Assessing Cardiovascular Disease Risk in Psoriatic Arthritis Patients

By M. Elaine Husni, MD, MPH, and Michael Lucke, MD

Risk for cardiovascular disease is elevated in patients with psoriatic arthritis (PsA) relative to the general population and is a major source of morbidity and mortality in these patients. Subclinical atherosclerosis in PsA has been shown to be prevalent even without existing classic cardiovascular risk factors, suggesting a role for systemic inflammation in patients with psoriatic skin and joint disease.

Unmet Needs in Cardiovascular Risk Assessment in PsA

The most commonly used methods of evaluating cardiovascular risk in the general population recently have been found to underestimate the risk of cardiovascular disease in patients with psoriasis, PsA and rheumatoid arthritis significantly. In spite of this, no clear guidelines exist for assessing or managing cardiovascular risk in patients with systemic rheumatic disease such as PsA.

There is an urgent need to identify coronary artery disease in its early forms, before clinical events, which will help guide therapy, particularly in patients with known increased risk, such as those with PsA. Carotid ultrasound findings have been shown in the general population to correlate highly with future cardiovascular events. As a result, physicians in Cleveland Clinic’s Department of Rheumatic and Immunologic Diseases are investigating whether screening of asymptomatic PsA patients for carotid plaque would alter medical management to address known cardiovascular risk.

Carotid Ultrasound as a Risk Screening Tool

We conducted a cross-sectional investigation of all PsA patients who were recruited for our Cardiometabolic Outcome Measures in Psoriatic Arthritis Study (COMPASS).

We identified PsA patients who were at least 18 years of age with subclinical cardiovascular disease from among 86 patients from our PsA registry who underwent voluntary carotid duplex ultrasound (CDU). Patients were screened for the presence of carotid artery plaque using the Mannheim consensus criteria, and arterial wall thickness was quantified by the carotid intima-media thickness measurement (Figure 1).

Figure 1. Carotid artery ultrasound images from a control patient (left) and from a PsA patient with carotid artery plaque and a thickened arterial wall CIMT measurement (right). CIMT = carotid intima-media thickness.

All patients also were offered a preventive cardiology consult automatically through the electronic health record, and results of the carotid scans were sent to the patient and his or her primary care physician. As per our PsA registry protocol, repeat CDU was performed at 12 to 24 months in 38 of the 86 patients. Demographics, cardiovascular risk factors, PsA history, disease activity, medication use, fasting glucose, C-reactive protein and lipid panels were recorded. CDU results and actual treatment protocols were assessed using our institution’s preventive cardiology guidelines regarding a minimal LDL cholesterol goal of 100 mg/dL and initiation of antiplatelet therapy and lifestyle counseling, as appropriate, in patients with PsA deemed at high risk for cardiovascular disease.

Prevalence of Carotid Plaque and Other Risk Factors

Carotid plaque was identified in 34 of 86 PsA patients (40 percent) at baseline carotid screening. This prevalence of carotid plaque is similar to that in other cohorts of PsA patients and higher than in the general population.

When we analyzed the 38 patients who underwent repeat carotid screening, 18 had plaque at baseline that persisted on the second scan. Of the remaining 20 patients without plaque at baseline, three (15 percent) had new plaque formation on repeat ultrasound. In the group with plaque, mean LDL cholesterol was 120 mg/dL (vs. 102 mg/dL in the no-plaque group), mean HDL cholesterol was 55 mg/dL (vs. 55 mg/dL) and mean triglycerides were 203 mg/dL (vs. 96 mg/dL). Mean ESR was 8 mm/hr in patients with plaque and 6 mm/hr in those without plaque.

Better Prevention Strategies Needed

Overall, 24 of 36 patients (67 percent) with repeat screening and LDL measurements had an LDL greater than 100 mg/dL, yet only 12 (33 percent) were on statin therapy and only 10 (27 percent) were on antiplatelet medication (Figure 2). Of the 21 patients identified with carotid plaque within the repeat-screening group, only seven (33 percent) were using statins; none were on maximum doses.

Despite the offer of automatic referral for all 86 patients screened, only 11 patients were seen by our preventive cardiology section. Fourteen others were seen by a cardiologist for other reasons, including hypertension, syncope, arrhythmias and valvular disease.

Figure 2. Among 36 patients in the repeat carotid ultrasound group, two-thirds exceeded preventive cardiology guidelines for goal LDL cholesterol (100 mg/dL) in PsA patients at elevated cardiac risk. In spite of this, only a third or less of the 36 patients were receiving statin therapy or antiplatelet therapy for primary prevention

Clinical Implications, Next Research Steps

Carotid ultrasound is a pragmatic modality that allows better estimation of cardiac risk than do traditional risk factors alone in PsA, and it presents an opportunity for early interventions. Low utilization of preventive services was observed even in patients with definitive evidence of atherosclerotic disease by plaque identification. A majority of patients exceeded stated preventive cardiology goals (in terms of LDL cholesterol), yet few were on statin or antiplatelet therapy.

Our research highlights the need to improve proactive modification of cardiovascular risk in PsA patients. Cleveland Clinic researchers are committed to characterizing these lapses in referral, and we recommend continued research to fill gaps in knowledge regarding short- and long-term cardiac risk assessment in our patients.

Accelerated cardiovascular disease remains a major problem for patients with PsA. Future work should focus on refining cardiac risk assessment tools to make them more specific for patients with systemic rheumatic diseases such as PsA.

The authors gratefully acknowledge the technical assistance of Alex Massiello

Dr. Husni is Director of the Arthritis and Musculoskeletal Treatment Center and directs Cleveland Clinic’s Psoriatic Disease Biobank. She can be reached at husnie@ccf.org or 216.445.1853.

Dr. Lucke is a senior rheumatology fellow in the Department of Rheumatic and Immunologic Diseases. He has been an active investigator in the area of cardiovascular risk stratification and subclinical atherosclerosis in patients with psoriatic arthritis.