Sex Related Differences in Electrocardiography.

Since its implementation into the clinical medicine by Willem Einthoven electrocardiography had become one of crucial diagnostic method in cardiology. In spite of this fact effects of gender differences on parameters of electrocardiographic recordings started to be studied only recently. Sex related differences in physiological ECG are only minimal in childhood but there are developing during adolescence reflecting rapidly evolving differences particularly in hormonal secretion and activity of an autonomic nervous system. The heart rate is approximately 7 % higher in women than in men, PQ and QRS intervals are longer in men while QT interval is longer in women. The ST segment in females is flatter but generally the sex-related differences in ST-T waveform patterns are relatively very small with higher level of ST segment and taller T wave in men. The effects of sex-related differences, including sex hormones, on cardiac cell injury and death and their influence in determining rhythmogenesis and action potential configuration and conduction play an important role in clinics. Women have a higher prevalence of sick sinus syndrome, inappropriate sinus tachycardia, atrioventricular nodal reentry tachycardia, idiopathic right ventricular tachycardia, and arrhythmic events in the long QT syndrome. In contrast, men have a higher prevalence of atrioventricular block, carotid sinus syndrome, atrial fibrillation, supraventricular tachycardia due to accessory pathways, Wolff-Parkinson-White syndrome, reentrant ventricular tachycardia, ventricular fibrillation and sudden death, and the Brugada syndrome.

A large arteriovenous fistula steals a considerable part of systemic blood flow during veno-arterial extracorporeal circulation support in a porcine model.

Background: Veno-arterial extracorporeal membrane oxygenation (V-A ECMO) is one of the most frequently used mechanical circulatory support devices. Distribution of extracorporeal membrane oxygenation flow depends (similarly as the cardiac output distribution) on regional vascular resistance. Arteriovenous fistulas (AVFs), used frequently as hemodialysis access, represent a low-resistant circuit which steals part of the systemic perfusion. We tested the hypothesis that the presence of a large Arteriovenous fistulas significantly changes organ perfusion during a partial and a full Veno-arterial extracorporeal membrane oxygenation support. Methods: The protocol was performed on domestic female pigs held under general anesthesia. Cannulas for Veno-arterial extracorporeal membrane oxygenation were inserted into femoral artery and vein. The Arteriovenous fistulas was created using another two high-diameter extracorporeal membrane oxygenation cannulas inserted in the contralateral femoral artery and vein. Catheters, flow probes, flow wires and other sensors were placed for continuous monitoring of haemodynamics and organ perfusion. A stepwise increase in extracorporeal membrane oxygenation flow was considered under beating heart and ventricular fibrillation (VF) with closed and opened Arteriovenous fistulas. Results: Opening of a large Arteriovenous fistulas (blood flow ranging from 1.1 to 2.2 L/min) resulted in decrease of effective systemic blood flow by 17%-30% (p < 0.01 for all steps). This led to a significant decrease of carotid artery flow (ranging from 13% to 25% after Arteriovenous fistulas opening) following VF and under partial extracorporeal membrane oxygenation support. Cerebral tissue oxygenation measured by near infrared spectroscopy also decreased significantly in all steps. These changes occurred even with maintained perfusion pressure. Changes in coronary artery flow were driven by changes in the native cardiac output. Conclusion: A large arteriovenous fistula can completely counteract Veno-arterial extracorporeal membrane oxygenation support unless maximal extracorporeal membrane oxygenation flow is applied. Cerebral blood flow and oxygenation are mainly compromised by the effect of the Arteriovenous fistulas. These effects could influence brain function in patients with Arteriovenous fistulas on Veno-arterial extracorporeal membrane oxygenation.

Comparing the hemodynamic effect of a large arteriovenous fistula during high and low cardiac output states.

Background: A large arteriovenous fistula (AVF) is a low-resistant circuit that affects organ perfusion and systemic hemodynamics even in standard conditions. The extent of its' effect in critical states has not been elucidated yet. We used norepinephrine to create systemic vasoconstriction, dobutamine to create high cardiac output, and rapid right ventricle pacing as a model of acute heart failure in a porcine model of high-flow AVF circulation. Methods: The protocol was performed on nine domestic female pigs under general anesthesia. AVF was created by connecting two high-diameter ECMO cannulas inserted in the femoral artery and vein. Continuous hemodynamic monitoring was performed throughout the protocol. Three interventions were performed-moderate dose of norepinephrine (0.25 ug/kg/min), moderate dose of dobutamine (10 ug/kg/min) and rapid right ventricle pacing to simulate low cardiac output state with mean arterial pressure under 60 mmHg. Measurements were taken with opened and closed arteriovenous fistula. Results: Continuous infusion of norepinephrine with opened AVF significantly increased mean arterial pressure (+20%) and total cardiac output (CO) (+36%), but vascular resistance remained virtually unchanged. AVF flow (Qa) rise correlated with mean arterial pressure increase (+20%; R = 0.97, p = 0.0001). Effective cardiac output increased, leading to insignificant improvement in organ perfusion. Dobutamine substantially increased cardiac output with insignificant effect on AVF flow and mean arterial pressure. Carotid artery blood flow increased significantly after dobutamine infusion by approximately 30%, coronary flow velocity increased significantly only in closed AVF state. The effective cardiac output using the heart failure model leading to decrease of carotid artery flow and worsening of brain and peripheral tissue oximetry. AVF blood flow also dropped significantly and proportionally to pressure, but Qa/CO ratio did not change. Therefore, the effective cardiac output decreased. Conclusion: In abovementioned extreme hemodynamic conditions the AVF flow was always directly proportional to systemic perfusion pressure. The ratio of shunt flow to cardiac output depended on systemic vascular resistance. These experiments highlight the detrimental role of a large AVF in these critical conditions' models.

Ten years of our translational research in the field of veno-arterial extracorporeal membrane oxygenation.

Extracorporeal life support is a treatment modality that provides prolonged blood circulation, gas exchange and can substitute functions of heart and lungs to provide urgent cardio-respiratory stabilization in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Generally, the therapy targets blood pressure, volume status, and end-organs perfusion. As there are significant differences in hemodynamic efficacy among different percutaneous circulatory support systems, it should be carefully considered when selecting the most appropriate circulatory support for specific medical conditions in individual patients. Despite severe metabolic and hemodynamic deterioration during prolonged cardiac arrest, venoarterial extracorporeal membrane oxygenation (VA ECMO) can rapidly revert otherwise fatal prognosis, thus carrying a potential for improvement in survival rate, which can be even improved by introduction of mild therapeutic hypothermia. In order to allow a rapid transfer of knowledge to clinical medicine two porcine models were developed for studying efficiency of the VA ECMO in treatments of acute cardiogenic shock and progressive chronic heart failure. These models allowed also an intensive research of adverse events accompanying a clinical use of VA ECMO and their possible compensations. The results indicated that in order to weaken the negative effects of increased afterload on the left ventricular function the optimal VA ECMO flow in cardiogenic shock should be as low as possible to allow adequate tissue perfusion. The left ventricle can be also unloaded by an ECG-synchronized pulsatile flow if using a novel pulsatile ECMO system. Thus, pulsatility of VA ECMO flow may improve coronary perfusion even under conditions of high ECMO blood flows. And last but not least, also the percutaneous balloon atrial septostomy is a very perspective method how to passively decompress overloaded left heart.

Hemodynamic adaptation of heart failure to percutaneous venoarterial extracorporeal circulatory supports.

Extracorporeal life support (ECLS) is a treatment modality that provides prolonged blood circulation, gas exchange and can partially support or fully substitute functions of heart and lungs in patients with severe but potentially reversible cardiopulmonary failure refractory to conventional therapy. Due to high-volume bypass, the extracorporeal flow is interacting with native cardiac output. The pathophysiology of circulation and ECLS support reveals significant effects on arterial pressure waveforms, cardiac hemodynamics, and myocardial perfusion. Moreover, it is still subject of research, whether increasing stroke work caused by the extracorporeal flow is accompanied by adequate myocardial oxygen supply. The left ventricular (LV) pressure-volume mechanics are reflecting perfusion and loading conditions and these changes are dependent on the degree of the extracorporeal blood flow. By increasing the afterload, artificial circulation puts higher demands on heart work with increasing myocardial oxygen consumption. Further, this can lead to LV distention, pulmonary edema, and progression of heart failure. Multiple methods of LV decompression (atrial septostomy, active venting, intra-aortic balloon pump, pulsatility of flow) have been suggested to relieve LV overload but the main risk factors still remain unclear. In this context, it has been recommended to keep the rate of circulatory support as low as possible. Also, utilization of detailed hemodynamic monitoring has been suggested in order to avoid possible harm from excessive extracorporeal flow.

Increasing Veno-Arterial Extracorporeal Membrane Oxygenation Flow Reduces Electrical Impedance of the Lung Regions in Porcine Acute Heart Failure.

Veno-arterial extracorporeal membrane oxygenation (VA ECMO) is a technique used in patients with severe heart failure. The aim of this study was to evaluate its effects on left ventricular afterload and fluid accumulation in lungs with electrical impedance tomography (EIT). In eight swine, incremental increases of extracorporeal blood flow (EBF) were applied before and after the induction of ischemic heart failure. Hemodynamic parameters were continuously recorded and computational analysis of EIT was used to determine lung fluid accumulation. With an increase in EBF from 1 to 4 l/min in acute heart failure the associated increase of arterial pressure (raised by 44%) was accompanied with significant decrease of electrical impedance of lung regions. Increasing EBF in healthy circulation did not cause lung impedance changes. Our findings indicate that in severe heart failure EIT may reflect fluid accumulation in lungs due to increasing EBF.

Selected sex related differences in pathophysiology of cardiovascular system.

The annual incidence of cardiovascular diseases is age-dependently increasing both in men and women, however, the prevalence is higher in men until midlife. The higher incidence of cardiovascular disease in men than in women of similar age, and the menopause-associated increase in cardiovascular disease in women, has led to speculation that gender-related differences in sex hormones might have a key role in the development and evolution of cardiovascular disease. There are several suggested pathways in which gender and sex hormones can affect human cardiovascular system to produce original sexually different pathophysiology between women and men. Sex steroid hormones and their receptors are critical determinants of cardiovascular gender differences. Also arterial blood pressure is typically lower in women than in men what could be explained particularly by greater synthesis of nitric oxide (NO) in women. Female cardiomyocytes have a greater survival advantage when challenged with oxidative stress, suggesting that female hormones may play an important role in antioxidative protection of myocardium. It was also demonstrated in animal models that combination of XX chromosomes versus an XY chromosomes enhances sex differences in higher HDL cholesterol. Women were found to have reduced sympathetic activity (reflected by lower total peripheral resistance) and pulmonary artery pressure and enhanced parasympathetic activity relative to men. Similarly, men were found to have higher plasma norepinephrine levels than women. Regarding differences between the sexes in electrophysiology of the heart, two principle mechanisms have been proposed to explain them: hormonal effects on the expression or function of ion channels or, conversely, differences in autonomic tone. To improve diagnosis and treatment of cardiovascular diseases, greater focus on understanding the molecular and cellular physiology of the sex steroid hormones and their receptors in the cardiovascular system will be required.

Severe acute heart failure - experimental model with very low mortality.

The growth in the experimental research of facilities to support extracorporeal circulation requires the further development of models of acute heart failure that can be well controlled and reproduced. Two types of acute heart failure were examined in domestic pigs (Sus scrofa domestica): a hypoxic model (n=5) with continuous perfusion of the left coronary artery by hypoxic deoxygenated blood and ischemic model (n=9) with proximal closure of the left coronary artery and controlled hypoperfusion behind the closure. The aim was a severe, stable heart pump failure defined by hemodynamic parameters changes: a) decrease in cardiac output by at least 50 %; b) decrease in mixed venous blood saturation to under 60 %; c) left ventricular ejection fraction below 25 %; and d) decrease in flow via the carotid arteries at least 50 %. Acute heart failure developed in the first group in one animal with no acute mortality and in the second group in 8 animals with no acute mortality. In the case of ischemic model the cardiac output fell from 6.70+/-0.89 l/min to 2.89+/-0.75 l/min. The saturation of the mixed venous blood decreased from 83+/-2 % to 58+/-8 %. The left ventricular ejection fraction decreased from 50+/-8 % to 19+/-2 %. The flow via the carotid arteries decreased from 337+/-78 ml/min to 136+/-59 ml/min (P

Outcome of resynchronization therapy on superficial and endocardial electrophysiological findings.

Cardiac resynchronization therapy (CRT) has proven efficacious in the treatment of patients with heart failure and dyssynchronous activation. Currently, we select suitable CRT candidates based on the QRS complex duration (QRSd) and morphology with left bundle branch block being the optimal substrate for resynchronization. To improve CRT response rates, recommendations emphasize attention to electrical parameters both before implant and after it. Therefore, we decided to study activation times before and after CRT on the body surface potential maps (BSPM) and to compare thus obtained results with data from electroanatomical mapping using the CARTO system. Total of 21 CRT recipients with symptomatic heart failure (NYHA II-IV), sinus rhythm, and QRSd >/=150 ms and 7 healthy controls were studied. The maximum QRSd and the longest and shortest activation times (ATmax and ATmin) were set in the BSPM maps and their locations on the chest were compared with CARTO derived time interval and site of the latest (LATmax) and earliest (LATmin) ventricular activation. In CRT patients, all these parameters were measured during both spontaneous rhythm and biventricular pacing (BVP) and compared with the findings during the spontaneous sinus rhythm in the healthy controls. QRSd was 169.7+/-12.1 ms during spontaneous rhythm in the CRT group and 104.3+/-10.2 ms after CRT (p<0.01). In the control group the QRSd was significantly shorter: 95.1+/-5.6 ms (p<0.01). There was a good correlation between LATmin(CARTO) and ATmin(BSPM). Both LATmin and ATmin were shorter in the control group (LATmin(CARTO) 24.8+/-7.1 ms and ATmin(BSPM) 29.6+/-11.3 ms, NS) than in CRT group (LATmin(CARTO) was 48.1+/-6.8 ms and ATmin(BSPM) 51.6+/-10.1 ms, NS). BVP produced shortening compared to the spontaneous rhythm of CRT recipients (LATmin(CARTO) 31.6+/-5.3 ms and ATmin(BSPM) 35.2+/-12.6 ms; p<0.01 spontaneous rhythm versus BVP). ATmax exhibited greater differences between both methods with higher values in BSPM: in the control group LATmax(CARTO) was 72.0+/-4.1 ms and ATmax (BSPM) 92.5+/-9.4 ms (p<0.01), in the CRT candidates LATmax(CARTO) reached only 106.1+/-6.8 ms whereas ATmax(BSPM) 146.0+/-12.1 ms (p<0.05), and BVP paced rhythm in CRT group produced improvement with LATmax(CARTO) 92.2+/-7.1 ms and ATmax(BSPM) 130.9+/-11.0 ms (p<0.01 before and during BVP). With regard to the propagation of ATmin and ATmax on the body surface, earliest activation projected most often frontally in all 3 groups, whereas projection of ATmax on the body surface was more variable. Our results suggest that compared to invasive electroanatomical mapping BSPM reflects well time of the earliest activation, however provides longer time-intervals for sites of late activation. Projection of both early and late activated regions of the heart on the body surface is more variable than expected, very likely due to changed LV geometry and interposed tissues between the heart and superficial ECG electrode.

Electrocardiographic outcome of resynchronization therapy.

Cardiac resynchronization therapy (CRT) has proven efficacious in reducing or even eliminating cardiac dyssynchrony and thus improving heart failure symptoms. However, quantification of mechanical dyssynchrony is still difficult and identification of CRT candidates is currently based just on the morphology and width of the QRS complex. As standard 12-lead ECG brings only limited information about the pattern of ventricular activation, we aimed to study changes produced by different pacing modes on the body surface potential maps (BSPM). Total of 12 CRT recipients with symptomatic heart failure (NYHA II-IV), sinus rhythm and QRS width >/=120 ms and 12 healthy controls were studied. Mapping system Biosemi (123 unipolar electrodes) was used for BSPM acquisition. Maximum QRS duration, longest and shortest activation times (ATmax and ATmin) and dispersion of QT interval (QTd) were measured and/or calculated during spontaneous rhythm, single-site right- and left-ventricular pacing and biventricular pacing with ECHO-optimized AV delay. Moreover we studied the impact of CRT on the locations of the early and late activated regions of the heart. The average values during the spontaneous rhythm in the group of patients with dyssynchrony (QRS 140.5+/-10.6 ms, ATmax 128.1+/-10.1 ms, ATmin 31.8+/-6.7 ms and QTd 104.3+/-24.7 ms) significantly differed from those measured in the control group (QRS 93.0+/-10.0 ms, ATmax 79.1+/-3.2 ms, ATmin 24.4+/-1.6 ms and QTd 43.6+/-10.7 ms). Right ventricular pacing (RVP) improved significantly only ATmax [111.2+/-10.6 ms (p<0.05)] but no other measured parameters. Left ventricular pacing (LVP) succeeded in improvement of all parameters [QRS 105.1+/-8.0 ms (p<0.01), ATmax 103.7+/-7.1 ms (p<0.01), ATmin 20.2+/-3.7 ms (p<0.01) and QTd 52.0+/-9.4 ms (p<0.01)]. Biventricular pacing (BVP) showed also a beneficial effect in all parameters [QRS 121.3+/-8.9 ms (p<0.05), ATmax 114.3+/-8.2 ms (p<0.05), ATmin 22.0+/-4.1 ms (p<0.01) and QTd 49.8+/-10.0 ms (p<0.01)]. Our results proved beneficial outcome of LVP and BVP in evaluated parameters (what seems to be important particularly in the case of activation times) and revealed a complete return of activation times to normal distribution when using these CRT modalities.

Detection of microembolic signals in the common carotid artery using Doppler sonography in the porcine model of acute heart failure treated by veno-arterial extracorporeal membrane oxygenation.

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a method used for the treatment most severe cases of decompensated heart failure. The purpose of this study was to evaluate the risk of the formation of microembolisms during VA-ECMO-based therapy. Heart failure was induced with simultaneous detection of microembolisms and the measurement of blood flow rate in the common carotid artery (CCA) without VA-ECMO (0 l/min) and at the VA-ECMO blood flow rate of 1, 2, 3 and 4 l/min. If embolisms for VA-ECMO 0 l/min and the individual regimes for VA-ECMO 1, 2, 3, 4 l/min are compared, a higher VA-ECMO flow rate is accompanied by a higher number of microembolisms. The final microembolism value at 16 min was for the VA-ECMO flow rate of 0 l/min 0.0 (0, 1), VA-ECMO l/min 7.5 (4, 19), VA-ECMO 2 l/min 12.5 (4, 26), VA-ECMO 3 l/min, 21.0 (18, 57) and VA-ECMO 4 l/min, 27.5 (21, 64). Such a comparison is statistically significant if VA-ECMO 0 vs. 4 l/min p<0.0001, 0 vs. 3 l/min p<0.01 and 1 vs. 4 l/min p<0.01 are compared. The results confirm that high VA-ECMO flow rates pose a risk with regards to the formation of a significantly higher number of microemboli in the blood circulation and that an increase in blood flow rates in the CCA corresponds to changes in the VA-ECMO flow rates.

Regional tissue oximetry reflects changes in arterial flow in porcine chronic heart failure treated with venoarterial extracorporeal membrane oxygenation.

Venoarterial extracorporeal membrane oxygenation (VA ECMO) is widely used in treatment of decompensated heart failure. Our aim was to investigate its effects on regional perfusion and tissue oxygenation with respect to extracorporeal blood flow (EBF). In five swine, decompensated low-output chronic heart failure was induced by long-term rapid ventricular pacing. Subsequently, VA ECMO was introduced and left ventricular (LV) volume, aortic blood pressure, regional arterial flow and tissue oxygenation were continuously recorded at different levels of EBF. With increasing EBF from minimal to 5 l/min, mean arterial pressure increased from 47+/-22 to 84+/-12 mm Hg (P<0.001) and arterial blood flow increased in carotid artery from 211+/-72 to 479+/-58 ml/min (P<0.01) and in subclavian artery from 103+/-49 to 296+/-54 ml/min (P<0.001). Corresponding brain and brachial tissue oxygenation increased promptly from 57+/-6 to 74+/-3 % and from 37+/-6 to 77+/-6 %, respectively (both P<0.01). Presented results confirm that VA ECMO is a capable form of heart support. Regional arterial flow and tissue oxygenation suggest that partial circulatory support may be sufficient to supply brain and peripheral tissue by oxygen.

A novel experimental model of acute respiratory distress syndrome in pig.

Acute respiratory distress syndrome (ARDS) is severe medical condition occurring in critically ill patients and with mortality of 33-52 % is one of the leading causes of death in critically ill patients. To better understand pathophysiology of ARDS and to verify novel therapeutical approaches a reliable animal model is needed. Therefore we have developed modified lavage model of ARDS in the pig. After premedication (ketamine and midazolam) 35 healthy pigs were anesthetized (propofol, midazolam, morphin, pipecuronium) and orotracheally intubated and ventilated. Primary ARDS was induced by repeated cycles of lung lavage with a detergent Triton X100 diluted in saline (0.03 %) heated to 37 °C preceded by pre-oxygenation with 100 % O(2). Single cycle included two subsequent lavages followed by detergent suction. Each cycle was followed by hemodynamic and ventilation stabilization for approx. 15 min, with eventual administration of vasopressors according to an arterial blood pressure. The lavage procedure was repeated until the paO(2)/FiO(2) index after stabilization remained below 100 at PEEP 5 cm H(2)O. In 33 pigs we have achieved the desired degree of severe ARDS (PaO(2)/FiO(2)<100). Typical number of lavages was 2-3 (min. 1, max. 5). Hemodynamic tolerance and the need for vasopressors were strongly individual. In remaining two animals an unmanageable hypotension developed. For other subjects the experimental ARDS stability was good and allowed reliable measurement for more than 10 h. The present model of the ARDS is clinically relevant and thus it is suitable for further research of the pathophysiology and management of this serious medical condition.

Novel porcine model of acute severe cardiogenic shock developed by upper-body hypoxia.

Despite the urgent need for experimental research in the field of acute heart failure and, particularly cardiogenic shock, currently there are only limited options in large animal models enabling research using devices applied to human subjects. The majority of available models are either associated with an unacceptably high rate of acute mortality or are incapable of developing sufficient severity of acute heart failure. The objective of our research was to develop a novel large animal model of acute severe cardiogenic shock. Advanced left ventricular dysfunction was induced by global myocardial hypoxia by perfusing the upper body (including coronary arteries) with deoxygenated venous blood. The model was tested in 12 pigs: cardiogenic shock with signs of tissue hypoxia developed in all animals with no acute mortality. Cardiac output decreased from a mean (+/- SD) of 6.61+/-1.14 l/min to 2.75+/-0.63 l/min, stroke volume from 79.7+/-9.8 ml to 25.3+/-7.8 ml and left ventricular ejection fraction from 61.2+/-4.3 % to 17.7+/-4.8 % (P

The development of selected cardiovascular parameters in patients with type 2 diabetes mellitus during a spa treatment.

Diabetes mellitus is not just a simple metabolic disorder, however, it is considered to be a cardiovascular disease of a metabolic origin. This is apparent especially when speaking about type 2 diabetes (DM II). The objective of our study was to determine whether a comprehensive spa treatment (procedures and drinking cure) may affect the level of the sympathetic tone of patients suffering from DM II. As an indicator of the sympathetic tone, selected electrocardiographic parameters derived from the heart rate variability and microwave alternans were chosen. There were 96 patients enrolled in our study: 38 patients with poorly controlled DM II and two control groups: 9 patients with compensated DM II and 49 patients, average age without diabetes or other disorders of the glucose metabolism. All received an identical spa treatment and continued their medical therapy. The electrophysiological examination of patients was performed before and after a three-week spa treatment using the KARDiVAR system. Parameters derived from the analysis of heart rate variability (HRV), microvolt T-wave alternans, and microvolt R-wave alternans were analyzed in order to evaluate the tones of the autonomic nervous system (ANS). The control group showed a slight increase of parameter the index of activity of regulatory systems (IRSA) (4.4+/-1.3 vs. 3.8+/-1.4; p=0.006) after the spa treatment, while increased heart rate (80.9+/-11.0 vs. 74.6+/-9.6; p=0.028), reduced index of centralization (IC) (1.3+/-0.6 vs. 2.9+/-1.4; p=0.027) and reduced index of myocardium (IM) (9.9+/-7.4 vs. 18.0+/-6.3; p=0.041) were found in patients with a compensated DM II. Patients with a poorly compensated DM II showed a decreased IM (10.9+/-8.6 vs. 16.9+/-5.2; p=0.001) and also a reduced IRSA (4.1+/-3.5 vs. 6.3+/-1.9; p=0.001). The results proved favorable changes in ANS cardiovascular control of patients with DM II after a spa treatment, especially in terms of reducing the sympathoadrenal system activity (decreased IRSA), improving electrical stability of the myocardium and increasing centrally controlled heart rate variability without overloading the cardiovascular system (drop of IM).

Head-up tilt rapidly compromises hemodynamics in healthy anesthetized swine.

The aims were to explore the effect of head-up tilt (HUT) to 30 and 60 degrees on hemodynamics and tissue oxygenation in anesthetized healthy swine. The data serve as a reference for a study of resuscitation efficacy at HUT such as during transport. Nine healthy swine (49+/-4 kg) were anesthetized and multiple sensors including myocardial pressure-volume loops catheter, carotid flow probe, blood pressure catheters, near infrared spectroscopy (NIRS) tissue oximetry and mixed venous oximetry (SVO2) catheter were introduced and parameters continuously recorded. Experimental protocol consisted of baseline in supine position (15 min), 30 degrees HUT (15 min), recovery at supine position (15 min) and 60 degrees HUT (5 min). Vacuum mattress was used for body fixation during tilts. We found that 30 and 60 degrees inclination led to significant immediate reduction in hemodynamic and oximetry parameters. Mean arterial pressure (mm Hg) decreased from 98 at baseline to 53 and 39, respectively. Carotid blood flow dropped to 47 % and 22 % of baseline values, end diastolic volume to 49 % and 53 % and stroke volume to 47 % and 45 % of baseline. SVO2 and tissue oximetry decreased by 17 and 21 percentage points. The values are means. In conclusions, within minutes, both 30 and 60 degrees head-up tilting is poorly tolerated in anesthetized swine. Significant differences among individual animals exist.

Electrocardiographic changes in diabetes mellitus.

Diabetes mellitus (DM) has been known for many years to be associated with poor cardiovascular prognosis. Due to the sensitive neuropathy, the coronary artery disease in diabetic patients is frequently asymptomatic. Also twelve leads resting ECG can be within normal limits even in an advanced stage of coronary artery disease. Therefore in addition to the standard ECG other electrocardiographic procedures started to be studied in order to find some typical signs of myocardial damages caused by DM. Repeatedly reported results showed in DM patients without cardiovascular complications the tachycardia, shortening of the QRS and QT intervals, increase of the dispersion of QT interval, decreased amplitudes of depolarization waves, shortened activation time of ventricular myocardium and a flattening of T waves confirmed by the lower value of maximum and minimum in repolarization body surface isopotential maps. Most of these changes are even more pronounced in patients with cardiac autonomic neuropathy. Comparison with similar ECG changes in other diseases suggests that the electrocardiographic changes in DM patients are not specific and that they are particularly caused by an increased tone of the sympathetic nervous system what was indirectly confirmed by the heart rate variability findings in these patients.

Are there any differences between stress hormone levels in non-stress conditions and in potentional stress overload (heart catheterisation) in sows?

In order to study a possible effect of mini-invasive heart intervention on a response of hypothalamo-pituitary-adrenal stress axis, we analyzed four stress markers (cortisol, cortisone, DHEA and DHEAS) in 25 sows using minimally invasive heart catheterisation as the stress factor. The marker levels were assessed in four periods of the experiment, (1) the baseline level on the day before intervention, (2) after the introduction of anesthesia, (3) after conducting tissue stimulation or ablation, and (4) after the end of the catheterisation. For statistical analyses we used the non-parametric Friedman test for four dependent samples (including all four stages of the operation) or three dependent samples (influence of operation only, baseline level was excluded). Statistically significant differences in both Friedman tests were found for cortisol and for cortisone. Significant differences for DHEA as well as for DHEAS were found for all tested stages but not for the effect of operation itself. We have concluded that cortisol levels are blunted by the influence of anesthesia after its administration, and therefore decrease back to the baseline at the end of the operation. The other markers (cortisone, DHEA and DHEAS) acted as balanced systems against the injurious stress effect.

Gender differences in electrophysiological characteristics of idiopathic ventricular tachycardia originating from right ventricular outflow tract.

It has become increasingly apparent in recent years that there are important differences of many cardiovascular disorders including ventricular tachycardias in men and women. Nevertheless, so far just few studies have addressed possible gender differences in electrophysiological characteristics of idiopathic ventricular tachycardia from right ventricular outflow tract (RVOT-VT), other than epidemiological ones. This study explored possible gender differences in electrophysiological characteristics and catheter ablation outcome in RVOT-VT patients. Ninety-three patients (mean age 38.7+/-15.5 years, 30 males) with idiopathic RVOT-VT were enrolled and analyzed in our study. Male patients had longer QRS width (99.9+/-19.4 ms vs. 88.4+/-20.7 ms, p=0.02). Female patients had lower right ventricular mean voltage (3.0+/-0.7 mV vs. 3.7+/-0.9 mV, p=0.03), and more low voltage zone over the right ventricular outflow tract free wall (27.0 % vs. 6.7 %, p=0.02). Eighty-one patients passed catheter ablation (23 males). The acute success rate, repeated catheter ablation rate and VT recurrence rate were similar in both genders. The present study provides evidence of the gender differences in electrophysiological findings in patients with idiopathic RVOT-VT. Studies on gender-specific differences in arrhythmia could lead to a better understanding of its mechanism(s) and provide valuable information for the development of optimal treatment strategies.

ECG body surface mapping in patients with gestational diabetes mellitus and optimal metabolic compensation.

Women with gestational diabetes mellitus (GDM) are at increased risk for cardiovascular diseases (CVD) events compared with women without GDM. The aim of the present study was to evaluate 200 parameters of the heart electric field in 35 women with GDM under optimal glycemic compensation compared to 32 healthy pregnant women. All examinations were performed in the 36th week of gestation. The parameters in ECG body surface mapping (BSM) were registered by the diagnostic system Cardiag 112.2. The absolute values of maximum and minimum in depolarization and repolarization isopotential, isointegral and isoarea maps were not significantly different between the groups. These findings correspond to the result of heart rate variability examination. However BSM revealed the significant prolongation of QRS complex (p=0.05), shortening of ventricular myocardial activation time (ICHVAT) (p=0.01), prolongation of mean QT duration (p=0.01) and increase of QT interval dispersion (p=0.01) in women with GDM. Duration of QRS and ICHVAT significantly correlated with interventricular septum and posterior wall thickness in GDM group, QTd interval correlated significantly with HbA1C level. We conclude that despite of optimal metabolic control several significant abnormalities detected by ECG BSM are still present in patients with GDM.