The aim – to study the features of longitudinal segmental displacement of left ventricular (LV) walls in patients with multiple types of hypertrophic cardiomyopathy.
Material and methods. 93 patients with hypertrophic cardiomyopathy and 35 patients without cardiac pathology have been involved into study. Common laboratory methods of examination and complex echocardiography, including Speckle-tracking echocardiography, have been carried out. Patients with hypertrophic cardiomyopathy have been assigned to 4 groups, according to the NYHA functional class and systolic gradient of the LV outflow tract.
Results. The study revealed that obstruction of the LV outflow tract is related to the signs of heart failure in patients with hypertrophic cardiomyopathy. Amplitude of the longitudinal displacement of the LV myocardium in normal condition and in hypertrophic cardiomyopathy in all walls was always the largest at the level of basal segments and achieved minimal level at the apex.
Conclusions. In hypertrophic cardiomyopathy the vector of longitudinal systolic displacement of LV walls is similar to normal ones. During the normal heartbeat and hypertrophic cardiomyopathy the peak values of longitudinal displacement were demonstrated by the basal segments of the LV, whereas the apex of the heart remained almost static. There is a direct relation between the value of systolic gradient in the LV outflow tract and number of segments with diminished function of longitudinal displacement, as well as the grade of circulatory deficiency. The indices of longitudinal displacement are lowering first in basal segments of anterior and septal regions. As the obstruction of the LV outflow tract increases, the rest segments are being involved into pathological process.
The purpose of the research was to look for additional laboratory markers and instrumental parameters associated with persistence of left ventricular (LV) systolic dysfunction and heart failure (HF) in acute diffuse myocarditis (ADM), and studying the possibilities of predicting the course of the disease after 12 months of follow-up. We examined 38 patients with ADM – 25 men and 13 women in the first month from the onset of the disease, after 6 and 12 months of follow-up. After 12 months 32 patients that survived were divided into 2 groups: 1st group – 17 patients with preserved systolic function – LV ejection fraction (EF) > 45 %, HF NYHA class ≤ I, 2nd group 15 patients with systolic dysfunction – LV EF ≤ 45 %, HF NYHA class ≥ II. In all patients we studied venous peripheral blood with measurement of antimyocardial antibody titers and blast-transformation lymphocyte activity against myocardium (BTLAm). In the supernatants of mononuclear cells we studied concentrations of the following cytokines: tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-2, interleukin-10 and interferon-γ. Additionally in serum we measured the activity of catalase and superoxidedysmutase. Echocardiography was performed with assessment of the indexes of LV end-diastolic volume, end-systolic volume and EF. Cardiothoracic index was measured by chest roentgen. Inflammatory cytokine concentrations on the 1st month after the ADM onset were higher than those after 6 months and appeared on average: for IL-1β 156.8±16.3 and 91.8±13,4 pg/ml (Р<0.05) respectively, for TNF-α 214.2±28.1 and 163.3±20.1 pg/ml (Р<0.05) respectively, and the BTLAm activity on the 1st month in comparison with the 6 months period was also higher: 6.90±0.52 and 4.90±0.51 % (Р<0.01) respectively. Activation of immunopathologic reactions and antioxidant enzyme activity depression at onset of the disease was accompanied by LV dilatation and systolic dysfunction. We built the prognostic model for the assessment of probability of LV systolic dysfunction at the first month after the disease onset and HF preservation after 12 months of disease course. In conclusion, LV dilatation and impairment of its systolic function is associated with activity of immune response and oxidative stress. We detected the most informative laboratory and instrumental markers which are useful for prediction of myocarditis course and built the prognostic model with high sensitivity and specificity.
The aim of the study was to evaluate intracardial haemodynamics parameters and remodeling of left and right heart in patients with essential hypertension (EH) of II stage with concentric left ventricular (LV) hypertrophy and mitral regurgitation (MR). 53 patients with EH and concentric LV hypertrophy were observed. Methods of investigation included blood pressure monitoring, transthoracic echocardiography, pulsed-wave, colour Dopplerography. MR 2nd stage was associated with left atrial remodeling studied by indexed volume, diameter and square parameters, as well as decreased left atrial ejection fraction. LV diastolic dysfunction was related to MR stage – it’s increase to stage 2 was associated with significant increase of LV early filling. In these patients increase of the right atrial diameter and square, right ventricular pressure, tricuspidal regurgitation, diminished acceleration time of pulmonary artery flow are the signs of initial pulmonary hypertension. MR 2nd stage was combined with complicated EH natural course, LV diastolic dysfunction increase and development of most unfavorable night-peaker type of blood pressure profile. In conclusion, the severity of MR in EH determines left and right heart remodeling stage.
The aim of the research was to investigate the effects of prolonged use of angiotensin-converting enzyme (ACE) inhibitor enalapril and angiotensin II receptor blocker (ARB) candesartan on the levels of aldosterone, N-terminal fragment of brain natriuretic peptide (NT-proBNP), tumor necrotic factor-α (TNF-α), apoptosis inducer Fas-Ligand (FasL) and pulmonary artery systolic pressure in patients with decompensated chronic pulmonary heart disease (CPHD). 74 patients (11 women and 63 men) with decompensated CPHD with heart failure (HF) NYHA Class III were examined. Their average age was 62.8±3.7 years. The patients were randomized into two clinical groups: the first (main) group consisted of 39 patients which received ACE inhibitor enalapril and additionally the ARB candesartan, while the second (control) group consisted of 35 patients which received only basic therapy and ACE inhibitor enalapril. Increase in blood levels of aldosterone, marker of HF NT-proBNP, proinflammatory cytokine TNF-α, and apoptosis inducer FasL is marked in patients with decompensated CPHD with HF NYHA Class III, in comparison with healthy individuals. The combined use of ACE inhibitor enalapril and the ARB candesartan within 6 months promotes reduction of levels of aldosterone, NT-proBNP, TNF-α, FasL and pulmonary artery systolic pressure, that leads to the delay of HF progression in patients with decompensated CPHD.
Sorry, this entry is only available in Українська.
Sorry, this entry is only available in Українська.
This article contains information about hypertrophic cardiomyopathy, about anatomic, physiologic and hemodynamic aspects of formation of obstructions in left ventricular outflow tract. Treatment algorithm in this pathology depends on stage of the disease and needs differentiated approaches, taking into account features of the disease clinical course. Using transcatheter alcohol ablation of the first septal branch of left coronary artery is one of the treatment methods in patients with hypertrophic obstructive cardiomyopathy. This method is used in the treatment of hypertrophic cardiomyopathy, depending on its stage and may be considered an alternative to the surgical treatment. The article presents immediate and long-term results in 25 patients with hypertrophic obstructive cardiomyopathy.
The aim of investigation was to study the expression of tyrosyl-tRNA synthase (TyrRS) in myocardium and to examine the peculiarities of autoimmune reactions against full-size TyrRS and its N- and C-terminal modules in
dilated cardiomyopathy (DCM). Recombinant proteins full-size TyrRS and its N- and C-terminal modules were isolated from the bacterial strains based on Escherichia coli BL21(DE)pLysE. TyrRS expression in myocardium
was identified by Western-blot analysis in pathomorphologic specimens of three DCM-affected human myocardia and samples of left ventricular myocardium of three practically healthy men who died from casual
trauma as a control. The level of specific circulating antibodies (Abs) against full-size TyrRS and its C- and N-terminal modules were measured by ELISA method in sera of 30 DCM patients with congestive heart failure.
Sera of 20 healthy donors were examined as a control. In order to study the effect of auto-Abs on TyrRS enzymatic activity we purified these Abs from DCM patients’ sera with immunoaffine chromatography and
analyzed their influence on the parameters of aminoacylation reaction of cognated tRNA catalyzed by TyrRS. The increased expression (by 43%) of TyrRS was revealed in total lysates and especially in nuclear subfraction
of DCM-affected cardiomyocytes compared to control. The increased levels of auto-Abs against full-size TyrARS (by 20.5%), against its N-terminal (catalytic) modules (by 21.1%) and C- (non-catalytic) modules (by
29.1%) were found in blood serum of DCM patients, compared with healthy donors.
Heat shock proteins (HSP) are a highly conserved family of proteins that are expressed at low level under normal physiological conditions but dramatically increased in response to different cellular online casino stresses. HSPs function primarily as molecular chaperones participating in different intracellular processes: proteins folding, prevention of protein aggregation, transporting of newly synthesized polypeptides to organelles, degradation of miss folding proteins, apoptosis regulation, etc. HSP hyper expression is a substantial mechanism of cytoprotection. Hsp60 one of representatives of HSP-family proteins, that participate in assembling and transporting of mitochondrial proteins and prevention of their aggregation. The aim of investigation was to study the peculiarities of Hsp60 expression and intracellular localization in the heart at dilated cardiomyopathy. In normal cardiomyocytes 70–80% of Hsp60 is located in mitochondria and 20–30% in cytoplasm. In our study we used GroEL – prokaryotic homology of Hsp60 (sequence homology > 50%). Hsp60 expression was evaluated by Western-blot analysis in pathomorphologic specimens of three DCM-affected human myocardia and samples of left ventricular myocardium of three practically healthy men who died from casual trauma as a control. The expression Hsp60 at mRNA level was determined by 3T-PCR. Anti-Hsp60 autoantibodies (autoAB) level was determined by ELISA method in sera of 24 DCM patients and 38 healthy donors as a control. We revealed no
differences in anti-Hsp60 autoAB”s level (both IgG and IgM) in DCM patients” and healthy donors sera. The results show the increased expression of Hsp60 in human DCM myocardium total lysates (more than twice –
2.36) compared to normal. It was also revealed the Hsp60 intracellular re-distribution at DCM – augmentation in mitochondrial (for 66%) and decrease in cytoplasmic fraction (for 59%) compared to normal hearts.