Carlos Garcia-De Los Ríos

Cardiovascular disease (CVD) is a main cause of death in patients with systemic lupus erythematous (SLE). Algorithms for cardiovascular risk stratification in general population underestimate the risk for CVD in SLE. Our study aimed to determine whether serum high-sensitivity cardiac troponin I (hs-cTnI) might help to identify SLE patients with subclinical atherosclerosis. Arterial stiffness was assessed measuring the carotid-femoral pulse wave velocity (PWV) in 68 SLE women with a normal or almost normal kidney function and in 71 controls of similar characteristics. None of the participants had a history of an overt CVD. Serum hs-cTnI level was measured using the chemiluminescence method. Factors associated with an increased PWV (iPWV) were identified and multivariate analysis was performed. When detectable, patients tended to have had higher hs-cTnI levels than controls [2.9 (2.3–4.0) vs 2.4 (2.2–4.1); p = 0.098] and were more likely to have detectable hs-cTnI [50% vs 28%, odds ratio (OR) 7.0; 95% confidence interval (CI) 0.008–0.013]. Also, patients with iPWV were more likely to have detectable hs-cTnI than those with normal PWV (OR 6.4; 95% CI 0.019–0.026). In the multivariate analysis, the age at SLE diagnosis (OR 1.24; 95% CI 1.04–1.48), systolic blood pressure (OR 1.28; 95% CI 1.10–1.48) and detectable hs-cTnI level (OR 2.04; 95% CI 1.18–3.50) were independently associated with an iPWV. The negative predictive value of having an iPWV with undetectable hs-cTnI levels was 88%. Hs-cTnI may be a useful biomarker for the identification of SLE patients with iPWV as a surrogated marker of subclinical atherosclerosis. Specifically targeted prospective studies are needed to confirm this hypothesis.

Secondary arterial hypertension (HTN) can be caused by primary hyperaldosteronism, renovascular disease, sleep apnea syndrome, chronic kidney disease, drug use, etc. In addition, some urological disorders such as hydronephrosis can cause hypertension due to an increase in intraglomerular pressure that activates the renin angiotensin system.