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Lege Artis Medicinae

NOVEMBER 10, 2008

Lege Artis Medicinae

SEPTEMBER 20, 2002

[QT dispersion - the surface ECG marker of arrhythmic risk]

KUN Csaba, CZURIGA István, LŐRINCZ István

[During the past decade numerous publications have reported the pathophysiological and clinical value of QT dispersion. Increased QT dispersion was observed to be associated with proarrhythmic drug effects, prediction of mortality in heart failure and risk assessment after acute myocardial infarction. Based on the results of the repolarization process research and other significant clinical studies, the meaning and the usefulness of QT dispersion seems to be challenged. The original concept of portraying QT dispersion as a direct measure of regional heterogeneity of myocardial refractoriness is seriously flawed. At the same time, disproving this concept is not a good reason for stating that QT dispersion does not exist. The measurement of QT dispersion seems to be an approximate expression of repolarization abnormalities and should not be taken as a gold standard for a noninvasive estimate of repolarization abnormalities. However, we presently have no decent and widely available alternative to address repolarization abnormalities in standard 12-lead ECG. The authors present the pathophysiological meaning of QT dispersion, the controversies of automatic and manual methodology and the possible clinical relevances based on the most recent studies.]

Lege Artis Medicinae

FEBRUARY 20, 2009

[Sudden cardiac death in athletes - cardiac electrophysiology point of view]

VARRÓ András

[Sudden cardiac death of athletes is very rare (1/50 000 to 1/100 000 annually) but it is still 2 to 4 times more frequent than that of the agematched normal population. In addition, it attracts peculiar media attention. Sudden cardiac death in athletes is supposed to not primarily have an ischemic origin but most likely relates to repolarization abnormalities. These may be caused by several independent and/or dependent factors such as benign cardiac hypertrophy developing normally in athletes (athlete’s heart), hypertrophic cardiomyopathy, increased sympathetic activity, genetic defects, seemingly harmless drugs, doping agents, food, and dietary supplements. These factors together can increase inhomogeneities in myocardial repolarization (“substrate”). In this case, an otherwise harmless extrasystole (“trigger”) occurring with unlucky timing may - although very seldomly - elicit fatal arrhythmias. Thus, effective prevention of sudden cardiac death may include new types of cost-effective cardiac electrophysiological screening methods (ECG or echocardiography) and, in case of a high level of suspicion, more costly genetic tests can be considered.]

Clinical Neuroscience

MAY 30, 2008

[EFFECT OF EPILEPTIC SEIZURES ON THE HEART RATE]

TÓTH Vanda, HEJJEL László, KALMÁR Zsuzsanna, FOGARASI András, AUER Tibor, GYIMESI Csilla, SZŰCS Anna, JANSZKY József

[Background - Sudden death appears in 8-17% of epilepsy patients non-responding to antiepileptic therapy. Some studies suggest that the most common cause of death is seizure-related cardiac arrhythmia. Aim of study - To analyze the alteration of the heart rate six hours before and after the seizures. Methods - Eighteen patients suffering from focal epilepsy were examined before epilepsy surgery. Video-EEG-ECG was carried out for 2-10 days, and 32 seizures were registered. Analysis of the heart rate was based on the 5- minute-long epochs of the ECGs taken at the 5-10-15- 30th minutes and at the 1-3-6th hours before and after seizures. Results - The heart rate increases (from average 69 beats/min to 92 beats/min, p<0.001) immediately after seizures, tough significantly higher heart rate was observed 3 hours after seizures. There were no patients with severe periictal bradycardia. In one of our patients, ectopic cardiac rhythm occurred after a generalized tonicclonic seizure. Conclusions - We can conclude that the sympathic activity increases while the parasympathic activity decreases after seizures. The observed alterations lasted for a long time and predict to fatal arrhythmias. These suggest that sudden death in epilepsy can be induced by cardiac arrhythmias connected with epileptic seizures.]

LAM Extra for General Practicioners

APRIL 20, 2010

[SUDDEN CARDIAC DEATH IN ATHLETES - CARDIAC ELECTROPHYSIOLOGY POINT]

VARRÓ András

[Sudden cardiac death of athletes is very rare (1/50 000 to 1/100 000 annually) but it is still 2 to 4 times more frequent than that of the agematched normal population. In addition, it attracts peculiar media attention. Sudden cardiac death in athletes is supposed to not primarily have an ischemic origin but most likely relates to repolarization abnormalities. These may be caused by several independent and/or dependent factors such as benign cardiac hypertrophy developing normally in athletes (athlete’s heart), hypertrophic cardiomyopathy, increased sympathetic activity, genetic defects, seemingly harmless drugs, doping agents, food, and dietary supplements. These factors together can increase inhomogeneities in myocardial repolarization (“substrate”). In this case, an otherwise harmless extrasystole (“trigger”) occurring with unlucky timing may - although very seldomly - elicit fatal arrhythmias. Thus, effective prevention of sudden cardiac death may include new types of cost-effective cardiac electrophysiological screening methods (ECG or echocardiography) and, in case of a high level of suspicion, more costly genetic tests can be considered.]

Clinical Neuroscience

NOVEMBER 30, 2006

[COMPLEX NON-INVASIVE HEMODYNAMIC SYSTEM FOR THE EVALUATION OF VASCULAR STATUS]

CSAPÓ Krisztina, BAJKÓ Zoltán, MOLNÁR Sándor, MAGYAR Tünde, CSIBA László

[The vascular diseases (myocardial infarct, stroke, peripheral occlusive disease) have a common pathophysiological background, the arteriosclerosis, that impairs the autoregulation of cerebral vessels, decreases the endothel mediated flow in the peripheral vessels. Therefore the assessment of the vascular damage or the follow-up of therapy need a complex and simultaneous approach. Currently the morphological and functional changes in the vascular system can be investigated with separated measuring systems, focusing either to cardiac or cerebral parameters (intermittent blood pressure measurement, ECG, cerebral blood flow by transcranial Doppler e.g.). Our purpose is to establish a complex non-invasive system for the simultaneous measurement and comparison of cardiac/cerebral/periheral hemodynamics. The hemodynamic parameters in hypertensive patients are examined with transcranial Doppler and cardiac monitoring during tilt-table test. Intima-media thickness, flow-mediated dilatation in brachial artery, augmentation index and pulse wave velocity are also measured. The measurement will be repeated after 6 and 12 months follow-up. Our preliminary results are similar to those found in the literature, that proves the reliability of our complex noninvasive hemodynamic system. It is assumed, that 12 months antihypertensive therapies with ACE inhibitors, calciumantagonist etc. might result in different effects on different vascular parameters. Our system enables the individualization of antihypertensive therapy.]

Hypertension and nephrology

SEPTEMBER 09, 2010

[The importance of assessing subclinical organ damage in risk prediction of hypertensive patients]

GODINA Gabriella, JÁRAI Zoltán

[As the cardiovascular risk influences the quality and intensity of blood pressure lowering therapy, the goal blood pressure values and the frequency of medical control of hypertensive patients, as well as global risk assessment has an important role in the management of hypertension. In the last couple of years many data have been accumulated showing the poor prognostic value of traditional cardiovascular risk factors. This is the reason why recent Hungarian and international guidelines on the management of hypertension advise the screening for subclinical organ damage. Our goal was to summarize the importance of subclinical organ damage by discussing recently published literature on this topic. An overview has been made on the markers of vascular subclinical damage, like carotid atherosclerosis proved with carotid ultrasonography, peripheral arterial disease assessed with ankle-brachial pressure index measurements and vascular rigidity defined with pulse wave velocity measurements. The prognostic values of myocardial hypertrophy assessed with ECG and/or echocardiography and renal damage proved with decreased estimated glomerular filtration rate and proteinuria are also discussed. Summing up what has been said so far, the assessment of subclinical organ damage has a role in cardiovascular risk prediction, however more randomized and prospective studies have to be performed to define the most suitable (i.e. the most reliable and the most cost-effective) markers for this purpose.]

Lege Artis Medicinae

NOVEMBER 30, 2006

[THE ROLE OF METABOLIC THERAPY IN THE TREATMENT OF STABLE RECURRENT ANGINA AFTER CORONARY REVASCULARIZATION]

TÓTH Csaba

[Current guidelines recommend drug treatment as firstline therapy for stable angina. If adequate symptom relief cannot be achieved with pharmacological management, or if myocardial ischaemia progresses, interventional revascularization procedures should be considered. Based on current guidelines, this should be either coronary artery bypass grafting or percutaneous coronary intervention. Recurrent angina refers to the persistence or reemergence of angina symptoms after a coronary revascularization procedure. This clinical situation indicates the repeat of coronarography as soon as possible. The repeated coronarography, however, often will not confirm progression or restenosis. The pathology of this clinical form of recurrent angina is not exactly known. As symptoms are frequently seen in the absence of abnormal coronary blood flow, vasodilator drugs are of limited effectiveness in recurrent angina. For this reason new, non-haemodynamic treatment approaches have been suggested. Among these, agents that help optimise cardiac metabolism are of particular interest. Trimetazidine acts on the energy metabolism of myocardial cells by reducing the reliance of myocardial metabolism on fatty acid oxidation and lifting the feedback inhibition of the glucose oxidation pathway. Moreover, trimetazidine reduces intracellular acidosis. These beneficial effects on cellular processes make trimetazidine the first representative of cardioprotective drugs. In randomized, placebo-controlled clinical trials on patients after revascularization, trimetazidine significantly reduced the number of angina episodes, decreased the ECG signs and the levels of biochemical markers of myocardial ischaemia, and improved exercise test parameters compared to placebo. The spectrum of benefits of this drug in stable angina ranges from decreasing the need for surgical intervention to improving the outcome and diminishing the symptoms of angina pectoris following revascularization.]

Lege Artis Medicinae

MARCH 20, 2011

[ECG artefacts]

TOMCSÁNYI János, BEZZEG Péter

[The recognition of ECG artefacts is becoming increasingly important for physicians working in the field of internal medicine. At the same time, however, very little information about artefacts is published in either articles or textbooks. The authors provide a summary of the generation, types and recognition of ECG artefacts. The aim of the article is to draw the attention of clinicians to the dangers of this increasingly common phenomenon. Unrecognised artefacts can often prompt further (unnecessary) investigations and may result in establishing wrong diagnosis as well as erroneous treatment decisions.]