Adiponectin resistance parameter as a marker for high normal blood pres-sure and hypertension in patients with metabolic syndrome.

INTRODUCTION: The different degrees of adiponectin/insulin sensitivity and dysfunctional adipose tissue lead to the development of hypertension (HT). This study aimed to determine adiponectin (AD) concentration in patients with metabolic syndrome (MetS) and high-normal blood pressure or hypertension and to investigate the importance of Homeostatic Model Assessment-AD (HOMA-AD) index in assessing adiponectin/insulin resistance in hypertension. METHODS: This cross-sectional study involved 150 subjects divided into two groups: with MetS (and high-normal blood pressure, n =50; and HT, n =50), and controls without MetS (n =50). In all subjects, serum adiponectin concentration was measured by enzyme-linked immunosorbent assay method. Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and HOMA-AD index were calculated. RESULTS: The results showed that, compared to the control group, serum AD concentrations were significantly lower in patients with MetS and high-normal blood pressure (p =0.008), and the lowest in group MetS and HT (p =0.001). High AD levels and low HOMA-AD were significantly associated with decreased blood pressure values. In patients with MetS, the value of HOMA-AD≥1.13 was associated with a higher risk of developing high-normal blood pressure. Furthermore, the value of HOMA-AD≥2.63 was associated with a higher risk of developing hypertension. CONCLUSIONS: Hypoadiponectinemia is associated with hypertension, especially in the early stages of the disease. The serum AD levels and HOMA-AD index may be useful markers for identifying patients at risk for high-normal blood pressure and hypertension. HIPPOKRATIA 2020, 24(1): 3-7.

High clinical accuracy of asymmetric dimethylarginine and symmetric dimethylarginine in patients with ischemic heart disease.

Elevated plasma concentrations of asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) were found in various clinical settings including coronary heart disease. To assess ADMA and SDMA diagnostic validity in patients with different stages of ischemic heart disease, we studied these markers in patients having stable angina pectoris (SAP), unstable angina (USAP), and acute myocardial infarction (AMI). The results were compared with the values of healthy individuals. Plasma ADMA and SDMA levels were measured by high-performance liquid chromatography. In all patient groups both markers were significantly elevated in comparison with control ones (p < 0.001). In SAP patients, the median ADMA value was 0.75 (0.31-2.73) µmol/L, and SDMA 1.11 (0.69-0.1.42) µmol/L, in USAP patients, the marker values were 0.94 (0.34-3.13) µmol/L and 1.23 (0.88-4.72) µmol/L, and in AMI patients, 0.98 (0.48-2.01) µmol/L and 1.26 (0.75-2.93) µmol/L, while in healthy subjects they were 0.31 (0.17-0.87) µmol/L and 0.29 (0.20-0.83) µmol/L, respectively. SDMA was found significantly different in SAP and AMI patients (p < 0.05). Diagnostic accuracy was determined by receiver operating characteristic (ROC) curve analysis. The highest area under the ROC (AUC) for ADMA was obtained in AMI patients (0.976), while for SDMA in USAP patients (1.000). There was no significant difference between the AUCs. The greatest sensitivity and specificity were found in the USAP group (95.65 and 96.30 % for ADMA, and 100 % for each characteristic of SDMA). Considering these results, SDMA showed better clinical accuracy in assessing ischemic disease, where it could be used as a valid marker and a therapeutic target.

Changes of lipid peroxides and antioxidative factors levels in blood of patients treated with ACE inhibitors.

In 14 patients (4 males and 10 females) with systemic hypertension plasma and erythrocyte lipid peroxides, plasma and erythrocyte catalase activity, plasma glutathione S-transferase (GST) activity, blood reduced glutathione (GSH) content and erythrocyte oxidant stress were investigated. All parameters were performed after clinical examination and then the patients were assigned to receive ACE inhibitor therapy, captopril (25-50 mg given twice per day) or enalapril (10-40 mg given twice per day). After six months the determination of lipid peroxides and antioxidative factors was repeated. At the beginning of the study both treated groups showed significantly higher plasma lipid peroxides compared to the control group. Both used ACE inhibitors produced significant decrease of plasma lipid peroxides after six months. Blood GSH content was also significantly higher in both patient groups before the treatment compared to the controls. Neither captopril nor enalapril produced any significant effect on GSH. Initial values of plasma GST activity in the patients were similar to the control group and did not significantly change after six month treatment. The patients assigned to receive enalapril showed significantly enhanced initial plasma catalase activity according to the controls. After six months treatment both ACE inhibitors significantly decreased plasma catalase activity. Erythrocyte lipid peroxides, erythrocyte catalase activity and oxidant stress of erythrocytes in both groups studied neither differ significantly at initial time of investigation according to the control group nor during or after six month treatment.

[Painless ST segment depression during exercise stress tests in patients after acute myocardial infarct]. / [Bezbolna depresija ST segmenta izazvana testom fizickim opterecenjem bolesnika s prebolelim akutnim infarktom miokarda.

A group of 125 patients (of the total of 400 patients) had ischaemic ST-segment depression (greater than or equal to 1 mm) on exercise electrocardiogram. Of 125 patients with ischaemic response on exercise electrocardiogram 83 (66.4%) patients had both ST-segment depression and anginal pain, and 43 (33.6%) patients were without ischaemic symptoms during exercise testing. There was no difference with regard to sex and age between patients with and without anginal pain. There was no difference in frequency of arterial hypertension, but diabetes mellitus was more frequent in patients with painless ST-segment depression than in patients with painful ST-segment depression. Left ventricular function was more deteriorated in patients with painless ST-segment depression (PEP/LVET = 0.390 +/- 0.028) than in symptomatic patients (PEP/LVET = 0.366 +/- 0.042; P/0.001). There was no difference in heart rate on peak exercise and in magnitude of ST-segment depression in patients with and without anginal pain.