Arterial hypertension (AH) and Osteoarthritis (OA) are related closely in elderly and associated with metabolic syndrome. They are regarded to be co-morbid, so have common aethiopathogenetic chains, coexist frequently, contribute to progression. In addition, treatment of one may also worsen course of other disease so it is vital to analyze modern literature as well as clinical, laboratory data related to course of AH and OA, estimate treatment results
138 patients with Ah with comorbid OA were examined. Full clinical investigation, ABPM, questionnatries related to life quality, VAS on symptoms degree, night sleep, life quality. blood chemistry, lipidogram, CRP level, adipokines level control were applied.
Hypocalcemia and hypercalciuria in AH influence mineral density of subchondral bone altering metabolic status of nearly located cartilage. Atherosclerotic lesions of arteries worsen ischemia state of synovial-cartilage complex and fail reparative mechanisms. Dysadipokinaemia that is worse in OA + AH increases oxidized LDL-induced increase of systemic production of reactive species of oxygen. Pain and inflammatory edema can mask manifestations of congestion in large circulation circuit in case of chronic heart failure. Hypodynamia that is result of pain facilitates development of obesity, which, in turn, switches on a lot of additional molecular interactions worsening course of basic pathology. Night symptoms of OA contribute into non-dipper profile change in OA and AH. Non-selective NSAIDs may increase blood pressure, selective - increase rate of heart-related acute events.
AH and OA have multiple symptoms masking the course one of another. Search for effective metabolic, cardio- and chondroprotective remedies is actual.