Nuclear receptors gene polymorphisms and risk of restenosis and clinical events following coronary stenting.

INTRODUCTION: Hereditary factors connected with inflammation and fibroproliferation may play important role in restenotic process after coronary stenting. Peroxisome proliferator-activated receptors (PPAR) and retinoic X receptors (RXR) regulate the transcription of crucial genes involved in the glucose and lipid metabolism, inflammation and cell differentiation. METHODS: In our angiographic and clinical study we assessed the association of gene polymorphisms of L162V for PPAR-alpha, C161T for PPAR-gamma and A(39526)AA for RXR-alpha with the risk of restenosis and cardiac events after coronary stenting. Primary endpoint was diameter stenosis > or = 50% at follow-up angiography. Secondary endpoints were death, myocardial infarction and/or target lesion revascularisation at 12 months, and clinical restenosis. The results were adjusted for known predictors of restenosis. The genotypes were analysed by polymerase chains reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. RESULTS: Control angiography was performed in 477 of 565 patients (84.4%) with following restenosis rates in genotype subgroups: CC 29.0% vs GC/GG 22.6% (p = 0.33) in L162V, CC 29.9% vs TC/TT 24.6% (p = 0.24) in C161T and A/A 26.9% vs A/AA + AA/AA 35.0% (p = 0.14) in A(39526)AA polymorphisms. The T allele ofC161T polymorphism was associated with lower frequency of clinical restenosis (p = 0.015). CONCLUSION: We could not find an association of L162V PPAR-alpha, C161T PPAR-gamma and A(39526)AA RXR-alpha gene polymorphisms with angiographic in-stent restenosis or major cardiac events. However, we found the relationship between C161T PPAR-gamma polymorphism and clinical restenosis deserving further study.

Mutation analysis of candidate genes SCN1B, KCND3 and ANK2 in patients with clinical diagnosis of long QT syndrome.

The long QT syndrome (LQTS) is a monogenic disorder characterized by prolongation of the QT interval on electrocardiogram and syncope or sudden death caused by polymorphic ventricular tachycardia (torsades de pointes). In general, mutations in cardiac ion channel genes (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2) have been identified as a cause for LQTS. About 50-60 % of LQTS patients have an identifiable LQTS causing mutation in one of mentioned genes. In a group of 12 LQTS patients with no identified mutations in these genes we have tested a hypothesis that other candidate genes could be involved in LQTS pathophysiology. SCN1B and KCND3 genes encode ion channel proteins, ANK2 gene encodes cytoskeletal protein interacting with ion channels. To screen coding regions of genes SCN1B, KCND3, and 10 exons of ANK2 following methods were used: PCR, SSCP, and DNA sequencing. Five polymorphisms were found in screened candidate genes, 2 polymorphisms in KCND3 and 3 in SCN1B. None of found polymorphisms has coding effect nor is located close to splice sites or has any similarity to known splicing enhancer motifs. Polymorphism G246T in SCN1B is a novel one. No mutation directly causing LQTS was found. Molecular mechanism of LQTS genesis in these patients remains unclear.

Age-dependent relationship between the carotid intima-media thickness, baroreflex sensitivity, and the inter-beat interval in normotensive and hypertensive subjects.

The interrelationship between baroreflex sensitivity expressed in ms/mm Hg (BRS) or in Hz/mm Hg (BRSf), carotid wall thickness (IMT), and age was investigated in hypertensive and normotensive subjects with respect to the mean inter-beat interval (IBI) and blood pressure (BP). BP monitoring was performed in 25 treated hypertensives (Hy; 47.4+/-9.2 years of age) and 23 normotensives (Norm; 44.5+/-8.1 years). IMT was measured by ultrasonography. BRS and BRSf were determined by the spectral method (five-minute non-invasive beat-to-beat recording of BP and IBI, Finapres, controlled breathing at a frequency of 0.33 Hz). Significant differences between Hy and Norm were detected in IMT (Hy: 0.624+/-0.183, Norm: 0.522+/-0.070 mm; p<0.01), BRS (Hy: 3.5+/-1.6, Norm: 5.7+/-2.3 ms/mm Hg; p<0.01), BRSf (Hy: 0.005+/-0.002, Norm: 0.009+/-0.004 Hz/mm Hg; p<0.01), systolic BP (Hy: 131+/-21, Norm: 116+/-17 mm Hg; p<0.01) and diastolic BP (Hy: 77+/-16, Norm: 64+/-12 mm Hg; p<0.01). A significant correlation was found between age and IMT (Norm: 0.523, p<0.05; Hy+Norm: 0.419, p<0.01), age and BRS (Norm: -0.596, p< 0.01; Hy+Norm: -0.496, p<0.01), age and BRSf (Norm: -0.555, p<0.01; Hy: -0.540, p <0.01; Hy+Norm: -0.627, p<0.01), age and IBI (Hy: 0.478, p<0.05), age and diastolic BP (Hy: -0.454, p<0.05), BRS and IMT (Hy+Norm: -0.327, p<0.05) and BRSf and IMT (Hy+Norm: -0.358, p<0.05). Hypertensive patients have increased IMT and decreased BRS and BRSf. The positive correlation between age and IMT and the negative correlation between age and BRS and BRSf are in agreement with the hypothesis that the age-dependent decrease of baroreflex sensitivity corresponds to the age-related structural changes of the carotid wall. Using two indices of baroreflex sensitivity, BRS and BRSf, we could show that baroreflex sensitivity in hypertensives is lower not only due to thickening of the carotid wall, but also due to aging.

[Care of patients with implanted cardioverters-defibrillators: what every physician should know]. / Péce o nemocné s implantabilními kardiovertery-defibrilátory: co by mel vedet kazdý lékar.

Implantable cardioverter defibrillators have become an integral part of treatment of patients with malignant chamber arrhythmias over last 10 years both in secondary and primary prevention of sudden deaths. Based on monitoring of a group of 182 patients and based on information in literature, authors present a survey of the most frequent situations, rules and complications related to therapy with implantable defibrillators. In the end they try to answer summary of the most frequent questions of internal medicine physicians and GPs concerning patients with this implanted device.

[Restrictive cardiomyopathy as a manifestation of primary amyloidosis]. / Restriktivní kardiomyopatie jako projev primární amyloidózy.

Primary amyloidosis is a rare disease, cardiac involvement occurs in up to 40% of patients. Diffuse amyloid deposits cause an impairment of myocardial systolic and diastolic function. In this paper we are presenting a case of a 54-year-old woman. The woman was admitted because of progressive fatigue, dyspnoea, chest pain, later she experienced hypotension, dyspepsia, and enterorrhagia. ECG showed decrease in QRS amplitude. We have found an echocardiographic evidence of wall hypertrophy. Right cardiac catheterization showed a restrictive situation. Immunobinding of serum and urine revealed monoclonal kappa light chains. The diagnosis was determined by rectal biopsy. Unfortunately, amyloid deposits caused progressive heart failure, hemorrhage, and death just before the diagnosis of primary amyloidosis could be determined on the basis of results of the immunofixations of serum and urine proteins (detection of the monoclonal light chains kappa) and from biopsy specimens taken from rectum (amyloid deposits).

[ST-segment resolution as a simple tool for the assessment of successful primary coronary intervention at a microvascular level]. / Ustup ST elevací jako jednoduchý nástroj pro posouzení úspesnosti primární koronární intervence na mikrovaskuláirní úrovni.

BACKGROUND: The primary success of the coronary artery reperfusion by primary coronary intervention (PCI) is almost angiographically assessed by TIMI flow score. The perfusion at a microvascular level can be inadequate despite the restoring of normal flow in the epicardial coronary artery. One of the options of successful reperfusion at a microvascular level is the measurement of ST-segment resolution (STR) after primary PCI. AIM: The assessment of ST-segment resolution in patients indicated for primary PCI and the comparison with clinical data. METHODS: The authors studied 149 patients (68.5 % men) with ST elevation acute myocardial infarction treated by primary PCI. The ECG was taken at the time of arriving patient at coronary unit and compared with ECG early after primary PCI. Patients were divided into 3 groups according to the grade of STR: with complete (> or = 70%), partial (30-69%) and none (< 30%) STR. The lead with maximal changes (STEmax) and sum of ST elevation (STEsum) were assessed. RESULTS: 42 (28.2 %) patients had complete STR, 55 (36.9%) partial STR and 52 (34.9%) patients didn't achieve STR. STR was connected with better left ventricular ejection fraction, which was in group with complete STR 50% compared with 39.4% in group without STR (p < 0.0001). Patients with symptoms of heart failure on admission (Killip II-IV) had complete STR only in 4 cases (10%) compared with patients without heart failure (Killip I), where was complete STR in 38 (34.8%), (p = 0.003). There wasn't noted significant difference in STR at dependence on glycoprotein IIb/IIIa inhibitors administration. A normal or mildly slower coronary flow (TIMI 2, 3) was achieved in 146 patients (98%), 3 patients (2%) had inadequate coronary flow after primary PCI (TIMI 0, 1). CONCLUSIONS: The evaluation of early ECG changes is simple method for the assessment of primary PCI success at the microvascular level. Our outcomes confirm a differences in achievement of optimal epicardial coronary flow and a perfusion at microvascular level.

[Comparison of various methods of correction of QT intervals during exercise in familial long QT interval syndrome]. / Srovnání ruzných metod korekce QT intervalu pri zátezi v rodinách se syndromem dlouhého QT intervalu.

BACKGROUND: Pathologic prolongation of QT interval is related to increased risk of arrhythmias. Changes of this parameter are influenced by many conditions, the most important is heart rate. Several formulas have been proposed for mathematical description of QT interval/heart rate relationship. The aim of this study was comparison of different QT interval correction formulas in families with congenital long QT syndrome (LQTS). METHODS: In 28 members of 6 families with LQTS occurrence bicycle ergometry testings were performed. QT and RR intervals were measured before exercise, at peak exercise and in the 1st and the 6th minute of restitution. For QT interval correction single-parameter formulas by Bazett, Fridericia, Malik and Framingham study were used. In 3 families the results could be correlated with genetically proved diagnosis (KCNQ1 gene mutations in 2 families, HERG-KCNH2 gene mutation in the other). RESULTS: In the described group the genetically established diagnosis of LQTS correlated at best with values obtained with correction by Bazett. All the mutation carriers were correctly identified only by this method. The Fridericia, Malik and Framingham formulas failed to identify 2 patients--mutation carriers (both KCNQ1 and HERG-KCNH2 mutations). DISCUSSION: Because of simplicity the Bazett formula remains the most common method of QT interval correction. Moreover, in our study this formula appeared to be the most sensitive for clinical diagnosis of LQTS.

[Failure of antiarrhythmia agents and understanding the phenomenon of proarrhythmia]. / Od selhání antiarytmik k pochopení fenoménu proarytmie.

The end of 80ies and the beginning of 90ies in arrhythmology was characterized by the demonstration of so called proarrhythmia, when drugs, particularly antiarrhythmic ones, induced serious, frequently fatal arrhythmias. The resulting pharmacotherapeutic skepsis in the treatment of, in particular, ventricular arrhythmias were accompanied at the same time by a powerful development of non-pharmacological modes of treatment of arrhythmias, especially by implantable defibrillators. The causes of proarrhythmia were identified with the evolution of knowledge in the genetic basis of hereditary syndrome of long QT interval. The first mutation was identified in 1991 and other mutations in the four subsequent years. The mutated genes controlling the synthesis of ionic membrane channels cause disorders in the repolarization phase of action potential. Their expression in individual types of myocytes is not homogenous, most affected being the M cells of ventricular myocardium. It results in a dispersion of repolarization which, together with induction of early after depolarization, causes the origin of polymorphic ventricular tachycardia--TdP. In the 90ies of 20th century there were increasingly frequent reports on sudden arrhythmic death in patients, who had been treated with non-cardiac drugs. They were caused by polymorphic ventricular tachycardia associated with the long QT interval. The syndrome was named as acquired syndrome of long QT interval, based on the drug-induced delayed repolarization of myocyte. The slowing-down is caused by affected membrane channels known from the syndrome of hereditary LQTS. The very low frequency of these fatal complications has been explained either by an obscure genetic defect or a disorder in metabolism of the therapeutic drug, but especially due to drug interactions metabolized in a similar way and similarly influencing the function of membrane channels. Sixty drug molecules with proarrhythmic potential have been identified so far, but the list is probably not complete yet.

[Glycoprotein IIb/IIIa platelet blockers in acute myocardial infarct treated with primary coronary angioplasty]. / Gp IIb/IIIa blokátory desticek u akutního infarktu myokardu léceného primární koronární angioplastikou.

BACKGROUND: Primary coronary angioplasty is at present accepted as the most effective reperfusion treatment strategy of the ST elevation acute myocardial infarction. The optimum approach appears to be combination of the interventional technique (mechanical reperfusion) with aggressive pharmacological treatment aimed at the platelets. Intravenous blockers of the glycoprotein receptors IIb/IIIa together with acetylsalicylic acid have the additive antiaggregant effect and are used more frequently as adjunctive therapy by coronary interventions in patients with acute coronary syndromes and the acute myocardial infarction. AIM: The assessment of safety and effectiveness of the IIb/IIIa platelet blockers in patients indicated to primary coronary angioplasty. METHODS: Since 1st January 2000 to 30th June 2001 the authors carried out the total of 912 coronary angioplasties in their cathlab, from which in 195 cases (21.4%) the primary angioplasty in acute ST elevation myocardial infarction was conducted. IIb/IIIa blockers were administered in the total of 53 cases (5.1% from the whole amount of coronary angioplasties), in 30 cases (15.4% from the total of 195 patients) of the primary coronary angioplasties, unlike the elective procedures, where these agents were given only in 9 patients (1.5% from the overall number of 621 coronary angioplasties) (p < 0.001). The authors in their work analyse the group of patients treated with primary coronary angioplasty with adjuvant treatment of IIb/IIIa platelet blockers. RESULTS: In the stated period the IIb/IIIa platelet blockers were given to 30 patients at the age of 60.3 +/- 11.3 on average (70% were men). The most frequent risk factors were smoking, in 18 patients (60%), and hypertension, in 14 patients (40%). At least one coronary stent was implanted in 20 patients (66.7%). Abciximab was administered in 27 cases (90%) and eptifibatid in 5 cases (10%). Solely in 5 cases (16.7%) the agents were administered at least 10 minutes before the intervention and therefore preventively, and in 25 cases (83.3%) the administration was rescue. The reason for preventive administration was in 3 cases determination of the angiographically high-risk coronary artery disease and in 2 cases the thrombosis of another non-infarction related artery. The most frequent reason for the rescue use was in 6 cases (22.2%) slow-flow or no-reflow fenomena even after the mechanical obstacles and in 5 cases (18.5%) that were successfully treated with further dilatation, the acute in-stent thrombosis was observed. The infarct-related artery was most often the left anterior descending coronary artery, namely in 16 cases (54%). CONCLUSION: IIb/IIIa platelet blockers in primary coronary angioplasty administered either preventively or as rescue therapy are highly effective, relatively safe and improve the effectiveness of mechanical reperfusion. The total in-hospital mortality of this group of patients was 10%.

[Implantable cardioverter-defibrillators in the prevention of sudden cardiac death]. / Implantabilní kardiovertory-defibrilátory v prevenci náhlé srdecní smrti.

The aim of this work is to characterize and analyse the spectrum of therapies delivered from implantable cardioverter-defibrillators (ICD), to evaluate their effectivity and to mark the most effective types of antitachycardia stimulations (ATP), cardioversion (CV) and defibrillation (CD). To compare our results with references and give precautions of trouble-shootings. Our patients had implanted ICDs according to standard criteria for ICD implantations. Before discharge from hospital we performed predischarge test of their ICD. Than we followed them periodically each three months. We have observed 72 ICD pts (55 M, 17 F) in the mean age of 62.7 +/- 12.2 years the with mean LVEF was 0.37 +/- 0.11. The mean follow-up was 21 +/- 12.8 months. Each examination was managed through anamnesis of symptoms accompanying the beginning of arrhythmia, the sensation of ICD therapy by patient, followed by interrogation of the ICD memory. All obtained episodes were analysed. During the follow-up 1023 episodes of malignant ventricular arrhythmias were detected and effectively terminated. 7 pts died. During the therapy the ATP reached 83% in comparison with CV, CD which reached only 17%. The dominating symptoms were palpitations and presyncopes. In comparison with initial arrhythmias leading to implantations of ICDs (ventricular fibrillations for most of the cases--54%) the significantly higher number of spontaneous episodes were caused by monomorphic ventricular tachycardias VT (92.0%). We had no sudden cardiac death in our pts. In the indicated pts with a high risk of sudden arrhythmic death, the ICD therapy is characterized as very effective and is associated with high safety, low discomfort and when up to date algorithms for detection being used, then only adequate part of the inappropriate therapies occurs (10% patients, 3.2% from the number of episodes). The therapy by implantable cardioverter-defibrillators has had an important role in treating pts with life-threatening ventricular arrhythmias.

[Pitfalls in the diagnosis of infectious endocarditis]. / Uskalí diagnostiky infekcní endokarditidy.

A group of 63 patients with infectious endocarditis (IE) (1991-1998) was subjected to a detailed retrospective analysis. The authors investigated the age of the patients, site of IE, type of infectious agent, incidence of coinciding diseases or interventions in the close premorbid period of IE, size of vegetation, incidence of embilizations, heart failure, indications for vital early cardiosurgery, number of deaths. From the clinical analysis it may be concluded: 1. There is a new group of patients with IE, who before development of the disease have no manifest cardiac disease who however frequently suffer from another coinciding disease; 2. There is a significant increase of dextrolateral IE (frequently "pacemaker" IE); 3. The ratio of staphylococcal strains in the etiopathogenesis of IE is rising; 4. The mean age of the affected patients is rising (as well as the age scatter); 5. IE is unfortunately frequently diagnosed only after embolization of the vegetation (mostly cerebrovascular attacks) in obscure febrile conditions.

[The role of ergometric testing in diagnosis of latent long QT syndrome]. / Postavení ergometrického vysetrení v diagnostice latentního syndromu dlouhého QT intervalu.

BACKGROUND: The long QT syndrome is a genetically determined disease based on mutations of ion membrane channel genes. The resulting prolongation of repolarization increases a risk of malignant ventricular arrhythmias and sudden death. The diagnosis is problematic in individuals with borderline or even normal corrected QT interval value. Ventricular arrhythmias in this syndrome are often provoked by exercise, therefore exercise testing is considered as a useful differential diagnostic method. METHODS: In a 24-member family an occurrence of the long QT syndrome was established clinically in 7 patients. In other 3 members borderline corrected QT interval values were found (0.44-0.46 s). In these individuals a stress testing by bicycle ergometry was performed. RESULTS: During exercise in a 28-year old man (patient III/6) the corrected QT interval prolonged to 0.53 s, in a 27-year old man (patient III/2) and in a 20-year old woman (patient III/9) physiological QT interval shortenings were observed (0.4 s during peak exercise). The diagnosis was confirmed by molecular genetic investigation. In patient III/6 (along with other symptomatic family members) a mutation in exon 7 of KCNQ1 (previously called KVLQT1) gene was found. In patients III/2 and III/9 no signs of KCNQ1 gene pathology were present. CONCLUSIONS: In families with clinically established diagnosis of long QT syndrome occurrence the exercise testing reveals previously asymptomatic individuals, at least in LQT1 type (which is the most common). In general stress testing and measurement of QT interval dynamics is a necessary part of arrhythmological investigation especially in young individuals with history of syncope.

Critical value of baroreflex sensitivity determined by spectral analysis in risk stratification after myocardial infarction.

The risk of cardiac death in patients after MI is predicted by a decreased baroreflex sensitivity (BRS). The critical value of BRS based on phenylephrine administration is 3 ms/mmHg. The aim of this study was to determine the critical value of BRS assessed by spectral analysis of spontaneous fluctuations in pulse intervals and blood pressure. Digital blood pressure was recorded noninvasively (3 min, controlled breathing 0.33 Hz) in 112 patients, 8-18 days after MI. Nine patients died during the first year after MI. BRS was determined as the gain between the spectrum of the variability of systolic blood pressure and the cross-spectrum between the variability of pulse intervals and systolic blood pressure. The gain at the frequency of 0.1 Hz was taken as the measure of BRS. Sensitivity, specificity, and the positive predictive value were calculated in the range of 1-10 ms/mmHg in steps of 1 ms/mmHg. The value of BRS above which sensitivity no longer increases and specificity decreases was taken as the optimal value. The critical value of BRS determined by spectral analysis was 3 ms/mmHg (sensitivity 77%; specificity 71%). In conclusion, the spectral critical value of BRS determined by spectral analysis of spontaneous fluctuations in pulse intervals and blood pressure corresponds to the value determined by the phenylephrine method.

Baroreflex sensitivity determined by spectral method and heart rate variability, and two-years mortality in patients after myocardial infarction.

Sympathetic overactivity and low parasympathetic activity is an autonomic dysfunction (AD) which enhances cardiac mortality. In the present study, the impact of AD on the mortality in patients after myocardial infarction was evaluated. We examined 162 patients 7-21 days after myocardial infarction, 20 patients of whom died in the course of two years. Baroreflex sensitivity (BRS) was estimated by spectral analysis of spontaneous fluctuations of systolic blood pressure and cardiac intervals (Finapres, 5 min recording, controlled breathing 20/min). The heart rate variability was determined as SDNN index (mean of standard deviations of RR intervals for all 5-min segments of 24-hour ECG recordings). BRS < 3 ms/mm Hg and/or SDNN index < 30 ms were taken as markers of AD. The risk stratification was performed according to the number of the following standard risk factors of increased risk of cardiac mortality (SRF): ejection fraction < 40%, positive late potentials and the presence of ventricular extrasystoles > 10/h. No difference in mortality between patients with AD (4%) and without AD (4.5%) was found in 92 patients without SRF, the mortality in 6 patients with three SRF was 66.6%. Five of these patients had AD. Out of 64 patients with one or two SRF, 32 had AD. The mortality of patients without AD was 6.25% and 31.2% of those with AD (p<0.025). It is concluded that AD enhanced two-years mortality five fold in our patients with moderate risks.

[Electric programmed ventricular stimulation using a permanent cardiac pacing system--a noninvasive method in arrhythmia]. / Elektrická programovaná stimulace komor provádená prostrednictvím trvalého kardiostimulacního systému--neinvazivní metoda v arytmologii.

BACKGROUND: Complex forms of ventricular arrhythmias often occur in patients with an implanted permanent cardiac pacing system. Some of the pacemakers are provided with software which allows electrophysiological testing of the cardiac conduction system by coupling with an external diagnostic pacemaker via their programmer. This method is non-invasive. METHODS AND RESULTS: In a group of 26 patients (19 males, 7 females) with an implanted pacemaker (Paragon III, Synchrony III, Sensorithm--all Pacesetter) complex ventricular arrhythmias were observed (class Lown IVa and higher). In these patients the electrical stability of the myocardium was tested by the described method (protocol: incremental pacing 90-220 bpm, pacing drives 110 bpm and 140 bpm with 1-3 extrastimuli). Complex ventricular arrhythmias were induced in 42% patients (n = 11), in this subgroup 55% (n = 6) was non-sustained ventricular tachycardia, 36% (n = 4) sustained ventricular flutter, 9% (n = 1) sustained ventricular tachycardia. Patients with non-sustained ventricular tachycardia were treated with beta-blockers, in the others the effective therapy was selected according to electrophysiological testing (amiodarone in 4 patients, ICD in 1 patient). During a 24-month follow-up the overall mortality was 7.7% (n = 2), sudden death mortality was 3.8% (n = 1). CONCLUSIONS: Programmed ventricular stimulation performed by a permanent cardiac pacing system is a simple and above all non-invasive method with no need for fluoroscopy. It can be repeated several times. It is not possible to pace from the right ventricle outflow tract. This is the main disadvantage. Nevertheless, by using non-invasive risk stratification methods (echocardiography, signal averaged ECG, heart rate variability, baroreflex sensitivity, dispersion of QT interval) the patients in need of an invasive study can be identified. This method can be considered an alternative screening method and a standard part of the investigation of the algorithm in patients with a previously implanted pacemaker.

[Role of determination of QT dispersal intervals in anti-arrhythmia therapy]. / Prínos hodnocení disperze QT intervalu v antiarytmické terapii.

In recent years attempts intensified to identify and treat patients with an increased risk of sudden cardiac death caused by malignant ventricular arrhythmias. An elevated dispersion value of the QT interval of surface ECG suggests non-homogeneous repolarization and thus the presence of an arrhythmogenic substrate. In patients with ischaemic heart disease and confirmed malignant arrhythmias after onset of antiarrhythmic therapy changes in the dispersion of the QT interval occur, depending on the antiarrhythmic agent used and the effectiveness of treatment. In the authors group of 40 patients the value of dispersion of the QT interval declined significantly after introduction of effective antiarrhythmic treatment in patients treated with amiodarone and beta-blocker. It may thus be stated that the value of the QT interval dispersion of surface ECG can be used not only as a non-invasive "marker" of sudden cardiac death but also as an auxiliary indicator of effectiveness of antiarrhythmic therapy.

[Solitary cardiac metastasis from carcinoma of the cervix]. / Solitární metastáza v srdci u karcinomu delozního cípku.

Authors report the case of 37 years old women after radiotherapy for spinocelular cervical carcinoma which was presented by a solitary metastasis in the right ventricle causing right ventricle output tract obstruction. Cardiosurgical intervention as well as chemotherapy were not indicated for the great extension of cardiac involvement. The patient died from a massive pulmonary embolism. Echocardiography, although limited by the discrimination ability, seems to be the best method for the cardiac metastasis detection.