The aim of this study was a comparison of risk stratification for death in patients after myocardial infarction (MI) and of risk stratification for malignant arrhythmias in patients with implantable cardioverter-defibrillator (ICD). The individual risk factors and more complex approaches were used, which take into account that a borderline between a risky and non-risky value of each predictor is not clear-cut (fuzzification of a critical value) and that individual risk factors have different weight (area under receiver operating curve - AUC or Sommers´ D - Dxy). The risk factors were baroreflex sensitivity, ejection fraction and the number of ventricular premature complexes/hour on Holter monitoring. Those factors were evaluated separately and they were involved into logit model and fuzzy models (Fuzzy, Fuzzy-AUC, and Fuzzy-Dxy). Two groups of patients were examined: a) 308 patients 7-21 days after MI (23 patients died within period of 24 month); b) 53 patients with left ventricular dysfunction examined before implantation of ICD (7 patients with malignant arrhythmia and electric discharge within 11 month after implantation). Our results obtained in MI patients demonstrated that the application of logit and fuzzy models was superior over the risk stratification based on algorithm where the decision making is dependent on one parameter. In patients with implanted defibrillator only logit method yielded statistically significant result, but its reliability was doubtful because all other tests were statistically insignificant. We recommend evaluating the data not only by tests based on logit model but also by tests based on fuzzy models., P. Honzík ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Myocardial Infarction (MI) also known as heart attack is one of the most dangerous cardiovascular diseases. Accurate early prediction can effectively reduce the mortality rate caused by MI. The early stages of MI may only have subtle indications which can be varied in variable risk factors and making diagnosis difficult even for experienced cardiologists. In this paper the computer aided detection system is proposed to find the risk level of MI using the supervised classifier. The MI prediction system is developed using Feed Forward Neural Network (FFNN), Cascade Correlation Neural Network (CNN), and Support Vector Machine (SVM). Genetic Optimized Neural Network (GAANN), Particle Swarm Optimized Neural Network (PSONN) and also the performance of the Computer Aided Detection system is analyzed using various performance metrics.
Chronic intermittent hypoxia (CIH ) is associated with increased production of reactive oxygen species that contributes to the adaptive mechanism underlying the improved myocardial ischemic tolerance. The aim was to find out whether the antioxidative enzyme manganese superoxide dismutase (MnSOD) can play a role in CIH-induced cardioprotection. Adult male Wistar rats were exposed to intermittent hypobaric hypoxia (7000 m, 8 h/day, 25 exposures) (n=14) or kept at normoxia (n=14). Half of the animals from each group received N-acetylcysteine (NAC, 100 mg/kg) daily before the hypoxic exposure. The activity and expression of MnSOD were increased by 66 % and 23 %, respectively, in the mitochondrial fraction of CIH hearts as compared with th e normoxic group; these effects were suppressed by NAC treatment. The negative correlation between MnSOD activity and myoc ardial infarct size suggests that MnSOD can contribute to the improved ischemic tolerance of CIH hearts., P. Balková ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Acute myocardial infarction (AMI) is one of the leading causes of death among adults in older age. Understanding mechanisms how organism responds to ischemia is essential for the ischemic patient’s prevention and treatment. Despite the great prevalence and incidence only a small number of studies utilize a metabolomic approach to describe AMI condition. Recent studies have shown the impact of metabolites on epigenetic changes, in these studies plasma metabolites were related to neurological outcome of the patients making metabolomic studies increasingly interesting. The aim of this study was to describe metabolomic response of an organism to ischemic stress through the changes in energetic metabolites and aminoacids in blood plasma in patients overcoming acute myocardial infarction. Blood plasma from patients in the first 12 h after onset of chest pain was collected and compared with volunteers without any history of ischemic diseases via NMR spectroscopy. Lowered plasma levels of pyruvate, alanine, glutamine and neurotransmitter precursors tyrosine and tryptophan were found. Further, we observed increased plasma levels of 3-hydroxybutyrate and acetoacetate in balance with decreased level of lipoproteins fraction, suggesting the ongoing ketonic state of an organism. Discriminatory analysis showed very promising performance where compounds: lipoproteins, alanine, pyruvate, glutamine, tryptophan and 3-hydroxybutyrate were of the highest discriminatory power with feasibility of successful statistical discrimination., Martin Petras, Dagmar Kalenska, Matej Samos, Tomas Bolek, Miroslava Sarlinova, Peter Racay, Erika Halasova, Oliver Štrbák, Jan Stasko, Ludovit Musak, Michaela Skorvanova, Eva Baranovicova., and Obsahuje bibliografii
Physical training (PT) is beneficial in cardiovascular diseases associated with NO deficiency such as coronary disease, hypertension, etc. However, it is not known whether PT can also prevent pathological conditions associated with excess NO and fall of blood pressure (BP) such as acute myocardial infarction (AMI). The aim was to compare the effect of AMI on BP and functional state of the endothelium in rats trained by swimming and in untrained animals. After AMI, BP fell from 110±2 to 74±4 mm Hg (p<0.05), the endothelium-dependent relaxation increased from 37±4 to 66±6 % (p<0.05) and the extent of contraction suppression by the endothelium was significantly greater than in the controls. PT itself increased the endothelium-dependent relaxation of rat aorta but left BP unaffected. PT limited the AMI-induced fall of BP to 87±3 mm Hg, the endothelium- dependent relaxation to 53±4 % and prevented the hyporesponsiveness of the aorta to norepinephrine. We suggest that the protective effect of PT is related to inhibition of inducible NO synthase by a negative feedback mechanism.
Adaptation to hypoxia is beneficial in cardiovascular pathology related to NO shortage or overproduction. However, the question about the influence of adaptation to hypoxia on NO metabolism has remained open. The present work was aimed at the relationship between processes of NO production and storage during adaptation to hypoxia and the possible protective significance of these processes. Rats were adapted to intermittent hypobaric hypoxia in an altitude chamber. NO production was determined by plasma nitrite/nitrate level. Vascular NO stores were evaluated by relaxation of the isolated aorta to diethyldithiocarbamate. Experimental myocardial infarction was used as a model of NO overproduction; stroke-prone spontaneously hypertensive rats (SHR-SP) were used as a model of NO shortage. During adaptation to hypoxia, the plasma nitrite/nitrate level progressively increased and was correlated with the increase in NO stores. Adaptation to hypoxia prevented the excessive endothelium-dependent relaxation and hypotension characteristic for myocardial infarction. At the same time, the adaptation attenuated the increase in blood pressure and prevented the impairment of endothelium-dependent relaxation in SHR-SP. The data suggest that NO stores induced by adaptation to hypoxia can either bind excessive NO to protect the organism against NO overproduction or provide a NO reserve to be used in NO deficiency., E. B. Manukhina, S. Yu. Mashina, B. V. Smirin, N. P. Lyamina, V. N. Senchikhin, A. F. Vanin, I. Yu. Malyshev., and Obsahuje bibliografii
The study of ischemia/reperfusion injury included 25 patients in the acute phase of myocardial infarction (19 perfused, 6 remained non-reperfused as evaluated according to the time course of creatine kinase and CK-MB isoenzyme activity) and a control group (21 blood donors). Plasma level of malondialdehyde was followed as a marker of oxidative stress. Shortly after reperfusion (within 90 min), a transient increase of malondialdehyde concentration was detected. The return to the baseline level was achieved 6 h after the onset of therapy. The activity of a free radical scavenger enzyme, plasma glutathione peroxidase (GPx), reached its maximum 90 min after the onset of treatment and returned to the initial value after 18 h. The specificity of the GPx response was confirmed by comparing with both non-reperfused patients and the control group, where no significant increase was detected. The erythrocyte Cu,Zn-superoxide dismutase (SOD) did not exhibit significant changes during the interval studied in perfused patients, probably due to the stability of erythrocyte metabolism. In non-reperfused patients, a decrease of SOD was found during prolonged hypoxia. These results help to elucidate the mechanisms of fast activation of plasma antioxidant system during the reperfusion after myocardial infarction., V. Mužáková, R. Kanďár, P. Vojtíšek, J. Skalický, Z. Červinková., and Obsahuje bibliografii
The aim of our study was to characterize resistance to ischemia/reperfusion (I/R) injury in Langendorff-perfused rat hearts and effectivity of ischemic preconditioning (PC) under condition of simulated acute hyperglycemia (SAHG) by perfusion of the hearts with Krebs-Henseleit (KH) solution with elevated glucose concentration (22 mmol/l). I/R injury was induced by 30- min coronary occlusion followed by 120-min reperfusion and PC by two cycles of 5-min occlusion/5-min reperfusion, prior to I/R. The severity of I/R injury was characterized by determination of the size of infarction (IS, expressed in % of area at risk size) and the amount of heart-type fatty acid binding protein (h-FABP, a marker of cell injury) released from the hearts to the effluent. Significantly smaller IS (8.8±1 %) and lower total amount of released h-FABP (1808±660 pmol) in PC group compared with IS 17.1±1.2 % (p<0.01) and amount of h-FABP (8803±2415 pmol, p<0.05) in the non-PC control hearts perfused with standard KH solution (glucose 11 mmol/l) confirmed protective effects of PC. In contrast, in SAHG groups, PC enhanced IS (21.4±2.2 vs. 14.3±1.3 %, p<0.05) and increased total amount of h-FABP (5541±229 vs. 3458±283 pmol, p<0.05) compared with respective non-PC controls. Results suggest that PC has negative effect on resistance of the hearts to I/R injury under conditions of elevated glucose in vitro., M. Zálešák, P. Blažíček, D. Pancza, V. Ledvényiová, M. Barteková, M. Nemčeková, S. Čarnická, A. Ziegelhöffer, T. Ravingerová., and Obsahuje bibliografii
The aim of our work was to study the opposite polarity of the PQ segment to the P wave body surface potential maps in different groups of patients. We constructed isointegral maps (IIM) in 26 healthy controls (C), 16 hypertensives (HT), 26 patients with arterial hypertension and left ventricular hypertrophy (LVH) and 15 patients with myocardial infarction (MI). We analyzed values and positions of map extrema and compared the polarity of maps using the correlation coefficien t. The IIM P maxima appeared mainly over the precordium, the minima mainly in the right subclavicular area. The highest ma xima were in the MI group, being significantly higher than in the HT and LVH groups. No differences concerning any values of other extrema were significant. The IIM PQ maxima were distributed over the upper half of the chest; the minima mainly over the middle sternum. A statistically significant opposite polarity between the IIM P and IIM PQ was found in 80 % of cases. The opposite polarity of the P wave and the PQ segment was proved in isointegral body surface maps. The extrema occurr ed in areas not examined by the standard chest leads. This has to be considered for diagnostic purposes., K. Kozlíková ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy