Therapeutic approach in patients with a floating thrombus in the right heart.

BACKGROUND: The occurrence of a floating thrombus in the right heart, although rare, is a life-threatening condition requiring a specific approach. In most cases, these thrombi are a result of embolization from deep venous thrombosis, and have lodged temporarily in the right heart. The management of this condition is variable, depending on whether or not there is a thrombus entrapped within a foramen ovale (FO). OBJECTIVES: To present the management of 2 patients with a free-floating thrombus in the right heart, and a third patient with an entrapped thrombus in the FO. CASE REPORTS: Two patients with a free-floating thrombus in the right atrium who were treated with thrombolytic therapy had an immediate excellent outcome. The patient with a thrombus entrapped within the FO was scheduled for surgical removal of the thrombus due to an unacceptable risk of systemic embolization if treated with thrombolytic and anticoagulant therapy. Unfortunately, he developed an ischemic stroke on the fifth day of presentation, just a few hours before the scheduled surgery, despite meticulous monitoring of continuous heparin infusion with activated partial thromboplastin time. CONCLUSION: Thrombolytic therapy is recommended in patients with a free-floating thrombus in the right heart. However, in patients with a thrombus entrapped within an FO, delaying surgical removal of the thrombus may be deleterious due to unpredictable systemic embolization.

The sex-specific association of Met62Ile gene polymorphism in P-selectin glycoprotein ligand (PSGL-1) with carotid plaque presence: preliminary study.

Atherosclerosis is known as an inflammatory disease in which a recruitment of leukocytes to the endothelium wall represents a preliminary step of the initiation and the development of disease. The P-selectin glycoprotein ligand (PSGL-1) seems to be the major molecule mediating leukocyte-endothelium interactions and leukocyte rolling on stimulated endothelium. There are limited number of studies reporting on association of Met62Ile SNP in PSGL-1 gene and the risk for atherosclerosis. The aim of this study was to analyze possible association of this polymorphism with an advanced carotid atherosclerosis and biochemical markers of inflammation and haemostasis. The 275 patients consecutively admitted for carotid endarterectomy with stenosis >70% and 256 controls of the same ethnic origin were included in the study. The Met62Ile genotypes were determined by PCR RFLP. The Ile/Ile homozygotes had significantly higher CRP compared to the other genotypes in patients. Female patients had Ile allele dose-dependent association with the carotid plaque presence (Met/Met vs. Met/Ile vs. Ile/Ile; OR 1, OR 2.02, CI 1.0-4.08, OR 4.08, CI 1.0-16.81, respectively, p = 0.04). Our results suggest the impact of PSGL-1 Met62Ile polymorphism on inflammation in advanced atherosclerosis. We observed the sex-differential association of Met62Ile with advanced carotid atherosclerosis. Studies in larger and different populations should validate and further examine the suggested role of genetic variations in PSGL-1 with atherosclerosis and thrombosis.

Apolipoprotein(a) gene polymorphisms (TTTTA)n and G/A-914 affect Lp(a) levels in ischemic heart disease patients from Serbia.

OBJECTIVES: Lipoprotein(a) (Lp(a)) concentration is determined primarily by the apolipoprotein(a) (apo(a)) gene. The pentanucleotide (TTTTA)n repeat and G/A-914 polymorphisms are in the 5' promoter region of the apo(a) gene. To elucidate whether these polymorphisms affect Lp(a) levels, a total of 211 Serbian adults were investigated. DESIGN: One hundred and eleven patients with ischemic heart disease and 100 healthy controls were genotyped and Lp(a) levels determined. RESULTS: Lp(a) concentrations differed according to the (TTTTA)n genotypes: among those having at least one allele 8, patients had significantly higher Lp(a) values than controls. A decreasing trend of Lp(a) values was associated with the -914A allele in controls but the opposite was true in patients. Patients with genotype TTTTA allele 8/AA-914 had significantly higher Lp(a) values than those without allele 8/AA (p < 0.05). The >8>8/GG genotype was not detected. Significant linkage disequilibrium between (TTTTA)n and G/A-914 polymorphism (p < 0.001) was found. In multivariate regression analysis, the G/A-914 polymorphism significantly (p < 0.05) affected Lp(a) levels in patients, after taking into account the (TTTTA)n polymorphism. CONCLUSION: These results indicate that (TTTTA)n and G/A-914 polymorphisms affect Lp(a) levels in ischemic heart disease as a consequence of the linkage disequlibrium.

Apolipoprotein E gene polymorphisms as risk factors for carotid atherosclerosis.

BACKGROUND/AIM: Atherosclerosis is still the leading cause of death in Western world. Development of atherosclerotic plaque involves accumulation of inflammatory cells, lipids, smooth muscle cells and extracellular matrix proteins in the intima of the vascular wall. Apolipoprotein E participates in the transport of exogenous cholesterol, endogenously synthesized lipids and triglycerides in the organism. Apolipoprotein E gene has been identified as one of the candidate genes for atherosclerosis. Previous studies in different populations have clearly implicated apolipoprotein E genetic variation (E polymorphisms) as a major modulator of low density lipoprotein cholesterol levels. Data considering apolipoprotein E polymorphisms in relation to carotid atherosclerosis gave results that are not in full compliance. The aim of present study was to investigate the apolipoprotein E polymorphisms in association with carotid plaque presence, apolipoprotein E and lipid serum levels in patients with carotid atherosclerosis from Serbia. METHODS: The study group enrolled 495 participants: 285 controls and 210 consecutive patients with carotid atherosclerosis who underwent carotid endarterectomy. Genotyping of apolipoprotein E polymorphisms were done using polymerase chain reaction and restriction fragment length polymorphism methods. RESULTS: Patients had significantly decreased frequency of the epsilon2 allele compared to controls. Patients who carry at least one epsilon2 allele had a significantly higher level of serum apolipoprotein E and significantly lower low density lipoprotein cholesterol levels compared to those who do not carry this allele. CONCLUSION: Our results suggest protective effect of apolipoprotein E epsilon2 allele on susceptibility for carotid plaque presence as well as low density lipoprotein cholesterol lowering effect in Serbian patients with carotid atherosclerosis. Further research of multiple gene and environmental factors that contribute to the appearance and the progression of atherosclerosis should be continued with respect to different populations.

The effects of acclimatization on blood clotting parameters in exertional heat stress.

BACKGROUND/AIM: Exertional heat stress is a common problem in military services. Considering the coagulation abnormalities are of major importance in development of severe heat stroke, we wanted to examine changes in hemostatic parameters in soldiers during exertional heat stress test as well as the effects of a 10-day passive or active acclimatization in a climatic chamber. METHODS: A total of 40 male soldiers with high aerobic capacity performed exertional heat stress test (EHST) either in cool [20 degrees C, 16 degrees C wet bulb globe temperature (WBGT)], or hot (40 degrees C, 29 degrees C, (WBGT) environment, unacclimatized (U) or after 10 days of passive (P) or active (A) acclimatization. Physiological strain was measured by tympanic temperatures (Tty) and heart rates (HR). Platelet count (PC), antithrombin III (AT), and prothrombin time (PT) were assessed in blood samples collected before and immediately after the EHST. RESULT: EHST in hot conditions induced physiological heat stress (increase in Tty and HR), with a significant increase in prothrombin time in the groups U and A. Platelet counts were significantly higher after the EHST compared to the basic levels in all the investigated groups, regardless environmental conditions and acclimatization state. Antithrombin levels were not affected by EHST whatsoever. CONCLUSION: In the trained soldiers, physiological heat stress caused mild changes in some serum parameters of blood clotting such as prothrombin time, while others such as antithrombin levels were not affected. Platelet counts were increased after EHST in all groups. A 10-day passive or active acclimatization in climatic chamber showed no effect on parameters investigated.

Increased inflammatory response in patients with the first myocardial infarction and nonsignificant stenosis of infarct-related artery.

INTRODUCTION/AIM: Atherosclerosis presents a serial of highly specific cellular and molecular responses, and could be described as inflammatory diseases. Accordingly, for development of acute myocardial infarction (AMI), structure and vulnerability of atherosclerotic plaque are more important than the extent of stenosis of infarct-related artery. Consequently, inflammation and atherosclerosis and its complications are in good correlation. C-reactive protein (CRP) as nonspecific inflammatory marker, has prognostic significance in coronary artery diseases. The aim of this study was to establish the correlation between inflammatory response expressed as levels of CRP and fibrinogen in serum and extent of coronary artery stenosis. METHODS: Study included 35 patients with acute myocardial infarction, as the first manifestation of coronary artery disease, which were treated with thrombolytic therapy according to the guidelines. All the patient had a reperfusion. The patients with acute or chronic inflammatory diseases, an increased value of sedimentation, fibrinogen, CK > or = 190 U/L, early and late complications of AMI were excluded. CRP was measured on admission, after 24, 48 and 72 hrs, and 21 days latter, while fibriogen only on admission. RESULTS: All the patients underwent coronary angiography, and were divided into two groups: the group 1 (23 patients), with significant stenosis of infarct-related artery (stenosis > or = 75%), and the group 2 (13 patients) without significant stenosis (< 75%). Mean value of CRP serum level on admission in the group 1 was 4.4 mg/L, and in the group 2 7.2 mg/L (p < 0.001). The mean value of fibrinogen on admission in the group 1 was 2.7 g/L, and in the group 2 3.0 g/L (p < 0.001). The mean CRP value after 48 hrs in the group 1 was 21.7 mg/L, and in the group 2 42.4 mg/L. (p < 0.001). After three weeks, the mean CRP value was 4 mg/L in the group 1 and 5.5 mg/L in the group 2 (p < 0.001). There was no significant difference between the groups 1 and 2 related to gender, age, localization of AMI, CK, EF value, and risk factors for coronary artery disease. CONCLUSION: The patients with nonsignificant stenosis of infarct-related artery had increased inflammtory responses according to the CRP value, as a result of inflammatory process in atherosclerotic plaque and/or enhanced individual reactivity.

The association of ACE I/D gene polymorphism with severe carotid atherosclerosis in patients undergoing carotid endarterectomy.

INTRODUCTION: The ACE I/D polymorphism was mostly investigated in association with intima-media thickness, rarely with severe atherosclerotic phenotype. MATERIALS AND METHODS: We investigated the association of I/D polymorphism with severe carotid atherosclerosis (CA) (stenosis > 70%) in asymptomatic and symptomatic patients undergoing carotid endarterectomy. The 504 patients subjected to endarterectomy and 492 healthy controls from a population in Serbia were investigated as a case-control study. RESULTS: The univariate logistic regression analysis revealed ACE DD as a significant risk factor for severe CA (odds ratio [OR] = 1.3, 95% confidence interval [CI] 1.0-1.7, p = 0.04). After adjustment for the common risk factors (age, hypertension, smoking, and HDL) ACE was no longer significant. However, we found a significant independent influence of DD genotype on plaque presence in a normotensive subgroup of patients (OR 1.8, CI 1.2-3.0, p = 0.01, corrected for multiple testing). In symptomatic patients D allele carriers were significantly more frequent compared with asymptomatic patients (OR 1.6 CI 1.0-2.6, p = 0.05). CONCLUSIONS: Our data suggests that ACE I/D is not an independent risk factor for severe CA. On the other hand, a significant independent genetic influence of ACE I/D appeared in normotensive and symptomatic patients with severe CA. This should be considered in further research toward resolving the complex genetic background of severe CA phenotype.

Elevation of troponin values in differential diagnosis of chest pain in view of pulmonary thromboembolism.

INTRODUCTION: Acute coronary syndrome, as unstable form of ischaemic heart disease, beside clinical presentation and electrocardiographic abnormalities, is characterized by increased value of troponin one of cardiospecific enzimes. Although troponin is a high specific and sensitive indicator of acute coronary syndrome, any heart muscle injury may induce its increasing, so there are some other diseases with the increased troponin value. CASE REPORT: We presented a female patient with chest pain, admitted because of suspicioun of acute coronary syndrome. Performed coronarography excluded ischemic heart disease. Considering symtomatology, electrocardiographic abnormalities, increased troponin and D-dimer values, as well as echocardiography finding we considered pulmonary embolism as a differential diagnosis, which was confirmed by pulmoangiography. CONCLUSION: Isolated increased troponin values are not enough for diagnosis of acute coronary syndrome.

[Impact of heart myxoma localization upon its clinical course and outcome].

INTRODUCTION: Primary heart tumors are very rare. They can be benign and malignant. Benign ones make about two thirds of all heart tumors. However, they are benign only by their biologic characteristics, but potentially malignant by their localization. About three forths of benign tumors are myxomas. Their growth is usually slow and they can be for a long time silent, particularly if they do not compromise vital functional parts of the heart. Myxomas grow in the atria, mostly in the left one and very rarely in the ventricles. CASE REPORT: We presented two patients with myxomas in the left, and, in the right atrium which are representative samples of the most common localization of heart myxoma considering previous knowledge of these tumors. Analysis of the clinical course in the two presented patients with characteristic localizations showed general characteristics of the clinical course of heart myxoma. The patients did not have characteristic symptoms for a rather long period of time and the findings obtained by standard examinations did not raise suspicion of heart tumor. Pulmonary symptomatology in one patient and cardial in the other, when tumor had already occupied almost the entire atrium, suggested necessity of cardiologic examination. Indication for operation was in both patients confirmed after performed echocardiography, computed tomography of the thorax and angiography with ventriculography. The size of the removed atrial tumors and their localization explained some of the patients' troubles, but it was also amazing that they had not caused more serious problems. Operation as the only method of treatment was successful in both female patients and its effect was permanent. At annual controls neither recurrence of the tumor nor troubles possibly associated with it were observed. CONCLUSION: Patients with heart myxoma usually pass through asymptomatic or oligosymptomatic phase, but when troubles become manifested, they do not much differ from those due to other causes. For this reason this tumor can be diagnosed just when complications caused by its localization and growth develop. Modern cardiologic diagnostics, primarily preventive non-invasive echocardiography, enables timely diagnosis and removal of the tumor because only then it may take a name benign tumor.

[Treatment of acute myocardial infarct with ST segment elevation with a combination of fibrinolytic therapy and abciximab]. / Primena kombinacije fibrinoliticke terapije i abciksimaba u lecenju akutnog infarkta srca sa elevacijom ST segmenta.

BACKGROUND: According to current knowledge, the best way to treat the acute myocardial infarction with ST elevation is primary transluminal coronary angioplasty, which can be performed only in the best equipped tertiary cardiology centers. As it was known that atherothrombosis wais the essence of the acute coronary syndrome we wanted to examine the efficacy and safety of combined therapy of tissue plasminogen activator and glycoprotein IIbIIIa platelet receptor antagonist abciximab. METHODS: The case is reported of combined abciximab and accelerate schedule of t-PA reperfusion therapy in a young patient with the extensive anterior acute myocardial infarction. Activated partial thromboplastin time and platelet count were regularly measured during therapy. RESULTS: The combination of these two drugs did not cause any complication in our patient. According to early noninvasive parameters, successful reperfusion was achieved. Postinfarction period was without complications. Coronary angiography was performed 15 days after and was without pathological findings. Eighteen months later the event patient had neither chest pain, nor other complaints with slightly reduced R waves in middle precordial leads and hypokinesis of anterior apical segment of the left ventricle showing the signs of important systolic function impairment. CONCLUSION: Controlled studies are needed to prove the safety and the benefit of such combined reperfusion therapy and to show which kind of treatment is appropriate in every case considering the patient conditions and the facilities of coronary care unit.

Primary percutaneous transluminal coronary angioplasty in the acute infarction of the right ventricle.

BACKGROUND: Predilection site for the acute myocardial infarction of the right ventricle, (AMI-RV) is the upper third of the right coronary artery and for this reason such an infarction is followed by numerous complications, primarily by conduction disorders and very often by sudden and rapid cardiogenic shock development. METHODS: Primary percutaneous transluminal coronary angioplasty (PPTCA) was performed on three patients, in whom the acute infarction of the right ventricular was diagnosed and who had been hospitalized six hours after the beginning of chest pain. In all three patients intracoronary stent was implanted. On the admission patients had been in the threatening cardiogenic shock, with the prominent chest pain and with the elevation of ST-segment in V4R > 2 mV. In the course of intervention patients were administered low-molecular intracoronary heparin, with direct platelet glycoprotein IIb/IIIa inhibitors (abciximab), according to the established procedure applied in such cases. RESULTS: The complete dilatation of the infarcted artery was established with the signs of reperfusion and the further clinical course was completely normal, there was no heart failure and patients had no subjective difficulties. CONCLUSION: Invasive approach in the treatment of AMI-RV is justifiable, and possibly the therapy of choice of these patients, providing well trained and equipped team is available.