[End stage renal disease and ventricular arrhythmia. Hemodialysis and hemodiafiltration differently affect ventricular repolarization]. / Végstádiumú vesebetegség és kamrai szívritmuszavarok. A hemodialízis és a hemodiafiltráció a kamrai repolarizációt eltéroen befolyásolja.

Various factors (hypertension [27%], diabetes mellitus [40%]) and their cardiovascular complications play an important role in the genesis of end stage renal disease. Furthermore, primary kidney diseases (glomerulonephritis, tubulointerstitial nephritis, obstructive uropathy, analgesic nephropathy, polycystic kidney disease, autoimmune diseases) have an unfavorable effect on the cardiovascular outcome of this particular population. Increased susceptibility for arrhythmias may be caused by intermittent volume overload, metabolic disturbance, renal anemia, structural and electrophysiological changes of the myocardium, inflammatory mechanisms that may worsen the mortality statistics of these patients. A novel renal replacement method, hemodiafiltration - based on a convective transport - ensures reduced mortality that may be attributed to a decreased occurrence of arrhythmias. The aim of this paper is to review the pathogenetic factors taking part in the arrhythmogenesis of end stage renal disease and to provide diagnostic and therapeutic opportunities that can help in the prediction and prevention of arrhythmias.

Hemodiafiltration beneficially affects QT interval duration and dispersion compared to hemodialysis.

BACKGROUND/AIMS: The prolongation of the QT interval and dispersion could predict ventricular arrhythmias. It is not yet established whether there is a difference between the effects of hemodialysis and hemodiafiltration on QT interval duration and dispersion. METHODS: Data of thirty patients was investigated while they were receiving hemodiafiltration over a period of 3 months; then the same group of patients was evaluated during treatment with conventional hemodialysis for at least another 3 months. Ionic parameters and surface electrocardiograms (ECG) were analyzed five times during each session, and 2D, M-mode echocardiography and Holter ECGs were performed to acquire additional information. RESULTS: QT interval duration (QTmax) and dispersion (QTd) showed a significant increase during hemodialysis, but not during hemodiafiltration. QTmax was 388.66 ± 31.81 ms at the beginning of hemodialysis and increased to 400.66 ± 39.12 ms even at the 30th minute (p < 0.05). QTd was found to be 31.33 ± 10.08 ms before the commencement of hemodialysis with the largest prolongation being seen at the 240th minute (51.33 ± 14.56 ms, p < 0.05). The occurrence of ventricular premature beats was significantly higher during hemodialysis (p = 0.018). The left atrial diameter significantly decreased at the end of hemodiafiltration (at the beginning 45.1 ± 5.25 mm, at the end 40.77 ± 5.76 mm; p < 0.05). CONCLUSION: Our results suggest a beneficial effect of hemodiafiltration on the studied electrocardiographic parameters compared to hemodialysis. The larger decrease in the left atrial diameter suggests a more efficient intracardiac volume-decreasing potential of hemodiafiltration.

Hemodialysis and hemodiafiltration differently modulate left ventricular diastolic function.

BACKGROUND: Renal replacement therapy may have a favorable effect on diastolic left ventricular function, but it is not clear whether hemodiafiltration is superior to hemodialysis in this field. Nitric oxide (NO) and asymmetric dimethylarginine (ADMA) may play a role in the changes of intracardiac hemodynamics, but it is not clear whether the different renal replacement methods have disparate influence on the metabolism of these materials. METHODS: Thirty patients on renal replacement therapy were investigated. First, data was analyzed while patients received hemodiafiltration over a period of three months. Then, the same patients were evaluated during treatment with hemodialysis for at least another three months. Echocardiography was performed before and after renal replacement therapy. RESULTS: No significant difference was found in the volume removals between hemodialysis and hemodiafiltration. The left atrial diameter and transmitral flow velocities (E/A) decreased significantly only during hemodiafiltration. A positive correlation was observed between the left atrial diameter and E/Ea representing the left ventricular pressure load during hemodiafiltration. Significant correlations between NO and A and E/A were observed only in the case of hemodiafiltration. CONCLUSION: Hemodiafiltration has a beneficial effect on echocardiographic markers representing left ventricular diastolic function. This could be attributed to the differences between the dynamics of volume removal and its distribution among liquid compartments.

[Molecular and genetic background of sudden cardiac death]. / A hirtelen szívhalál molekuláris és genetikai háttere.

Despite recent findings on the functional, structural and genetic background of sudden cardiac death, the incidence is still relatively high in the entire population. A thorough knowledge on susceptibility, as well as pathophysiology behind the development of malignant arrhythmias will help us to identify individuals at risk and prevent sudden cardiac death. This article presents a review of the current literature on the role of altered intracellular Ca2+ handling, acute myocardial ischaemia, cardiac autonomic innervation, renin-angiotensin-aldosterone system, monogenic and complex heritability in the pathogenesis of sudden cardiac death.

[Microvolt T-wave alternant: pathomechanism and evaluation of a new marker of arrhythmia risk]. / A fokozott arrhythmiarizikó új markere: a mikrovolt T-hullám-alternáns patomechanizmusa és vizsgálati módszerei.

Microvolt T-wave alternant (microV-TWA) is a beat-to-beat fluctuation in the amplitude of T-wave at a microvolt level. The amount of variation is small, on the order of microvolts, so sensitive digital signal processing techniques are required to detect microV-TWA. The appearance of microV-TWA has been suggested as a predictor of susceptibility to lethal ventricular tachyarrhythmias, and sudden cardiac death in different patients' populations. During the last decade, theoretical, experimental and clinical research efforts have focused primarily on microV-TWA, examining its mechanisms and predictive value using time-invariant cutoff values. The cellular mechanisms involved are not well-defined and are the subject of this investigation. This review discusses the bench-to-bedside literature that, over decades, has linked alternans of repolarization in cellular, whole-heart, and human studies with spatial dispersion of repolarization, alternans of cellular action potential, and fluctuations in ionic currents, intracellular calcium regulation, role of the beta adrenergic receptors and connexins that may lead to ventricular arrhythmias. This review then provides a contemporary framework for the use of microV-TWA methods to enhance risk stratification for sudden cardiac death, identifying populations for whom microV-TWA is best established.

The effect of sleep apnea on QT interval, QT dispersion, and arrhythmias.

BACKGROUND: QT interval (QT) and QT dispersion (QTd) are electrocardiograph (ECG) parameters for the evaluation of myocardial repolarization. The inhomogeneity of ventricular repolarization is associated with ventricular arrhythmias. An increased QT, QTd, and increased incidence of nocturnal cardiac rhythm disturbances have been described in patients with obstructive sleep apnea (OSA), while other investigators did not find a relationship between ventricular arrhythmias and OSA. HYPOTHESIS: The aim of this study was to examine the occurrence of ventricular arrhythmias and to measure QT parameters in patients with untreated OSA using an ambulatory Holter-ECG. METHODS: A total of 25 patients with untreated OSA were studied. After routine biochemical investigation and 2-dimensional, M-mode echocardiography, a 24-hour Holter-ECG was recorded to detect cardiac arrhythmias and QT parameters. QT parameters were measured by the QT Guard system. RESULTS: Only the QT interval increased significantly during the nighttime period (nocturnal QT interval: 423.1 +/- 34.6 ms, daytime QT interval: 381.6 +/- 33.8 ms, 24-hour QT interval: 394.7 +/- 31.1 ms). However, during the nighttime QT interval (422.8 +/- 14.9 ms), QTd (31.2 +/- 11.0 ms) and QT dispersion (30.5 +/- 10.2 ms) did not show any change compared to 24-hour (QTc interval: 423.7 +/- 14.2 ms, QTd: 28.8 +/- 9.4 ms, QTcd: 30.5 +/- 9.43 ms) and daytime levels (QTc interval: 423.9 +/- 14.3 ms, QTd: 27.3 +/- 10.7 ms, QTcd: 29.9 +/- 11.1 ms). None of the patients had ventricular arrhythmias. CONCLUSIONS: QTd and QTcd did not increase during the nighttime period. Our study did not show an increased risk of ventricular arrhythmias in this population during the monitoring period.

Myocardial adrenergic innervation in patients with vasovagal syncope measured with 123I-MIBG uptake.

BACKGROUND: Data about biochemical abnormalities (catecholamines) during vasovagal syncope (VVS) are available, but adrenergic myocardial structural damage may be hypothesized as well. AIM: To study the global and regional adrenergic myocardial innervations in patients with VVS that was shown by head-up tilt table testing. PATIENTS AND METHODS: Fifteen adult patients with VVS were studied. The age of patients was 44+/-18 years (17-73), nine were female and six were male. According to the tilt test results, five patients had cardioinhibition, six patients had vasodepressor syncope and four patients suffered from mixed-type VVS. Ischemic heart diseases were excluded by normal Tc-MIBI rest-stress dipyridamol single-photon emission computed tomography (SPECT) results. A control group was formed from six healthy adult volunteers. To investigate cardiac sympathetic innervations 250-370 MBq iodine-123 meta-iodobenzylguanidine (I-MIBG) was used. Fifteen minutes after the intravenous administration of I-MIBG early, and 2-3 h later, delayed planar myocardial and tomographic (SPECT) scintigraphies were performed. The heart-to-mediastinum count ratio (H/M) was calculated for both early and delayed images, together with the decay-corrected change rates. The regional I-MIBG uptake was visualized on SPECT slices and polar map images. The regional uptake was considered pathological below 50% compared with normal uptake sites. RESULTS: Delayed H/M ratios significantly depended on group (analysis of variance: P=0.005), whereas early H/M values did not. Although the decay-corrected myocardial MIBG uptake increased in time in controls, less wash-in or even wash-out could be observed in the VVS groups; however, difference from the controls was significant only in the vasodepressor group (Dunnett's t-test: P<0.05). All patients had regional I-MIBG uptake deficit in different regions. CONCLUSION: In our patients with VVS, global I-MIBG deficit was present frequently, and all patients had regional adrenergic nerve function deficit. These alterations may play a role in causing clinical symptoms and have importance in staging and treatment planning.

[Atrial fibrillation and the autonomous nervous system]. / A pitvarfibrilláció és a vegetatív idegrendszer.

The autonomic nervous system has a crucial role in the genesis, maintenance and abruption of atrial fibrillation. The substrate and trigger mechanism of atrial fibrillation can be influenced by the changing autonomic tone. The authors summarize the current knowledge on the relationship between autonomic nervous system and atrial fibrillation. The special neuroanatomical status and the role of autonomic reflexes and baroreflex in the initiation, maintenance, and termination of arrhythmia are reviewed. Furthermore, the mechanism and consequences of autonomic effect of the curative radiofrequency catheter ablation of pulmonary vein with atrial vagal neuroablation are discussed. At the end we also summarize the pharmacologic therapy of atrial fibrillation. Classification of atrial fibrillation, as either vagal or adrenergic, has only limited impact on current management.

[Arrhythmias in patients with obstructive sleep apnea]. / Szívritmuszavarok obstruktív alvási apnoéban.

The authors summarize the current knowledge on the types, prevalence, reasons, diagnosis and current therapy of arrhythmias occurring in patients with obstructive sleep apnea. Most of the patients with obstructive sleep apnea have nocturnal bradycardia (5-50%), paroxysmal tachyarrhythmia (atrial 35%; ventricular 0-15%), or both. The frequency of rhythm disturbances associated with the severity of the sleeping disorder. It is important to recognize the factors predisposing to arrhythmias and the early appropriate therapy of patients is essential, in order to protect patients from life threatening arrhythmias which may worsen the clinical outcome.

[Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone]. / A hyperthyreosis cardiovascularis manifesztációi es az amiodaron-kezelés okozta pajzsmirigybetegség.

Cardiovascular manifestations of thyrotoxicosis and thyroid dysfunction caused by amiodarone. The cardiovascular symptoms of thyrotoxicosis were described more than two hundred years ago and remained the basis of diagnosis in modern medicine. Myocardium, peripheral circulation and sympathetic nerve system, all affecting cardiovascular hemodynamics, are influenced by thyroid hormones in many ways. Sub-clinical hyperthyroidism is characterized by suppressed thyroid stimulating hormone and normal free triiodothyronine and free thyroxine levels. Cardiovascular symptoms: elevation of heart rate, myocardial contractility, stroke volume, myocardial oxygen consumption, systolic blood pressure and reduction in systemic vascular resistance and diastolic blood pressure can be often seen even in case of subclinical hyperthyroidism. Thyrotoxicosis exacerbates the symptoms of a preexisting heart disease, but it can also cause complaints in case of a structurally normal heart. The most common cardiac complications are arrhythmias (mainly atrial fibrillation), heart failure and hypertension. Amiodarone is used for the treatment and prevention of several arrhythmias. It is safely applicable even in case of left ventricular dysfunction. The more common application is limited by its side effects that can develop even at low doses and may involve several organs (thyroid gland, lungs, liver, heart, nerve system among others). The complex effect of amiodarone on thyroid function ranges from mild abnormalities of thyroid function tests to overt thyrotoxicosis or hypothyroidism.