CMS) by the 
nurse. The study will be approved by the respective Ethics Committees of each hospital and all patients will 
provide written consent.  
 
Clinical assessment 
At baseline and then every 3 to 6 months up to 1 year, the following clinical variables and questionnaires 
will be assessed: erythrocyte sedimentation rate (mm/h1st), CRP (mg/L), number of swollen joints (0–28 for 
RA, 0-66 for PsA), number of tender joints (0–28 for RA, 0-68 for PsA), number of damaged joints, visual 
analogue scale (VAS) for pain (0-10=most pain), VAS for patient’s global assessment (0-10=worst score), 
and VAS for physician’s global assessment (0-10=worst score). Functional disability will be assessed by 
the disability index of Health Assessment Questionnaire (HAQ) (0-3=most functional disability). Overall 
disease activity will be assessed using 28-joint assessment (DAS28) for established RA (symptom onset 
greater than 2 years), simplified disease activity score (SDAI) for early RA (symptom onset less than 2 
years), and Disease Activity in Psoriatic Arthritis (DAPSA),  Bath Ankylosing Spondylitis Functional Index 
(BASFI) Test and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) for PsA. Quality of life 
outcome will also be assessed at baseline and month 12 by Short Form (36) Health Survey and EQ5D. 
PsA patients will also complete the Dermatology Life Quality Index (DLQI) and Ankylosing Spondylitis 
Quality of Life (AsQoL) questionnaire. 
 
Cardiovascular assessments  
The following anthropomorphic assessment will be performed for all patients at baseline and at the end of 
the study. Anthropomorphic measurements include body heights, body weight, waist and hip 
circumferences, two consecutive blood pressure (BP) readings in sitting position and heart rate. 
Hypertension status is defined as systolic blood pressure (SBP) ≥140mmHg or diastolic blood pressure 
(DBP) ≥90mmHg or the use of antihypertensive agents. Other data collected at baseline include 
menopausal status, smoking and drinking habits, social economic status, history of diabetes, hypertension, 
hypercholesterolemia, dyslipidemia, overt CVD and cerebrovascular diseases, peptic ulcer disease and 
family history of CVD, diabetes and cerebrovascular diseases in first-degree male relatives <55 years of 
age or first-degree female relatives <65 years of age. Drug history is retrieved from case notes or elicited 
during the clinical assessment. Body weight and blood pressure will also be measured during each visit to 
the rheumatologist. 
Laboratory assessment at baseline include fasting blood glucose, fasting lipid profile (total cholesterol [TC], 
low-density lipoprotein-cholesterol [LDL-C], high-density lipoprotein-cholesterol [HDL-C], triglycerides [TG]), 
fibrinogen, thyroid function test, creatinine kinase and uric acid. Fasting sugar and lipid profile will also be 
measured at 6 and 12 months. Hemoglobin A1c levels will be measured at baseline and 12 months for 
patients with known diabetes. 
 
Rationale for choosing FRS and the level of cut off for intervention 
Evidence is scarce with regard to the validity of disease specific CVD risk prediction models to accurately 
predict risk in individual patients with RA and PsA, and it is therefore currently recommended to perform 
risk evaluation according to general population guidelines. Currently, no national guideline is available in 
Hong Kong. In our previous study to evaluate the performances of different CV risk scores in detecting high 
CV risk in PsA patients identified by coronary plaques on CCTA, we categorized patients as having either 
low or elevated 10-year CV risk using the 10% threshold for the FRS and found that FRS provided better 
discrimination of PsA patients with significant coronary artery plaque on CCTA than 3 other commonly used 
risk scores (25). Therefore, FRS was chosen to predict CV risk and a cut off of 10% was chosen to identify 
high risk individuals for interventions such as lipid-lowering treatment. 
 
Arterial stiffness as alternate CV risk indicator 
Apart from FRS, arterial stiffness was suggested to be an alternative measurement of CV risk. An increase 
in aortic PWV by 1 SD corresponds to an age-, sex- and risk factor-adjusted risk increase of 47%, 47% and 
47% in total cardiovascular events, cardiovascular mortality and all-cause mortality, respectively.(26) AIx 
has emerged as a surrogate marker for CVD. A 10% increase of central AIx is associated with a relative 

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risk of 1.4 for all-cause mortality.(27) Therefore, arterial stiffness measurement could serve for additional 
CV risk indication apart from FRS and/or subclinical carotid atherosclerosis by ultrasound. 
 
Intervention of CV risk in the nurse-led clinic  
All patients will receive a one-on-one nurse-led intervention at baseline and month 12 including:  
(1) Detection of CV risk factors (eg, hypertension, diabetes, hypercholesterolaemia).  
(2) Calculation of the FRS. We will follow the recommendation to adapt for patients with RA by a 1.5 
multiplication factor (5).  
(3) The implementation of the recommendation for the detection (eg, yearly evaluation of CV risk factors) 
and/or management of such comorbidities at baseline. Nurses will be given a booklet to be used for the 
systematic identification and assessment of the comorbidities associated with RA and PsA. In case of a 
detected risk factor (eg, hypertension) and/or a non-optimally managed comorbidity (eg, Hba1c > 7), the 
nurse reminds the patient the interest of the management of such comorbidity and advises the patient to 
visit her/his general practitioner and/or rheumatologist to take care of it. In parallel, a report of this visit will 
be given to the patient to hand-over to the rheumatologist of each evaluated patient during their next clinical 
visit. 
(4) The report of the presence of newly developed CV comorbidities at month 12. 
(5) The number of new measures taken against comorbidities at month 12. The following measures against 
comorbidities are considered for the definition of the secondary objective of the trial: purchase of BP self-
measurement devices, attending education class by dietitian and initiation of a diet because of overweight 
+/- hyperlipidemia, smoking cessation, initiation of lipid-lowering therapy, initiation of antiplatelet therapy, 
referral to a nephrologist because of renal insufficiency (chronic kidney disease stage IIIb). 
(6) adherence of lipid-lowering and antiplatelet therapy at month 12. 
 
Carotid intima-media thickness (IMT) and plaque  
All patients will have the carotid intima-media thickness (IMT) and plaque assessed at baseline and 12 
months at the Prince of Wales Hospital. Carotid IMT will be measured using a high-resolution B-mode 
ultrasound machine (Philips EPIQ7). Briefly, duplex carotid ultrasound will be performed by an experienced 
sonographer blinded to all clinical information using a 30-MHz linear vascular probe (Philips L12-3 
broadband linear array transducer). The IMT will be measured offline in the distal common carotid artery 
(the arterial segment 1 cm proximal to the carotid bulb), bulb, and proximal internal carotid artery (the 
arterial segment 1 cm distal to the carotid bifurcation) using dedicated software (Philips Xcelera Cardiology 
Enterprise Viewer Client 4). The values of maximal thickness will be recorded, not including plaques, for 
the following calculation. Plaque is defined as a localized thickening >1.2 mm that do not uniformly involve 
the whole artery. The mean and maximal IMT values of 6 arterial segments will be calculated for further 
analysis. Reproducibility of IMT in our center was 0.97 (13).   
A report of this visit will be given to the patient to hand-over to the treating rheumatologist during their next 
clinical visit. All participating rheumatologist will attend a briefing session on the importance of carotid 
ultrasound screening and the risk represented by carotid plaque in order to avoid under-appreciation of CV 
risk. Moreover, while the results of the US scan will be provided to the patient’s primary rheumatologist, an 
interpretation of the findings regarding level of CV risk will also be provided. 
 
Pulse wave velocity (PWV) and pulse wave analysis (PWA)  
Arterial stiffness will be measured by baPWV, cfPWV and AIx at baseline and month 12 for all subjects(28). 
Participants receive PWA examination in the morning, having fasted overnight; having a light meal 4h 
before measurement and avoid tobacco, alcohol, and caffeine with 3h before measurement. Participants 
rest in sitting position in a quiet room for at least 10 minutes before examination. BP is measured 3 times 
at the right brachial artery using a validated oscillometric device (Omron HEM-757 - UK). PWA is performed 
using the pressure cuff and analog system (VICORDER Version 3.1 - UK). The central aortic arterial pulse 
wave is transferred from the peripheral arterial pulse wave automatically. Since AIx in an individual patient 
varies by heart rate, it is standardized to a heart rate of 75 beats-per-minute (b.p.m.) (AIx@75).  
Carotid femoral PWV (cfPWV) is a gold standard of arterial stiffness and will be measured by VICORDER 
system as well. cfPWV will be measured in the supine position by a sphygmomanometer cuff in bilateral 
carotid and femoral position. The VICORDER machine measures and records results of pulse waveforms 

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of carotid and femoral arteries automatically. cfPWV is defined as the mean speed of bilateral blood 
pressure wave traveling between carotid and femoral artery. The distance between sampling points are 
measured manually. 
Brachial-ankle PWV (baPWV) is another measure of arterial stiffness and will be assessed non-invasively 
in subjects in the supine position by a dedicated tonometry system (Non-Invasive Vascular Profile Device 
VP-2000; Omron Healthcare, Inc. Bannockburn, Illinois, USA). In brief, this device record PWV, blood 
pressure, electrocardiogram (ECG), and heart sounds simultaneously. Sphygmomanometer cuffs are 
applied on both arms just above the level of elbows and on both legs just above the ankles. ECG electrodes 
are placed on both wrists, and a heart sound microphone is placed on the left sternal border. The machine 
measures and records results of electrocardiogram, phonocardiogram and blood pressure of limbs as well 
as pulse waveforms of carotid and limb arteries automatically. baPWV is defined as the speed of the blood 
pressure wave traveling between brachium and ankle. The distance between sampling points of brachial-
ankle PWV are calculated automatically according to the height of the subject. All PWA measurements are 
made by a single skilled operator. Intra-observer reliability is 0.86 (28). The reports will also be hand over 
to the attending rheumatologist in their subsequence visit, and to further evaluate the CV risk. 
Treatment protocol  
There are no formal guidelines on the management of patients with high CV risk or identified carotid plaque 
in Hong Kong. The following management plan was formulated after a general discussion with practicing 
rheumatologists and cardiologists locally. 
 
Use of statins 
Group 1 patients will be prescribed statin when FRS > 10%; while group patients will be prescribed statin 
upon presence of carotid plaque as reported from carotid ultrasound. The decision will solely be made base 
on the randomized group by either FRS>10% or presence of carotid plaque. 
We choose atorvastatin 20 mg daily since generic atorvastatin is available in the Hong Kong Hospital 
Authority drug formulary. Each tablet cost HK $ 0.28 and the yearly cost is HK $ 102.2 (around US $ 13) 
per person. Atorvastatin 20 mg is recommended as the preferred initial high-intensity statin to use because 
it is clinically and cost effective for the primary prevention of CVD according to the national institute for 
Health and Care Excellence (NICE) guideline from the United Kingdom. Nonetheless, similar data is lacking 
in Hong Kong. 
No trials to date that have evaluated effects on CVD events have tested any medication in combination with 
statins or treatment to specific LDL-C goals, therefore we do not intensify the regimen for any particular 
level of LDL-C response. Measuring LDL-C response after initiating therapy in this study is mainly to assess 
adherence. In this primary prevention trial, in patients who do not tolerate statins, no lipid-lowering therapy 
will be administered. Potential interventions include lifestyle modification and, in higher-risk patients, 
antiplatelet therapy. 
Use of Aspirin 
For low-risk patients (ie, men and women whose 10-year absolute risk of a first coronary heart disease 
event is <10 percent), the absolute benefit of a reduction in CV events is unlikely to exceed the absolute 
risk of major bleeding. For moderate- and high-risk patients (ie, men and women whose 10-year absolute 
risk of a first CVD event is ≥10 percent), randomized data on benefits and risks are sparse. Nonsteroidal 
anti-inflammatory drug (NSAID) therapy combined with aspirin use increases the risk for serious 
gastrointestinal (GI) bleeding compared with aspirin use alone (29). The gastrointestinal harms may offset 
the CV benefits in our group of patients on long-term NSAID where the GI risk is high and the CV risk is 
low. Therefore, aspirin for primary prevention in this trial will be highly individualized based on a benefit/risk 
ratio assessment for each patient and a clinician-patient discussion regarding potential benefits, potential 
harms, and patient preferences. 
Use of DMARDs 
Disease activity should be controlled optimally in order to lower CVD risk in all patients with RA or PsA (5). 
All participants will receive a 1-year protocolized treatment (Appendix 2 and 3) with the aim to achieve 
remission. The protocol was developed based on the EULAR recommendations, the Hong Kong Society of 
Rheumatology recommendation and the Hong Kong guideline for the use of biologics. When patient cannot 
achieve treatment goal within 3 to 6 months of therapy, the treatment therapy will be escalated to the next 
step according to the protocol, unless the patient declined or toxic effects preclude this approach.  

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Toxicity monitoring 
To monitor the possible side effect of the NSAID, biologic and synthetic DMARDs, statins and aspirin, 
patients will be asked about various symptoms (such as myalgias or weakness for statins; coffee ground 
vomiting, melaena and dyspepsia for NSAID and aspirin). Complete blood count, liver function tests and 
renal function tests will be performed during every clinic visit. Creatinine kinase will be measured in patients 
who complain of myalgias or weakness after staring statins. Chest X-rays will be obtained at baseline and 
at the end of the study. The treating physician record all adverse events and serious adverse events and, 
if necessary, make treatment adjustments in accordance with the protocol. Serious adverse events are 
defined as any adverse reaction resulting in any of the following outcomes: a life-threatening condition or 
death, a significant or permanent disability, a malignancy, hospitalization or prolongation of hospitalization, 
a congenital abnormality, or a birth defect. 
 
Outcome measures 
The primary outcome is the change in FRS. Although this algorithm was developed for prediction of 
absolute coronary risk among patients without clinical manifestations of CAD, they combine the following 
major risk factors recognized for coronary and other atherosclerotic CVD (ASCVD): age, sex, high BP, 
smoking, dyslipidemia, and diabetes status. We use risk scores as a composite measure of change in 
modifiable major risk factors, rather than as a predictor of risk. This approach has been previously used in 
evaluating effects of nurse- and dietitian-led case management program to reduce CV risk (30). Baseline 
age will be applied when calculating the FRS at 12 months.  
 
Secondary end points included  
1) Change in arterial stiffness in subjects 
2) Change in individual modifiable risk factors (systolic and diastolic BP; TC, LDL-C, HDL-C and TG 
levels; TC/HDL ratio; and hemoglobin A1c value in patients with diabetes) 
3) The number of measures taken against comorbidities.  
4) Proportions of patients achieving remission. 
5) Changes in IMT and proportion of plaque progression in subjects between 2 groups 
 
The trial will be conducted with compliance to ICH-GCP and Declaration of Helsinki. 
 

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Statistical analysis: 
Descriptive statistics will be used for demographic and clinical variables included frequencies, percentage, 
means and standard deviations, median and interquartile range. Comparisons in demographic and clinical 
characteristics at baseline will be performed using chi-square test, independent samples t-test or Mann-
Whitney U test, depending on distribution of data. We will compare the proportion of participants eligible for 
statin treatment using FRS >10% vs carotid ultrasound criteria using the McNemar test. The intervention 
effect on the primary and secondary outcomes will be examined at 12 months on an intention-to-treat basis 
using a mixed-effects regression model adjusted for baseline FRS. The model will also take into account 
random effects associated with physicians and clinics in a hierarchical structure. The magnitudes and 
patterns of missing data will be examined by the randomized group. Missing outcomes at the 12-month 
follow-up will be imputed using the method of the baseline observation carried forward. The same mixed-
effects model will be used for subgroup analyses defined by sex and underlying diseases. All statistical 
analyses will be conducted using IBM SPSS Statistics Version 23 (IBM, Armonk, NY, USA). A level of 
significance of p =0.05 is used. 
 
Sample size calculation: 
The sample size is estimated by the Power Analysis and Sample Size for Windows software (PASS 2000, 
NCSS, Utah, USA). All calculations will use a two-sided α of 0.05 and β=0.2 achieving 80% power. From 
our previous cohort study, standard deviation of FRS was 8. Taking population variance of FRS as 64, and 
suppose 4 unit drop in FRS is clinically meaningful. A sample size of 63 is required in each group. Assuming 
a drop-off rate of 10%, a total sample size of 140 (i.e. 70 per arm) would be sufficient. 
 
 
(G)  
Purpose and potential for implementation of results 
Elevated CVD risk is a significant public health problem that contributes greatly to the increased morbidity 
and shortened lifespan of individuals with RA and PsA. Over the past decades, there has been great 
progress into the understanding of the severity of CVD risk in these patients but these risk factors are not 
well managed. The development of the high-risk strategy is therefore necessary, with more intensive 
therapy reserved for patients identified as high-risk, e.g. because they have high-risk FRS. However, these 
risk scores under-estimated CV risk in patients with RA and PsA. An intermediate approach is to use 
quantification of preclinical vascular disease to further identify high-risk patients. Results from this study will 
provide clinical implications in terms of detecting and managing cardiovascular morbidity in patients with 
RA and PsA. 
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