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Focus on the Fasting Lipid Profile

There has been much discussion of late regarding the important topic of how best to manage the independent cardiovascular risk associated with rheumatoid arthritis and other rheumatic diseases. This issue has been well covered on RheumNow, most recently in the article by Dr. Kathryn Dao (September 18), by Drs. Janet Pope and Jack Cush (podcast, September 8), and by Drs. Janet Pope, Jeff Curtis, Jon Giles and Roy Fleischmann (Tuesday Nite Rheumatology, September 6). The question that has been asked is: 

How best do we communicate this risk to other members of the treating team, most particularly the Primary Care Physicians (PCPs; known as ‘General Practitioners’ (GPs) here in Australia)?

Do we communicate this risk to them individually for each patient (and how do we add that to our already busy schedule?), or do we take on the mantle of responsibility for cardiovascular disease management, as suggested by the European League Against Rheumatism (EULAR) in their guidance in 2016?

After some experimentation, I have come up with an approach that seems to work and which does not take up much time. I would be grateful for your feedback, so that together, as a community, we might refine the best approach.

In the past, I have written to PCPs advising that they consider rheumatoid arthritis as akin to diabetes mellitus when assessing cardiovascular risk. This approach did not work and I found myself having to add CV risk management to my existing workload. Much better, I thought, to bring the PCP on board to assist. There are many details we could choose to communicate (see Drosos et al. EULAR recommendations for cardiovascular risk management in rheumatic and musculoskeletal diseases, including systemic lupus erythematosus and antiphospholipid syndrome. Ann Rheum Dis 2022; 81(6):768-779. doi: 10.1136/annrheumdis-2021-221733); however, I chose to focus on lipids.

My new strategy since January has elicited a very positive response from PCPs. My approach has been to check a fasting lipid profile and then respond to the result by sending the following letter. I have integrated this template into my EMR so that it takes all of 10 seconds to modify and send for each individual patient (the patient's name is automatically included by my EMR and I then choose the risk multiplier and replace 'rheumatic disease' with the patient's diagnosis). Please feel free to use this yourself and modify it as you see fit:

“Please find a copy of PATIENT's fasting lipid profile below. Whilst this forms part of the standard cardiovascular risk calculation, PATIENT's rheumatic disease does not. When calculating PATIENT's cardiovascular risk, please consider adding a risk multiplier of 1.5/2.0/2.5 for rheumatic disease.

Evidence base for recommendation

A population-based study of the risks for 12 different cardiovascular disease outcomes in patients with autoimmune and rheumatic diseases found that the risk for cardiovascular disease was increased for people with rheumatic diseases by an average of 68%, compared with people without rheumatic diseases (Conrad et al. Ann Rheum Dis 2022; Published Online First: 28 November 2022. doi: 10.1136/ard-2022-223315; Conrad et al. Lancet 2022; 400(10354):733-743. doi: 10.1016/S0140-6736(22)01349-6). This study examined electronic health records of 446,449 individuals with autoimmune diseases and matched them to 2,102,830 individuals without autoimmune disease. This included 160,217 individuals with seven rheumatic diseases: rheumatoid arthritis, polymyalgia rheumatica, vasculitis, systemic lupus erythematosus, Sjögren's syndrome, ankylosing spondylitis, and systemic sclerosis. The authors suggested that cardiovascular risk guidelines should consider a risk multiplier of 2.5 for systemic sclerosis, 2.0 for lupus, and 1.5 for any other rheumatic disease. While they recognize that risk multipliers aren't perfect, "they are the best available option until personalized risk prediction tools are developed specifically for patients with RMDs."

Why do rheumatic diseases increase the risk of cardiovascular disease?

That rheumatic diseases (particularly when poorly controlled) are major independent risk factors for cardiovascular disease has been documented in multiple previous studies. Why? In my opinion, the two main drivers of increased cardiovascular risk in patients with rheumatic disease are likely to be a) biochemical inflammation and b) corticosteroid use.

A collaborative analysis of 31,245 patients from three statin trials found that inflammation assessed by high-sensitivity CRP was a stronger predictor for risk of future cardiovascular events and death than cholesterol assessed by LDL (Ridker et al. Lancet 2023; 401(10384):1293-1301. doi: 10.1016/S0140-6736(23)00215-5). Multiple studies have identified prednisolone, even at doses as low as a mean of 2.8mg as a major independent risk factor for cardiovascular disease, heart failure and death (eg: Roubille et al. Rheumatology (Oxford) 2021; 60(8):3738-46; George et al. Ann Intern Med 2019; May 21. doi: 10.7326/M18-2217; George et al. Ann Rheum Dis 2020; March 24, doi: 10.1136/annrheumdis-2019-216802; Wu et al. CMAJ 2019; 191(25):E680-88; DOI:

Scleroderma and lupus have their own unique risks. Scleroderma is characterised in part by vasculopathy, and, as with lupus, can sometimes be associated with antiphospholipid antibodies (aPL). Even in patients without lupus, aPL are an independent risk factor. A cohort study has shown that aPL Abs are found in a substantial proportion of adults with atherosclerotic cardiovascular disease (ASCVD) events and finding both positive aCL IgA and anti-beta-2GPI IgA Abs independently predicted future ASCVD events (Zuo et al. JAMA Netw Open. 2023;6(4):e236530. doi:10.1001/jamanetworkopen.2023.6530).


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Dr Paul Anthony John Russo is a Fellow of the Royal Australasian College of Physicians (qualified in both rheumatology and clinical immunology and allergy) and a Fellow of the American College of Rheumatology. Paul obtained 1st Class Honours in Immunology at the University of Sydney prior to studying medicine. During his training, Paul also spent time in Edinburgh (Scotland), Kiel (Germany) and Papua New Guinea. Paul has published over 40 papers in the peer-reviewed literature and since 2011 has lived in Adelaide with his wife and young family. Since 2014, Paul has worked privately as a sole practitioner in the Adelaide foothills, not far from the McLaren Vale.