Ambulatory blood pressure monitoring and parallel polysomnographic study were performed in 116 adult males divided into 6 groups. Thirty blood-pressure (BP) and polysomnographic variables were measured to test their usefulness for screening for both arterial hypertension and sleep apnea-hypopnea syndrome (SAHS). The development of severe breathing disorders and hypoxemia during sleep was attributed to SAHS, when compared with measurements in healthy controls and in patients with arterial hypertension. Such disorders manifested as an increased apnea-hypopnea index, apnea index, duration of arterial oxygen saturation of less than 85%, and decrease of average arterial oxygen saturation that correlated with nocturnal average diastolic BP (p=0.0049, p=0.0027, p=0.049 and p=0.0457, respectively). These respiratory disorders resulted in various nocturnal, rather than diurnal, and diastolic and systolic BP variables. The acute antihypertensive effect of continuous positive airway pressure therapy for SAHS significantly reduced the episodes of apnea and hypopnea and the secondary component of hypertension caused by excessive sympathetic stimulation. For the SAHS-induced, dose-dependent component of hypertension that responded to continuous positive airway pressure, the following variables, in decreasing significance, were useful: nocturnal average systolic and diastolic BP and 24-hour average systolic and diastolic BP, as well as percent time elevation and mean blood pressure load. The monitoring of these variables could contribute to early diagnostic and prognostic stratification of complications and adequate therapy of the secondary component of hypertension caused by SAHS.
In the current study, we evaluated the dynamics of oxidative stress markers in patients with acute myocardial infarction (AMI) treated by primary percutaneous coronary intervention (PCI). Thirty consecutive patients with AMI with ST elevation were included. Plasma lipid peroxidation end product malondialdehyde (MDA) and total antioxidant capacity (TAC) in blood plasma were evaluated. Peripheral venous blood samples were obtained prior to reperfusion and at five time points after reperfusion. The control group consisted of 20 ischemic patients without acute coronary syndrome. TAC in the AMI group at admission was lower than in control patients (1.26 + 0.32 vs. 1.52 + 0.24 mmol/l). Within 1 h after reperfusion, in most cases, values significantly declined (1 min, 1.10 + 0.33 mmol/l; 1 h, 1.06 + 0.21 mmol/l [p= 0.03]). After 3 h, values began to increase (1.14 + 0.29 mmol/l) and returned to basal values after 3 d (1.29 + 0.24 mmol/l). MDA levels in AMI patients at admission were higher than in control patients (1.66 + 0.55 vs. 1.44 + 0.55 mmol/l) but showed a sustained decrease over the 3 h after reperfusion of the occluded artery (1 min, 1.57 + 0.37 mmol/l; 1 h, 1.50 + 0.35 μmol/l; 3 h, 1.35 + 0.59 μmol/l [p = 0.03]). Reperfusion of the occluded coronary artery by PCI in AMI lead to an immediate decrease in TAC, suggesting formation of reactive oxygen species. However, the MDA level significantly decreased after reperfusion. This may suggests less reperfusion injury after PCI.
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