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The paper presents an algorithm of cardio complex classification as part of processing the data of continuous cardiac monitoring. R-wave detection concurrently with cardio complex sorting is discussed. The core of this approach is the use of prior information about. cardio complex forms, segmental structure, and degree of kindness. Results of the sorting algorithm testing are provided.

The present study was aimed to investigate neuroprotective effects of early and late ischemic preconditioning in the acute phase of ischemic brain damage in rats. It was found that a single five-minute ischemic episode of early ischemic preconditioning did not lead to significant neuroprotective effects in comparison with control group, while three five-minute ischemic episode early ischemic preconditioning accompanied by a significant increase in neurological deficit and growing damage rate in CA1 hippocampus neurons. In contrast, later ischemic preconditioning in form of single five-minute episode 24 hours before ischemia modeling, provided a significant neuroprotective effect, manifesting reduced neurological deficit and maintaining viability of CA1 hippocampus neurons.

The purpose of the present investigation was to study the time course of changes in myocardial blood flow (MBF) in response to cold stimulation. Thirty-eight patients having risk factors of cardiovascular complications were examined. The time course of MBF changes was estimated by positron emission tomography (PET) using 13N-ammonium at rest and during a cold test (CT). Endothelium-dependent vasodilation of the brachial artery was determined from the results of a reactive hyperemia test, by applying ultrasound duplex scanning. No significant MBF increase in response to the cold test was an indicator of coronary arterial endothelial dysfunction at cardiac 13N-ammonium PET. Agreement of the results of brachial arterial ultrasonography during reactive hyperemia and cardiac 13N-ammonium PET in the presence of the cold test suggests that endothelial dysfunction is generalized. Cardiovascular risk factors, such as left ventricular hypertrophy, smoking, dyslipidemia, and diabetes mellitus, substantially affect coronary arterial function. Left ventricular hypertrophy is an independent factor that influences the amount of the coronary reserve and, in combination with endothelial dysfunction, worsens coronary microcirculation.

Unlabelled: The purpose of this investigation is to evaluate the influence of purified highly-concentrated omega-3 polyunsaturated fatty acids (90% omega-3 polyunsaturated fatty acids 1 g/day) on the severe ventricular arrythmias in patients with stable coronary heart disease (CHD) without concomitant left ventricular contractivity impairment., Materials and Methods: 43 patients with stable CHD (26 male and 17 female, aged 66.2 +/- 8.3) with ejection fraction above 45% with unstable paroxysms of ventricular tachycardia detected at Holter ECG monitoring that received 1 g/day omega-3 polyunsaturated fatty acids during 1 month. 23 patients continued treatment for one month extra, while 20 stopped receiving after one month. ECG monitoring was repeated monthly., Results: In one month after started receiving 90% omega-3 polyunsaturated fatty acids the mean heart rate reduced by 2.4%, the number of single extrasystoles reduced by 20.1% (p=0.01), the number of paired extrasystoles reduced by 47% (p=0.0018) and the number of paroxysms reduced by 49% (p=0.0029). In 41.9% patients no paroxysms have been registered after one month. When continuously receiving omega-3 polyunsaturated fatty acids during the second month, the treatment efficiency increases, while the receiving been stopped after one month, the effect is reduced but remains., Conclusion: 1 g/day omega-3 polyunsaturated fatty acids application in patients with stable CHD without myocardium contraction dysfunction suffering from ventricular arrhythmias (4B grade after B.Lown) with no direct indications for implantable cardioverter defibrillator therapy results in significant reduction of arrhythmia.

Traditionally infarction size reduction by ischemic preconditioning is estimated in duration of test ischemia. This approach limits the understanding of real antiischemic efficacy of ischemic preconditioning. Present study was performed in the in vivo rat model of regional myocardial ischemia-reperfusion and showed that protective effect afforded by ischemic preconditioning progressively decreased with prolongation of test ischemia. There were no statistically significant differences in infarction size between control and preconditioned animals when the duration of test ischemia was increased up to 1 hour. Preconditioning ensured maximal infarction-limiting effect in duration of test ischemia varying from 20 to 40 minutes.

Present study was aimed at investigation into the role of sodium-calcium exchanger (NCX) in myocardial ischemia-reperfusion injury and ischemic preconditioning (IPC). Experiments were performed in vivo rat model of regional myocardial ischemia-reperfusion. It was shown that inhibition of reverse mode of NCX with selective blocker KB-R7943 at a dose of 10 mg/kg resulted in significant decrease in occurrence and severity of ischemic ventricular tachyarrhythmias. Furthermore, administration of KB-R7943 caused potentiation of the antiarrhythmic effect exerted by single episode of IPC. However, KB-R7943 exerted no effect on myocardial infarction size nor affected infarction size limitation by IPC. In conclusion, inhibition of reverse mode of NCX conferred significant antiarrhythmic effect against ischemic rhythm disorders but it was ineffective in terms of infarction size limitation.

The present investigation was to study the time course of changes in myocardial blood flow (MBF) in response to cold stimulation. Thirty-eight patients having risk factors of cardiovascular complications were examined. The time course of MBF changes was estimated by positron emission tomography (PET) using 13N-ammonium at rest and during a cold test (CT). Endothelium-dependent vasodilation of the brachial artery was determined from the results of a reactive hyperemia test, by applying ultrasonic duplex scanning. No significant MBF increase in response to the cold test was an indicator of coronary arterial endothelial dysfunction at cardiac 13N-ammonium PET. Agreement of the results of brachial arterial ultrasonography during reactive hyperemia and cardiac 13N-ammonium PET in the presence of the cold test suggests that endothelial dysfunction is generalized. Cardiovascular risk factors, such as left ventricular hypertrophy, smoking, dyslipidemia, and diabetes mellitus, substantially affect coronary arterial function. Left ventricular hypertrophy is an independent factor that influences the size of the coronary reserve and, in combination with endothelial dysfunction, worsens coronary microcirculation.

Data on myocardial tolerance of ischemia in the animals with experimental diabetes are controversial. In our study, myocardial sensitivity to ischemia and infarction-limiting effect of ischemic preconditioning have been investigated in the in vivo rat model of myocardial infarction in alloxan-induced insulin-dependent diabetes mellitus. It has been shown that in 6 weeks after alloxan injection in the diabetic rats infarction size as determined by TTC staining was significantly smaller than in healthy controls (39.8 +/- 8.8 and 62.3 +/- 6.6%, respectively, p < 0.01). Also, occurrence of ischemic tachyarrhythmias was more rare in diabetic rats than in controls. A single episode of ischemic preconditioning in diabetic rats showed a much lesser protection against infarction than in controls. Therefore, the data obtained support the existence of endogenous protective myocardial phenotype in diabetes, although the effectiveness of ischemic preconditioning in diabetes is reduced.

Phenomenon of ischemic post-conditioning of the myocardium (attenuation of myocardial damage during reperfusion resulting from interruption of early reperfusion period by repetitive short episodes of ischemia) was discovered in 2003. This paper contains presentation of protective effects of ischemic post-conditioning during ischemia-reperfusion of the myocardium, data on antiarrhythmic effects of post-conditioning in relation to persistent tachyarrhythmias during reperfusion, analysis of possible mechanisms of infarct-limiting effect of post-conditioning, and perspectives of its clinical application.

In experimental arrhythmias induced in rabbits by strophanthin, epinephrine, and calcium chloride the high antiarrhythmic efficacy of Naloxone was proved. No antiarrhythmic activity of Naloxone was observed in aconitine models. The intravenous administration of Naloxone to normal adults (0.4 - 0.8 mg) increased the sinus cycle length, sinus node recovery time (SNRT), CSNRT, and sinoatrial conduction time.

Using the results of a prospective follow-up of 106 patients with angina, the authors examined the factors influencing the prognosis of coronary heart disease, including the prognostic value of dynamic coronary occlusion detected during an intravenous ergometrine test. The indicators that are most typical of patients groups with varying outcomes were identified by using the discriminant analysis. The highest value is shown by the factors associated with the extent of coronary occlusion in the prediction of a fatal outcome. A tendency to vasoconstrictive reactions shown as a high sensitivity to ergometrine is a risk factor of myocardial infarction and acute heart failure in individuals highly tolerant to exercise.

A study of 157 patients with verified or suspected coronary disease, subjected to the intravenous ergometrin test, is reported. A clear-cut correlation is demonstrated between the rate of clinically and electrocardiographically positive tests, the pattern of the pain syndrome and the clinical course of the disease. Vasospastic response was particularly common in patients with unstable angina. Of those, patients prone to attacks of acute coronary insufficiency in the presence of progressive angina with recent clinical coronary manifestations were particularly sensitive to ergometrin. Among patients with stable angina, angina of the higher functional classes was associated with a considerable rate of positive ergometrin tests. Vasoconstrictive response was rather uncommon in individuals with intact stress tolerance and spontaneous chest pains, suggestive of spontaneous angina. There were no vasospastic reactions in patients with the atypical pain syndrome.

Ninety-five coronary patients were studied, including 44 patients with stable angina and 51 with unstable angina. All patients underwent bicycle ergometry and the intravenous ergometrin test. An anginal attack developed in response to bicycle ergometry in 63.5% of patients with stable angina and in 74.4% of patients with progressive coronary insufficiency. The threshold capacity achieved was directly related to the functional class of stable angina, and dependent on the clinical variety of unstable angina. The ergometrin test was positive in 70.4% of patients with stable angina and 82.4% of patients with unstable angina. An ergometrin-induced anginal attack developed where the double product was significantly smaller than that of threshold stress. The differences were the highest in patients with progressive angina and attacks of acute coronary insufficiency.

To study the role of the vasospastic factor in the etiology of CHD pain forms a total of 326 patients were examined using coronary angiography, of them a test with i. v. administration of ergometrine was made to 117. An analysis of the peculiarities in the CHD course showed that angina destabilization usually associated with the addition of a dynamic component, could occur in a different duration of disease. The first clinical signs of CHD in more than half of the cases in a stable and unstable course of angina developed in the marked obstructive involvement of the coronary bed. Obvious vasospastic reactions in the ergometrine test were more frequently noted with recently developed unstable angina however they could occur in a different period of disease. The data obtained indicated that in most cases two mechanisms were involved in the development of angina: fixed coronary obstruction as a morphological basis of coronary insufficiency and spasm of the coronary arteries which could be a leading factor in a number of patients or determine angina instability.

An attempt has been made to elucidate causes of heart rate change during exercise in anginal patients, using multifactorial mathematical analysis. Seventy-one patients underwent bicycle ergometry and the intravenous ergometrin test. Heart rate variation was found to be unrelated to the type of stress (bicycle ergometry or Master's test), or the presence or absence of ischemic ECG changes during an attack of pain. During exercise, heart rate shifts preceding an anginal attack are similar to those in patients with painless response to stress. At the onset of pain, an abrupt rise in heart rate is seen, its magnitude being particularly great in postmyocardial infarction patients with low physical stress tolerance and high sensitivity to ergometrin. Myocardial insufficiency may be the cause of excessive tachycardia in this category of patients. In patients with high stress tolerance in the absence of ergometrin sensitivity, increased sensitivity to endogenic catecholamines may be a cause of tachycardia during an anginal attack.