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H Wysocki

Publications and source records attributed to H Wysocki.

At least 19 recordsLinked to original sources
PubMed2006

Myocardial perfusion SPECT with dipyridamole stress test in cardiac syndrome X.

UNLABELLED: Cardiac syndrome X defines patients with typical anginal chest pain, a positive exercise ECG stress test and angiographically normal coronary arteries. AIM of this study was to evaluate the role of myocardial perfusion SPECT with dipyridamole stress in the diagnosis of cardiac syndrome X. PATIENTS, METHODS: 68 patients with syndrome X aged 32 to 60 years were subjected to myocardial imaging using (99m)Tc-MIBI according to the two-days protocol: at rest and after dipyridamole infusion. Semiquantitative evaluation of the images was based on the assessment of (99m)Tc-MIBI uptake in 17 myocardial segments using a 5-points scale (0 point -- normal uptake, 4 points -- no uptake). Scores obtained in each segment were summed up, constituting the summed rest score (SRS) and summed stress score (SSS). RESULTS: Mean SRS was 7.9 +/- 4.8 and mean SSS was 7.2 +/- 4.4 (non-significant difference). Individual comparison of SRS and SSS values revealed three patterns of scintigraphic images: 1) in 25 patients (36.8%), a paradoxical improvement of perfusion at stress images was found, 2) in 23 patients (33.8%), the myocardial perfusion deteriorated after dipyridamole, 3) in 20 patients (29.4%), no significant change of the myocardial perfusion between rest and stress images occurred. CONCLUSIONS: In cardiac syndrome X, myocardial SPECT with dipyridamole stress shows different patterns of myocardial perfusion that reflects heterogeneity of this pathology.

Electrocardiography↗
PubMed2005

Augmentation index, pulse pressure amplification and superoxide anion production in patients with coronary artery disease.

BACKGROUND: Free oxygen radicals appear to be involved in several processes that contribute to atherogenesis and increased arterial stiffness. METHODS: The aim of our study was to evaluate arterial stiffness and the production of superoxide anions by activated polymorphonuclear neutrophils (PMN) obtained from patients with stable coronary artery disease (CAD). Thirty four consecutive patients were studied (21 men, 13 women, mean age 58 years) who underwent coronary angiography. Arterial stiffness was assessed by pulse wave analysis using a validated system (Sphygmocor Mx, AtCor Medical). Superoxide anion production by activated neutrophils was determined by a spectrophotometric method involving the measurement of cytochrome C reduction. The extent of coronary narrowing was estimated by calculation of the Gensini score. RESULTS: Superoxide anion production by stimulated PMN showed a significant positive correlation with the augmentation index (AIx) and a significant negative correlation with pulse pressure amplification (PPA), (r=0.4, p=0.02; r=-0.5 and p=0.0026 respectively). In multivariable analyses, after adjustment for age, gender and Gensini score, superoxide anions and BMI were significant predictors of AIx (R2=57.37%, p=0.001) and PPA (R2=49.04%, p=0.008). Superoxide anion production was significantly higher in the middle (52.0+/-5.8 nmol O2-/2.5x10(6) PMN/30 min) and upper teriles (62.7+/-5.6) of AIx in comparison with the first tertile 31.8+/-4.1 (p< or =0.05, p< or =0.001). Moreover, superoxide anion production in the highest tertile of PPA was significantly lower (35.6+/-4.3 nmol O2-/2.5x10(6) PMN/30 min) than that in the tertile (60.8+/-6.2, p< or =0.05). Neither the augmentation index nor pulse pressure amplification correlate with the severity of coronary atherosclerosis as indicated by the Gensini score. CONCLUSIONS: markers of arterial stiffness, AIx and pulse pressure amplification correlate with superoxide anion production but not with the severity of atherosclerosis in coronary arteries.

Biomarkers↗
PubMed2005

The influence of growth hormone (GH) therapy on cardiac performance in patients with childhood onset GH deficiency.

OBJECTIVE: There is accumulating evidence that growth hormone (GH) plays an important role in the maintenance of normal cardiac growth and function. Abnormalities in left ventricular diastolic function and impairment of systolic function have also been reported in patients with GHD. In this study, we investigated the effects of 12 months GH replacement therapy on cardiac functional indices measured by echocardiography, the ECG stress test and SPECT imaging. DESIGN: Sixteen patients with childhood onset GHD (age 42.3+/-13.1 years, 10 males) were investigated before, and after, 12 months of GH treatment at a dosage of 0.02 IU/kg/day (7 microg/kg/day). The GH administration resulted in serum IGF-I levels within the normal range in all the patients. The following investigations were performed initially and after 12 months: electrocardiography, systolic and diastolic blood pressure, heart rate measurement, a complete Doppler-echocardiographic examination, treadmill exercise test and Technetium-99m sestamibi single-photon emission computer tomography (SPECT) imaging at rest and after exercise. RESULTS: Echocardiography showed improvement in left ventricular systolic function after GH treatment. End-systolic volume fell from 29.9+/-12.4 to 24.4+/-6.9 ml (p<0.05) and the ejection fraction increased from 56.2+/-7.2% to 63.2+/-6,1% (p<0.01). Left ventricular diameter and wall thickness did not change after GH treatment, although systolic increase in interventricular septum thickness (IVS%) and systolic increase in posterior wall thickness (PWT%) increased significantly (IVS% 52.2+/-31.9% vs. 67.3+/-30.4% and PWT% 48.7+/-20.2% vs. 58.0+/-17.7%, p<0.01, p<0.01, respectively). Contractile function, measured at midwall level, improved as left ventricular midwall fractional shortening (MWS) increased (16.11+/-6.55 vs. 23.30+/-5.89 %, p<0.01) and stress-corrected MWS increased between the examinations performed before and after 12 months of GH treatment (90.97+/-36.66 vs. 133.10+/-32.84 %, p<0.01). Diastolic function did not change, as assessed by early diastolic flow (E), diastolic flow secondary to atrial contraction (A), or the E/A ratio. The LV-mass index did not change significantly after GH treatment (78.4+/-22.1 vs. 81.9+/-21.1g/m(2)). After 12 months of GH treatment the myocardial performance index (MPI) decreased significantly from 0.483+/-0.146 at baseline to 0.410+/-0.086 at the end of the study (p<0.05). There was a trend towards an increase in exercise duration and capacity after GH treatment but the differences did not reach levels of statistical significance. SPECT imaging basally and after 12 months showed normal myocardial perfusion at rest and after exercise in all the patients. In conclusion, GH replacement therapy in adults with GHD demonstrated the beneficial effects on cardiac functions.

Adolescent↗
PubMed2004

Dipyridamole inhibits hydroxylamine augmented nitric oxide (NO) production by activated polymorphonuclear neutrophils through an adenosine-independent mechanism.

Polymorphonuclear neutrophils (PMN) are thought to play a role in reperfusion injury and ischemia. These effects are partly mediated by toxic oxygen species (superoxide anion, hydrogen peroxide and hydroxyl radical) acting at the level of the endothelium. It was demonstrated recently that the superoxide anion reacts with nitric oxide (NO) and that interaction leads to the generation of highly toxic peroxynitrite. Several drugs were tested so far in order to affect PMN function. It was demonstrated that dipyridamole (2,6-bis-diethanolamino-4,8-dipiperidinopyrimido-(5,4-d)-pyrimidine) can influence neutrophil function by inhibiting adenosine uptake. However, this action can not fully explain all of the observed effects of dipyridamole action on PMN metabolism. The aim of our study was to evaluate the influence of dipyridamole on nitric oxide production by activated polymorphonuclear neutrophils. Incubation of PMNs with hydroxylamine (HA) and phorbol myristate acetate (PMA) generated nitrite (36.4+/-4.2 nmol/h 2x10(6) PMN), dipyridamole at 100 micromol/l, 50 micromol/l and 10 micromol/l caused a considerable drop in nitrite production (11.8+/-1.8, 19.7+/-2.7 and 27.4+/-3.2 nmol/h, respectively). Neither adenosine nor the adenosine analogue could mimic the dipyridamole effect. Moreover theophylline, an adenosine inhibitor could not reverse the dipirydamole action on PMN metabolism. We also found that dipyridamole inhibited hydrogen peroxide release from neutrophils. Catalase that scavenges hydrogen peroxide also largely abolished nitric oxide release from PMN. It is evident that dipyridamole inhibits hydroxylamine-augmented nitric oxide production by activated polymorphonuclear neutrophils through an adenosine-independent mechanism.

Adenosine↗
PubMed2003

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.

Angioplasty, Balloon, Coronary↗
PubMed2001

Hydrogen peroxide and superoxide anion production by polymorphonuclear neutrophils in patients with chronic periapical granuloma, before and after surgical treatment.

Chronic periapical granuloma represents a localized tissue injury with well established signs of systemic immunological reactions. The aim of the study was to investigate changes in superoxide anion and hydrogen peroxide production by polymorphonuclear neutrophils (PMN) in patients with chronic periapical granuloma before and after surgical treatment. The affected teeth were extracted from 20 patients with chronic periapical lesions. Blood samples were obtained at admission, before extraction and on day 14. PMNs were isolated from blood samples and superoxide anion (O2-) and hydrogen peroxide (H2O2) production were estimated without stimulation and after stimulation of the cells with opsonized zymosan. Similar procedures were performed with blood samples obtained from 20 healthy controls. Superoxide anions as well as hydrogen peroxide production by unstimulated cells obtained from patients before treatment were significantly higher in comparison with controls. Fourteen days after extraction O2- production by unstimulated cells was higher than the controls and significantly lower in comparison to PMNs obtained before treatment, while H2O2 production was not significantly higher when compared to controls and significantly lower in comparison with PMNs obtained before extraction. The results obtained strongly imply the termination of a generalized inflammatory response after elimination of local inflammation by tooth extraction.

Adult↗
PubMed2001

Stimulation of neutrophil activation during coronary artery bypass grafting: comparison of crystalloid and blood cardioplegia.

BACKGROUND: During myocardial ischemia, activation of polymorphonuclear neutrophils (PMNs) results in the production of free oxygen radicals, which increase myocardial injury. It has been shown that PMNs also produce nitric oxide. It is not clear whether PMNs become activated as a result of their direct contact with ischemic/reperfused myocardium or if PMN activation and free oxygen radical production are effects of specific stimuli released during coronary artery bypass grafting (CABG). The aim of the current study was to evaluate plasma-mediated neutrophil stimulation and production of superoxide anion (O2) and nitric oxide in patients undergoing CABG, and to verify whether crystalloid and blood cardioplegia can modify such stimulation. METHODS: Coronary sinus, peripheral arterial, and venous plasma samples were collected from 50 patients who underwent CABG and were divided into 2 equal groups which received either crystalloid or blood cardioplegia: directly before myocardial ischemia and aortic cross-clamping; at the beginning of reperfusion after aortic clamp release; and 30 minutes after reperfusion. O2 and nitric oxide production by PMN was evaluated by standard methods. RESULTS: There was a significant (p < 0.05) increase in O2 production by PMN incubated with plasma obtained from the coronary sinus immediately after reperfusion in patients receiving crystalloid cardioplegia compared to blood cardioplegia. No difference was observed in plasma stimulation of nitric oxide production by PMN in the 2 groups of patients at different times during the procedure. CONCLUSIONS: Cardioplegia may affect release of neutrophil-oriented stimuli from ischemic myocardium and modify neutrophil activation during coronary artery bypass grafting.

Adult↗
PubMed2001

The influence of short-term treatment with simvastatin on the inflammatory profile of patients with hypercholesterolaemia.

BACKGROUND: Treatment with 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors can reduce cardiovascular mortality of patients with atherosclerosis. This effect is probably due not only to a decrease in concentration of cholesterol, but also to non-lipid-involving mechanisms elicited by the action of statin drugs. OBJECTIVE: To investigate the influence of short-term therapy with simvastatin on markers of inflammation and oxidation processes in patients with hypercholesterolaemia. DESIGN: We administered 20mg simvastatin daily for 12 weeks to 19 patients with hypercholesterolaemia (250-400 mg/dl). Peripheral blood samples for evaluation of plasma concentrations of thiobarbituric acid reactive substances (malonaldehyde), stable metabolites of nitric oxide (NOx) and interleukin 6 (11-6) were taken before and after the therapy. RESULTS: Plasma levels of malonaldehyde decreased significantly (from 4.533+/-0.428 versus 3.690+/-0.310 micromol/l, P = 0.04) during the study period. Similarly, there was a significant decrease in the plasma concentrations of NOx (from 33.477+/-4.352 micromol/l versus 25.919+/-2.561 micromol/l, P = 0.02). There were significant positive correlations between concentrations of total cholesterol and NOx in plasma (r = 0.4397, P = 0.008) and of low-density lipoprotein and NOx (r = 0.3987, P = 0.02). The plasma level of interleukin 6 remained unchanged by the intervention (1.837+/-0.200 versus 1.820+/-0.169 pg/ml, P = 0.54). CONCLUSIONS: Short-term therapy with simvastatin decreases the plasma concentrations of markers of peroxidation of lipids and of stable metabolites of nitric oxide in hypercholesterolaemic patients, but leaves levels of interleukin 6 unaffected.

Female↗
PubMed2000

The influence of treatment of hypercholesterolemic patients with simvastatin on plasma chemotactic activity and adherence of neutrophils.

BACKGROUND: there is some evidence to indicate that statins may affect the function of immune and inflammatory cells. This study investigates the influence of short term treatment with simvastatin on plasma chemotactic activity and adherence of polymorphonuclear neutrophils in hypercholesterolemic patients. METHODS AND RESULTS: 20 hypercholesterolemic patients (250-400 mg/dl) were given simvastatin (20 mg daily for 12 weeks). Peripheral blood samples were taken before and after 4 and 12 weeks of the therapy. The percentage of neutrophils adhering to plastic surface coated with albumin was significantly higher when cells were incubated with plasma obtained after 12 weeks of treatment with simvastatin in comparison with plasma collected before the therapy (unstimulated neutrophils: 5.945+/-0.475% vs. 8.155+/-0.96%, P=0.0477, stimulated neutrophils: 39.09+/-4.540% vs. 29.18+/-3.702%, P=0.032). There was a significant negative correlation between adherence of stimulated neutrophils and total cholesterol levels ((r)=-0.2796, 95% CI -0. 4999 to -0.02526, r(2)=0.07817, P=0.032). Migration of neutrophils towards plasma obtained after 12 weeks of treatment with simvastatin was significantly higher than towards plasma collected before the therapy (7.038+/-1.127 vs. 4.505+/-0 618 P=0.0475). CONCLUSION: treatment of hypercholesterolemic patients with simvastatin increases the chemotactic activity of plasma and augments the adherence of human neutrophils.

Anticholesteremic Agents↗
PubMed2000

Stimulation of neutrophil integrin expression during coronary artery bypass grafting: comparison of crystalloid and blood cardioplegic solutions.

OBJECTIVES: This study was designed (1) to evaluate the influence of plasma obtained from patients undergoing coronary artery bypass grafting on L-selectin, CD11b, and CD18 expression on human neutrophils and (2) to determine the influence of the use of crystalloid or blood cardioplegia during bypass grafting on plasma-mediated expression of adhesion molecules on polymorphonuclear neutrophils. PATIENTS AND METHODS: Patients undergoing coronary artery bypass grafting were divided into 2 groups to receive crystalloid or blood cardioplegic solutions. Peripheral vein, radial artery, and coronary sinus blood samples were drawn at aortic crossclamping, aortic crossclamp release, and 30 minutes after reperfusion. Human neutrophils were incubated with patients' plasma, and the expression of CD11b, CD18, and L-selectin was determined with flow cytometry. RESULTS: In patients receiving crystalloid cardioplegic solutions, plasma samples collected from the coronary sinus at aortic clamp release and 30 minutes thereafter induced significantly higher expression of neutrophil CD11b and CD18 than plasma samples obtained from a peripheral vein or artery at the same time points. The expression of L-selectin on polymorphonuclear neutrophils was significantly reduced with plasma obtained 30 minutes after reperfusion as compared with samples collected at aortic crossclamp release. In the group receiving blood cardioplegia, no significant differences in CD11b, CD18, or L-selectin expression were found. CONCLUSIONS: (1) Ischemia/reperfusion after coronary artery bypass grafting is associated with the release of factors capable of neutrophil activation from myocardium into the circulating blood. (2) The release of soluble stimuli for neutrophils during bypass grafting may be modified by the cardioplegic solution.

Adult↗
PubMed2000

Effects of trimetazidine on clinical symptoms and tolerance of exercise of patients with syndrome X: a preliminary study.

BACKGROUND: Trimetazidine diminishes angina and improves tolerance of exercise of patients with ischemic heart disease, and has no influence on blood pressure and heart rate. OBJECTIVE: To determine the effect of trimetazidine on angina symptoms and exercise tolerance in patients with syndrome X. METHODS: We investigated the effect of trimetazidine on the clinical symptoms and tolerance of exercise of 34 patients (20 women and 14 men, aged 32-60 years) with syndrome X (angina pectoris, positive result of exercise test, and normal coronary angiogram). The exercise test was performed before initiation of oral administration of trimetazidine therapy (20 mg three times a day) and 1 and 6 months thereafter. RESULTS: We obtained negative results of exercise treadmill tests for four patients (11.76%) after 1 month and five patients (14.71%) after 6 months of trimetazidine treatment. There was also a decrease in the incidence of effort angina after 6 months of treatment (26 patients or 76.47% before treatment versus 13 patients or 38.23% after 6 months of treatment). The drug had no significant influence on the heart rate and blood pressure. The duration for which patients could exercise was significantly prolonged by 1 month (652.9 +/- 206.2 versus 563.4 +/- 190.4 s, P = 0.0047) and 6 months (650.3 +/- 207.8 s, P = 0.0094) of treatment with trimetazidine. CONCLUSION: Treatment with trimetazidine decreases signs of angina during exercise and improves tolerance of exercise of patients with syndrome X.

Adult↗
PubMed1999

Endothelin-1 is involved in plasma mediated stimulation of neutrophil adherence during coronary artery bypass grafting.

OBJECTIVE: Myocardial ischaemia followed by reperfusion during coronary artery bypass grafting (CABG) is known to result in the activation of polymorphonuclear neutrophils (PMN). The activation of PMN during ischaemia/reperfusion may be a result of their direct contact with activated endothelial cells and/or an effect of stimuli released from ischaemic myocardium. Increased expression of adhesion molecules on the PMN surface, after activation, leads to coronary capillary plugging with a subsequent decrease in blood flow. The purpose of the study was to evaluate plasma-mediated stimulation of PMN adhesion during CABG and to verify if endothelin-1 (ET-1), known to be a potent stimulus for PMN, is involved in stimulation of neutrophils adhesion mediated by integrins. METHODS: Coronary sinus, peripheral artery and peripheral venous plasma samples were taken from 11 patients undergoing coronary surgery before aortal cross-clamping, at the beginning of reperfusion and 30 min thereafter. PMN isolated from five healthy volunteers were incubated with the plasma (20 samples per patient) in the presence of saline or a specific ET-1 receptor blocker, and PMN adherence to a microtiter plate covered with a monoclonal antibody against CD 18 antigen (beta-subunit of the integrin family of adhesion molecules) was evaluated. RESULTS: We have observed a significant increase in adhesion of PMN incubated in the presence of saline with the plasma taken from coronary sinus at the beginning of reperfusion (7.79+/-1.64% of adhering cells) as compared with plasma obtained before aortal cross-clamping from the same place (6.78+/-1.3%, P = 0.04) and from peripheral artery at the beginning of reperfusion (6.64+/-1.1%, P = 0.04, means +/- SEM). ET-1 receptor blocker, significantly decreased stimulation of PMN adhesion by coronary sinus plasma obtained at the beginning of reperfusion (6.7+/-1.51%, P = 0.02). Plasma levels of ET-1 (ELISA) in the samples taken from coronary sinus at the beginning of reperfusion, were higher than in samples obtained before myocardial ischaemia or 30 min after reperfusion. CONCLUSIONS: We conclude, that soluble stimuli capable of stimulation of PMN adhesion are released following myocardial ischaemia during CABG and ET-1 may be involved in PMN stimulation.

Adult↗
PubMed1999

Plasma-mediated stimulation of neutrophil superoxide anion production during coronary artery bypass grafting: role of endothelin-1.

BACKGROUND: Activation of polymorphonuclear neutrophils (PMN) and subsequent release of free oxygen radicals, including the superoxide anion (O2-) has been shown to result in postischaemic myocardial dysfunction during coronary artery bypass grafting (CABG). Several neutrophil-oriented stimuli are known to be released from myocardium during ischaemia and reperfusion. Release of endothelin-1 has been documented during CABG. The aim of the current study was to evaluate plasma-mediated neutrophil stimulation and to verify whether endothelin-1, known to be a stimulus for PMN, is involved in plasma-mediated stimulation of PMN during coronary artery bypass grafting. METHODS: Plasma samples from peripheral artery, peripheral vein, and coronary sinus were obtained from 21 patients undergoing CABG before aortic clamping (global ischaemia), immediately after beginning reperfusion, and 30 min after reperfusion as well as from healthy controls. Plasma was incubated with PMN isolated from healthy donors preincubated in the presence of saline or specific endothelin-1 receptor antagonist (ET-A). PMN O2- production was measured spectrophotometrically. RESULTS: Plasma samples taken from the coronary sinus at the beginning of reperfusion were capable of higher stimulation of neutrophil superoxide anion production (24.2 +/- 2.0 nmol/5 x 10(6)PMN/30 min) than plasma obtained before reperfusion (15.6 +/- 1.5; p < 0.05) or plasma taken from peripheral artery (17.1 +/- 1.7; p < 0.05). Preincubation of PMN with endothelin-1 receptor antagonist decreased superoxide anion production by cells exposed to plasma taken from coronary sinus at the beginning of reperfusion (17.6 +/- 2.0, p < 0.05). CONCLUSIONS: Transcardiac release of soluble stimuli for PMN occurs as a result of myocardial ischaemia during CABG. Endothelin-1 may be involved in the plasma-mediated stimulation of neutrophil superoxide anion production.

Adult↗
PubMed1999

The effects of dipyridamole stress test on plasma levels of soluble adhesion molecules intracellular adhesion molecule-1, vascular cell adhesion molecule-1, E-selectin and L-selectin in patients with ischemic heart disease and patients with syndrome X.

BACKGROUND: Adhesion of activated leukocytes to the endothelium as a result of myocardial ischemia/reperfusion has been shown to be involved in the development of tissue injury. Leukocyte adhesion to the endothelium occurs via adhesion molecules expressed on the surface of both cell types. Upon cell activation these proteins may be released into the circulation and measured in a soluble form. AIM: To verify whether the dipyridamole stress test, performed in patients with ischemic heart disease (IHD) and in patients with syndrome X, modifies plasma levels of the soluble adhesion molecules vascular cell adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1), E-selectin and L-selectin. METHODS: Plasma levels of the soluble endothelial adhesion molecules ICAM-1, VCAM-1 and E-selectin, as well as of the soluble leukocyte adhesion molecule L-selectin, were measured in venous blood samples taken before and 7 min after administration of dipyridamole in patients with IHD, patients with syndrome X and healthy individuals. Myocardial perfusion was evaluated using single photon emission tomography. The plasma levels of soluble VCAM-1, ICAM-1, E-selectin and L-selectin were all measured using enzyme-linked immunosorbent assays. RESULTS: After infusion of dipyridamole, plasma levels of ICAM-1 increased significantly in patients with IHD, whereas they remained unchanged in patients with syndrome X and in the control group. In patients with IHD, the initial plasma levels of VCAM-1, E-selectin and L-selectin, before administration of dipyridamole, were higher than those observed in patients with syndrome X and than those in the control group. Plasma levels of soluble VCAM-1, E-selectin and L-selectin decreased significantly in patients with IHD following the dipyridamole stress test, whereas they remained unchanged in patients with syndrome X, and in the control group. CONCLUSION: In patients with IHD, administration of dipyridamole induces myocardial ischemia resulting in modification of plasma levels of the soluble adhesion molecules.

Adult↗
PubMed1999

Fibrinolytic therapy and n-acetylocysteine in the treatment of patients with acute myocardial infarction: its influence on authentic plasma hydroperoxide levels and polymorphonuclear neutrophil oxygen metabolism.

Recently it has been demonstrated that the administration of n-acetylocysteine (NAC), in combination with streptokinase, significantly diminished oxidative stress in patients with myocardial infarction. The aim of our study was to assess the influence of NAC treatment, as adjunct therapy in an evolving myocardial infarction, on the polymorphonuclear count, superoxide anion and hydrogen peroxide levels and nitric oxide production by PMNs and authentic plasma hydroperoxide (ROOH). Treatment of patients with NAC in addition to reperfusion therapy was accompanied by a significant decrease in the number of circulating polymorphonuclear neutrophils. However, the oxygen metabolism of PMNs was not affected by NAC administration. The concentration of authentic plasma hydroperoxide was significantly reduced by the administration of NAC which suggests diminished oxidative stress during acute myocardial infarction.

Acetylcysteine↗
PubMed1998

Exercise-induced increase in hydrogen peroxide plasma levels is diminished by endurance training after myocardial infarction.

We have investigated the influence of physical training on exercise-induced changes in free radical activity in patients after myocardial infarction. Seventeen patients admitted to the cardiac rehabilitation center performed a bicycle ergometry before and after a 3-week endurance training program. The oxygen consumption and carbon dioxide production were measured and the ECG and the systemic blood pressure were monitored during the tests. Blood samples for acid-base equilibrium, lactic acid levels and hydrogen peroxide concentrations were collected directly before and after each exercise test. Exercise-induced increases in systolic blood pressure, heart rate and rate-pressure product as well as lactic acid concentrations were significantly less marked during the bicycle ergometry performed after the rehabilitation program. During the initial exercise test hydrogen peroxide levels increased significantly from 7.15+/-0.74 micromol/l before to 9.09+/-1.04 micromol/l 3 min after the test (P=0.0229). In contrast, no significant changes in hydrogen peroxide concentrations were observed during the exercise test performed after the training (6.31+/-1.05 micromol/l before the test, 5.85+/-1.08 micromol/l after the test, P=0.201). These observations suggest that physical training may have a beneficial influence on free radicals' generation in patients after myocardial infarction.

Acid-Base Equilibrium↗
PubMed1998

Plasma chemotactic activity during dipyridamole induced myocardial ischemia.

BACKGROUND: We have previously reported that transient myocardial ischemia induced during exercise or dipyridamole challenge leads to the release of increased amounts of hydrogen peroxide into circulating blood. It would indicate that the temporary functional changes within myocardial cells may constitute there a sterile inflammatory area. Therefore we decided to evaluate the chemotactic properties of plasma in patients undergoing dipyridamole provocative test, as a sign of released inflammatory mediators. The ischemia occurrence was evaluated with 99mTc-SestaMIBI followed by single photon emission computed tomography (SPECT). METHODS: Blood samples were obtained from the peripheral vein of 42 patients (18 men and 24 women, mean age 61 years). Plasma chemotactic activity was determined by the use of the Boyden chamber method: immediately before dipyridamole challenge (time 0), 7, and 30 min after drug infusion. The migration of control polymorphonuclear neutrophils towards evaluated plasma samples was estimated. RESULTS: Chemotaxis of control PMNs towards plasma isolated from patients without signs of myocardial ischemia 7 min after dipyridamole administration was significantly diminished in comparison with baseline values (p=0.003). Plasma obtained 7 min after dipyridamole infusion from patients manifesting signs of myocardial ischemia by SPECT attracted control PMNs significantly more intensively in comparison to plasma isolated at time 0 (p=0.0005). CONCLUSIONS: The obtained results indicate that transient myocardial ischemia induced by dipyridamole challenge leads to generation of chemotactic factors detectable in peripheral blood plasma.

Angina Pectoris↗