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Heart rate turbulence (HRT) is modulated by the baroreceptor reflex and it was suggested that it could be used as a measure of autonomic dysfunction. Impaired HRT is of a significant prognostic value in humans after myocardial infarction, suffering from dilated cardiomyopathy and patients with heart failure. So far no studies were performed assessing the importance of HRT in dogs. The aim of this study was to prospectively evaluate the HRT turbulence onset (TO) and the turbulence slope (TS) in healthy dogs and in dogs with DCM and to compare the HRT in dogs with DCM that died during the first 30 days of observation and dogs with DCM that survived the first 30 days after the HRT analysis. The current study was aimed at determining reference value of the TO and TS of HRT in healthy dogs (control group) and dogs with dilated cardiomyopathy (DCM group). The tests were carried out on 30 healthy dogs and 30 dogs with DCM composed of Boxers, Doberman pinschers and Great Danes, of different sexes and body weights from 22 to 72 kg, aged between 1.5 and 11.5 years, submitted to the 24-hour Holter monitoring. HRT parameters were calculated using an HolCard software algorithm. TO is a percentage difference between the heart rate immediately following ventricular premature complex (VPC) and the heart rate immediately preceding VPC. TS corresponds to the steepest slope of the linear regression line for each sequence of five consecutive normal intervals in the local tachogram. The average TO in healthy dogs was determined as -13.55 ± 11.12%, TS was 21.33 ± 9.66 ms/RR. TO in dogs with DCM was determined as - 2.61 ± 2.1% and TS was 6.15 ± 3.86 ms/RR. Parameters of HRT were statistically significantly decreased (p<0.01) in dogs with DCM. HRT TO and TS were statistically significantly decreased in dogs with DCM. Dogs with DCM that survived more than 30 days of observation had HRT statistically significantly decreased in comparison to dogs with DCM that died after the 30’th day of observation. Decreased HRT parameters in dogs with DCM suggest an autonomic neuropathy which principally consists of the withdrawal of the cardiac parasympathetic tone. The more the autonomic neuropathy is advanced the faster the death of the dog with DCM might occur, with no correlation with the level of the heart failure.
Vascular endothelial growth factor (VEGF-A) is one of the most important proangiogenic factors. It has many isoforms encoded by one gene. The occurrence of these isoforms is associated with the process of alternative splicing of mRNA. Some of the splice forms are perceived as tissue specific. The aim of this study was to determine the alternative splicing of VEGF-A mRNA in dilated cardiomyopathy, especially at the level of particular myocardial layers. The assessment of post-transcriptional modifications of VEGF-A mRNA was made on specimens taken from the explanted hearts of patients undergoing cardiac transplantation. Molecular and histopathological studies were perfomed on particular layers of the myocardial muscle (endocardium, myocardium, epicardium). A molecular analysis of cardiac samples was performed by quantitative analysis of the mRNA of the studied VEGF-A isoforms (VEGF121, -145, -165, -183, -189, and -206) using QRTPCR with an ABI-PRISM 7700-TaqMan sequence detector. 72 cardiac specimens taken from the explanted hearts were analyzed. Each of the studied VEGF-A splice forms was present in the evaluated hearts, but the types of alternative splicing of mRNA were different in particular layers. Quantitative analysis revealed different amounts of the studied isoforms. Generally, significantly increased expression of the VEGF-A isoforms was observed in samples taken from hearts with post-inflammatory etiology of cardiomyopathy. Our conclusions are: 1. All the studied VEGF-A isoforms were found in the human hearts, including those thusfar considered characteristic for other tissues. 2. Significant differences were observed in the expression of the VEGF-A splice forms with respect to the myocardial layers and the location of the cardiac biopsy. 3. Repetitive and comparable results for samples with post-inflammatory etiology were obtained, and they revealed considerably higher amounts of VEGF-A isoforms compared to specimens with idiopathic etiology.
 In the pathogenesis of dilated cardiomyopathy (DCM) in Emery-Dreifuss muscular dystrophy (EDMD) matrix metalloproteinases (MMPs) are supposed to be involved and may have diagnostic/prognostic value. Serum levels of MT1-MMP, MMP-2 and MMP-9 were quantified by ELISA and zymography in 22 EDMD patients and 15 age-matched controls. In the autosomal-dominant EDMD MMP-2 and MT1-MMP were increased in all cases, and MMP-9 was increased in two of the eight examined patients. In the X-linked EDMD MMP-2 expression was increased in all the cases, MMP-9 level was elevated in 3 of the 14 cases, and MT1-MMP was decreased in eight of these patients. There was no evident correlation between the MMPs level and the different cardiac parameters including left-ventricular end-diastolic diameter, left atrial diameter and left ventricular ejection fraction in either form of EDMD. The presented results indicate that a changed level of matrix metalloproteinases, especially that of MMP-2 in serum, may be of value for detection of cardiac involvement in EDMD patients, especially in those patients with no evident subjective cardiac symptoms. Further follow-up studies of MMPs are needed to check if their determination is of value for monitoring of the progression of atrial/ventricular dilatation. MMPs determinations may also be useful for monitoring DCM treatment by synthetic MMPs inhibitors.
The case of a 12-year-old boxer dog, with an infiltrating tumour in cardiac base and dilated cardiomyopathy was described. Morphological and biochemical examinations of the blood, ECG, and USG of the heart were performed. In the resting ECG record, atrial fibrillation was detected with rapid action of ventricles. Echocardiography demonstrated distension of all cardiac cavities and a decreased contractility of the left ventricular myocardium. Despite intense treatment, the condition of the dog deteriorated: anaemia and renal insufficiency appeared and asphyxia intensified. At the owners' request, the dog was subjected to euthanasia. On autopsy, a tumour in the cardiac base was detected, which infiltrated the left atrial wall. Histopathology and immunohistochemistry permitted to diagnose neoplastic hypertrophy of chemodectoma type.
Atrial light chain 1 (ALC-1) is expressed in embryonic and hypertrophied human ventricles but not in normal adult human ventricles. We investigated the effects of recombinant human atrial light chains (hALC-1) on the structure and enzymatic activity of synthetic filaments of ventricular myosin. The endogenous ventricular myosin light chain 1 (VLC-1) was partially replaced by recombinant hALC-1 yielding hALC-1 levels of 12%, 24% and 42%. This reconstitution of ventricular myosin with hALC-1 did not change the length of synthetic myosin filaments but led to more rounded myosin heads in comparison with those of control filaments. Actin-activated ATPase activity of myosin, a parameter of functional activity of molecular motor, amounted to 79.5 nmol Pi/mg per min in control myosin filaments. Reconstitution with hALC-1 caused a profound increase of the actin-activated myosin ATPase activity in a dose dependent manner, for example, synthetic myosin filaments formed with 12%, 24% and 42% hALC-1 reconstituted myosin revealed the actin-activated ATPase activity increased by 18%, 26% and 36%, respectively, as compared to control. These results strongly suggest that in vivo expression of ALC-1 enhances ventricular myosin function, thereby contributing to cardiac compensation.
Genetic manipulation conducted for many years has resulted in breeding turkeys with very intensive growth rate and high percentage of muscle tissue. These features promote dysfunctions in the cardiovascular system. The aim of this article was to present current data on the etiology of cardiovascular system diseases in turkeys. In this paper the most recent data on dilated cardiomyopathy (round heart disease), spontaneous aortic rupture and perirenal hemorrhage syndrome are described.
Echocardiography is a valuable tool for the evaluation of systolic and diastolic cardiac function. A high correlation between measurements of diastolic mitral inflow parameters analyzed with Doppler echocardiography and invasive methods makes the former valuable. The aim of this study was to ascertain if significant differences occur in diastolic myocardial parameters between dogs with no heart disease and dogs with subclinical or clinical dilated cardiomyopathy. Furthermore the aim of the study was to determine whether heart failure in dilated cardiomypathy is a result of systolic dysfunction alone or both systolic and diastolic dysfunction. Eleven parameters were analyzed: E wave, E-AT, E-DT, E time, A wave, A-AT, A-DT, A time, E+A time, E/A ratio, and IVRT. The study confirmed the value of noninvasive echocardiographic assessment of diastolic function in dogs with dilated cardiomyopathy. Significant differences were found in E wave, E-AT, E time, E/A ratio and IVRT between healthy dogs and dogs with dilated cardiomyopathy. All are characterized by a significant decrease compared to healthy dogs after taking into account age and body weight except for the E/A ratio, which significantly increased in value. There were no significant changes in any of the Doppler parameters for diastolic evaluation in subclinical cases of DCM. Advanced heart failure in dilated cardiomyopathy entails systolic and diastolic dysfunction.
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