Mental stress, heart rate and endothelial function in patients with syndrome X.

BACKGROUND: The aim of the study was to determine whether the baseline heart rate (HR) and changes in HR after mental stress (MS) can influence endothelial function in syndrome X. METHODS: Forty four patients with syndrome X (F/M: 21/23, mean age: 55.4 +/- 10.7 years) were examined. The endothelium-dependent flow-mediated dilation (FMD) was defined as the percentage change in the brachial artery diameter during reactive hyperaemia related to baseline (%FMD). The %FMD was assessed before and after (at 10, 30, and 45 min) standardised three-minute MS. HR and blood pressure were monitored simultaneously. The %FMD values were compared between subgroups characterised by baseline HR, maximum HR and DHR, and HR after MS below and over the median values. RESULTS: The values of %FMD measured at 10, 30 and 45 min after MS (4.39 +/- 5.4%, 4.99 +/- 3.9%, 4.03 +/- 3.5%, respectively; p < 0.001) were significantly lower than baseline values (7.73 +/- 4.9%). Impaired vasodilatation after MS was observed in the following subgroups of patients: those with baseline HR below the median (< 71.5 bpm; baseline: 8.35 +/- 5.8%; 10 min: 2.87 +/- 3.6%, 45 min: 4.56 +/- 3.9%; p < 0.001); those with HR after MS below the median (< 76.5 bpm; baseline: 8.19 +/- 5.5; 10 min: 3.88 +/- 4.3%, 45 min: 4.59 +/- 3.7%; p < 0.01); and those with maximum HR after MS below the median (< 84 bpm; baseline: 8.88 +/- 5.6%; 10 min: 3.88 +/- 3.8%, 30 min: 5.88 +/- 3.9%, 45 min: 4.51 +/- 3.8; p < 0.01). CONCLUSION: The stress-induced endothelial dysfunction syndrome X is related to the baseline HR and the changes in HR after MS, suggesting that the autonomic nervous system plays a part in its pathogenesis. (Cardiol J 2007; 14: 180-185).

Inflammatory markers in a 2-year follow-up of coronary artery disease.

Our study was designed in an attempt to determine the dynamics of changes in serum tumor necrosis factor (TNF)-alpha, soluble forms of its receptors (sTNFR 1, sTNFR 2), and adhesion molecules (sE-selectin, sP-selectin, sVCAM-1, sICAM-1) over a 2-year follow-up of patients with coronary artery disease (CAD). The study involved 70 patients with stable CAD (stable angina class II/III according to the Canadian Cardiovascular Society) and 20 apparently healthy subjects. Over the follow-up period a marked attenuation of angina (P<0.001) was observed. Interventional treatment (percutaneous coronary intervention, coronary artery bypass grafting) was used in 53 CAD patients. Laboratory analysis revealed a significant decrease of serum TNF-alpha and sTNFR1 at 2 years (TNF-alpha: 12.1+/-0.7 pg/ml; sTNFR 1: 1306+/-46 pg/ml) as compared to baseline levels (16.5+/-0.7 pg/ml, P=0.030; 1551+/-82 pg/ml, P=0.048, respectively). The levels of sP-selectin (159+/-7 vs 201+/-14 ng/ml, P<0.01) and sICAM-1 (133+/-4 vs 153+/-6 ng/ml, P<0.05) were found to be significantly increased as compared to the baseline. Interventional procedures resulted in suppression of both cytokine (TNF-alpha, sTNFR 2) and adhesion molecule (sE-selectin, sP-selectin) activation in the CAD group. The baseline and post-follow-up TNF-alpha and sTNFR 1 levels showed persistent elevation in CAD patients as compared to the controls (9.0, 956.3 pg/ml, respectively; P<0.01). There were no differences between baseline and final cytokines and adhesion molecules in healthy subjects. The course of CAD as modified by a clinically effective therapy is characterized by changes of immune markers activation. Revascularization seems to be an important factor suppressing both cytokine and adhesion molecule activation in CAD patients.

[Immunologic activity in coronary heart disease and atherosclerosis of the lower extremities]. / Aktywacja immunologiczna w chorobie wiencowej i miazdzycy naczyn konczyn dolnych.

Cytokine activation may be connected to increase of clinical symptoms both of coronary heart disease and lower limbs atherosclerosis. Our aim is to determine the influence of the atherosclerosis generalization upon immune activation in coronary heart disease, with regard to ECG stress test. 127 patients have been included in the study: 21 with stable angina and peripheral artery disease (PAD)--group A, and 106 with stable angina--group B. 20 healthy persons comprised the control group (group K). The serum concentration of TNF alpha, sTNFR 1, E-selectin and sVCAM-1 has been measured before and after the ECG stress test, using the ELISA method. Serum concentration levels of TNF alpha (A: 17.8 +/- 6.2 pg/ml, B: 17.4 +/- 3.8 pg/ml) and sTNFR 1 (A: 1678.5 +/- 600 pg/ml, B: 1376.4 +/- 558 pg/ml) have been significantly higher in both research groups than in the control group K (8.3 +/- 1.4 pg/ml, p < 0.001; 1093.9 +/- 457 pg/ml, p < 0.01). The sTNFR 1 concentration has been significantly higher in group A than in group B (p < 0.05). A significant post-exercise increase in E-selectin serum concentration has been observed, regardless to coincidence of lower limbs atherosclerosis. The atherosclerosis generalization level, e.g. the prevalence of PAD, in patients with coronary heart disease has an influence on immune activation--patients with lower limbs atherosclerosis are characterized by higher sTNFR 1 serum level. The ECG stress test induces the increase of E-selectin serum concentration in coronary patients, regardless of PAD.