[Repolarization homogeneity in patients after acute myocardial infarction assessed from long-term 12-lead electrocardiographic recordings]. / Homogenita repolarizace u patientu po akutním infarktu myokardu hodnocená z dlouhodobých 12svodových elektrokardiografických záznamu.

BACKGROUND: Abnormal heterogeneity of myocardial electrophysiologic processes increases the risk of malignant arrhythmias. The aim of the studywas to assess changes ofrepolarization homogeneity in patients after acute myocardial infarction (MI) using morphological parameters obtained from long-term 12-lead electrocardiographic recordings. METHODS: In the group of 200 patients (45 females, 155 males) a long-term (10 minutes supine) 12-lead electrocardiographic recording (SEER MC, GE Medical) was performed 48-72 hours after acute myocardial infarction. The following parameters were calculated using experimental software: total cosine R to T (TCRT) and Twave residuum (TWR). The results were correlated with Q wave evolution and left ventricular ejection fraction (LVEF). RESULTS: Distinguishing the MI type (Q vs nonQ) the following values were obtained: TCRT: 0.17 +/- 0.61 vs 0.16 +/- 0.49, p = 0.52, absolute TWR: 21,200 +/- 21,700 vs 25,700 +/- 29,300, p = 0.3, relative TWR: 0.0012 +/- 0.0017 vs 0.0017 +/- 0.0026, p = 0.28. Stratification according to LVEF (< or = 40% vs > 40%) led to: TCRT: -0.03 +/- 0.66 vs 0.25 +/- 0.54, p = 0.01, absolute TWR: 29,700 +/- 32,400 vs 21,300 +/- 21,500, p = 0.14, relative TWR: 0.0021 +/- 0.0047 vs 0.0013 +/- 0.0021, p = 0.48. CONCLUSION: TCRT is a robust measurement of the spatial angle between the QRS complex and T wave loops which is related to LVEF. The results concerning TWR might indicate that this parameter is independent of LVEF, which needs to be confirmed in further analyses in a larger population.

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.

[QT dynamicity in risk stratification in patients after myocardial infarction]. / QT dynamicita v rizikové stratifikaci u pacientu po infarktu myokardu.

BACKGROUND: Ventricular repolarization abnormalities are associated with increased risk of sudden cardiac death in patients after myocardial infarction. The aim of this study is to assess QT dynamicity - QT/RR relationship - in patients after myocardial infarction and its contribution to risk stratification of sudden cardiac death. METHODS: In a group of patients with diagnosis of acute myocardial infarction a long term ECG recording was performed 48-72 hours after myocardial infarction (MARS Unity Workstation, GE Medical Information Technologies). Patients with unstable circulation, artificial pulmonary ventilation, left bundle brach block, atrial fibrillation and paced rhythm were excluded. Analysis of QT dynamicity was performed by QT Guard software (GE Medical Information Technologies). QT/RR relationship is expressed by linear regression as QT = = aRR + b where "a" is termed "slope". RESULTS: Assessment of QT dynamicity was possible in 215 ECG recordings. In 6-month follow-up 2 patients died and another was successfully resuscitated for primary ventricular fibrillation. Six-month mortality resp. mortality + resuscitation was 0.9 %, resp. 1.4 %. Therefore statistical evaluation was not possible. In the 3 mentioned individuals the slope values were 0.333, 0.249 and 0.342. CONCLUSIONS: Mortality of up-to-date-treated patients after myocardial infarction is low. Therefore, in such patients it is not possible to assess QT dynamicity as a risk factor in midterm follow-up. Limitation of the method is the necessity of substantial selection of patients elegible for analysis and dependance on necessary equipment.

[Extension of QT interval as a consequence of risk factor accumulation--case study]. / Prodlouzení QT intervalu jako dusledek kumulace rizikových faktoru: kazuistika.

BACKGROUND: Many non-cardiovascular drugs have a potential for QT interval prolongation. This phenomenon can be related to occurence of ventricular tachycardia torsades de pointes, syncopi and even sudden death. DESCRIPTION OF THE CASE: A female patient treated with antracycline cytostatics developed a depression of left ventricle ejection fraction. At the same time she was administered 2 common drugs with proarrhythmic potential--terfenadine and itraconazole. In this patient hypokalemia also occured. Combination of the above mentioned risk factors led to QT interval prolongation and frequent ventricular tachycardias torsades de pointes degenerating in ventricular fibrillations with need of repeated defibrillations. Both drugs were withdrawn and dysiontaemia corrected. Then arrhythmias disappeared and QT interval completely normalized. In this patient the congenital long QT syndrome was not proved. DISCUSSION AND CONCLUSIONS: In proarrhythmic effect of non-cardiovascular drugs the following factors play role: predisposition of a particular individual, "repolarization reserve", interindividual differences in drug metabolism. The risk factors are age, sex, dysiontaemia, heart disease and drug interactions. By different choice of medication and attention to risk factors teh life threat to the described patient could have been avoided.

[Mutational analysis of LQT genes in individuals with drug induced QT interval prolongation]. / Mutacní analáza LQT genu u jedincu s polékovým prodlouzením QT intervalu.

BACKGROUND: In a long list of non-cardiovascular drugs a risk of QT interval prolongation and thus an increased risk of malignant arrhythmias has been described. The precise mechanism remains unclear. Many of these drugs are potent blockers of cardiac ion channels. Thus, prolongation of repolarization could be caused by latent ion channel genes mutations which are revealed under stress conditions. GROUP OF PATIENTS AND METHODS: Patients were recruited in screening of antipsychotic drugs with proarrhythmic potential, another sporadic cases were reffered from regional hospitals. In 13 individuals pathologic values of corrected QT interval (> 0.44 s in males, > 0.46 s in females) were observed. Eleven patients gave their consent to mutational analysis of KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2 and KCNJ2 genes (associated with congenital long QT syndrome). RESULTS: At present complete results of mutational analysis are available in 8 patients. In 5 individuals changes in DNA sequence were found which are considered normal variants according to the literature (nucleotide and aminoacid polymorphisms, intronic variants). In 1 male a KCNQ1 gene mutation A590T was identified (yet not reported in literature). CONCLUSION: Mechanisms of drug-induced QT interval prolongation is complex and it cannot be explained simply by ion channel disorders.

[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.

[Significance of vegetative nerve tone in patients with vasovagal neurocardiogenic syncope]. / Význam vegetativního nervového tonu u nemocných s vazovagální neurokardiogenní synkopou.

The timely provided and precise diagnostic of the syncopal states as well as their causal therapy is a main subject of many medical branches interest within last time. Our work was concentrated on a vasovagal neurocardiogenic syncope. The definition of the vegetative nervous tonus participation on its development by a method of evaluation of the heart rate variability as well as the review of a possibility to the application of quantification these results to a prediction of vasovagal reaction, respective of its malignant variant, was the main aim of our effort. Our results enable a conclusion, that the observation of aquiet autonomic nervous tonus does not represent a contribution to a differential diagnostics of syncope of uncleared etiology with a suspicion on vasovagalous neurocardiogenous syncope, because the basal vagal tonus does not allow the forecast of head upright tilt table testing results as well as determination of the type of respectively provocated vasovagal neurocardiogenic syncope. However, a correlation between an actual reactive vageous tonus surveyed by the SD index for patients with vasovagal neurocardiogenic syncope of the type I and IIa in comparison with healthy persons, was found out. It allows to draw a conclusion, that the vasovagal neurocardiogenic syncope is not homogeneous nosological unit, what results in efforts to it's more detailed classification.

[Neural syncope--a current therapeutic problem]. / Neurálne zprostredkovaná synkopasou--soucasný terapeutický problém.

Syncope, a state performed by transient loss of consciousness connected with postural tone decrease present still an important therapeutical problem. It can vary from a benign physiological body reaction to a life-limiting situation. The authors of the article present HUT-testing to be a simple, useful and safe method for discovering vasovagal mechanism of the syncope. They notice the experiences with treatment according to the HUT results. The most frequent types of therapy are the pharmacological and the pacing ones, when the former is appropriate for I and III class of VVS the latter then for the II. class. There are some big studies in progress now which should bring more information about this clinical problem.