Table 1 Points to consider in cardiovascular disease risk management among South African black and white patients with RA

 1.1 We suggest to perform overall CVD risk assessment in all RA patients irrespective of population origin and socioeconomic status.

3

C

 1.2 We suggest to perform overall CVD risk assessment upon initial presentation and subsequently at least every 5 years in RA patients at low risk, and at least yearly in those at high or very high risk.

3

C

 1.3 We suggest that the treating rheumatologist performs primarily CVD risk assessment and management in patients with RA.

3

C

 1.4 We suggest that (1) cardiovascular risk profiles and (2) potential benefits, (3) side effects and (4) drug-drug interactions as well as (5) patient preferences are consistently discussed between the clinician and RA patient in order to facilitate informed decision making and intervention adherence and non-discontinuation.

3

C

 2.1 RA control

 2.1.1 We suggest targeting optimal RA control and, in the absence of contraindications, to consider including (hydroxy) chloroquine in DMARD regimens to reduce CVD risk in RA patients.

1B-3

A-C

 2.1.2 We suggest considering the use of intra-articular glucocorticoids as bridge therapy upon initiating or intensifying conventional synthetic DMARD in order to reduce CVD risk in RA.

3

C

 2.1.3 We suggest using NSAID sparingly in patients with RA, particularly amongst those at high or very high CVD risk including the presence of chronic kidney disease, and with hypertension.  We recommend the preferential use of naproxen (with a proton pump inhibitor).  NSAID use is not recommended in RA patients with heart failure.

 1A-3

B-C

 2.2.1 In RA patients with very high CVD risk comprising (1) established CVD, (2) diabetes mellitus with target organ damage or major CVD risk factors, and (3) severe chronic kidney disease, we suggest using high dose statin therapy targeting an LDL-C level of 1.8 mmol/l. In RA patients with high CVD risk comprising (1) diabetes without target organ damage or other major CVD risk factors, (2) moderate chronic kidney disease, and (3) severe dyslipidemia (total cholesterol >/= 8.0 mmol/l or/and LDL-C level >/= 4.9 mmol/l), we suggest using moderate to high dose statin therapy targeting an LDL cholesterol level of 2.5 mmol/l.  

 1A-3

 B-C

 2.2.2 In RA patients without (1) established CVD, (2) diabetes, (3) moderate or severe chronic kidney disease, or (4) severe dyslipidemia, we suggest refining CVD risk assessment by carotid and femoral artery ultrasound when accessible to identify plaque presence, which represents very high CVD risk and an indication for high dose statin therapy. This is particularly important in black African RA patients.

3

C

 2.2.3 In black RA patients without access to carotid and femoral ultrasound, we suggest to consider the presence of a CKD-EPI estimated estimated glomerular filtration rate of < 80 ml/min/1.73m² as an indication for high-dose statin therapy.

3

C

 2.2.4 In white RA patients without access to carotid and femoral ultrasound, we suggest to consider the presence of a Framingham score score of > 7.5% as an indication for high-dose statin therapy.

3

C

 2.2.5 In black RA patients without (1) CVD, (2) diabetes, (3) moderate or severe chronic kidney disease, (4) severe dyslipidemia and (5) carotid or/and femoral plaque existence, we suggest to consider the presence of a CKD-EPI determined glomerular filtration rate of < 80 ml/min/1.73m² as an indication for moderate dose statin therapy.

1A

B

 2.2.6 In white RA patients without (1) CVD, (2) diabetes, (3) moderate or severe chronic kidney disease, (4) severe dyslipidemia and (5) carotid or/and femoral plaque, we suggest to consider the presence of a Framingham score of > 7.5% as an indication for moderate dose statin therapy.

1A

B

 2.2.7 When affordable, we suggest the additional use of ezetimibe in RA patients when the LDL-C target is not met despite maximally tolerated statin doses. In RA patients who are intolerant to statin therapy, we suggest the alternative use of ezetimibe. When affordable, we suggest referral to a lipidologist for consideration of additional treatment with a proprotein convertase subtilisin/kexin 9 inhibitor in RA patients with established ACVD and severe dyslipidemia that have persistently high LDL-C levels despite maximally tolerated statin therapy and ezetimibe.

1B-3

B-D

 2.2.8 We suggest lipid profile re-evaluation in RA patients subsequent to (1) obtaining low RA activity or remission due to changes in DMARD therapy, (2) major changes in life style factors and (3) one to three months after initiation or intensification of lipid lowering therapy to determine whether the LDL-C target is met. We suggest lifelong use of lipid lowering agents in RA patients with very high or high CVD risk.

1A-3

B-C

 2.3.1 We suggest considering the use of antihypertensive agents in RA patients with a SBP of 130–139 mmHg or/and DBP of 80–89 mmHg and elevated overall CVD risk, and in all patients with SBP > 140 mmHg or/and DBP > 90 mmHg. Preferred first line agents comprise angiotensin converting enzyme inhibitors, angiotensin receptor blockers, calcium channel blockers and diuretics.  Preferred second line agents include spironolactone, hydralazine and minoxidil.  We suggest that calcium channel blockers should be included in initial antihypertensive combination regimens in black Sub-Saharan African RA patients.  We suggest yearly, monthly and three monthly blood pressure measurement in normotensive RA patients, and those with uncontrolled and controlled hypertension, respectively.

 1B-3

 B-C

 2.4.1 We suggest using low dose aspirin as secondary prevention in RA patients with established atherosclerotic CVD. We suggest not to use aspirin as primary intervention in RA patients without CVD.

1A-3

B-C

 2.5 Lifestyle factors

 2.5.1 We suggest to address the importance of healthy eating habits, adequate physical activity, stress and depressive symptom control and smoking and smokeless tobacco cessation with consideration of Sub-Saharan Africa specific aggravating factors and in order to reduce CVD risk at presentation and thereafter at least yearly in patients with RA.

1A-3

B-C