Aims: The aim of the study was to evaluate the correlations between clinical symptoms (pain), physical examination, ultrasound (US), and radiological findings in patients with bilateral knee osteoarthritis (OA). Material and methods: Knee pain was appreciated during medial and lateral palpation of each knee joint and using visual analogue scale (VAS) and The Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). US evaluation (osteophytes, meniscal protrusion, synovial fluid, femoral hyaline cartilage thickness) and radiological assessment (osteophytes, femoral-tibial space, Kellgren-Lawrence [K-L] score, enthesopathies) were performed by two examiners blinded to the clinical results and to each other. All these findings were scored with a five-point scale. Results: A total of 52 consecutive patients aged 63.44±9.49 were examined, 33 (80.5%) being females. In patients with bilateral knee OA the pain, evaluated by WOMAC score and VAS, was correlated with the presence of osteophytes and cartilage thickness but no association with medial meniscal protrusion and effusion was demonstrated. Pain produced by palpation of the knee was strongly associated with the presence of medial osteophytes. VAS and WOMAC scores increased with the severity of radiological and US findings. The presence of osteophytes and articular cartilage damage at US examination were strongly and positively correlated with radiological K-L score. US examiners agreement was good for osteophytes and moderate for meniscal protrusion, cartilage damage, and synovial fluid. The cartilage damage score was the only independent predictor for VAS scale; for WOMAC score the sex, cartilage damage, the presence of medial osteophytes and lateral meniscal protrusion were the independent predictors. Conclusion: Pain intensity was correlated with the severity of US findings, cartilage damage score being an independent predictor for both VAS and WOMAC scores. Medial osteophytes and lateral meniscal protrusion and are independent predictors for WOMAC score.
Cardiovascular autonomic neuropathy is a common form of autonomic dysfunction in diabetes mellitus (DM) and associates abnormalities in heart rate control and in vascular dynamics. This study evaluates the impact of diabetes mellitus on left ventricular diastolic dysfunction (LVDD) and heart rate variability in a group of type 2 diabetes mellitus without signs of cardiovascular disease. The study group consisted of 58 patients, aged 61 ± 8 years, diagnosed with type 2 DM. The subjects were selected from a series of 104 consecutive diabetic patients. All the subjects were on oral therapy or on diet for DM, and ECG was normal for all the subjects. The control group consisted of 45 healthy subjects, matched for age and sex. Heart rate variability was measured using a 24-h ECG monitoring system, and standard 2D and Doppler echocardiography was performed in all the subjects. There are significant differences between groups regarding disease duration, longer in patients with impaired relaxation (11.22 ± 9.17 vs. 8.31 ± 8.95 years), and disease control, worse in impaired relaxation group. Heart rate in impaired relaxation group is significantly higher than in controls, and higher, but not significantly, when compared with normal group (91 ± 10, vs. 88 ± 11 and 71 ± 11, respectively). Cardiac autonomic neuropathy was associated with LVDD in patients with type 2 DM, but without clinically manifest heart disease. Twenty-four-hour ECG monitoring and echocardiography can detect diabetic cardiomyopathy in early stages and should be performed in all subjects.
Hyperuricemia is usually associated with hypertension, diabetes mellitus, metabolic syndrome and chronic kidney disease. Accumulating data from epidemiological studies indicate an association of increased uric acid (UA) with cardiovascular diseases. Possible pathogenic mechanisms include enhancement of oxidative stress and systemic inflammation caused by hyperuricemia. Arterial stiffness may be one of the possible pathways between hyperuricemia and cardiovascular disease, but a clear relationship between increased UA and vascular alterations has not been confirmed. The review summarizes the epidemiological studies investigating the relationship between UA and arterial stiffness and highlights the results of interventional studies evaluating arterial stiffness parameters in patients treated with UA-lowering drugs.
Adipokines are active molecules with pleiotropic effects produced by adipose tissue and involved in obesity-related metabolic and cardiovascular diseases. Arterial stiffness, which is a consequence of arteriosclerosis, has been shown to be an independent predictor of cardiovascular morbidity and mortality. The pathogenesis of arterial stiffness is complex but incompletely understood. Adipokines dysregulation may induce, by various mechanisms, vascular inflammation, endothelial dysfunction, and vascular remodeling, leading to increased arterial stiffness. This article summarizes literature data regarding adipokine-related pathogenetic mechanisms involved in the development of arterial stiffness, particularly in obesity, as well as the results of clinical and epidemiological studies which investigated the relationship between adipokines and arterial stiffness.
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