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The authors present a case of a 70-year-old woman in whom clinical picture of an acute coronary syndrome with ST segment elevation was suggestive of takotsubo cardiomyopathy (TC). Chest pain, extensive ECG changes and typical TC left ventricular contraction pattern were preceded by emotional and physical stress, while in coronary angiography no atherosclerotic lesions were found. There was however left anterior descending coronary artery myocardial bridging with total systolic compression. Following treatment with beta-blocker and diltiazem, spectacular left ventricle function improvement, with near total recovery after 6 months was observed. Magnetic resonance imaging detected the presence of subendocardial late gadolinium enhancement indicative of postmyocardial scar.

Quantitative analysis of blood viscosity was performed on the basis of mathematical models of non-Newtonian fluid shear flow behavior (Casson, Ree-Eyring and Quemada). A total of 100 blood samples were drawn from clinically stable survivors of myocardial infarction, treated with aspirin or acenocoumarol and controls to these drugs. Whole blood and plasma viscosity were measured at a broad range of shear rates using a rotary-oscillating viscometer Contraves LS40. Numerical analysis of the experimental data was carried out by means of linear (for Casson) and non-linear regression for the remaining models. In the evaluation of the results, both the fit quality and physical interpretation of the models' parameters were considered. The Quemada model fitted most precisely with the experimental findings and, despite the controversies concerning the relationship between in vivo tissue perfusion and in vitro rheological measurements, seemed to be a valuable method enhancing investigation possibilities of cardiovascular patients. Our results suggest that aspirin does not affect blood rheological properties, while acenocoumarol may slightly alter red cell deformability and rouleaux formation.

Ischaemic stroke in thromboembolic mechanism may be a first sign of neoplastic disease, as in the presented case of a 56-year-old woman. Progressive trombocytopenia, anaemia with reticulocytosis and schistocytes in peripheral blood smear, elevated serum LDH activity as well as coexisting myocardial infarction initially suggested Moschcowitz syndrome. However, plasma exchange did not improve her neurological status and D-dimer values increase in subsequent evaluations indicated chronic DIC. At the same time, on transesophageal echocardiography, thrombotic endocarditis was diagnosed. Screening for cancer showed high CA 125 marker and chest computed tomography revealed lung tumor, not visible on earlier chest X-ray. In further treatment she underwent palliative radiotherapy and continued low molecular weight heparin. The neoplastic process had an unfavorable course and she died after four months. The authors point out that in case of multifocal ischaemic stroke and coexistent thrombocytopenia, neoplastic hypercoagulable state and thrombotic endocarditis should be considered.

Introduction: The glycoprotein complex Ia/IIa (GP Ia/IIa) is a major collagen receptor on platelets and other cell types. Recently, linked polymorphisms within the coding region of the GP Ia gene (C807T and G873A) related to GP Ia/IIa surface expression have been identified. The 807T/873A allele is associated with high expression, whereas the 807C/873G allele is associated with low surface expression of GP Ia/IIa. Subsequently, the 807T allele was found to be associated with coronary artery disease (CAD) and cerebral infarction in younger patients. Moreover, platelet thrombus formation is significantly influenced by genetic variations of the GPIb alpha and GPIa receptors and is dependent on the blood flow rate., Aim: 1. To determine the frequency of C807T polymorphism of the GPIa gene in young survivors of myocardial infarction (MI) and 2. to evaluate the relationship between the intensity of CAD in the coronary angiography examination and the 807C/T genetic status of the patients., Methods: 102 young male survivors of MI (YSMI) -- mean age 43, range 29-49 years, mean age at the time of the first episode 37+/-3 years -- were studied. Obesity was found in 15%, diabetes in 14%, hyperlipidemia in 87%, hypertension in 22% and smoking history in 90% of cases. Familial CAD and/or MI were confirmed in 50% of patients. The control group consisted of 106 healthy volunteers with a negative family history of CAD, both medical staff members and blood donors (mean age 40, range 18-42 years). The genetic study was performed using genomic DNA obtained from peripheral blood leukocytes. The C807T polymorphism of platelet glycoprotein Ia (GPIa) was investigated using the PCR method introduced by Santoso et al., Results: Coronary angiography (Siemens Bicor system) revealed single-artery disease in 34%, two-artery disease in 36% and three-artery disease in 26% of patients. In two patients there were no signs of CAD. The C807T polymorphism of GPIa was found in 73.5% of investigated patients (heterozygotes CT 59.8%, homozygotes TT 13.7%). The CC genotype was confirmed in 26.5% of patients. A similar analysis performed in the group of healthy men showed C807T polymorphism of the GPIa gene in 73.6% (CT in 58.5% and TT in 15.1% of persons, ns). CC genotype was found in 26.4% of persons. Interestingly, the T genotype frequency was similar in patients with three- or two-artery disease in comparison with patients with single-vessel or without CAD (49.3% vs. 50.7%, respectively, ns). In 75 YSMI carrying C807T polymorphism of the GPIa gene additional genetic abnormalities were confirmed in 21 patients - BclI polymorphism of b-chain fibrinogen gene, G4070A and G1691A (FV Leiden) mutation of factor V gene and C677T polymorphism of methylenetetrahydrofolate reductase gene. Partial occurrence of combined polymorphisms was found. This was confirmed independently of the number of coronary arteries involved., Conclusions: Our results may question the potential role of C807T the GPIa anomaly as a single genetic abnormality predisposing young men to coronary artery disease.

Profound thrombocytopenia after abciximab administration in acute myocardial infarction and stent thrombosis. This article presents a case of a 62-years-old man with acute anterior myocardial infarction, treated with PCI and stent implantation, in whom profound acute thrombocytopenia was observed after abciximab administration. Nadir platelet count was 6 G/L (before treatment: 250 G/L). Pseudothrombocytopenia was excluded. The remaining antiplatelet drugs (heparin, ASA, clopidogrel) were discontinued. There were no symptoms of bleeding, but next morning (platelet count: 14 G/L) a gross hematoma at femoral puncture site was observed. The patient received 5 U transfusion of platelets. On the 4th day, when the platelet count reached 64 G/L, he was started again on ASA (150 mg) and clopidogrel (75 mg). On the 7th day (platelet count: 138 G/L) he developed anterior ischemia and stent reocclusion was diagnosed. After p.o. clopidogrel (300 mg), balloon PCI with i.c. heparin was performed and ischemia symptoms subsided. The platelet value before the patient's discharge, on subsequent therapy with ASA and clopidogrel, increased to 300 G/L. A review of current literature on this topic is provided.

The viscosity of whole blood taken from patients suffering from different diseases was studied. The measurements of blood viscosity were performed in the shear rate range 0.01-100 s-1 in three groups of patients. The first group consisted of 60 patients without known cardiovascular disorders referred for a non-vascular minor surgery (patients did not take any drugs influencing vascular system). The second group (30 persons) consisted of patients after cerebral ischemic episode, remaining under permanent medical control. The third group consisted of 100 patients after myocardial infarction. In the group of patients suffering from vascular system disorders (second and third) the blood viscosity has been significantly lower then in the first group. Such results might suggest that in patients with vascular system disorders blood viscosity has been decreased in the way of specific feedback mechanism, whereas the beneficial hemorrheological influence of secondary prevention seems to be questionable.

Background: Several polymorphisms in the genes encoding for three separate chains of fibrinogen have been described. Some of them (Hae III and B854) are associated with elevated fibrinogen plasma level., Aim: To determine the frequency of BclI polymorphism in the fibrinogen beta-chain gene (BclI betaFb) in young survivors of myocardial infraction (MI) and to assess the relationship between allele status, plasma fibrinogen concentration and the number of affected coronary arteries., Methods: The study group consisted of 99 male patients (mean age 43.5, range 29-49 years) with premature coronary artery disease (CAD) diagnosed by coronary angiography who had MI in the mean age of 37.4+/-3.2 years. The control group involved 78 age- and gender-matched healthy volunteers. DNA was extracted from peripheral blood leukocytes using standard methods. Fibrinogen blood concentration was determined using biuretic method. The BclI polymorphism in the fibrinogen beta-chain gene was investigated using polymerase chain reaction (PCR)., Results: Obesity was found in 15%, smoking - in 89%, hypertension - in 21%, diabetes - in 14% and hyperlipidemia - in 86% of MI patients. A family history of MI was present in 50% of patients. Coronary angiography revealed single-vessel disease in 34%, two-vessel disease in 36%, and three-vessel disease in 16% of patients. In two patients coronary angiography was normal. The frequency of BclI polymorphism of the beta-fibrinogen gene was significantly higher in MI patients than in controls (40.4% vs 29.5%, p<0.01). Moreover, in MI patients carrying the mutant allele a higher concentration of blood fibrinogen was found in comparison to patients without this anomaly (3.87 vs 3.55 g/L, p=0.05). There was no evidence of an association between the number of affected coronary arteries and polymorphism of BclI betaFbg gene status. However, all patients carrying BclI polymorphism of betaFbg gene had abnormal coronary angiography, contrary to patients without any defect., Conclusions: 1. Polymorphism of BclI betaFbg gene is associated with an increased fibrinogen plasma level. 2. There is no association between BclI polymorphism of betaFbg gene and the number of affected coronary arteries. This may confirm the hypothesis of multi-factorial aetiology of CAD in young patients suffering MI.

The aim of this study was to compare fibrinolytic parameters in two subgroups of young survivors of myocardial infarction: group A (n = 14) with silent myocardial ischaemia and group B (n = 15) without silent myocardial ischaemia, as assessed by 24 h Holter electrocardiogram monitoring. Only men aged 33-46 years who were in a stable condition at least 6 months after the acute event were included in the survey. All patients were normolipaemic or had only mild hyperlipidaemia, non-diabetic, normotensive, non-current smokers and with a normal body mass index. The control group consisted of 15 age-matched healthy men. Blood samples were taken at 7.30 a.m. In the group A patients, we found higher mean levels of tissue plasminogen activator (t-PA) total antigen (11.1 versus 6.9 ng/ml, P < 0.01), its inhibitor plasminogen activator inhibitor-1 (PAI-1) antigen (58.1 versus 34.8 ng/ml, P < 0.01), PAI-1 activity (4.9 versus 3.4 U/ml, P < 0.05) and tPA-PAI-1 complexes (5.1 versus 3.5 ng/ml, P < 0.05) as well as a lower level of t-PA activity (0.5 versus 0.8 IU/ml, P < 0.01) and free t-PA antigen (0.8 versus 1.3 ng/ml, P < 0.01) compared with the controls. However, group A patients exhibited higher PAI-1 antigen levels (58.1 versus 41.6 ng/ml, P < 0.05) than those without silent ischaemia. There were no differences between group B and controls in any of the parameters measured. Our results indicate that patients with more severe disease, as revealed by silent myocardial ischaemia, had lower levels of free t-PA as a result of the excess of PAI-1.

The platelet factor 4 (PF4) mobilisation properties of low molecular weight heparin (Fraxiparine, Sanofi Winthrop, France) in young survivors of myocardial infarction (YSMI) and healthy volunteers have been investigated. The study group consisted of 42 YSMI less than 44 years old, all of them with angiographically proven occlusive coronary artery disease, studied 6 to 24 months after the acute event. The control group was composed of 30 healthy men of similar age. Subjects from the study and control groups were allocated to the following subgroups: those receiving 60 or 120 IU/kg b.w. of standard heparin (Polfa Kutno, Poland) and those receiving 60, 120 or 180 IC anti-Xa U/kg b.w. of low molecular weight heparin (Fraxiparine, Sanofi Winthrop, France) as a single intravenous injection. Additionally, in five YSMI patients the influence of prolonged aspirin administration (0.3g daily for more than 30 days) on the Fraxiparine mobilsable pool of PF4 and beta-thromboglobulin (beta-TG) concentration in the plasma was determined after injection of 180 IC anti-Xa U/kg b.w. of the drug. The PF 4 and beta-TG concentration in the plasma was evaluated using enzyme immunoassay methods before heparin or Fraxiparine intravenous injection and 2, 5, 10, 20, 30 and 60 min after. In both, the control and YSMI groups baseline PF4 levels were found to be normal. Moreover, similar marked dose-dependent increases of PF4 concentration in the plasma measured after 60 and 120 IU/kg b.w. of heparin as well as after 60 and 120 IC anti-Xa U/kg b.w. of Fraxiparine was found. The administration of 120 IU/kg b.w. of heparin resulted in a reduced rise in plasma PF 4 in YSMI as compared to healthy controls. The same phenomenon was observed when 180 IC anti-Xa U/kg b. w. of Fraxiparine was injected intravenously. In YSMI treatment with aspirin had no influence on the Fraxiparine mobilisable pool of PF 4 or the beta-TG concentration in the plasma. These results suggest that mobilisable pool of platelet factor 4 in young survivors of myocardial infarction derives from the "nonplatelet pool" and that reduction of heparin- or Fraxiparine-releasable pool of PF4 may reflect an impaired endothelium function, probably due to atherosclerosis.

In 53 patients with recent (< 6 hrs) acute myocardial infarction a study was undertaken to evaluate the safety of conjunctive therapy with streptokinase (1.5 mln U), aspirin (150 mg) and low molecular weight heparin (Fraxiparine). Patients were treated with Fraxiparine 250 U anti-Xa IC/kg/24 hrs iv for 2 days (with bolus 12.5 U anti-Xa IC/kg), and 125 U anti-Xa IC/kg twice a day sc for 5 subsequent days. Clinical course in one-year observation was compared regarding the time the therapy was initiated. In the group undergoing therapy 3-6 hrs after the infarct had occurred 4 (7.5%) patients died (2 during hospitalization, 2 after discharge). In 31 patients treated within 3 hrs of the myocardial infarction there were fewer cases of recurrent myocardial infarction, unstable angina or congestive heart failure necessitating rehospitalization their (9.1%) than in 22 patients included in the treatment regimen between 3 rd and 6th h of the infarction (27.3%). Earlier thrombolysis was also connected with higher left ventricular ejection fraction (55 +/- 8% vs 49 +/- 10%) and more frequent peak CK-MB values 12 hrs after thrombolysis (81% and 68% of patients respectively). Neither symptomatic deep vein thrombosis nor pulmonary embolism was detected. The left ventricular thrombosis was diagnosed by echocardiography in 4 of 20 patients (20%) with the first anterior myocardial infarction. There was neither bleeding requiring blood transfusion nor cerebrovascular stroke. The treatment with Fraxiparine did not induce the prolongation of APTT values. Conjunctive thrombolytic therapy with low molecular weight heparin was safe and followed by a favorable outcome of the acute myocardial infarction, especially if instituted within the first 3 hrs after the onset of infarction.

Hemovasal produced by Manetti-Roberts, Florence, Italy, is a glycosaminoglycan obtained from porcine intestinal mucosa which belongs to the family of heparan sulfates. The substance was examined On 36 male survivors of myocardial infarction with an interval of at least 6 months after the acute event. No anticoagulants were given and ASA was withdrawn at least 2 weeks before the trial. Hemovasal was administered in 3 different i.m. doses as single injections. A further group received a daily oral dose of 300 mg for one week. A comparable placebo group of patients as well as a group of healthy volunteers was run in parallel. The coagulation profile showed only a slight prolongation of the aPTT, a trace of diminution of Antithrombin III and no activation of Heparin cofactor II. The fibrinolytic system showed an enhancement of the diurnal increase of t-PA without an alteration of the total increase of this activity. There was a considerable and highly significant diminution of the PAI-1 activity. This was dose dependent and could be found after i.m. as well as after oral administration. It was assumed that the thrombolytic effect which was repeatedly described was a consequence of the diminution of PAI-1.

The studies involved 102 male patients, aged between 23 and 40 years, with a history of one myocardial infarction. Behaviour pattern was determined with The Jenkins Activity Survey questionnaire. Total serum cholesterol, triglycerides, glucose, and uric acid concentrations were assayed, both diastolic and systolic blood pressures were measured, all patients were weighed, and reported the number of smoked cigarettes. A mean number of risk factors per patient was calculated as well as their incidence in various behaviour patterns. It was found behaviour pattern A predominates in young male patients with a history of myocardial infarction. However, serum total cholesterol, triglycerides, and uric acid levels were lower in this group in comparison with those representing behaviour patterns B and X. The authors suggest that behaviour pattern A may be an independent risk factor for myocardial infarction in young subjects. Further studies are, therefore, needed within the programs of circulatory diseases prevention.

The study was aimed at an evaluation of individualized indications for antithrombotic therapy for secondary prevention in a group of 40 young survivors (aged 30-40 years) of myocardial infarction, presenting a stable phase of coronary disease. The control group consisted of 19 healthy men, of approximately similar age distribution. The determinations concerned the following: in vitro ADP and collagen induced platelet aggregation, plasma fibrinogen concentration, factor VII, VIII and antithrombin III activity, protein C concentration, spontaneous fibrinolytic activity and fibrinolytic activity after venostasis, plasminogen and alpha-2 antiplasmin activity. Moreover, to determine correlations with hemostatic parameters lipids, apolipoproteins, glucose, uric acid plasma concentration as well as percentages of lipoproteins and glycolyzed hemoglobin were also studied. In the study group various hemostasis disturbances were found: an increased platelet aggregation induced by low concentrations of ADP, increased plasma fibrinogen concentration and factor VII activity, decreased protein C concentration and impaired plasma fibrinolytic activity after venostasis. Some correlations between hemostatic and lipids parameters were also observed. Results of the study have suggested necessity for the individualized antithrombotic prevention in young survivors of myocardial infarction with antiplatelet and/or anticoagulant drugs.

Selected parameters of platelet function as well as their relationship with metabolic coronary risk factors are studied in a group of 40 young survivors (aged 30-40 years) of myocardial infarction, now presenting stable coronary disease. Nineteen healthy men, of approximately similar age-span, constituted the control group. The following parameters were determined: platelet survival half-time (via non-isotope method), intraplatelet activity of cyclooxygenase and lipoxygenase pathway of arachidonic acid (by measurements of malondialdehyde concentration before and after incubation with acetylsalicylic acid acid) and 125-I-fibrinogen binding to platelets. Moreover, the plasmatic concentration of total cholesterol, HDL-cholesterol, triglycerides, phospholipids, Apo A and B, total beta lipoproteins, glucose, uric acid as well as percentages of beta, prebeta, alpha lipoproteins and glycosylated hemoglobin were also studied. Platelet survival half-time in patients was significantly shortened (3.64 +/- 1.37 days) when compared with the control group (4.97 +/- 1.7 days). A higher intraplatelet activity of lipoxygenase pathway (2.02 +/- 0.62 and 1.49 +/- 0.54 nmol MDA/10(9) platelets, respectively) was also found. However, activity of cyclooxygenase pathway of arachidonic acid and 125-I-fibrinogen binding to platelets remained unchanged. Shortened platelet survival half-time and the hyperactivity of intraplatelet lipoxygenase pathway correlated with a reduced plasmatic concentration of HDL-cholesterol (r = 0.323, p less than 0.05 and r = -0.451, p less than 0.05, respectively). The remaining parameters of platelet function were not statistically related to metabolic risk factors. The values of platelet function indicators in subgroups of patients divided according to family history of coronary heart disease, oral glucose load test result, and submaximal exercise test result did not differ significantly.(ABSTRACT TRUNCATED AT 250 WORDS)