Search PubMed⌕ Search

Biomedical subjects

N R Paleev

Publications and source records attributed to N R Paleev.

At least 91 records · Page 5Linked to original sources

[Various factors determining the fatal outcome in myocarditis].

A study of 38 patients with infectious-allergic myocarditis included clinical laboratory investigation, echocardiography, catheterization of the right heart compartments and the pulmonary artery and endomyocardial biopsy. It has identified adverse factors contributing to fatal outcome: increased end-diastolic pressure in the pulmonary artery, low cardiac output, signs of macrofocal fibrosis and small ejection fraction.

Adult↗

[Central hemodynamic status and left ventricular contractile function in patients with chronic obstructive lung diseases and stable pulmonary hypertension (based on data from radionuclide study methods)].

Systemic, central and intracardiac hemodynamics and left-ventricular contractility were studied radiocardiographically and radioventriculographically in 22 patients with stable pulmonary hypertension, developing in the presence of chronic obstructive pulmonary diseases. A tendency to increased circulating blood volume, significantly elevated end diastolic and end systolic indices, reduced total ejection fraction, and a tendency to decreased segmental ejection fractions were demonstrated. A significant reduction of the speed and percentage of left-ventricular myocardial circular fibre contraction is another evidence of incompetent left-ventricular contractility, in addition to the reduced ejection fraction.

Adult↗

[Principles and methods of the treatment of pulmonary hypertension in chronic nonspecific lung diseases].

A critical review of medication to control pulmonary hypertension associated with chronic nonspecific pulmonary diseases is presented along with the authors' own experience with the use of long-acting nitrates and calcium antagonists, suggesting that such drugs are warranted as a long-term treatment in combination with agents controlling bronchial obstruction.

Antihypertensive Agents↗

[Mechanism of the occurrence of ventricular bigeminy].

Twenty-seven patients, aged 15 to 77, with a variety of cardiovascular diseases and bigeminy, and 3 normal subjects were investigated, using exercise and atropin tests. Electrocardiograms were recorded at pre-ectopic intervals of no more than 0.55 sec in bigeminy and polygeminy. The common divisor for interectopic intervals, ectopic complex interpolation, P-Q and Q-T intervals of the main complex and the presence of a wave on the ascending or descending slope of the R wave in sinus QRS complex were determined. Three mechanisms were identified to explain ventricular bigeminy developing during the third phase of action potential and the supernormal myocardial excitation period. A risk group was identified with respect to persistent bigeminy, incorporating patients with the short P-Q syndrome and signs of the typical or atypical Wolff-Parkinson-White syndrome.

Action Potentials↗

[Mechanisms of the occurrence of parasystole and extrasystole].

Mechanisms involved in the development of parasystole and extrasystole are substantiated on the basis of vast clinical material (261 patients with parasystole and 45 with extrasystole). The use of functional tests employing exercise and atropine contributed to both the correct diagnosis of parasystole and extrasystole and a logical explanation of the mechanisms governing their development. Prolonged ECG recording identified, for the first time ever, the limits of the maximum admissible coupling interval for normotopic extrasystole, as the preliminary diagnosis of the nature of the arrhythmia was only made after the said tests. Parasystole was shown to be rooted in a pathologic automatism, and extrasystole, in the summation of extrasystolic focus potentials and the principal pacemaker potential during movement as well as the principal pacemaker impulse along the route of the minor circular wave on Purkinje' level. The localization of ectopic foci in parasystole and extrasystole confirms the hypothesis of the mechanisms involved in these arrhythmias. A parallel study of parasystole and extrasystole defined parasystole as active heterotopia, and extrasystole, as passive heterotopia incapable of generating a rhythm.

Arrhythmias, Cardiac↗

[Pulmonary hypertension and cardiac lesions in chronic nonspecific lung diseases].

Clinical and instrumental criteria for pulmonary and intracardiac hemodynamic disorders within the lesser circulation, associated with chronic nonspecific pulmonary disease (CNPD) are presented. It is demonstrated that right-ventricular (RV) hypertrophy is not an obligatory sign of hemodynamic disorders complicating chronic pulmonary disease, therefore selecting it as the principal sign of an intricate complex of pulmonocardiac disorders is a mistake that interferes with prospective early clinical diagnosis of pulmonocardiac disturbances associated with CNPD and reduces the efficiency of their treatment. The nature of CNPD-associated pulmonocardiac disturbances is adequately reflected in the term "secondary pulmonary hypertension".

Cardiomegaly↗

[Hemostatic system in obstructive lung diseases and its changes in the course of treatment with low heparin doses].

A decrease in antithrombin III activity was noted in exacerbation of chronic obstructive bronchitis and bronchial asthma. It was assessed as a criterion of intravascular activation of the blood coagulation system. The absence of dependence of the clinical effect of heparin on its anticoagulant properties was shown in these diseases. The use of small doses of heparin was shown to result in a rise of antithrombin III activity in the plasma irrespective of an obvious clinical effect of treatment.

Adolescent↗

[Differential diagnosis of linked parasystole and extrasystole].

The differentiation between linked parasystole and extrasystole was based on functional tests with exercise and atropin as stimuli. A total of 116 patients (71 with parasystole and 45 with extrasystole) were investigated. Two mechanisms involved in parasystole with fixed links between ectopic complexes were identified: 1) a mechanism of simple quantitative correlation between two pace-makers, 2) a mechanism of the principal pace-maker being discharged with impulses from the parasystolic one. Extrasystole is based on the trigger mechanism of relationship between ectopic excitation and the impulse from the principal pace-maker. Prolonged ECG recording established limits for the maximum interval of links between monotopic extrasystoles and the interectopic interval for paired extrasystole. Extrasystole was shown to be incapable of generating a pace of its own, i.e. a succession of three or more ectopic complexes of similar morphology.

Arrhythmias, Cardiac↗