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Biomedical subjects

J Vítovec

Publications and source records attributed to J Vítovec.

At least 19 recordsLinked to original sources
PubMed2006

Prevalence and pathogenicity of Cryptosporidium suis in pre- and post-weaned pigs.

A total of 4338 faecal samples, 135 of sows, 3368 of pre-weaned and 835 of post-weaned piglets from eight farms in South Bohemia, Czech Republic were collected and examined for Cryptosporidium infection. No sow, but 5.7% pre-weaned and 24.1% post-weaned piglets were positive for Cryptosporidium infection. No relationship was found between diarrhoea and Cryptosporidium infection in any of the different age groups (pre- and post-weaned piglets). Four piglets, which were sporadically shedding cryptosporidia in faeces, were necropsied. Neither clinical signs of diarrhoea nor macroscopical changes were found. Histologically, a moderate infection of cryptosporidia was detected in the glandular epithelium along the large intestine, with predisposition to the ansa centralis of the colon. No inflammatory response in the lamina propria was observed. Cryptosporidia were also commonly found in the glandular epithelium of submucosal lymphoglandular complexes in the colon. Cryptosporidium isolates from all farms were identified as Cryptosporidium suis using molecular markers (SSU rRNA). All of the C. suis strains obtained were larger [6.2 (6.0-6.8) x 5.5 (5.3-5.7) microm] than any isolate described so far [4.6 (4.4-4.9) x 4.2 (4.0-4.3) microm] and did not appear to be infective for neonatal BALB/c mice.

Animals↗
PubMed2006

[Pharmacogenetics of chronic heart failure--beta blockers].

BACKGROUND: Activation of the renin-angiotensin (RAS) cascade and sympathetic nervous systems adversely affect heart failure progression. ACE deletion allele (ACE D) of insertion/deletion polymorphism in the gene coding for angiotensin-1 converting enzyme is associated with increased renin-angiotensin activation. The aim of the study was to test pharmacogenetic associations of I/D ACE genotype with beta blockers therapy in patients with chronic heart failure. METHODS AND RESULTS: A total of 241 patients were included in the study, 63% with betablocker therapy and 37% without it. Using polymerase chain reaction (PCR) method, I/D genotype was detected in 2% agarose electrophoretic gel in UV light. Patients with chronic heart failure and with the II genotype of polymorphism I/D ACE were younger, with more frequent administration of betablockers and diuretics, with less regular administration of aspirin and with lower glycemia and plasma TNFalpha level. A significant difference in genotype distribution and allele frequency between patients with recommended dose and patients without betablockers therapy was proved, when a decrease of the D allele in patients with betablockers had been observed. Contemporary evaluating of AC inhibitor and betablocker therapy, a decrease of ID+DD genotypes in patients with lower than 50% recommended dose compared with the others was found. CONCLUSIONS: In this study, we proved statistically significant interactions between genotypes in I/D ACE polymorphism, betablocker administration, its dosing and pharmacogenetic interaction with ACE inhibitors in patients with chronic heart failure.

Adrenergic beta-Antagonists↗
PubMed2006

[Interval and continuous training in cardiovascular rehabilitation].

The objective of the study was to evaluate the physiological effectiveness and the influence of two modifications of aerobic training (interval and continuous) on the physical performance in the patients with coronary heart disease. 38 males with coronary heart disease (age 60 +/- 10.2 years) passed three months training programme of 60 min 3 times a week (10 min of warm up phase, 25 min of aerobic phase, 15 min of resistance training, 10 min of relaxing phase). Patients with coronarographically verified stenosis > 50% luminal diameter and/or left ventricular ejection fraction lower than 40 % (n = 22) had in terms of aerobic phase interval training prescribed (30 second work phases with work load intensity on the level of anaerobic threshold alternating with 60 second recovery phases with intensity of 5 W); other patients (n = 16) passed aerobic phase of the programme with continual work load of intensity on the level of ventilatory anaerobic threshold. After the determination of three month rehabilitation programme the maximal achieved performance as well as aerobic capacity evaluated by spiroergometric examination statistically significantly increased in the group of patients with interval training and also in the group with continuous training. Despite the group with interval training performed 2.5-3 times less work in each training unit (p < 0.01), the performance and aerobic capacity parameters after the termination of three month programme did not statistically significantly differ from the group with continuous training. The advantage of the continuous training is a possibility to achieve an improvement also in the patients with left ventricular dysfunction and chronic coronary heart disease who could have worse tolerance of the continual work load.

Exercise Therapy↗
PubMed2005

MORE--MOexipril and REgression of left ventricle hypertrophy in combination therapy A multicentric open label clinical trial.

AIM: To evaluate the effect of ACE inhibitor moexipril if added to combination therapy in patient with poorly controlled hypertension. PATIENTS: Four hundred twenty patients with hypertension treated with monotherapy or two dug combination without an ACE inhibitor or AII antagonist and with blood pressure >/=140/90 mm Hg. DESIGN: Single-blind, multicenter, open, with a double-blind echocardiographic examination. METHODS: Basic cardiological examination including echocardiography was performed before including into the study. If the patient fulfilled inclusion criteria, ACE inhibitor moexipril was added to the therapy and uptitrated according to BP values. BP measuring, clinical examination, and basic laboratory were performed every month, echocardiography was repeated after 6 months. RESULTS: Sitting BP decreased from 161.43+/-12.84/96.72+/-7.74 mm Hg to 135.87+/-9.98/82.36+/-5.83 mm Hg (p<0.0001), heart rate from 73.08+/-9.87 to 69.80+/-7.91 (p<0.0001). Three hundred forty patients (81%) had BPd <90 mm Hg after 6 months. Left ventricle mass decreased from 263.24+/-94.69 to 246.71+/-89.08 g (p<0.0001), left atrium decreased from 39.78+/-5.40 to 38.89+/-4.98 mm (p<0.0001), and E/A ratio increased from 0.91+/-0.28 to 0.94+/-0.27 (p<0.0005). Plasma cholesterol level decreased from 5.67+/-0.87 to 5.44+/-0.68 mmol/l (p<0.0001) and plasma triglycerides decreased from 1.92+/-1.07 to 1.78+/-0.80 mmol/l (p<0.001). A greater effect on blood pressure reduction was observed in combination ACE-I+diuretics than in combination ACE-I+betablocker or ACE-I+Ca blocker (statistically borderline). A statistically greater effect on left ventricle mass was observed if moexipril was added to a diuretic than to Ca blocker (p=0.02) or betablocker (p=0.04). SUMMARY: ACE inhibitor moexipril added to combination therapy of hypertension had similar effect on blood pressure reduction and left ventricle mass as in monotherapy trials. The most effective combination is ACE ihibitor+thiazide diuretic. A very small number of adverse events was observed; cough was reported in 2.14% of patients. Decreased heart rate and improvement in lipid parameters were observed in the whole group.

Adrenergic beta-Antagonists↗
PubMed2004

Big endothelin in chronic heart failure: marker of disease severity or genetic determination?

The first objective of the study was to compare the levels of big endothelin and endothelin-1 and other noninvasive parameters used for evaluation of disease severity in patients with stable chronic heart failure (CHF). Endothelin-1 and big endothelin plasma concentrations were measured in 124 chronic heart failure patients. The second objective of the study was to prove an association between endothelin-1 and big endothelin plasma levels and two frequent polymorphisms in the endothelin-1 coding gene (6p21-23) -3A/-4A and G (8002) A in patients with chronic heart failure. Thirdly, we tried to associate other noninvasive parameters of CHF, especially cardiothoracic index (CTI), NYHA classification, signs of pulmonary congestion (PC) and ejection fraction (EF) with determined genotypes of the two ET-1 polymorphic variants. There were significant differences between big endothelin levels in NYHA II versus IV (P<0.001) and NYHA III versus IV (P<0.001) and endothelin-1 in NYHA II versus IV (P<0.001) and NYHA III versus IV (P<0.001). No associations between plasma levels of endothelin-1 and big endothelin and polymorphisms G (8002) A and -3A/-4A in gene coding endothelin-1 were found. In patients with CHF with CTI above 60% the number of carriers of genotypes with ET-1 8002A (AA and AG genotypes) increases. Concerning on the -3A/-4A ET-1 polymorphism, we observed a significant difference in genotype distribution as well as in allelic frequency in the group of patients with CTI above 60% between patients without and with pulmonary congestion. The allelic frequency of 3A allele is twice elevated in the patients with pulmonary congestion (37.8 vs. 78.1%, respectively).

Analysis of Variance↗
PubMed2003

Prevalence and pathogenicity of Cryptosporidium andersoni in one herd of beef cattle.

Over a 35-week period from January to July 2002, a breed of Hereford beef cattle (H) and their hybrids were monitored. Five hundred and ninety-nine individual fecal samples from calves and 96 samples from their mothers were examined. First excretion of Cryptosporidium andersoni oocysts in calves was found in the 9th week after the start of calving (a calf 63-day old). The prevalence of C. andersoni in calves ranged from 11.1 to 92.9% depending on age. The mean prevalence in their mothers was found to be 43.8%. The size of oocysts was 8.48 +/- 0.78 x 6.41 +/- 0.59 microm. Infection intensity in calves ranged from 32 000 to 4 375 000 oocysts per gram (OPG) and in mothers from 78 000 to 2 552 000 OPG. Three cases of abomasal cryptosporidiosis slaughtered at the age of 81, 157 and 236 days were examined histologically and ultrastructurally [transmission electron microscopy (TEM) and scanning electron microscopy (SEM)]. Cryptosporidium infection of the abomasum was located in the upper half of the mucosal glands in the plicae spirales of the fundus, corpus and near the ostium omasoabomasicum. Cryptosporidia were not located in the glandular epithelium of the pars pylorica in the abomasum minimally 10 cm from pylorus. Histopathological changes in the site of cryptosporidial infection in the abomasum had a non-inflammatory character and included distinctive dilatation of infected parts of the glands with atrophy and metaplasia of the glandular epithelial cells, goblet cell activation and mucus hyperproduction. The TEM revealed a relatively small number of Cryptosporidium life cycle stages attached to glandular epithelial cells. In SEM the inner mucosal abomasal surface appeared swollen but was never infected by cryptosporidia.

Animals↗
PubMed2003

[Disorders of laminins in diseases of myocardial and skeletal muscles].

UNLABELLED: The Emery-Dreifuss muscular dystrophy is caused by muscular lesions and disorders of cardial rhythm and/or by cardiomyopathy. An autosomal dominant form is related to mutations of genes, which are coding for lamins A/C. GROUP AND METHODS: In the group A the authors examined 37 patients with the diagnosis of dilatation cardiomyopathy (DKMP) and the mean ejection fraction 28.4; 8.8%. In the group B of 13 patients a cardiac stimulator was implanted for a rhythm disorder. Both groups were subjected to cardiological, neurological, clinical and electromyographic (EMG) examinations. A muscle biopsy from m. vastus lateralis was made and the sample was evaluated by histology, histochemistry and immunohistochemistry. The coding sequences of genes for lamins were amplified by polymerase chain reaction and the products were analyzed by the DHPLC method (denaturing higher performance liquid chromatography). RESULTS: In the group A there was a clinically myopathic picture in three patients, while EMG examination revealed a myogenic finding in 12 patients and a marginally myogenic one in five patients. The histological finding in 12 patients was evaluated as myogenic and marginally myogenic in six. In one patient the mutation analysis revealed mutation in the gene for lamin A/C. A myogenic finding in this patient was determined by EMG as well as by histological examination and the autosomal dominant form of the Emery-Dreifuss muscular dystrophy was therefore diagnosed. In the group B one patient displayed a myopathic neurological finding and a myogenic finding during EMG. A subsequent mutation analysis revealed a mutation in the gene for lamin A/C. The case was therefore the autosomal dominant form of the Emery-Dreifuss muscular dystrophy. In the other patients the clinically marginal myopathic finding was observed once, a marginally myogenic finding during EMG was seen five times, histology and immunochemistry revealed a myogenic finding once and a marginally myogenic finding also once. The other findings were within normal range. CONCLUSIONS: A careful neurological examination including EMG determined symptoms of skeletal muscle myopathies in a surprisingly high percentage of our cardiological patients. This observation draws attention to the need of neurological examination in patients with DKMP in order to discovered disorder in this area in time. In two patients mutations in genes coding lamins A/C were detected. It would be useful to analyze also genes coding for other cytoskeletal proteins in the future.

Adult↗
PubMed2003

[Atrial fibrillation].

Atrial fibrilation is the most frequent arrhythmia, the occurrence increasing with age and associated diseases. The incidence at the age below 60 years is markedly lower than one per cent, whereas in persons above 80 years of age it exceeds six per cent. The occurrence in patients with heart failure is from 10% (NYHA II) up to 50% (NYHA IV). Atrial fibrillation is classified into that observed for the first time and permanent, respectively, while transient forms include paroxyzmal and persistent atrial fibrillation. The diagnosis is based on ECG recording, while echocardiography is most significant. The therapy includes two basic questions--anticoagulant or anti-aggregation treatment and the control of rhythm or frequency. The anticoagulant therapy should be introduced in all patients, where contraindications are not present, being necessary before every cardioversion, provided atrial fibrillation lasts more than two days. In patients without any heart disease and with a physiological echocardiogram it is possible to administer only anti-aggregation treatment. Cardioversion (the control of rhythm) is recommended to all symptomatic patients, in other cases and especially in older persons the control of frequency is safer and of more advantage. Electrical cardioversion is more effective that a pharmacological treatment, the sinus rhythm is preferably controlled by dofetilid, ibutilid, propafenon and amiodaron. For the control of heart rate beta-blockers, diltiazem, verapamil and digitalis are recommended.

Atrial Fibrillation↗
PubMed2003

[Diabetes mellitus and chronic heart failure].

Diabetes mellitus is one of the significant risk factors for many cardiovascular diseases. Diabetes mellitus is 3-4 times more frequent in patients with heart failure compared to patients without heart failure. Prognosis of patients with heart failure and diabetes mellitus is worse than prognosis of non-diabetic patients with the same left ventricular dysfunction. The term diabetic cardiomyopathy refers to a relation between diabetes mellitus and heart disease, but it probably isn't a separate morphology unit. In treatment of patients with diabetes mellitus general rules apply to heart failure management. The effect of ACE inhibitors was in majority of studies stronger in diabetics than in non-diabetics, the effect of beta blockers was comparable or smaller. Treatment is based on good compensation of metabolic parameters, blood pressure, titration of ACE inhibitors into recommended doses, and an optimal dose of a beta blocker. Type II diabetics with heart failure will, due to decreased resorption and metabolism, need insulin more often than diabetics without heart failure.

Cardiomyopathies↗
PubMed2002

The double heterozygote of two endothelin-1 gene polymorphisms (G8002A and -3A/-4A) is related to big endothelin levels in chronic heart failure.

The aim of this study was to focus on the relationship among the associated genotypes of G (8002) A and -3A/-4A endothelin-1 (ET-1) gene polymorphisms and some clinical and/or biochemical parameters in Czech (Caucasian) patients with chronic heart failure. Included in the study were 103 patients with chronic heart failure (functional classes NYHA II-IV, ejection fraction < 40%). The ET-1 gene polymorphisms were detected by polymerase chain reaction (PCR) and restriction fragment length polymorphism methods. A significant decrease in the ET-1-associated genotype AG3A4A number (double heterozygote) was observed in CHF patients with plasma big endothelin levels above 0.7 pmol/L compared to those with levels below 0.7 pmol/L (OR = 0.19; 95% confidence interval = 0.06-0.57; P = 0.005; Pcorr = 0.03). We found a significant decrease in the AG3A4A genotype number in the other groups compared to the group of patients with both big endothelin and endothelin-1 levels under 0.7 pmol/L (OR = 0.22; 95% confidence interval = 0.07-0.79; P = 0.02). The double heterozygote variants of two ET-1 gene polymorphisms were associated with significantly less risk for chronic heart failure with higher levels of big endothelin.

Adult↗
PubMed2002

[Big endothelin and chronic heart failure].

In a group of 124 patients the authors investigated the importance of assessment of plasma levels of big endothelin and endothelin 1 in patients with chronic heart failure as compared with other currently used non-invasive parameters. A six fold increase of plasma levels of both substances was found in patients in functional class NYHA IV as compared with patients in class NYHA II-III. But even patients in the milder stage of NYHA had twice as high values as compared with the standard of the healthy population. Similarly patients with interstitial pulmonary oedema had a twice as high level of both parameters as compared with patients who had a normal finding on X-ray or merely a redistribution of the pulmonary vascularization. The sensitivity of assessment of plasma levels is such that this examination could become part of the basic diagnosis.

Biomarkers↗
PubMed2002

[Acetylsalicylic acid (ASA)--is everything clear?].

The authors summarize results of trials with acetysalicyl acid (ASA) in patients with ischaemic heart disease and in particular with chronic cardiac failure. They draw attention to the relatively frequent use this drug in common practice, although so far not a single trial was completed which would prove the effect of acetylsalicyl acid on long-term mortality. The authors discuss also possible interactions of acetylsalicyl acid and ACE inhibitors which in retrospective analyses indicate possible veakening of the ACE-I when administered concurrently with ASA in cardiac failure. The authors mention also other antiaggregation drugs, which similarly as ASA, significantly reduce the mortality in acute coronary syndrome. Their long-term administration is however not associated with further improvement of the diagnosis. Trials are mentioned which compare antiaggregation and anticolagulation treatment in patients with ischaemic heart disease. They analyze also the effect of dosage (benefit vs. risk). After ASA > 300 mg there are more frequent complications, and without a proved effect on total mortality, while doses < or = 100 mg seem to be safer but there is evidence that they are effective in reducing the total mortality of patients with IHD and/or cardiac failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

[HOTEL P--Hypertension Optimal Treatment with Enalapril Lachema-Pliva. Optimal treatment of hypertension with Enalapril Lachema--Pliva].

The authors investigated in a one-year multicentric open study the effect of enalapril (Enalapril Lachema-Pliva) in 653 patients with mild to moderate hypertension treated in ambulance of 128 general practitioners and specialists in internal medicine. The blood pressure was checked after 6 weeks during the first six months and every 3 months during the second six months. Normal levels of diastolic pressure were achieved in 576 (82%) patients, whereby a combination of antihypertensive drugs had to be used in 383 (59%) patients. Complete renal functions were assessed in 51 patients, microalbuminuria declined from 91.8+/- 37.8 to 72.1 +/- 13.1 mg/l (p < 0.001), glomerular filtration was not affected. Parameters of insulin sensitivity were assessed in 117 patients, the complete lipid spectrum in 253 patients. IRI declined from 12.29 +/- 5.40 to 11.57 +/- 5.42 (p = 0.06) and glycosylated haemoglobin from 6.98 +/- 2.39 to 6.69 +/- 1.97 (p = 0.03), which slows improved insulin sensitivity. Total-cholesterol, LDL-cholesterol and triglycerides decreased significantly and HDL increased (p < 0.001). The left ventricle mass declined significantly after treatment, using Dewereux's calculation, by 17.2 %. The left ventricular diastolic function was not affected by the treatment, however, the lef aulium and left ventricle diminished in volume.

Antihypertensive Agents↗
PubMed2000

Effects of controlled-release metoprolol on total mortality, hospitalizations, and well-being in patients with heart failure: the Metoprolol CR/XL Randomized Intervention Trial in congestive heart failure (MERIT-HF). MERIT-HF Study Group.

CONTEXT: Results from recent studies on the effects of beta1-blockade in patients with heart failure demonstrated a 34% reduction in total mortality. However, the effect of beta1-blockade on the frequency of hospitalizations, symptoms, and quality of life in patients with heart failure has not been fully explored. OBJECTIVE: To examine the effects of the beta1-blocker controlled-release/extended-release metoprolol succinate (metoprolol CR/XL) on mortality, hospitalization, symptoms, and quality of life in patients with heart failure. DESIGN: Randomized, double-blind controlled trial, preceded by a 2-week single-blind placebo run-in period, conducted from February 14, 1997, to October 31, 1998, with a mean follow-up of 1 year. SETTING: Three hundred thirteen sites in 14 countries. PARTICIPANTS: Patients (n = 3991) with chronic heart failure, New York Heart Association (NYHA) functional class II to IV, and ejection fraction of 0.40 or less who were stabilized with optimum standard therapy. INTERVENTIONS: Patients were randomized to metoprolol CR/XL, 25 mg once per day (NYHA class II), or 12.5 mg once per day (NYHA class III or IV), titrated for 6 to 8 weeks up to a target dosage of 200 mg once per day (n = 1990); or matching placebo (n = 2001). MAIN OUTCOME MEASURES: Total mortality or any hospitalization (time to first event), number of hospitalizations for worsening heart failure, and change in NYHA class, by intervention group; quality of life was assessed in a substudy of 741 patients. RESULTS: The incidence of all predefined end points was lower in the metoprolol CR/XL group than in the placebo group, including total mortality or all-cause hospitalizations (the prespecified second primary end point; 641 vs 767 events; risk reduction, 19%; 95% confidence interval [CI], 10%-27%; P<.001); total mortality or hospitalizations due to worsening heart failure (311 vs 439 events; risk reduction, 31%; 95% CI, 20%-40%; P<.001), number of hospitalizations due to worsening heart failure (317 vs 451; P<.001); and number of days in hospital due to worsening heart failure (3401 vs 5303 days; P<.001). NYHA functional class, assessed by physicians, and McMaster Overall Treatment Evaluation score, assessed by patients, both improved in the metoprolol CR/XL group compared with the placebo group (P = .003 and P = .009, respectively). CONCLUSIONS: In this study of patients with symptomatic heartfailure, metoprolol CR/XL improved survival, reduced the need for hospitalizations due to worsening heart failure, improved NYHA functional class, and had beneficial effects on patient well-being.

Adrenergic beta-Antagonists↗
PubMed2000

First-dose hypotension after angiotensin-converting enzyme (ACE) inhibitors in chronic heart failure: a comparison of enalapril and perindopril. Slovak Investigator Group.

BACKGROUND: First-dose hypotension refers to an observed reduction in blood pressure after the administration of the first dose of ACE inhibitors in patients with congestive heart failure. AIM: To compare the first-dose responses of low-dose enalapril and perindopril in patients with stable symptomatic chronic heart failure. METHODS: Single blind, randomised, multicenter, parallel, prospective study. Patients (N=298) with chronic heart failure due to ischemic heart disease or dilated cardiomyopathy, NYHA II-IV, ejection fraction<40%, age>18 years, naive to ACE inhibitors or ATI-receptor blocker, were randomised to receive a single dose of 2. 5 mg enalapril or 2.0 mg perindopril. Baseline laboratory and clinical examinations were performed before entry into the study. Ambulatory blood pressure monitoring started 2 h before the study medication was given, and continued for at least 10 h after the medication. RESULTS: The maximum drop in blood pressure appeared approximately 4 h after dose administration in both groups, and was more pronounced in the enalapril group. Patients in the enalapril group had a significantly higher incidence of asymptomatic hypotension. No symptomatic hypotension requiring a change in medication or a prolongation of hospitalisation was observed. CONCLUSION: A low dose of perindopril is well-tolerated at initiation of ACE inhibitor therapy in patients with chronic heart failure and causes less first-dose hypotension than a low dose of enalapril.

Aged↗
PubMed2000

[Beta-blockers in the treatment of chronic heart failure. How should results of clinical studies be introduced into clinical practice].

The long-term action of elevated catecholamine concentrations on the heart muscle causes a number of adverse effects from apoptosis to malignant arrhythmia or terminal failure of the cardiac pump. Recently completed mortality studies with beta-blockers (BB) in chronic heart failure CIBIS II and MERIT HF confirmed the conclusions of pilot studies with carvedilol that in stabilized chronic heart failure BB reduces the mortality rate as well as the need of hospital admission on account of deteriorating heart failure. Proper selection of patients for administration of BB is necessary, assessment of absolute and relative contraindications. It is also necessary to define the initiation and increase of dosage and the target dose of the beta-blocker. The sooner treatment with beta-blockers is started, the greater the foreseen benefit for the patient.

Adrenergic beta-Antagonists↗