Клиничко-дијагностички пристап кон проценка на коронарна атерогенеза кај болни со системски лупус еритематозус

Abstract

Introduction: Numerous epidemiological and clinical studies confirm the strong proatherogenic potential of systemic lupus erythematosus (SLE), with an accelerated course of atherogenesis, the dominantion of its subclinical form, and the impact on the younger population of patients. The unfavorable signs of SLE associated atherosclerosis are explained by the exaggerated effect of the associated traditional proatrogenic risk factors and lupus specific risk factors of atherosclerosis: the severity of the underlying disease and the inflammatory vascular process, the poor control of the disease, the adverse effects of corticosteroid therapy on the risk factors, associated endothelial dysfunction, and a procoagulant tendency. Theese days prolonged survival of patients with SLE allows the progression of the atherosclerotic process, with more frequent destabilization of atheroma plaques and occurrence of a premature type of infarction in asymptomatic, young and premenopausal women. The motive for the scientific research of the problem of CAD in patients with SLE is derived from the stated specificities of atherosclerosis in SLE and from the insufficient risk-stratification diagnostic procedures for early diagnosis. Some of these procedures are: monitoring of risk factors for atherosclerosis, biological markers of inflammation and endothelial dysfunction, and in particular the inclusion of diagnostic techniques - nonvisual and visual, for morphological and functional evaluation of CAD. In addition to screening of these diseases in patients with SLE, world literature is also focused on preventing them through prevention of risk factors - traditional and SLE-specific and good control of the underlying disease. The aim of this scientific research was to examine the proatherogenic profile (representation of the traditional and SLE-specific risk factors of atherogenesis), the intensity of vascular inflammation and endothelial dysfunction (CRP, endothelin) in the subjects with SLE, in the younger and the elderly, and control subjects (without SLE) and correlate with the status of myocardial perfusion and left ventricular function. Material and methods: 120 patients were included in this study, 60 with SLE and 60 control subjects (without SLE), grouped into age groups under and over 45 years. The proterogenic profile of the patients was assessed on the basis of the clinical and laboratory data for the status of the underlying disease - SLE (antibody values, procoagulant markers, CRP, endothelin) and clinical and laboratory data of interest for prediction of CAD (traditional risk factors for atherogenesis). All included subjects with SLE, independently of the clinical and biochemical prediction of the existence of CADs, were subjected to an assessment of myocardial perfusion with 99mTc MIBI ECG synchronized SPECT Myocardial Perfusion Scintigraphy (MPS) (one-day standalone Dipyridamole Protocol) for the detection of CAD, quantitative evaluation of the intensity and extent of CAd, left ventricular volumes, global and regional function, indexes of transient ischemic dilatation. Results. Pathological MPS finding was more commonly observed in SLE subjects (45% of all) compared with control group (31.7% of all), or SLE subjects had 1.8 times higher risk of myocardial perfusion disorders. In the risk profile of SLE examinees, the traditional risk factors such as HTA, HLP, DM are more common than in the general population, therefore they have significant pathogenic role in atherogenesis, but are not solely responsible for the higher prevalence of pathological MPS among these patients. Only patients with pathological MPS compared to those with normal MPS findings, had high significant differences to some of the SLE specific risk factors such as high disease activity, significantly higher LOOP index, hcCRP, endothelin, less aggressive drug treatment. These features are very likely to explain the fact that SLE appears as a strong, independent risk factor for atherosclerosis. A pathological MPS finding with the same prevalence occurs also in the group of elderly and younger than 45 years patients, with an almost identical proteroegenic risk profile. Myocardial perfusion disorders in our SLE and control subjects, otherwise oligosymptomatic, with a low to moderate risk for CAD, are predominantly mild and moderate, reversible, less fixed, with single-vessel LAD involvement, possible from microcirculatory nature. A complex of features: fatigue, increased RV, lower LV volumes, and absence of cardiac reserve in SLE subjects (significantly different compared to the control group) indicate initial diastolic and probably systolic LV dysfunction in SLE examinees, both in the elderly and younger groups. Conclusion: SLE patients have more risically proatherogenious profile based on a higher prevalence of traditional risk factors such as HTA, CLP, DM, but an even more significant impact on atherogenesis as an additional risk for atherosclerosis, especially in young, premenopausal women with SLE and they have specific risk factor such as high activity of the disease (high SLEDAI-2K scores), high inflammatory activity (hcCRP), endothelial dysfunction (endothelin) and less aggressive therapeutic approach - monotherapy, especially without antimalarials. MPS as a highly sensitive and specific method for assessing myocardial microcirculatory perfusion can become an integral diagnostic method in evaluating young, premenopausal women with SLE with a present risic proatherogenous profile, especially if they are asymptomatic for the CAD or with symptoms of atypical chest pain and fatigue. Depending on the degree of abnormality, MPS findingс may stratify these patients in group with low risk (1-5% in the case of mild and moderate pathological MPS) and a group with high risk (over 5% in moderate and severe pathologic MPS) of vascular events. Also, when SLE patients with low proteroegenic risk, MPS show a normal finding, it has a more favorable prognostic information for MI risk of less than 1% in the next 2 year period).