Background Cardiovascular comorbidities are a major contributor of damage in patients with SLE. They are driven by classical, as well as SLE-related risk factors, i.e. disease activity and immunosuppressive treatment.
Objectives We aimed to analyze cardiovascular damage (CVD) in a group of 90 deceased SLE patients regularly followed-up in a routine academic setting at our Department, and to identify features associated with accrual of CVD.
Methods We retrospectively observed 90 SLE patients (68 females) deceased within the 2002–2011 period. All patients were ≥18 years of age and Croatian residents at the time of death, fulfilling ≥4 classification criteria of the American College of Rheumatology (ACR). We identified patients with CVD, including the following components of the Systemic Lupus International Collaborating Clinics (SLICC)/ACR damage index: cardiovascular damage as defined by the index (cardiac damage), peripheral vascular damage, cerebrovascular accident, pulmonary infarction, bowel infarction and avascular necrosis. An extensive set of variables was compared between patients with and without CVD: demographics, ACR criteria at diagnosis and death, damage (according to the SLICC/ACR index) and its components one year following diagnosis and at the time of death, disease activity at diagnosis (according to the European Consensus Lupus Activity Measurements index, ECLAM), as well as features of the metabolic syndrome, smoking and immunosuppressive treatment. Frequencies were compared using the χ2 and Fisher's exact test, and continuous variables using the t-test and Mann-Whitney U test. Variables associated with CVD in the univariate analysis were included in a multivariate logistic regression model.
Results We identified 63/90 patients with CVD, including 46/63 (73%) with cardiac damage, 19/63 (30%) with peripheral vascular damage, 21/63 (33%) with cerebrovascular accident, 4/63 (6%) with bowel infarction, 14/63 (22%) with avascular necrosis and a single patient with pulmonary infarction (Figure 1). Patients with CVD had a higher disease duration at time of death compared to patients without CVD (12±8 vs. 7±6 years), as well as higher cumulative proportions of hematologic disorder (60/63 vs. 15/27), lymphopenia (48/63 vs. 10/27), pulmonary damage (19/63 vs. 1/27), fractures (25/63 vs. 2/27), higher overall damage (6.0±3.0 vs. 2.4±2.0) and a higher proportion of secondary antiphospholipid syndrome (14/63 vs. 1/27) (p<0.05). Conversely, patients with CVD had a lower proportion of discoid lupus at diagnosis (7/49 vs. 9/24) and a lower proportion of skin damage one year following diagnosis (2/63 vs. 5/27) (p<0.05). Parameters associated with cardiovascular damage in the multivariate model were cumulative fulfillment of lymphopenia as a classification criterion (odds ratio, OR 4.7 (95% confidence interval, CI 1.3–17.0)) and accrual of pulmonary damage (OR 13.1 (95% CI 2.2–76.3)).
Figure 1. Distribution of cardiovascular damage in the analyzed group (numbers represent frequencies of each subtype of cardiovascular damage)
Conclusions More than two thirds of deceased patients accrued CVD over the disease course. Lymphopenia and pulmonary damage may be associated with CVD in deceased SLE patients.
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Disclosure of Interest None declared