MICRO- AND MACROVASCULAR ALTERATIONS IN RHEUMATOID ARTHRITIS COMPARED TO TYPE 2 DIABETES MELLITUS: EVIDENCE OF SIMILAR DEGREE OF ORGAN DAMAGE

Abstract

Objective: Rheumatoid arthritis (RA) is characterized by excess cardiovascular risk attributed to the chronic inflammatory load in combination with the accumulation of traditional cardiovascular risk factors. RA is being currently perceived as a cardiovascular risk factor equivalent to type 2 diabetes mellitus (DM2), although recent relevant studies have provided conflicting results. The aim of the present study was to compare markers of micro- and macrovascular dysfunction between patients with relatively well-controlled RA and patients with DM2. Design and method: Patients with RA who presented low levels of systemic inflammation and patients with DM2, who were free from cardiovascular comorbidities including hypertension, were studied. A control group that comprised of healthy volunteers was additionally included. All participants underwent applanation tonometry (Sphygmocor device) to assess a) carotid-femoral pulse wave velocity (PWV), b) augmentation index corrected for 75 bpm (AIx@75), c) central systolic/diastolic blood pressure (cSBP/cDBP) as markers of large artery stiffening. Subendocardial viability ratio (SEVR) or Buckberg index was measured with the same device as a functional marker of microvascular myocardial perfusion. In addition, carotid ultrasound was applied to evaluate a) carotid intima-media thickness (cIMT), as a marker of systemic atherosclerosis, and b) beta-stiffness index, as a marker of local stiffness in the carotid arteries. Results: We studied 31 patients with RA at remission or low disease activity, 32 patients with DM2 and 69 controls matched for age and office blood pressure. Significant differences were observed in several outcomes of the study between patients and controls; by contrast, none of the studied parameters (PWV, AIx@75, cSBP/cDBP, cIMT, beta-stiffness index, and SEVR) significantly differed between patients with RA and patients with DM2 (Table 1). Conclusions: Patients with RA present impaired markers of micro- and macrovascular dysfunction, even in the absence of cardiovascular comorbidities including hypertension and whilst at remission or low disease activity. Moreover, the degree of divergent micro- and macrovascular alterations in this well-characterized group of RA patients appears comparable to that associated with DM2. These findings are line with the widely held perception that RA should be regarded as a novel cardiovascular risk factor equivalent to DM2.