Lack of ST-segment depression normalization after PCI is a predictor of 5-year mortality in patients with ST-elevation myocardial infarction.

BACKGROUND: The significance of dynamic changes in a depressed ST-segment in the reciprocal changes after percutaneous coronary intervention (PCI) of patients with ST-elevation myocardial infarction (STEMI) is unknown, so the aim of this study was to evaluate the significance of reciprocal ST-segment depression normalization (STN) on long-term mortality in patients with STEMI treated with primary PCI. METHODS AND RESULTS: Data for 247 consecutive patients with STEMI were analyzed; 84 patients were excluded because of exclusion or incomplete inclusion criteria, so finally, 163 patients successfully treated with primary PCI were included. The study group was divided into 3 subgroups according to percentage of STN: poor STN (<30%), partial STN (30-70%), complete STN (>70%). Complete STN occurred in 63%, partial in 24% and poor in 13% of patients. STN correlated with late mortality (15% vs 28% vs 38% respectively, p=0.012). Patients who died during the follow-up period had a lower mean percentage reduction of initial ST-segment depression after PCI (50% vs 75%, p=0.001). Percentage reduction of initial ST-segment depression after PCI was a significant and independent risk factor of long-term mortality (odds ratio 1.01; 95% confidence interval: 1.00-1.02; p=0.02). CONCLUSIONS: These data revealed the use of reciprocal changes normalization as a novel tool for assessment of long-term risk of death in patients after successful primary PCI for STEMI.

Transfer with GP IIb/IIIa inhibitor tirofiban for primary percutaneous coronary intervention vs. on-site thrombolysis in patients with ST-elevation myocardial infarction (STEMI): a randomized open-label study for patients admitted to community hospitals.

AIMS: Our study aimed to compare two reperfusion strategies in patients with ST-elevation myocardial infarction (STEMI) admitted initially to a community hospital without catheterization facilities. METHODS AND RESULTS: Four hundred and one patients with STEMI admitted to community hospital (13 hospitals, radius 20-150 km from cath-lab) were randomized to on-site thrombolysis or to transport with tirofiban (10 microg/kg bolus i.v. + i.v. infusion 0.1 microg/kg/min) for primary PCI in single invasive centre. Primary endpoints were total mortality, recurrent MI (re-AMI), and stroke during 1 year follow-up. Delay to reperfusion defined as interval between admission and start of fibrinolysis or primary PCI was 35 and 145 min (P < 0.0001). Mean time of tirofiban administration to PCI in transfer group was: 122.3 +/- 35.7 min. Mortality was not different during hospitalization and at 30th-day, with trend towards lower mortality at 1 year in transport group (12.5 vs. 7.0%, P = 0.061). There were no differences in the rate of re-AMI and stroke, with trend towards lower incidence of re-AMI in transfer group at 1 year (7.5 vs. 3.5%, P = 0.073). Composite of death/re-AMI/stroke was higher in on-site group during follow-up (15.5 vs. 8.0%, P = 0.019; 21.5 vs. 11.4%, P = 0.006, respectively, at 30th-day and 1 year). CONCLUSION: Outcomes at 1 year follow-up suggest that transportation with adjunctive therapy with GP IIb/IIIa inhibitor tirofiban for primary PCI is superior to on-site thrombolysis for patient with STEMI presenting to hospital without catheterization facilities.

Is transport with platelet GP IIb/IIIa inhibition for primary percutaneous coronary intervention more efficient than on-site thrombolysis in patients with STEMI admitted to community hospitals? Randomised study. Early results.

INTRODUCTION: The advantage of primary percutaneous coronary intervention (pPCI) in the management of ST-elevation myocardial infarction (STEMI) over thrombolytic therapy has been demonstrated. However, an optimal medical treatment of STEMI patients admitted to regional hospitals without catheterisation facilities has not yet been established. Delay in initiation of pPCI resulting from transportation to the catheterisation laboratory may diminish the benefits of such therapy in comparison with thrombolysis administered in a regional hospital. Early initiation of therapy with platelet glycoprotein IIb/IIIa receptor inhibitor, which provides protection for the transportation, may be a reasonable solution to maintain the advantage of pPCI over thrombolysis alone in STEMI patients. METHODS: The studied group comprised patients with STEMI (infarct duration time <12 hours, typical clinical and electrocardiographic criteria of MI) who were randomly assigned in 13 regional hospitals located 20 to 150 km from invasive centre to one of two subgroups, either to thrombolysis in the community hospital or to transport after thrombolysis initiation with platelet GP IIb/IIIa receptor inhibitor (tirofiban; 10 mg/kg in intravenous bolus in the emergency room of the community hospital followed by continuous intravenous infusion of 0.1 mg/kg/min during transport as well as coronary procedure) in order to receive pPCI. All patients with cardiogenic shock on admission were routinely treated with PCI and were excluded from the study. RESULTS: 341 patients were included in the study (169 were randomised to receive thrombolytic therapy and 172--transport with intention to perform PCI). Mean time between onset of MI and randomisation was similar in the transport and thrombolysis groups, (139+/-133 min. vs 143+/-117 min., respectively, p=0.94). Mean infusion time of tirofiban to the beginning of PCI in the transport group was 121+/-36 min. Anterior MI was present in 42.6% of patients in the PCI group and in 41.5% in the thrombolytic group (p=0.085). Mean time from randomisation to pPCI was 158+/-60 min., and to thrombolysis initiation in 44+/-43 min. (p <0.0001). None of the patients died during transfer. In a 30-day follow-up we noted (pPCI vs thrombolytic group, respectively): mortality 3.49% vs 8.88% (p=0.04); reinfarction 1.16% vs 5.92% (p=0.02), stroke 0.58% vs 1.18% (p=0.55). In-hospital stay was significantly shorter in the transport group (9+/-3 days vs 14+/-7 days, p <0.0001). During hospitalisation, 17 (10.05%) patients initially assigned to thrombolysis alone had to be transferred to the catheterisation laboratory to undergo PCI (rescue PCI or PCI for postinfarction angina). Combined end-point (death/reinfarction/stroke) was reached more frequently in the thrombolytic group (15.98% vs 5.23%, p=0.001). CONCLUSIONS: A strategy of invasive therapy involving transport with GP IIb/IIIa receptor inhibitor and pPCI in STEMI patients admitted to hospital without catheterisation facilities was found to be more effective than thrombolytic therapy alone employed in the regional hospitals.

The effect of glycoprotein IIIa A1/A2 gene polymorphism on one-year outcome in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention.

INTRODUCTION: Glycoprotein IIb/IIIa (GP IIb/IIIa) is a platelet receptor composed of two subunits coded by individual genes. GP IIIa gene has two alleles: A1 and A2. The A2 allele determines higher platelet activity and was investigated many times as a potential risk factor of ACS. The influence of A1/A2 polymorphism on the prognosis in patients with ST-segment elevation myocardial infarction (STEMI) has not been analysed so far. AIM: Evaluation of the relationship between GP IIb/IIIa A1/A2 gene polymorphism and one-year prognosis in patients with STEMI treated with primary percutaneous coronary intervention (pPCI). METHODS: 171 patients (23.9%--women, 39.7%--anterior MI) with STEMI treated successfully with pPCI as well as 121 healthy subjects from a reference group were enrolled in the study. Genotyping was performed using restriction fragment length polymorphism analysis (RFLP). In one-year follow-up the primary end point included deaths and infarctions. The following methods were used in statistical analysis: chi(2) as well as Mann-Whitney test, Kaplan-Meier survival analysis, Cox regression model and multivariate analysis. RESULTS: The percentage of A2 allele carriers was similar in STEMI patients and in subjects from the reference group (27.4% vs. 21.5%, p=0.24). No statistically significant difference in the incidence of primary end point between the A1A1 homozygotes and A2 allele carriers (A1A2/A2A2 genotype) was observed among STEMI patients. In Cox regression analysis, the variables associated with death or MI were: ejection fraction (RR 0.912, p=0.01) and systolic blood pressure on admission (RR 0.97, p=0.049). The variables categorised as unfavourable predictors included: Killip class >2 and heart ratio on admission >100/min (p <0.05, log-rank test). CONCLUSION: No relationship between GP IIb/IIIa A1/A2 gene polymorphism and STEMI incidence as well as one-year prognosis in patients with STEMI treated with pPCI was documented.

The prognostic significance of early dobutamine echocardiography in patients with acute myocardial infarction treated with primary coronary angioplasty.

BACKGROUND: The prognostic significance of early dobutamine echocardiography (DE) after successfully treated acute myocardial infarction (AMI) with primary coronary angioplasty (PTCA) is still unclear. Patients who respond to DE may have better left ventricular function improvement and possibly a better clinical outcome. AIM: To assess whether early DE can predict spontaneous functional recovery in patients treated successfully with primary PTCA and whether responders to DE have a better clinical outcome. METHODS: DE (5 and 10 ug/kg/min) was performed in 110 consecutive patients (61+/-10 years) 4+/-1 days after successful primary PTCA (TIMI 3, stenosis <30%). Left ventricular ejection fraction (LVEF) and wall motion index (WMSI) were measured. Patients underwent clinical assessment and two-dimensional echocardiography at 3 and 6 months. RESULTS: In the DE responders (76 pts), LVEF increased significantly from 41%+/-9% at baseline to 47%+/-10% at 6 months (p<0.0001), whereas the improvement found in nonresponders (34 pts) was insignificant (from 36.3%+/-9% at baseline to 38.8%+/-10% at 6 months, p=0.4). The nonresponders to DE had a higher incidence of subsequent revascularisation (4/34 (11.8%) vs 3/76 (3.9%) p=0.12), reinfarction (5/34 (14.7%) vs 2/76 (2.6%), p=0.28) and death (3/34 (9%) vs 0/76 (0%), p=0.0086). The incidence of combined end-point (revascularisation, reinfarction and death) was significantly lower in the group of responders to early DE (p=0.03). CONCLUSIONS: Early DE can precisely predict functional recovery and the extent of irreversibly damaged myocardium in patients with AMI in whom anterograde flow is fully restored. A positive response to early DE is associated with a better clinical outcome and prognosis.

Does gastro-esophageal reflux provoke the myocardial ischemia in patients with CAD?

BACKGROUND: Gastro-esophageal reflux disease (GERD) may cause chest pain. The aim was to determine the correlation between ischemia and gastro-esophageal reflux in patients with CAD and to assess the influence of short-term "anti-reflux" therapy on the ischemia in patients with GERD and CAD. METHODS: Fifty patients with angiographically proven CAD underwent simultaneous 24-h continuous ECG and esophageal pH monitoring. We assessed the number of ST-segment depression episodes (ST dep.) and total duration of ischemic episodes, expressed as total ischemic burden (TIB). In pH-metry, we assessed: time percentage of pH lower than 4, total time of pH lower than 4 and the number of pathological refluxes (PR). Patients fulfilling the GERD criteria received a 7-day therapy with omeprazole 20 mg bid. On the 7th day of therapy, simultaneous Holter and esophageal pH monitoring was repeated. RESULTS: Total number of 224 PRs in 42 patients (84%) was recorded during esophageal pH-metry. GERD criteria were fulfilled in 23 patients (46%). Out of 218 episodes of ST dep., 45 (20.6%) correlated with PR. GERD patients had larger TIB and higher number of ST dep. (p<0.015 and p<0.035, respectively). The anti-reflux therapy reduced all analyzed parameters of esophageal pH monitoring (p<0.0022) as well as the number of ST dep. (p<0.012) and TIB (p<0.05). CONCLUSIONS: Gastro-esophageal reflux disease is common in patients with CAD and may provoke myocardial ischemia. Short-term proton pump inhibitors therapy that restores normal esophageal pH significantly reduces myocardial ischemia, possibly due to elimination of acid-derived esophago-cardiac reflex compromising coronary perfusion-the phenomenon known as "linked angina".

[Peripartum cardiomyopathy--a case report]. / Kardiomiopatia okoloporodowa. Opis przypadku.

Peripartum cardiomyopathy -- a case report. A case of a 32-year old woman, previously healthy, with heart failure symptoms occurring during third pregnancy, is described. In spite of standard pharmacological treatment, her condition worsened and the pregnancy had to be terminated at 28 hbd by cesarean section. The patient's condition improved and three months later normal left ventricular function as well as good exercise tolerance were observed.

Supraventricular tachycardia and pulmonary hypertension at the presentation of Hodgkin's disease.

A 27-year-old pregnant woman was admitted with supraventricular tachycardia (SVT) and symptoms of heart failure. Echocardiography revealed pulmonary hypertension due to a tumour infiltrating the left atrium and compressing the pulmonary veins. After delivery by Caesarean section, the paroxysmal SVT was controlled by amiodarone. Thoracic CT scan showed mediastinal masses compressing the pulmonary arteries and veins, and a preliminary diagnosis of Hodgkin's disease was later confirmed by mediastinoscopy and lymph node biopsy. Following two courses of chemotherapy the masses diminished. The lumen of the left atrium increased, pulmonary hypertension and SVTs receded.

Normalisation of elevated ST segment predicts return of left ventricular systolic function and improved outcome in patients with acute myocardial infarction, treated with primary coronary angioplasty.

BACKGROUND: It has been shown that normalisation of elevated ST segment after primary percutaneous coronary interventions (PCI) is associated with the achievement of reperfusion at the tissue level. AIM: To assess prospectively the return of left ventricular (LV) systolic function and the outcome of patients with acute myocardial infarction (AMI), treated with primary PCI, in relation to the early normalisation of the ST segment. METHODS: The study group consisted of 110 consecutive patients (33 females, 77 males, mean age 56 years) with AMI who were successfully treated with primary PCI (TIMI flow grade 3 and residual stenosis <30%) within 12 hours from the onset of symptoms. The patients were divided into two groups according to normalisation or lack of normalisation of an elevated ST segment. The mean time from the onset of symptoms to the restoration of blood flow in an infarct-related artery (pain-to-balloon time) was similar in both groups. LV echocardiographic parameters (ejection fraction EF and wall motion score index WMSI) and clinical status directly after PCI as well as 3 and 6 months later were assessed. RESULTS: Directly after primary PCI, LV impairment (low EF and high WMSI) was significantly more often present in patients without rather than with ST segment normalisation. Afterwards, LVEF and WMSI improved significantly only in patients with ST segment normalisation whereas in the remaining patients no such improvement was observed. During 6-month follow-up period, major cardiac events (death, new AMI or need for revascularisation) occurred more frequently in patients without rather than with ST segment normalisation (p=0.03). CONCLUSIONS: 1. Rapid resolution of ST segment elevation following effective primary PCI identifies patients with a favourable outcome. 2. ST segment normalisation predicts a return of LV systolic function in patients with AMI treated with primary PCI.

Safety and feasibility of a novel dosing regimen of tirofiban administered in patients with acute myocardial infarction with ST elevation before primary coronary angioplasty: a pilot study.

BACKGROUND: Intravenous glycoprotein GP IIb/IIIa receptor antagonists administered to patients with acute coronary syndromes limit platelet-dependent thrombus formation and vasoconstriction and lower the complication rate of PCI. The efficacy of glycoprotein IIb/IIIa inhibitors critically depends on appropriate suppression of platelet aggregation. A growing body of evidence indicates that regimen of tirofiban used in several recent trials may be suboptimal. We investigated if a novel regimen of dosage of tirofiban administered to patients with acute myocardial infarction with ST elevation (STEMI) before primary angioplasty is safe, feasible and whether such treatment improves coronary flow in infarct-related artery. METHODS: It was an open-label, non-randomized, prospective observational study. 253 consecutive patients with STEMI, qualified to PCI were included. 104 of patients (group 1) received heparin plus tirofiban at a novel regimen (10 microg/kg bolus, followed by 0.4 microg/kg/min for 30 min and then 0.1 microg/kg/min for 12-24 hours) and the remaining 149 of the patients (group 2) received a standard dose of heparin prior to PCI. Bleeding complications were recorded. The primary end point of the study was combined TIMI 1 + 2 + 3 grade flow at the time of first contrast medium injection during angiography for primary PCI. RESULTS: Heparin was administered 50.3 +/- 58.1 minutes (group 1) or 62.3 +/- 67.3 minutes (group 2) ( p = 0.205). Tirofiban was administered for an average of 14.5 +/- 14.4 minutes before TIMI assessment (group 1). In patients treated with heparin + tirofiban the rate of combined TIMI 1 + 2 + 3 coronary flow was higher (38.4% vs. 24.8%, p = 0.020) as compared to patients treated with heparin alone. The difference in the rate of TIMI > or = 2 coronary blood flow between the groups 1 and 2 (24.0% vs. 20.1%) has not reached statistical significance ( p = 0.459). At the same time the significant difference in the rate of TIMI 1 coronary blood flow between the groups 1 and 2 was noted (14.4 vs. 4.7%, p = 0.007). In hospital mortality in the groups 1 and 2 was similar (5.3 vs. 4.8%, p = 0.838). Significant difference was noted between the groups 1 and 2 with regard to minor bleeding complications (17.3 vs. 8.7%, p = 0.041). CONCLUSION: In patients undergoing primary angioplasty for acute myocardial infarction the novel regimen of tirofiban is well tolerated and feasible, and is associated with improvement in coronary blood flow in the infarct related artery. Larger studies assessing the effects of tirofiban on clinical outcomes of patients with AMI undergoing primary angioplasty seem worthwhile.

Platelet inhibition by increased tirofiban dosing during primary coronary angioplasty for ST elevation myocardial infarction.

BACKGROUND: Platelet receptor IIb/IIIa inhibition during percutaneous coronary interventions (PCI) decreases incidence of major adverse cardiac events (MACE). These effects directly result from the level of platelet inhibition. Due to existing data indicating that standard dosing of tirofiban is insufficient for optimal platelet inhibition, we proposed a novel, experimental dosing. AIM: In this study we assessed, with the use of Ultegra Rapid Platelet Function Assay (RFPA), the level of platelet inhibition with increased tirofiban dosing during primary PCI for ST elevation myocardial infarction (STEMI). METHODS: Twenty eight patients (22 males, 6 females, mean age 63 years, range 32-78 years) with STEMI were included into the study. All patients received 300 mg of aspirin, iv. heparin in a dose of 10 000 IU, which was followed by platelet receptor GP IIb/IIIa inhibitor tirofiban - 10 micro g/kg iv bolus, 0.4 micro g/kg/min for 30 min and infusion 0.1 micro g/kg/min continued for 12-24 h. Platelet function was assessed with RFPA before tirofiban administration and after 10, 30, 90 minutes as well as 8 hours from the initial dose of tirofiban. Baseline fibrinogen binding to platelet receptor IIb/IIIa was defined as PAU (platelet aggregation unit) and the effects of tirofiban on platelets were expressed as a percentage of platelet inhibition. RESULTS: During in-hospital stay, no deaths, re-infarction nor recurrences of ischaemia requiring intervention were noted. The mean total duration of tirofiban administration was 21 hours. Thrombocytopenia was not observed in any patient. Bleeding complications occurred in 5 (17.9%) patients. Blood transfusion was required in three patients. The percentages of platelet inhibition measured at the pre-specified time-points were 95%, 94%, 91% and 87%, respectively. In 32% of patients an inhibition of platelet exceeding 95%, measured 10 minutes from the onset of tirofiban infusion, was not achieved. At the same time, platelet inhibition <90% was found in only 3 (11%) patients. Eight hours from the initiation of tirofiban, platelet inhibition <70% was found in 3 (11%) patients; of them, two had platelet inhibition <95% when measured 10 minutes from the onset of therapy with tirofiban. CONCLUSIONS: 1. Increased dosing of tirofiban resulted in an enhanced platelet inhibition. 2. Optimal platelet inhibition, especially during first minutes of drug administration, was not achieved in a substantial number of patients. 3. Increased IIb/IIIa inhibitor dosing resulted in a high partial and normal baseline coronary flow in an infarct-related artery. 4. Increased tirofiban dosing resulted in a relatively high bleeding complications rate.

[Recurrent systemic embolisation in a patient with a large thrombus in left ventricular aneurysm--case report]. / Nawracajaca zatorowosc systemowa u chorej z duza skrzeplina w pozawalowym tetniaku lewej komory.

A case of a 47-year-old female with the aneurysm of the left ventricle is presented. Several days prior to the hospitalization signs of femoral embolism emerged, which was treated with embolectomy. Echocardiographic examination revealed large thrombus in the cavity of the aneurysm with pedunculated surrounding echo. On the second day after the admission the symptoms of renal artery embolism occurred. Due to recurrent symptoms of peripheral emboli and the lack of a consent for the interventional treatment, fibrinolysis (Actilyse) was applied resulting in the reduction of the thrombus mass in the left ventricle. Subsequent Doppler ultrasound of the renal arteries showed normal flow pattern. During hospitalization general condition has gradually improved and the patient was discharged.

[Is Q-wave on admission associated with microvascular injury in patients with acute myocardial infarction treated with primary angioplasty?]. / Czy obecnosc patologicznego zalamka Q przy przyjeciu predysponuje do poreperfuzyjnego uszkodzenia mikrokrazenia u pacjentów ze swiezym zawalem miesnia sercowego, leczonych pierwotna angioplastyka wiencowa?

INTRODUCTION: Impaired microvascular flow, despite patent epicardial artery (no-reflow phenomenon), leads to greater left ventricular dysfunction after myocardial infarction (MI). Predictive factors associated with no-reflow remain largely unexplored. Q-wave on admission (Q(A)) is a sign of extensive ischemia probably predisposing to no-reflow. The aim of the study was to explore possible relation between Q(A) and electrocardiographic signs of no-reflow in patients with first MI. MATERIAL AND METHODS: The study group was composed of 108 patients (81 men; mean age 60+/-11 years), with first ST-segment elevation MI, treated successfully with primary angioplasty (p-PTCA). ECG tracings were obtained before and 30 minutes after p-PTCA. The sum of ST-segment elevations (sum(ST(el))) in 3 contiguous leads with the highest ST(el) was calculated. Lack of 50% reduction of the sum(ST(el)) 30 minutes after angioplasty was defined as ECG sign of no-reflow. Presence of Q(A) was estimated in leads with ST(el). RESULTS: Q(A) was found in 42 (39%) patients. Q(A) was more often observed in patients with ECG signs of no-reflow (38% vs. 18%; p<0.05). Group with Q(A) showed larger damage of left ventricle estimated with ECG QRS score (7.7+/-4.4 vs. 6.1+/-3.4; p<0.05) as well as worse ejection fraction (42% vs. 46%; p=0.05). CONCLUSIONS: Patients with Q(A) have more often ECG signs of no-reflow than other patients with MI. Previously described worse function of left ventricle in this group, may be partially caused by more frequent no-reflow occurring in those patients. This fact suggests that adjunctive therapy preventing no-reflow could be beneficial in this group of patients.

[Assessment of possible correlations between endogenous androgens and the extent of coronary heart disease and left ventricle function]. / Badanie korelacji stezenia meskich hormonów plciowych ze stanem zaawansowania choroby wiencowej i funkcja lewej komory serca.

In men, androgens and especially testosterone are considered responsible for the much higher rate of coronary artery disease. The male gender is an independent coronary artery disease risk factor. An adverse correlation between endogenous testosterone levels and the extent of coronary atherosclerosis has been demonstrated in just one study. In our study, we investigated the associations between endogenous sex hormone levels and the extent of coronary atherosclerosis, ejection fraction of the left ventricle and coronary heart disease risk factors.

[Massive haematoma following rescue coronary angioplasty in a patient with acute myocardial infarction - a case report]. / Masywne krwiaki jako powiklanie ratunkowej angioplastyki u chorej ze swiezym zawalem serca.

A case of a 79 year old female with acute myocardial infarction, treated with rescue coronary angioplasty, is presented. The patient received also thrombolysis, followed by heparin and IIb/IIIa platelet receptor blocker. The hospital stay was complicated by a massive groin haematoma and ecchymoses in the other parts of the lower and upper limbs, requiring blood transfusion.

An assessment of correlations between endogenous sex hormone levels and the extensiveness of coronary heart disease and the ejection fraction of the left ventricle in males.

This clinical study investigated the possible associations of male sex hormone with the extensiveness of coronary artery lesions, coronary heart disease risk factors and ejection fraction of the heart. Ninety six Caucasian male subjects were recruited, 76 with positive and 20 with negative coronary angiograms. Early morning, prior to haemodynamic examination all of them had determined levels of total testosterone, free testosterone, free androgen index (FAI), sex hormone-binding globulin (SHBG), oestradiol, luteinizing hormone, follicle-stimulating hormone, plasma lipids, fibrinogen and glucose. The ejection fraction and the extensiveness of coronary lesions of each subject was assessed on the basis of x-ray examination results using Quantitative Coronary Angiography (QCA) and Left Ventricular Analysis (LVA) packages on the TCS Acquisition workstation, Medcon. Men with proven coronary heart disease had significantly lower levels of total testosterone (11.9 vs 21.2 nmol/l), free testosterone (45.53 vs 86.10 pmol/l), free androgen index (36.7 vs 47.3 IU) and oestradiol (109.4 vs 146.4 pmol/l). The level of testosterone was negatively associated with the DUKE Index. The most essential negative correlation was observed between SHBG and atherogenic lipid profile (low high-density lipoprotein, high triglycerides). Ejection fraction was substantially lower in patients (51.85 vs 61.30) (without prior myocardial infarction) with low levels of free-testosterone (23.85 vs. 86.10 pmol/l) and FAI (28.4 vs 47.3 IU). A negative correlation was observed between total testosterone, free testosterone, FAI and blood pressure, especially with diastolic pressure. Men with proven coronary atherosclerosis had lower levels of endogenous androgens than the healthy controls. For the first time in clinical settings it has been demonstrated that low levels of free-testosterone was characteristic for patients with low ejection fraction. Numerous hypothesies for this action can be proposed but all require a proper evaluation process. The main determinant of atherogenic plasma lipid was low levels of SHBG suggesting its main role in developing atheroscerotic lesions.

Oxidative stress and neutrophil activation--the two keystones of ischemia/reperfusion injury.

The widespread introduction of fibrinolytics and recently also PTCA in the treatment of myocardial infarction has changed the picture of modern cardiology. But this therapy also raises new problems and challenges. One of them is the occurrence of extensive tissue injury caused by reperfusion. Reinstitution of oxygen to the ischemic tissues initiates various processes leading to generation of reactive oxygen species (ROSs). Acting on the plasma membrane ROS damage its organization and release various proinflammatory agents. Different proteins, including receptors, ionic channels, transporters or components of transduction pathways are substrates of oxidation by ROSs. Their changed structure results in altered functioning and disruption of vital cellular processes. Another key factor of reperfusion injury is activation and infiltration of infarcted area by polymorphonuclear leukocytes (PMNs). Multiple studies identified consecutive stages of PMN activation and substances being involved in it. Main interest lies in cellular adhesion molecules, particularly selectins and beta2 integrins, as their antagonists were repeatedly found to diminish neutrophil activation and infarct size. Nevertheless new publications strike at the foundations of the established order and confront the relation between neutrophil infiltration and infarct size. PMNs are linked by close ties to other cells involved in inflammatory response. Seemingly also in cardiac ischemia-reperfusion injury, the activity of neutrophils is modulated by lymphocytes and macrophages. The article describes mutual interactions between different factors involved in the reperfusion injury that may enable preparing new treatments, hopefully as effective and successful as reperfusion therapy.

[Ischemic heart disease and gastro-oesophageal reflux disease--simultaneous 24 monitoring of ECG and oesophageal pH]. / Choroba niedokrwienna serca a choroba refluksowa przelyku-ocena za pomoca jednoczasowego 24-godzinnego monitorowania EKG i pH w przelyku.

AIM: To determine the correlation between episodes of ischaemia in ECG recordings with pathologic gastro-esophageal reflux during simultaneous 24 hour monitoring of ECG and oesophageal pH. METHODS: Simultaneous 24 hour monitoring of ECG and oesophageal pH was performed in 30 patients (p) (26 M/4F, aged 39-74) with coronary artery disease of CCS class II-III, CAD was confirmed in coronary angiography. Analysis of the oesophageal pH was performed by using the Polygram programme (PW-version 2.04 Esophogram-version 2.01). ST depression > 1 mm and lasting at least 1 min was regarded as significant in ECG monitoring. Pathologic gastro-esophageal reflux was defined as a drop in pH < 4 lasting more than 5 min. Gastrooesophageal reflux disease (GERD) was diagnosed when a drop in pH < 4 lasted for more than 5% of the monitoring period. Gastro-oesophageal reflux dependent ST depression was defined as an ST depression that occurred during reflux episode and lasted up until 10 min from the end of the reflux. RESULTS: 26 patients (87%) had a total of 116 episodes of ST depression and 21 out of the 116 episodes (18%) were Gastro-oesophageal reflux time dependent. Fifteen patients (50%), had at least one episode of ST depression, depending on the time of reflux. Pathologic gastro-esophageal reflux was present in 25 patients (85%). In 14 patients (46.6%), the GERD pH criteria were fulfilled. In this group of patients, there was a significantly longer time of total ST depression (total ischaemic burden). CONCLUSIONS: 1. GERD is a frequent disease in patients with angiographically proven coronary artery disease. 2. Pathological gastroesophageal reflux can induce myocardial ischaemia, which can be determined by analysis of ST depression during 24 hour monitoring of ECG.