Routine pretreatment with abciximab versus standard periprocedural therapy in mechanically ventilated cardiogenic shock patients undergoing primary percutaneous coronary intervention: Subanalysis of the PRAGUE-7 study.

BACKGROUND: The clinical outcome of patients with myocardial infarction (MI) complicated by cardiogenic shock (CS) who require mechanical ventilation (MV) is poor. OBJECTIVE: To analyze the impact of abciximab pretreatment in this high-risk population of MI patients. METHODS: The present study was a retrospective subanalysis of the multicentre randomized Routine Upfront Abciximab Versus Standard Peri-Procedural Therapy in Patients Undergoing Percutaneous Coronary Intervention for Cardiogenic Shock (PRAGUE-7) study, which included 80 MI patients in CS undergoing primary percutaneous coronary intervention (PCI). Patients were randomly assigned into group A (routine pretreatment with an abciximab bolus followed by a 1 h abciximab infusion) and group B (standard therapy). The subanalysis included 37 patients requiring MV. Seventeen patients were in group A and 20 were in group B. The primary end point (death/stroke/reinfarction/new severe renal failure) at 30 days, procedural success (thrombosis in myocardial infarction [TIMI] flow) and frequency of bleeding were assessed. The χ(2) and Student's t tests were used for statistical analysis; P<0.05 was considered to be statistically significant. RESULTS: The primary end point occurred in nine (53%) patients in group A and 12 (60%) patients in group B (P=0.66). TIMI flow after primary PCI was higher in group A (2.75 versus 2.31; P<0.05). Major bleeding occurred in 12% of patients in group A versus 10% of patients in group B (P=0.86). Minor or minimal bleeding was more common in group A (29%) compared with group B (5%; P<0.05). CONCLUSION: The results of the present study suggest that routine pretreatment with abciximab before primary PCI in mechanically ventilated patients with MI complicated by cardiogenic shock was associated with better angiographic results but also with a higher incidence of bleeding.

Glycogen phosphorylase BB as a potential marker of cardiac toxicity in patients treated with anthracyclines for acute leukemia.

OBJECTIVES: The aim of the presented study was to assess plasma glycogen phosphorylase BB (GPBB) concentrations in acute leukemia patients treated with anthracycline containing chemotherapy. BACKGROUND: Anthracyclines represent the highest risk for development of cardiotoxicity. GPBB belongs to proposed biomarkers of cardiac injury with a very limited experience in this context. METHODS: Totally, 24 adult patients with acute leukemia were enrolled. Plasma GPBB concentrations were measured by ELISA at diagnosis (before chemotherapy), after first chemotherapy with anthracyclines and 6 months after the completion of treatment. The cut-off value for GPBB positivity was 10.00 µg/L as recommended by the manufacturer. RESULTS: Before chemotherapy, the mean plasma GPBB concentration was 5.25±3.81 µg/L, increased above the cut-off in 1 patient (4.2 %). After the first chemotherapy, the mean GPBB was 6.61±5.54 µg/L, positive in 7 (29.2 %) patients. Six months after treatment, the mean GPBB was 10.06±11.41 µg/L, positive in 8 (33.3 %) patients. Six months after treatment, we found a significant correlation between elevation in GPBB and diastolic left ventricular dysfunction on echocardiography (r=0.621; p<0.0001). The differences in plasma GPBB between healthy blood donors and patients treated for acute leukemia were statistically significant (p<0.01 in all cases). CONCLUSION: Our results suggested that GPBB could become a potential biomarker for detection of acute and chronic cardiotoxicity associated with anthracycline containing chemotherapy. The predictive value for development of treatment-related cardiomyopathy in future is not clear and will be evaluated during the follow-up. Further studies are needed to define the potential role of GPBB and other biomarkers in the assessment of chemotherapy-induced cardiotoxicity (Ref. 21). Text in PDF www.elis.sk.

European Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatment.

AIMS: To develop quality indicators (QIs) for the evaluation of the prevention and management of cancer therapy-related cardiovascular toxicity. METHODS AND RESULTS: We followed the European Society of Cardiology (ESC) methodology for QI development which comprises (i) identifying the key domains of care for the prevention and management of cancer therapy-related cardiovascular toxicity in patients on cancer treatment, (ii) performing a systematic review of the literature to develop candidate QIs, and (iii) selecting of the final set of QIs using a modified Delphi process. Work was undertaken in parallel with the writing of the 2022 ESC Guidelines on Cardio-Oncology and in collaboration with the European Haematology Association, the European Society for Therapeutic Radiology and Oncology and the International Cardio-Oncology Society. In total, 5 main and 9 secondary QIs were selected across five domains of care: (i) Structural framework, (ii) Baseline cardiovascular risk assessment, (iii) Cancer therapy related cardiovascular toxicity, (iv) Predictors of outcomes, and (v) Monitoring of cardiovascular complications during cancer therapy. CONCLUSION: We present the ESC Cardio-Oncology QIs with their development process and provide an overview of the scientific rationale for their selection. These indicators are aimed at quantifying and improving the adherence to guideline-recommended clinical practice and improving patient outcomes.

Application of proteomics in biomarker discovery: a primer for the clinician.

Ever since proteomics was proven to be capable of characterizing a large number of differences in both protein quality and quantity, it has been applied in various areas of biomedicine, ranging from the deciphering molecular pathogenesis of diseases to the characterization of novel drug targets and the discovery of potential diagnostic biomarkers. Indeed, the biomarker discovery in human plasma is clearly one of the areas with enormous potential. However, without proper planning and implementation of specific techniques, the efforts and expectations may very easily be hampered. Numerous earlier projects aimed at clinical proteomics, characterized by exaggerated enthusiasm, often underestimated some principal obstacles of plasma biomarker discovery. Consequently, ambiguous and insignificant results soon led to a more critical view in this field. In this article, we critically review the current state of proteomic approaches for biomarker discovery and validation, in order to provide basic information and guidelines for both clinicians and researchers. These need to be closely considered prior to initiation of a project aimed at plasma biomarker discovery. We also present a short overview of recent applications of clinical proteomics in biomarker discovery.

[Multi-marker approach in the diagnostics of cardiac diseases by protein biochip technology]. / Multianalytový prístup k diagnostice srdecních chorob technologií proteinových biocipu.

BACKGROUND: Multi-marker approach is recommended for rapid diagnostics and risk stratification of acute coronary syndrome. We tested the analytical performance of protein biochip technology for determination cardiac markers. METHODS: Analysis of cardiac markers: CK-MB mass, cTnl, myoglobin, glycogen phosphorylase BB (GPBB), heart type of fatty acid binding protein (h-FABP) and carbonic anhydrase III (CAIII) was performed by system Evidence Investigator (Randox). Analytical parameters of Cardiac array were tested. The Evidence Investigator results were compared with Elecsys 2010 (Roche) CK-MB mass and myoglobin methods. Markers of myocardial injury were determined in 28 blood donors, 28 patients with acute myocardial infarction diagnosis and 21 patients after chemotherapy containing anthracyclines (monitoring of cardiotoxicity). RESULTS: The Passing-Bablok regression shows statistically significant differences in results. The reasons for these differences are poor standardization of methods and discrepancies between calibrations. New substances h-FABP and GPBB are promising early markers of acute myocardial infarction and diagnostic sensitivity of h-FABP would be better than myoglobin test. These markers can be useful for monitoring of cardiotoxicity of anthracyclines. CONCLUSIONS: In future, the use of biochip technology in cardiology diagnostic represents an important challenge but it is a necessary standardization of immunochemical methods.

[High sensitivity cardiac troponin assays 2009: clinical potential, current practice and benefits, the future]. / High-sensitivity metody stanovení srdecních troponinu 2009: klinický potenciál, soucasná praxe a prínos, perspektiva.

At present, determination of cardiac troponins (cTn) is the biomarker method of choice for diagnostics and risk stratification in patients with a myocardial injury. Past clinical practice had provided sound evidence that low cTn concentrations, measured with unacceptable imprecision by the currently used methods, hold important clinical, diagnostic and stratification potential. The new generation cTn assays, so called high-sensitivity assays, enable determination of very low cTn concentrations with satisfactory analytical precision and open the way to early identification of small but often prognostically important myocardial damage. Introduction of high-sensitivity cTn assays in practice is, however, associated with some difficulties: their superior diagnostic sensitivity to identify small injuries to myocardium is often linked to lower specificity, higher incidence of elevated cTn concentrations is frequently associated with less obvious clinical symptomatology (overdiagnosis), resulting in greater demand for further patient assessment (overcrowding), repeated analyses and trend monitoring of cTn fluctuation. These initial difficulties cannot lessen the by now indisputable, established benefit of high-sensitivity cTn assays that we briefly describe in the present paper.

Re-expression of nestin in the myocardium of postinfarcted patients.

Intact cardiac muscle cells in the adult heart do not express intermediate filament nestin. In this study, we report on widespread expression of intermediate filament nestin in human myocardium of patients who died from the myocardial infarction. Nestin was detected in cardiomyocytes, endothelial cells, and few interstitial cells. Elevated levels of nestin were observed in cardiac muscle cells in all specimens, although the intensity of immunoreactivity and distribution of the signal differed. The strongest immunoreactivity was observed from 4 days after myocardial infarction in the infarction border zone where nestin was distributed homogeneously in the entire sarcoplasm of cardiac muscle cells. Within the following week, nestin in immunoreactive cardiomyocytes was redistributed and restricted to small subsarcolemmal foci and to intercalated discs. Angiogenic capillaries that grew between vital nestin-positive cardiomyocytes and entered the necrotic area expressed also high levels of nestin. Nestin-positive endothelial cells were often observed in mutual interactions with nestin-positive cardiac muscle cells. These findings document a crucial role of nestin in remodeling cytoskeleton of cells in the human postinfarcted myocardium.

Multimarker approach to evaluation of cardiac toxicity during preparative regimen and hematopoietic cell transplantation.

Cardiac toxicity of preparative regimen (PR) containing high-dose Cyclophosphamide (120 mg/kg) followed by hematopoietic cell transplantation (HCT) was evaluated with 6 biomarkers of cardiac injury: N-terminal pro brain natriuretic peptide (NT-proBNP), creatine kinase MB (CK-MB mass), cardiac troponins (cTnT, cTnI), heart-type fatty acid binding protein (H-FABP), glycogen phosphorylase BB (GPBB). Twenty-three patients (mean age 44.5+/-10.6 years, 15 males) with acute leukemia were studied. All biomarkers were measured the day before PR, the day after PR, the day after HCT and 14 days after HCT. We found NT-proBNP elevations above 500 ng/L in 6 (26.1 %) patients after PR, in 9 (39.1 %) after HCT and in 7 (30.4 %) 14 days after HCT. GPBB became elevated (above 7.30 microg/L) in 5 (21.7 %) patients after PR, remained elevated in 5 (21.7 %) after HCT and in 2 (8.7 %) 14 days after HCT. A significant correlation between elevation in NT-proBNP and GPBB was found. Other markers remained within the reference range early after PR and HCT. Our findings show that administration of PR and HCT for acute leukemia is associated with acute neurohumoral activation of cardiac dysfunction (significant rise in NT-proBNP) and may lead to GPBB elevation. These changes could indicate acute cardiac toxicity due to treatment and require further follow-up. The predictive value for development of cardiomyopathy in the future is unclear. Further studies will be needed to define the potential role of new biomarkers in this context.

[Biomarkers of myocardial ischemia and necrosis in 2008]. / Biomarkery ischemie a nekrózy myokardu v roce 2008.

In the review article, the authors present current knowledge of biomarkers of myocardial ischemia and necrosis. They comment new definition of myocardial infarction resulted as consensus of European Society of Cardiology and American Heart Association. They added clinically interested data about routinely used cardiomarkers (cardiac troponins and creatinkinase). At the second part, the authors focused on new biomarkers (fatty acids binding proteins, ischemia-modified albumin, glycogen phosphorylase isoenzyme BB) and its significance in diagnosis of myocardial ischemia/necrosis and their prognostic significance. Some of new promising molecules are discussed in the last part of the article.

Identification of novel biomarker candidates for hypertrophic cardiomyopathy and other cardiovascular diseases leading to heart failure.

In-depth proteome discovery analysis represents new strategy in an effort to identify novel reliable specific protein markers for hypertrophic cardiomyopathy and other life threatening cardiovascular diseases. To systematically identify novel protein biomarkers of cardiovascular diseases with high mortality we employed an isobaric tag for relative and absolute quantitation (iTRAQ) proteome technology to make comparative analysis of plasma samples obtained from patients suffering from non-obstructive hypertrophic cardiomyopathy, stable dilated cardiomyopathy, aortic valve stenosis, chronic stable coronary artery disease and stable arterial hypertension. We found 128 plasma proteins whose abundances were uniquely regulated among the analyzed cardiovascular pathologies. 49 of them have not been described yet. Additionally, application of statistical exploratory analyses of the measured protein profiles indicated the relationship in pathophysiology of the examined cardiovascular pathologies.

The use of biochemical markers in cardiotoxicity monitoring in patients treated for leukemia.

Cardiotoxicity is a serious and relatively frequent complication of anti-tumorous treatment. Anthracyclines represent the greatest risk. Biochemical markers of structural and functional myocardial damage have been gaining ground in cardiotoxicity monitoring. The aim of the study was to monitor cardiotoxicity of induction chemotherapy in acute myeloid leukemia (AML) patients and to assess the potential for use of biochemical markers in early diagnostics of cardiotoxicity. Fifteen consecutive adult patients with a newly diagnosed AML were studied. All patients received induction chemotherapy containing Idarubicin (IDA) 3 x 12 mg/m2 and intermediate doses of Cytarabine (8 x 1.5 g/m2). Serial measurements of plasma N-terminal pro brain natriuretic peptide (NT-proBNP) values were performed at the baseline, the day following each IDA infusion, after 14 days and after circa 1 month, i.e. before the next chemotherapy. Cardio-specific markers (cTnT, CK-MB mass) were measured at the baseline and after the last IDA infusion. The mean baseline value of NT-proBNP in newly diagnosed AML patients was 129.7+/-59.6 pg/ml. The mean NT-proBNP value increased after the first IDA infusion to 307.3+/-171.4 pg/ml (p=0.02). In most of the patients, the second and the third IDA infusions were not associated with a further increase in the NT-proBNP value and levels after 2 and 4 weeks were not significantly different from the baseline. However, in one of the patients the NT-proBNP values were increasing after each IDA infusion (after the last one 786.2 pg/ml) and within 14 days he developed congestive heart failure due to left ventricular diastolic dysfunction as assessed by echocardiography. At that time, the NT-proBNP value was 1,184.0 pg/ml; after diuretics it decreased significantly. In all patients, plasma cTnT and CK-MB mass concentrations were within the reference interval at the baseline and after the induction chemotherapy. Our results suggest that induction chemotherapy in AML (IDA 36 mg/m2 and intermediate doses of Cytarabine): 1. does not cause detectable damage of the myocyte structure, 2. is in all patients associated with acute neurohumoral activation (transient elevation of NT-proBNP) indicating acute subclinical cardiotoxicity, 3. may lead to congestive heart failure and NT-proBNP seems to be a promising early marker and predictor of this complication.

[Present view on the stem cell plasticity and cell therapy]. / Soucasný pohled na plasticitu kmenoých bunek a bunecnou terapii.

The most controversial problem in the present biology and medicine is the existence of stem cell plasticity. Experimental biology and medicine have been working with stem cells and stem cell therapy more than twenty years. The term plasticity, as it is understood, is the potential of stem cell phenotypes that is much broader that phenotypes of differentiated cells of their original tissues. Many laboratories have documented the existence of stem cell plasticity; however, many objections to the reported results still exist. Here, we present some of these objections questioning the data on stem cell plasticity. We wish to point out some problems associated with plasticity of stem cells, transdifferentiation and cell fusion. Recent experimental results indicate that stem cells may have a key role in stem cell therapy. This review is an introductory discussion on the stem cell plasticity and stem cell therapy.

[Contemporary view on the plasma natriuretic peptide assessment in the clinical practice]. / Soucasný pohled na stanovení mozkového natriuretického peptidu v klinické praxi.

Plasma natriuretic peptide assessment became a part of the routine clinical practice because of the laboratory methods development. After a brief historical overview of natriuretic peptides discovery, the article focuses on the brain natriuretic peptide (BNP). BNP plays an important role in the pathophysiology of many diseases of cardiovascular system due to its effects on the circulation (natriuresis, diuresis, inhibition of renin-angiotensin system, etc). The authors describe process of BNP synthesis, factors leading to its release into circulation. The main emphasis is done on the clinical significance of BNP and NT-proBNP assessment for the-diagnosis in cardiovascular diseases, risk stratification and monitoring of the treatment.

[Acetylsalicylic acid (ASA) resistance in patients with ischemic heart disease (IHD) as bioindicator of the treatment strategy]. / Rezistence na kyselinu acetylosalicylovou u nemocných s ischemickou chorobou srdecní jako bioindikátor lécebné strategie.

BACKGROUND: The interest in aspirin resistance has been increasing during the last few years, with researchers earnestly pursuing alternative anti-platelet therapies and devices for measuring platelet aggregation. The recent studies suggest that 5-45% of patients taking aspirin do not experience adequate anti-platelet effects. METHODS AND RESULTS: There is scant evidence proving that aspirin resistance has some clinical consequences. To assess the prevalence of aspirin resistance in patients with ischemic heart disease (IHD) two independent methods were used: platelet aggregation in platelet rich plasma (PRP) after induction by propylgallate (CPG), and assessment of platelet function by PFA 100 method. The study population consisted of 424 patients treated for IHD on the 2nd Dept. of Medicine, Teaching Hospital, Hradec Kralove. The age, gender, diagnosis and effect of therapy were characterized in this group of the patients. Daily ASA dose was 100 mg. We used two methods to monitor ASA treatment efficacy: a) thrombocyte aggregation after induction by CPG, b) the assessment of platelet function by PFA 100 method. a) Of the patients studied by CPG platelet aggregation, 51 (12.1%) pts were resistant to ASA dose 100 mg/day, and 32 (7.6%) pts remained resistant even after increasig the dose to 200 mg/day. In 80 (20%) pts, the daily ASA dose of less than 100 mg was sufficient to inhibit platelet function. b) Although the PFA-100 system is not able to detect the difference between low and high ASA dose, we found 53 (15.2%) patients aspirin resistant using this method. CONCLUSIONS: In the patients with IHD treated with 100 mg of ASA per day, our study has shown that the prevalence of aspirin resistance was 12.1% using CPG method, and 15.2% using PFA-100 method. Aspirin resistance was dose dependent. Prevalence of ASA resistance in patients treated with 200 mg of ASA per day was only 7.6% using the CPG method.

[Ischemia-modified albumin: new marker of myocardial ischemia?]. / Ischémií modifikovaný albumin: nový marker ischémie myokardu.

The Albumin Cobalt Binding Test is a quantitative in vitro diagnostic test used on human serum that detects ischemia-modified albumin by measuring the cobalt binding capacity of albumin in human serum. Ischemia modified albumin is intended for use in conjunction with ECG and cardiac troponin as an aid to short term risk stratification of patients presenting with chest pain suggestive of cardiac origin. Thus, in patients with chest pain or equivalent symptoms suggestive of cardiac origin, with non-diagnostic ECG and normal troponin, a negative IMA can be used as an aid to rule out acute coronary syndrome (ACS) in low risk patients.

Cytokines and adhesion molecules in the course of acute myocardial infarction.

The plasma levels of interleukin 1 beta (IL 1beta), interleukin 6 (IL 6), interleukin 8 (IL 8), tumor necrosis factor alpha (TNF-alpha), E-selectin, ICAM 1 and C-reactive protein (CRP) have been studied in 24 patients with acute myocardial infarction in the course of 96 h. The plasma IL 1beta and IL 6 levels were continually elevated during the 96 h study period (the peak of plasma IL 1beta level was 22.2 pg/ml, S.D. 8.6, P < 0.001, normal values of IL 1beta are less than 10 pg/ml, the mean peak plasma concentration of IL 6 was 184.9 pg/ml, S.D. 134.7, vs. normal values of 15.57 pg/ml, S.D. 2.4, P < 0.001). The mean plasma IL 8 level was increased for the duration of the study, the mean plasma IL 8 level was 103.0 pg/ml, S.D. 23.4 (normal value was below 30 pg/l, S.D. 8.0) P < 0.001. The plasma TNF-alpha level was elevated throughout the time of observation without any significant peak. The mean plasma TNF-alpha concentration was 46.8 pg/ml, S.D. 2.13, vs. normal value 4.35 pg/ml, S.D. 1.23, P < 0.001. The plasma E-selectin level reached the mean level of 145.1 ng/ml, S.D. 75.4, vs. normal value 29.1-63.4 ng/ml, P < 0.001 at an interval of 15-42 h after the onset of the symptoms. The plasma ICAM 1 level showed only a slight significant increase during the first 36 h. The plasma CRP concentration increased later than IL 6, and reached a peak at 42 h after the onset of the symptoms (69.2 mg/l, S.D. 29.9, vs. 1.2 mg/l, S.D. 4.7, P < 0.0001). We conclude that cytokines and adhesion molecules can play an important role in the mechanisms of tissue injury in the process of ischemia and reperfusion.

The prognostic significance of intermediate QRS prolongation in acute myocardial infarction.

Complete right and left bundle branch block and advanced atrioventricular block present on admission electrocardiograms of patients with acute myocardial infarction, are associated with poor short and long-term outcome. Little is known about the impact of intermediate QRS prolongation (0.09-0.11 s) on the prognosis of acute myocardial infarction. In this study, among 1100 consecutive patients with acute myocardial infarction treated with thrombolysis, the QRS duration on admission electrocardiogram was <0.09 s in 536 (48%) patients, between 0.09 and 0.11 s in 496 (45%) patients and >0.11 s in 78 (7%) patients. QRS duration was strongly associated with 7-day (0.6%, 6%,18%, P<0.001), 30-day (1%, 8%, 22%, P<0.001) and 1-year (3%, 11%, 26%, P<0.001) all-cause mortality. After adjustment for significant variables associated with 1-year mortality, including age, female gender, diabetes mellitus, systemic hypertension, previous myocardial infarction, anterior myocardial infarction and Killip class> or =2 on admission, both levels of QRS prolongation remained significant independent predictors of short and long-term all-cause mortality.

The effect of reperfusion on plasma tumor necrosis factor alpha and C reactive protein levels in the course of acute myocardial infarction.

Severe acute response, the synthesis of human acute-phase proteins and the increase of plasma cytokines and adhesion molecules occur in patients in the course of acute myocardial infarction. We examined the plasma tumor necrosis factor alpha (TNF alpha), plasma creatinkinase (CK) and C-reactive protein (C-RP) levels in patients with acute myocardial infarction (AMI) in the course of 96 hours. Venous blood samples were taken at 3-hour intervals during the first 48 hours, and at 6-hour intervals during the next 48 hours. All patients were treated using thrombolytic therapy (streptokinase). Detection of the reperfusion was based on the method of measuring the time to achieve peak serum creatinkinase activity. The study was done on a group of 24 patients. Plasma levels of the parameters were compared between the group of patients with expected reperfusion versus the group of patients in which reperfusion is not suggested. The plasma TNF alpha level was elevated constantly without any significant peak. The mean plasma TNF alpha concentration was 46.8 pg/ml, SD 2.13, vs. normal level 4.35 pg/ml, p < 0.001. The plasma TNF alpha level in the group of patients with reperfused coronary artery showed a significant decrease especially during the 3rd and 4th day (the mean peak plasma TNF alpha concentration was 35.2 pg/ml, SD 15.8, vs. 66.9 pg/ml, SD 38.3 pg/ml, p < 0.005). The plasma C-RP levels were elevated throughout the time of observation in the both groups. The elevation of the plasma C-RP levels was more significant in the group of patients without successful reperfusion (80.6 mg/ml, SD 31.2, the mean plasma C-RP level of the group of the patients with successful reperfusion was 45.7 mg/ml, SD 18.1, p < 0.005). We conclude, that TNF alpha can play a role in the mechanisms of tissue injury. The successful reperfusion of coronary artery leads to significant decrease of plasma TNF alpha and C-RP levels.

The effect of trimetazidine on C-reactive protein, cytokines and adhesion molecules in the course of acute myocardial infarction.

The aim of this randomised, double-blind, placebo controlled, parallel group study was to assess the effect of trimetazidine (TMZ), a potent antiischaemic drug, on plasma C-reactive protein (C-RP), cytokine and adhesion molecule levels. The study population consists of 18 patients (16 males, 2 females, average age 56.45 +/- 10.97 years) with acute myocardial infarction admitted within 6 hours after onset of symptoms and treated with streptokinase. Blood samples were taken at 3-hour intervals during the time of treatment. All patients were randomised blindly using a centralised randomisation process, between trimetazidine (40 mg bolus i.v. then 60 mg per day for 48 hours intravenously in glucose infusion) or placebo group. Plasma C-RP level was significantly lower in TMZ group (39.5 mg/ml +/- 9.7 mg/ml) as compared to placebo (75.7 +/- 29.4 mg/ml, p < or = 0.001) and peaked 28 hours later in TMZ group. Plasma interleukin 6 (IL 6) level showed a sharp peak 9 hours after the onset of the symptoms in TMZ group (116.9 +/- 180.2 pg/ml vs. 45.4 +/- 37.9 pg/ml) and was increased up to 30 hours after the onset of the symptoms. Plasma interleukin 1 beta (IL 1 beta) was also higher in TMZ group notably 21 hours after the onset of symptoms (26.4 +/- 9.3 pg/ml vs. 16.2 +/- 2.4 pg/ml). TMZ group showed lower plasma E-selectin levels. Plasma IL 8, TNF alpha and ICAM 1 levels were without statistical significant differences. The present study demonstrates a significant reduction of plasma C-reactive protein level in the course of acute myocardial infarction treated with streptokinase and intravenous trimetazidine infusion compared with the group of patients without trimetazidine treatment.

Inflammatory response to acute myocardial infarction complicated by cardiogenic shock.

We report a case of a 60-year-old man with acute myocardial infarction (AMI) treated using thrombolysis, and complicated by cardiogenic shock (CS). Plasma interleukin (IL) 1 beta, IL 6, IL 8, tumor necrosis factor alpha (TNF alpha), and soluble adhesion molecule (sICAM 1, sE-selectin) levels were measured at 3-h intervals. This observation showed the effect of AMI and CS on the plasma interleukin levels. Remarkable changes were found in the plasma TNF alpha level, which reached two significant peaks. The peak of the first elevation caused by AMI (80.11 pg/ml, vs. normal value 4.35 pg/ml, SD 21.3 pg/ml) was seen 6 h after the onset of the symptoms. After the period of significant decrease, TNF alpha level was increasing until the end of the observation period because of CS (the last TNF alpha level was 204.1 pg/ml). The plasma IL 1 beta level was continually increased during the period of observation (maximal IL 1 beta level 32.1 pg/ml, normal value < 10 pg/ml). The plasma IL 6 level reached the first peak caused by AMI nine hours after the onset of the symptoms (362.85 pg/ml, normal value (10 pg/ml). Because of CS, after the short period of decrease, the plasma IL 6 level was increasing until the end of the observation period (the last IL 6 level was 859.61 pg/ml). The plasma IL 8 level was also elevated throughout the time of observation (max. value 1652 pg/ml, vs. normal value < 30 pg/ml). The soluble adhesion molecule levels (sE-selectin and sICAM 1) were elevated throughout the period of observation without any significant peak.