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The publisher regrets that this was an accidental duplication of an article that has already been published in Eur. J. Echocardiogr., 4 (2003) 262-271, . The duplicate article has therefore been withdrawn.
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.
UNLABELLED: Objective of the work is to determine the relation of G8002 polymorhism in endothelin 1 gene to the incidence of diabetes mellitus (DM), ischemic disease of lower limbs (ID LL) and myocardial infarction (MI) at the patients with heart failure. METHODICS: There were observed 224 patients, 176 males, 48 females, average age 55 +/- 12 years, NYHA II/III/IV 82/131/11, average EF LK 25 +/- 7 %, diagnosis ischemic heart disease (IHD) 133, dilatation cardiomyopathy (DCMP) 91. RESULTS: Patients with IHD had higher incidence of hypertension (p < 0.0007), diabetes mellitus (p < 0.00007) and hyperlipoproteinemy (p < 0.0006) than patients with DCMP. Patients with IHD who experienced MI had a difference in the distribution of G8002A genotypes for endothelin 1 gene: G 0.718 and A 0.282 alleles vs ischemic patients without MI G 0.882 and A 0.118 (p < 0.05) alleles. Ischemic patients with DM had G allele in 0.67 and A 0.33 unlike ischemic patients without DM G allele 0.791 and A 0.209 (p < 0.03). Ischemic patients with synchronous ID LL had G allele in 0.718 and A 0.282 vs ischemic patients without ID LL G allele 0.882 and A 0.118 (p < 0.0004). At the patients with DCMP there was not found a difference in G8002A genotype and the presence of DM or ID LL. RESULTS: At the patients with heart failure on the basis of ischemic heart disease there was found a difference in endothelin G8002A genotype distribution depending on other accessory diseases. There was more frequently present an A allele and less present G allele in the ischemic patients with DM, who had experienced MI or ID LL than in the ischemic patients without these diseases. Genotype with A allele is connected with higher risk of all accessory diseases.
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).
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Since its beginning in 1967 heart transplantations have become in 80s of the 20th century a routine treatment method of an advanced heart failure. In spite of the successes in transplantations a range of possible topics and research goals still has to be disclosed to improve quality of life and survival of patients. New horizons in heart transplantations can be summarised in following points: 1 Search of new more efficient immunosuppressives with less adverse effects. Classically a combination of Cyclosporin, Azathioprin, and corticoids have been used. Mycophenolate mofetil starts to be used in treatment instead of Azathioprin, Tacrolimus has been introduced as a drug for resistant rejections and also Rapamycin or Baziliximab are planned to be used in future. Use of Rapamycin seems desirable in patients suffering from nephropathy because it makes possible to lower doses of Cyclosporin or Tacrolimus or to stop taking them. 2 Diagnostics of rejection episodes without endomyocardial biopsy. From noninvasive methods echocardiography methods are looked for--tissue doppler imaging, densitometry, contrast echocardiography, strain and strain rate or assessing levels of some of the humoral agents: interleukin, cerebral natriuretic peptide or troponin T or direct assessment of donor DNA release in receptor's blood. 3 Earlier diagnostics of vasculopathy (here intravascular ultrasound is possible to use), particularly its pharmacology prevention. Statin treatment has been preventively introduced. 4 Xenotransplantation as a possible way of a heart replacement with an animal heart. Progresses in gene engineering lead to a development of transgenic animals, particularly pigs, with human proteins inserted in their genome and regulating activation of immune system. This way hyperacute rejection could be prevented. A range of unclear questions still remains in this area, particularly ethical ones and a risk of animal diseases transfer onto a human together with transplanted tissue. 5 Transplantation of cells from skeletal muscles (myoblasts) or marrow stem cells. 6 Development of apparatuses able to substitute heart function--total artificial heart. However, a range of questions is still unanswered in this area: a suitable material or source for long-term operation is needed to be found. Heart transplantation has become in last two decades a well-established treatment method of a serious heart failure. In spite of numerous difficulties it extends life of patients and improves its quality. Future will show whether we are able to replace it with other procedures.
AIMS: We sought to assess whether the peak systolic and diastolic tricuspid annular velocities as indicators of the right ventricular systolic and diastolic function are of prognostic importance in patients with symptomatic heart failure. METHODS AND RESULTS: The study included 139 consecutive patients with symptomatic heart failure. Their mean left ventricular ejection fraction was 24% (range, 10-39%); 107 patients (77%) were in functional class III according to the New York Heart Association. All patients underwent clinical and laboratory examination, standard echocardiography completed by the Doppler tissue imaging of the tricuspid annular motion, and the right-sided heart catheterization. They were followed up for cardiac-related death and non-fatal cardiac events including the need for implantation of a cardioverter-defibrillator and hospitalization for heart failure. The median follow-up was 11 months (range, 1-48 months). There were 17 cardiac-related deaths and 23 non-fatal cardiac events. The multivariate stepwise Cox regression modelling revealed three effective predictors for both survival and event-free survival: aetiology of heart failure, left ventricular end-diastolic diameter, and the peak systolic tricuspid annular velocity (Sa). Patients with Sa<10.8cms(-1) exhibited worse survival (P=0.048) and event-free survival (P<0.001) compared with those having Sa>/=10.8cms(-1). Risk values of Sa (<10.8cms(-1)) and the left ventricular end-diastolic diameter (>70mm) were found to be of additive simultaneous influence leading to a very poor prognosis, mainly if aetiology of heart failure was idiopathic dilated cardiomyopathy (P<0.001). CONCLUSION: The Sa represents a significant independent predictor of survival and event-free survival in patients with symptomatic heart failure. Its combination with the left ventricular end-diastolic diameter provides a very powerful tool for patient risk stratification.
The objective was to establish whether an intravascular volume increase leads to a heart rate (HR) increase without increased sympathetic tonus. HR changes at rest and at deep breathing (6/min - simulated increase of atrial filling pressure) were measured in patients after heart transplantation. Evaluation of dependency of HR changes on breathing depth was done through a new time series methodology. The data was evaluated through graphs displaying a significant increase in the graph area at deep breathing, when compared with breathing at rest (p<0.01). We presume that an increase in HR corresponds to increased intravascular volume and malfunctioning kidneys.
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.
UNLABELLED: ECG examination belongs to basic procedures in the care of patients with heart failure. The Euroheart Survey study followed the data and therapy of hospitalized patients with chronic heart failure (CHF) with participation of 116 hospitals from 25 European countries and surveyed documentation of 45,993 patients dismissed from internal wards. A new atrial fibrillation or supraventricular tachycardia affected 25.3% of patients, chronic fibrillation was encountered in 23%. Bradyarrhythmia occurred in 10.8% and pacemaker was applied in 8.5% of patients. Ventricular arrhythmias were present in 8.4%, implantable cardiovertor-defibrillator in 1.5%. Syncope was reported in 15% and the arrhythmic death was described in 1.83%. The patients with heart failure suffer from a high incidence of ventricular arrhythmias. About 40-50% of death events in patients with CHF are estimated to be associated with a sudden death or arrhythmia. Large clinical studies investigate the occurrence of and influence upon the sudden death as indices of therapy. The disorders of rhythm as well defects of ventricular conduction may be the risk factors of survival in patients with CHF. The Italian registry of heart failure includes examinations of 5 517 patients. A complete blockade of the left bundle branch block (LBBB) was present in 25.2% patients, whereas a complete blockade of the right bundle branch block (RBBB) occurred in 6.1%. The patients differed in the CHF cause: the group with LBBB suffered more frequently from dilatative cardiomyopathy, whereas IHD more present more frequently in patients without the blockade. The groups also differed in the severity of the disease. The patients with LBBB had a higher prevalence of heart weakness NYHA III and IV (32.8% and 26.4%, respectively, P < 0.001), lower systolic blood pressure, more frequently third heart sound (34.2% versus 22.2%, P < 0.001), cardiomegaly classified as a cardiothoracic index higher that 0.55 (63.2% versus 55%, P < 0.04). In the course of one-year observation 11.9% of patients died, death being evaluated as sudden in 46%. The one-year mortality in patients those with LBBB was 16.1% in contrast to 10.5% in those who had not suffered from the blockade. A sudden death affected 5.5% of patients in the whole cohort, the frequency being again in LBBB (7.3% vs. 4.9%). The risk further increased with a simultaneous atrial fibrillation. After heart transplantation, ECG is also of importance for revealing an acute rejection. In the bilateral operation technique a direct alteration of the sinus node could be the cause of dysfunction. Various bradyarrhythmias developed in later periods of time. A modification of the operation technique has been used in the last 10 years. The application of bicaval method eliminated brachycardiac complications after heart transplantation. A cardiostimulator proved to be necessary in 5 to 15% of patients when biatrial technique was used, whereas it was virtually not required with the bicaval technique. The blockade the left bundle branch block is an unfavorable prognostic factor in the same way as in CHF, whereas of the right bundle branch block is critical in the heart transplantation. It is supposed to be caused by surgical or thermal damage or it is also associated with different degree of the right ventricular dysfunction and a higher number of rejections. The blockade is also associated with worse one-year survival (74% vs. 92%, P < 0.03). CONCLUSION: ECG retains its position even in modern times not only in the diagnosis of conditions responsible for heart failure, in the diagnosis of disorder of rhythm and conduction, but it is also of prognostic value. It also retains its position in the same areas as in heart failure, i.e. in the diagnosis and prognosis in heart transplantation.
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.
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.
UNLABELLED: One of the most serious complications after orthotopic transplantation of the heart (OTH) is graft rejection. Its early detection can help successful control. The diagnostic gold standard is myocardial biopsy, it is however not always supreme. We tried to find out whether some modern echocardiographic methods can provide further valuable information. At the same time we were concerned with the follow up of basic variables of the circulation and echocardiographic indicators of left ventricular function. MATERIAL AND METHODS: The authors examined repeatedly 22 patients where in 1998-2000 OTH was performed, who did not have an acute severe rejection, who had at least one myocardial biopsy between the first and second month after OTH without signs of rejection and who were easily examined by echocardiography. In addition to the standard follow up according to a routine pattern they were subjected to clinical and echocardiographic examination during the 1st-2nd month after OTH, 6 months after the first examination and one year after the second examination. Classical echocardiography, acoustic densitometry and Doppler tissue examination of the movement of the mitral ring were used. RESULTS: The patients had throughout the investigation period clinical cardiological complications. Between the first and second examination the systolic pressure rose from 125.4 +/- 9.5 to 135.4 +/- 13.5 mm Hg (p < 0.05), the diastolic pressure from 79.6 +/- 8.2 to 86.4 +/- 9.5 mm (p < 0.05), during the third examination it dropped again to original values. During the follow up no significant differences developed in indicators of classical echocardiography, acoustic densitometry and Doppler tissue echocardiography. Of 22 patients however myocardial biopsy of the right ventricle proved rejection only in two. In those the authors did not observe any echocardiographic changes during rejection. In one patient who died echocardiography revealed a decline of left ventricular function and a non-specific bioptic finding, and on necropsy severe cellular vascular rejection. CONCLUSIONS: Blood pressure rises early in some patients after OTH, it is therefore important to monitor it carefully and to administer early and systematic treatment of hypertension. In non-complicated patients the echocardiographic findings did not change. Because of the low number of rejections the authors were not able to prove the importance of some new echocardiographic methods. In view of discrepancies between methods in some patients with rejection a comprehensive diagnostic approach is still necessary: myocardial biopsy supplemented by further examinations, in particular echocardiographic ones.
AIMS: Rapid, accurate, and widely available non-invasive evaluation of right ventricular function still presents a problem. The purpose of the study was to determine whether the parameters derived from Doppler tissue imaging of tricuspid annular motion could be used as indexes of right ventricular function in patients with heart failure. METHODS: Standard and pulsed Doppler tissue echocardiography were obtained in 44 patients with heart failure (mean left ventricular ejection fraction 24 +/- 7%) and in 30 age- and sex-matched healthy volunteers. The tricuspid annular systolic and diastolic velocities were acquired in apical four-chamber views at the junction of the right ventricular free wall and the anterior leaflet of the tricuspid valve using Doppler tissue imaging. Within 2 h of Doppler tissue imaging, the first-pass radionuclide ventriculogram, determining right ventricular ejection fraction and equilibrium gated radionuclide ventriculography single photon emission computed tomography, were performed in all patients. RESULTS: In patients with heart failure, the peak systolic annular velocity was significantly lower and the time from the onset of the electrocardiographic QRS complex to the peak of systolic annular velocity was significantly greater than the corresponding values in healthy subjects (10.3 +/- 2.6 cm. s(-1) vs 15.5 +/- 2.6 cm.s(-1), P < 0.001, and 198 +/- 34ms vs 171 +/- 29 ms, P < 0.01, respectively). There was a good correlation between systolic annular velocity and right ventricular ejection fraction (r = 0.648, P <0.001). A systolic annular velocity < 11.5 cm.s(-1)predicted right ventricular dysfunction (ejection fraction < 45%) with a sensitivity of 90% and a specificity of 85%. CONCLUSION: We conclude that the evaluation of peak systolic tricuspid annular velocity using Doppler tissue imaging provides a simple, rapid, and non-invasive tool for assessing right ventricular systolic function in patients with heart failure.
UNLABELLED: The objective of the investigation is to assess the safety and contribution of physical training in patients with chronic heart failure and to assess the effect of training on central haemodynamics, left ventricular function evaluated by echocardiography and humoral substances. PATIENTS AND METHODS: Patients with cardiac failure NYHA II and III incl. 17 on t he background of IHD and 21 on the background of dilatation cardiomyopathy. All patients had the ejection fraction below 40% and pVO2 below 20 ml/kg/min. They were divided into groups enagaged in training (T) and controls (K). Before training and after its termination the patients were subjected to clinical examination, basic laboratory tests, echocardiography amd dextrolateral catheterization at rest and during ergometry and levels of humoral agents were assessed. The training was pursued three times per week for a period of two months on a bicycle ergometer. RESULTS: Before training there were no statistically significant differences between the groups. After training the groups did not differ in echocardiographic and haemodynamic parameters. In the training group there was as compared with the onset of the experiment a decline of the maximal median pressure (123.6 +/- 11.9 vs. 113 +/- 10.2 mm Hg, p < 0.04) the maximal pulse rate (112.5 +/- 18.7 vs. 108.4 +/- 20.1 p <0.02). In the control group, on the other hand there was an increase of big endothelin (52.2 +/- 4 9.1 vs. 88.0 +/- 76.7 pg/ml, p < 0.04) and an increase of pulmonary vascular resistance (102.8 +/- 71.7 vs. 149.2 +/- 69.5 dyn.s/cm5, p < 0.002). CONCLUSION: Physical training was well tolertaed by patients, it led to a subjective improvement of their conditionn, to a reduction of the chronotropic response to a load and thus to more economical cardiac activity.
UNLABELLED: In recent years evidence is increasing on the usefulness of physical loads and controlled physical training in patients with chronic heart failure (CHSS). In the presented work the authors assessed changes of the functional capacity and muscular strength after training on a bicycle ergometer. The group comprised 38 patients with CHSS due to IHD or dilatation cardiomyopathy NYHA II-III, EF lower than 40%, with a peak oxygen consumption (pVO2) lower than 20 ml/kg/min. The group was subdivided in a random fashion to subjects participating in training (T) and the control group (K). The patients were subjected to clinical examination, examination by common laboratory methods, spiroergometry, dynamometry. By the puncture technique a specimen of the m. vastus lateralis was taken for histological and histochemical examination of the muscle. The patients trained on the bicycle ergometer three times per week for a period of eight weeks, one exercise session lasted 30 minutes and was at the level of the anaerobic threshold. After completion of the training period the examinations were repeated. RESULTS: Before the onset of training the groups did not differ in any indicators. After termination of training they increased in group T: pVO2 from 18.9 +/- 4.8 to 22.13 +/- 15.72 ml/kg/min. (p < 0.0004), the oxygen consumption at the level of the anaerobic threshold (VO2AT) from 13.4 +/- 3.4 to 15.96 < or = 3.75 ml/kg/min. (p < 0.0006), the respiratory quotient (RQ) from 0.93 +/- v0.09 to 0.97 +/- 0.006 (p < 0.05), the maximal tolerated load from 0.72 +/- 0.72 to 1.08 +/- 0.33 W/kg (p <0.002), the maximal voluntary contraction of the femoral quadriceps muscle (MVC START) from 291.2 +/- 70.1 to 328.1 +/- 66.0 N (p<0.01), the maximal voluntary contraction of this muscle after 20 mins. of repeated contractions (MVC END) from 157.6 +/- 109 to 290.1 +/- 64.9 N (p < 0.01), the decrease of the maximal contraction after 20 minutes of repeated contractions was from 52.8 +/- 32.1 to 12.4 +/- 5.0% (p < 0.01). After training there were statistically significant differences between groups in VO2AT (p < 0.01), in pVO2 (p < 0.03) and in the decrement of the maximal muscular contraction (p < 0.01). The authors found a trend towards normalization of the diameter of muscle fibres I and II and of their ratio. The ventilation equivalent for carbon dioxide VE/VCO2 during the maximal tolerated load correlated significantly with the systemic and pulmonary vascular resistance, with RQ, VO2AT, pVO2, with the maximal tolerated load and with the blood level of prostaglandin F. CONCLUSION: Controlled physical training in patients with CHSS was safe, led to a significant improvement of spiroergometric indicators, load tolerance and muscular strength. After training there was a trend towards normalization of pathological changes in skeletal muscle. Based on the authors' experience and findings of other authors it is advisable to recommend training as part of treatment of patients with CHSS.
The causes of chronic heart failure at the end of the 20th century are quite different from those 30 or 50 years ago. The last data from the Framingham study indicate that ischaemic heart disease and/or hypertension are the main cause in as many as 90% patients. The prevalence of chronic heart failure in European countries, 0.4-2%, implies 40-200,000 patients in the Czech Republic. Pharmacological treatment during the last 15 years revealed clearly that the drugs of choice which prolong life are inhibitors of the angiotensin converting enzyme (ACE-I) which are combined with other drugs as needed by the patient. A combination of five drug groups (ACE-I, digitalis, diuretics, beta-blockers, and spironolactone) are nowadays the basic treatment. In the 4S study (Scandinavian Simvastatin Survival Study--4,444 patients with ischaemic heart disease followed up for 5.4 years) 412 (9.2%) developed chronic heart failure requiring treatment, i.e. 228 (10.3%) in the placebo group and 184 (8.3%) patients in the group treated with simvastatin (p < 0.015). In the group of patients with signs of heart failure 73 of 228 died the placebo group and 47 of 184 in the simvastatin group (reduction of the relative risk by 19%, p = 0.014), to save one life (NNT) it was necessary to treat 15 patients for a period of 5 years. From the aspect of the number of patients it was necessary to treat six times as many patients without heart failure than with heart failure to save one life in five years. Hypolipidaemic treatment should be an obvious part of treatment of heart failure due to ischaemic heart disease. Hyperlipoproteinaemia is described in 60-80% patients after transplantation of the heart. Treatment involves diet, reduction or discontinuation of corticoids, maintenance of cyclosporin at the lowest effective level and treatment wit statins.
Transplantation of the heart has become an accepted method for the treatment of terminal cardiac failure. Despite obvious advances in the care of patients after trasplantation a number of problems exist. The authors summarize their experience with the long-term follow-up of 100 adult patients with transplantations made in the Brno Centre of Cardiovascular and Transplantation Surgery. One-year survival in the group of patients is 80%, three-year survival 69%. The authors discuss indications and contraindications of cardiac transplantations, necessary preoperative and postoperative examinations, they follow-up the most serious complications during the posttransplantation period. They mention therapeutic possibilities and outline briefly the perspectives of care of patients after cardiac transplantation. Despite the number of problems encountered transplantation of the heart is for indicated patients with cardiac failure a unique chance to improve the prognosis of survival and the quality of life.