Henryk Wysocki

Impairment of Endothelial Function in Unipolar and Bipolar Depression

BACKGROUND Previous studies have suggested an association between abnormal endothelial function and depression. We therefore tested this hypothesis in patients with depression in the course of mood disorders and assessed the effect of antidepressant treatment. METHODS Psychometric evaluation and hemodynamic and endothelial function studies using pulse wave analysis were performed on a group of 31 patients with unipolar or bipolar depression. The control group consisted of 18 healthy subjects, age- and gender-matched. RESULTS Arterial endothelial function was impaired in patients compared with that in control subjects, both during a depressive episode and when in remission after pharmacological treatment. The diagnosis, intensity of depression, and type of antidepressant drugs did not influence the results. CONCLUSIONS The impairment of endothelial function might constitute a trait marker of the biological make-up of patients with mood disorders and might contribute to the increased frequency of cardiovascular conditions observed in these patients.

Prospective evaluation of hydroperoxide plasma levels and stable nitric oxide end products in patients subjected to angioplasty for coronary artery disease

BACKGROUND Oxidative stress appears to be involved in several processes that contribute to atherogenesis and restenosis following vascular intervention. METHODS The aim of our study was to evaluate prospectively the plasma concentrations of a hydroperoxide (ROOH) and nitric oxide end product (NO(x)) in patients subjected to coronary angioplasty (PTCA) and routine control angiography 6 months after the initial procedure. We prospectively studied 48 consecutive patients (39 men, nine women, mean age 52 years) with stable angina who underwent successful elective angioplasty. A vascular segment was considered successfully treated when the residual luminal narrowing in the dilated segment immediately after angioplasty was <50%. Angiographic follow-up was obtained in all of the patients. Plasma samples were drawn at baseline (before angioplasty) and serially after angioplasty (1, 3 and 6 months afterwards). Hydroperoxides were determined by the FOX II assay (ferrous oxidation in xylenol orange, Pierce Rockford, IL). Nitrate was converted in the presence of NO3 reductase. The Griess reagent was used for the measurement of NO2. RESULTS The overall angiographic restenosis rate was 35%. There were no significant differences in clinical variables between the patients with or without restenosis. The baseline levels (0.8+/-0.09 vs. 0.6+/-0.2 micromol/l) as well as the concentrations of authentic lipid hydroperoxide in plasma after 1 month (0.7+/-0.09 vs. 1.0+/-0.2 micromol/l) and 6 months (0.8+/-0.1 vs. 1.0+/-0.2 micromol/l) were similar in both groups. Three months after the angioplasty a significant increase in the ROOH level was noticed in the patients with restenosis (0.9+/-0.1 vs. 1.4+/-0.2, P=0.04). Plasma levels of NO(x) were similar in both groups at baseline (23.6+/-2.1 vs. 22.7+/-2.6 micromol/l) and 1 month after procedure (24.4+/-2.2 vs. 23.4+/-3.3 micromol/l). However, in patients with restenosis significant decreases in stable NO end products were observed 3 and 6 months after PTCA (18.1+/-1.5 vs. 13.3+/-1.7, P=0.04; 14.2+/-1.0 vs. 8.7+/-1.3, P=0.02, respectively). CONCLUSIONS In patients with angiographic restenosis a significant increase in lipid peroxidation accompanied by a reduction in the stable end products of nitric oxide in plasma is observed several months after PTCA.

J-wave formation in patients with acute intracranial hypertension

Various electrocardiographic changes are found in patients with increased intracranial pressure. The most common findings are sinus bradycardia, QT prolongation, ST-segment changes, and T- or U-wave abnormalities. The presence of J wave is reported rarely. We describe 3 patients with increased intracranial pressure caused by different cerebral pathologies accompanied by the dynamic formation of J waves in time.

Add-On Therapy with a Nighttime Dose of Doxazosin in Patients with Uncontrolled Hypertension: Effects on Autonomic Modulation of the Cardiovascular System

This study was designed to determine whether or not the addition of a single nighttime dose of doxazosin in extended-release form (GITS; gastrointestinal therapeutic system) would affect the autonomic modulation of the cardiovascular system in patients with uncontrolled hypertension treated with a multi-drug regimen. Resting 5-min noninvasive finger blood pressure and ECG signals, as well as 24-h Holter ECGs, were recorded in 30 patients with uncontrolled hypertension on multi-drug treatment before and after 16-week add-on therapy with doxazosin GITS. Cardiovascular autonomic modulation was evaluated by spectral analysis of heart rate variability (HRV) and a cross-correlation method for spontaneous baroreflex sensitivity (BRS) in 5-min resting recordings, and by the analysis of Poincaré plots and phase-rectified signal averaging of the duration of cardiac cycles in 24-h ECG recordings. This combined therapy significantly reduced systolic pressure (19.4±3.5 mmHg; p<0.0001), diastolic blood pressure (9.4±2.0 mmHg; p=0.0003), and pulse pressure (10.0±2.8 mmHg; p=0.0021). Concomitantly, there was a significant increase in resting spontaneous BRS (p=0.0191) and increases in 24-h short-term (p=0.0129) and total (p=0.0153) HRV, but with no significant change in heart rate or other measures of HRV. The improvements in HRV and BRS were observed mainly in patients already treated with thiazide diuretics. There was a significant association (r=0.49; p=0.0065) between the degree of change in diastolic blood pressure and short-term HRV caused by the combined treatment. The addition of 4 mg doxazosin GITS to multi-drug antihypertensive therapy is associated with an improvement in cardiovascular autonomic control.

The influence of electrical cardioversion on superoxide anions (O2−) production by polymorphonuclear neutrophils, hydrogen peroxide (H2O2) plasma level and malondialdehyde serum concentration

We studied the influence of electrical cardioversion on unstimulated and stimulated superoxide anion production by polymorphonuclear neutrophils in 22 patients with atrial flutter or atrial fibrillation. We also estimated hydrogen peroxide plasma level, as well as malondialdehyde serum concentration, in these subjects. We noted an increase in spontaneous production of superoxide anions from 14.9 +/- 1.8 nmol/10(6) neutrophils per 20 min to 21.37 +/- 2.7 nmol/10(6) neutrophils per 20 min (P = 0.002) in neutrophils obtained after electrical cardioversion. Similarly, stimulated production of O2- also increased after electrical cardioversion (41.8 +/ 3.4 nmol/10(6) neutrophils per 20 min vs. 59.0 +/- 5.9 nmol/10(6) neutrophils per 20 min, P = 0.0027). Moreover, hydrogen peroxide plasma level increased significantly after electrical cardioversion (39.9 +/- 6.2 mumol/l vs. 53.4 +/- 7.6 mol/l, P = 0.003). Serum malondialdehyde concentration also increased after countershock (2.56 +/- 0.26 nmol/ml vs. 2.94 +/- 0.26 nmol/ml, P = 0.023). These results seem to indicate that electrical cardioversion may lead to polymorphonuclear neutrophils activation, increased H2O2 production and lipid peroxidation.

Albuminuria and VEGF as early markers of cardiovascular disturbances in young type 1 diabetic patients

AIMS The aim of the study was to assess myocardial perfusion by means of non-invasive diagnostic methods and measurement of the plasma concentration of vascular endothelial growth factor (VEGF) in patients with long-lasting type 1 diabetes. METHODS AND RESULTS The study was performed on 41 Type 1 diabetic patients (23 females, 18 males), aged 30±7.6 with a duration of disease 15.2±5.5years. 17 patients exhibited microalbuminuria (10 females, 7 males) and 24 subjects were without microalbuminuria (13 females, 11 males). The methods used included a 24-h ECG tape, an exercise treadmill test, echocardiological evaluation with dobutamine and atropine challenge and single photon emission computer tomography (SPECT) at rest, and after dipyridamol induction of ischemia. All the exercise and stress echocardiography tests were negative. There were significant differences between microalbuminuric and normoalbuminuric subjects in the duration of their exercise tests (586.9±110.5 vs. 664.9±133.2s, p=0.027), performed work (11.4±1.6.vs. 12.6±1.8 METs, p=0.045), achieved pulse limit (89.1±3.6 vs. 92.6±5.2%, p=0.037), rest ejection fraction (55.8±8.7 vs. 62.0±4.4%, p=0.040), abnormal changes in SPECT (53 vs. 21%, p=0.047) and VEGF concentration (101.5±7.8 vs. 75.15±16.5pg/ml, p<0.05). The presence of retinopathy increased 12-fold the probability of significant changes in the SPECT (OR 12.1, 95% CI 1.38-105.64, p=0.02) and nephropathy (OR 4.27; 95%CI 1.09-16.83, p=0.03). CONCLUSION Asymptomatic patients with long lasting type 1 diabetes may have disturbances in myocardial perfusion, especially these with microalbuminuria.

Neutrophils are active in total joint implant loosening.

Background Polymorphonuclear neutrophils (PMN) are the first cells to take part in the local foreign body reaction in aseptic loosening of endoprostheses. The aim of this study was to evaluate the systemic host reaction to total joint replacement by measuring the production of nitric oxide by neutrophils before and after total joint replacement.Patients and method Blood samples were collected from 33 patients (27 hips and 6 knees) before surgery, and 2 weeks, 2 months and 2.5–3 years after surgery. The levels of nitric oxide produced by PMN were measured by the method described by Markert et al. (1994).Results Patients reporting pain in the region of the implant 3 years after surgery, and also patients with radiographic signs of loosening, had higher production of NO in the early period and 3 years after the implantation than those with good clinical results.Interpretation We propose that elevated levels of nitric oxide production by PMNs may serve as a marker of total joint prosthesis loosening.

Aortic excess pressure and arterial stiffness in subjects with subclinical white matter lesions

a Department of Radiology, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland b Department of Cardiology-Intensive Therapy, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland c Institute of Physics, University of Zielona Gora, 4a Szafrana, 65-516 Zielona Gora, Poland d Department of Surgery, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland

Contribution of arterial excess pressure and arterial stiffness to central augmentation pressure in healthy subjects.

pressure in healthy subjects J. Piskorski , T. Krauze , K. Katulska , M. Wykretowicz , A. Milewska , D. Przymuszala , H. Wysocki , A. Wykretowicz ⁎, P. Guzik b a Institute of Physics, University of Zielona Gora, 4a Szafrana, 65-516 Zielona Gora, Poland b Department of Cardiology-Intensive Therapy, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland c Department of Radiology, University School of Medicine, 49 Przybyszewskiego, 60-355 Poznan, Poland