[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.]

[Asymptomatic hyperuricemia is frequent in hypertension and its prevalence is increasing. Authors studied the incidence of serum uric acid levels and its correlation with age, risk factors, anthropological, metabolic characteristics, blood pressure, blood pressure target, organ damage, age-related co-morbidity in 47,372 hypertensive patients (22,688 males, 24,694 women). In the second part of their analysis the prevalence of hyperuricemia was 13.8% in hypertensive men and 21.6% in women. The age, BMI, waist diameter, systolic and diastolic blood pressure and onset of hypertension, serum cholesterol, triglyceride, blood glucose and serum creatinine were slightly higher, but serum HDL cholesterol and eGFR were slightly lower in hyperuricemic hypertensive patients, independently of their gender. Among hypertension mediated organ damage ischemic and left ventricular hypertensive ECG alterations, mild chronic kidney disease and proteinuria, among hypertension associated diseases diabetes associated ischemic heart disease, chronic kidney disease associated diabetes and both ischemic and chronic kidney disease associated diabetes were significantly more frequent in hyperuricemic hypertensive patients.]

[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.]

[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.]