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Biomedical subjects

S Dhein

Publications and source records attributed to S Dhein.

At least 19 recordsLinked to original sources
PubMed1996

Fosinopril improves regulation of vascular tone in mesenteric bed of diabetic rats.

Because diabetes mellitus leads to vascular dysfunction, we examined the microvascular endothelial and smooth muscle function in long-term diabetes and a possible influence of fosinopril treatment (10 mg/kg). We investigated isolated perfused mesenteric beds of diabetic rats (4 groups: control, control + fosinopril, diabetes, diabetes + fosinopril; diabetes of 6-month duration, induced by streptozotocin, STC) were investigated using computer-assisted microvideoangiometry. Vascular diameter of four different vascular regions [classified as conductive (G1, 303 +/- 6.5 mu m and G2, 239 +/- 6.3 mu m) and resistance (G3, 192 +/- 4.5 mu m and G4, 124 +/- 2.6 mu m) vessel generations; resting conditions, control group] were increased in diabetes by approximately 20%. However, the endothelium-dependent relaxation in response to 1 mu M acetylcholine (ACh) was reduced from 38-44% to 20-25% (diabetes mellitus) with maximal impairment in G4 vessels. This could be significantly antagonized by fosinopril treatment. Similarly, vasodilation in response to 1 mu M glyceroltrinitrate (GTN) was reduced from 50-58 to 20-30%, but was partially prevented by fosinopril (32-38%), whereas potassium chloride (KCl)-induced vasoconstriction did not show differences between the groups. Inhibition of nitric oxide (NO) synthesis by 3 mu M L-NG-nitro arginine (L-NNA) resulted in a slight vasoconstriction of all vessels (12-25%), with maximum response in G3/G4. This was not altered by disease or treatment. We conclude that (a) long-term diabetes leads to endothelial and smooth muscle dysfunction with reduced capability of vasodilation and either an impairment of NO release or a reduced smooth muscle responsiveness to and (b) a predominant impairment of NO-dependent regulation in small resistance vessels, and (c) that fosinopril treatment can at least partially prevent this vascular dysfunction.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

Electrocardiological profile and proarrhythmic effects of quinidine, verapamil and their combination: a mapping study.

Quinidine and verapamil are widely used as antiarrhythmic agents and their combination is often used in the treatment of supraventricular tachycardia. This study was undertaken to clarify, whether these drugs exert proarrhythmic effects on the ventricles in therapeutic concentrations and whether possible arrhythmogenic effects might be enhanced by combination. Isolated rabbit hearts perfused according to the Langendorff technique were treated with increasing concentrations of quinidine (0.05 to 3.5 microM) or verapamil (5 to 50 nM) or of their combination (70:1 or 10:1, quinidine:verapamil) corresponding to common low, medium and high free therapeutic concentrations. The epicardial activation process was measured using a computer assisted mapping system for unipolar multichannel recording (256 channels simultaneously). Both substances prolonged the atrioventricular conduction time PQ. This effect was even more pronounced if the 70:1 combination was administered. The activation pattern was altered by both drugs and their combination to the same extent as became obvious from analysis of local activation vectors and of localisation of breakthroughpoints of epicardial activation for heart beats under control conditions and under drug treatment. The epicardial potential durations were prolonged by quinidine and to the same degree by the combinations, but not by verapamil alone. The total activation time was prolonged under the influence of quinidine and if the 70:1 combination was given. Both substances exerted a negative inotropic effect which was enhanced in an additive manner if both drugs were combined. In parallel the coronary flow was diminished.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Actions of 1,4-dihydropyridines in isolated mesenteric vascular beds.

Recent studies indicate that the vasorelaxation induced by nitrendipine may be mediated partially by increased release of nitric oxide (NO). To study this effect in more detail and to examine the vasodilating effect of other 1,4-dihydropyridines (1,4-DHP) with regard to a possible involvement of NO, we investigated the effects of nitrendipine, nifedipine, nisoldipine, and nimodipine on isolated mesenteric vascular bed an the influence of L-NG-nitroarginine (L-NNA) on 1,4-DHP-induced vasorelaxation. Perfusion with these 1,4-DHP resulted in a concentration-dependent increase in global flow and vascular diameter in all vessel branches. Nifedipine exhibited a more pronounced effect on G4 vessels, whereas the actions of the other 1,4-DHP on the investigated vascular tree were more homogeneous. The dilating and flow increasing effects of nitrendipine and nifedipine could be significantly antagonized by treatment with LNNA. The vasodilating effects of nisoldipine and nimodipine could also be antagonized with L-NNA. We conclude that NO release plays an additional role in the relaxation of small resistance vessels by 1,4-DHP.

Animals↗
PubMed1995

The contribution of neutrophils to reperfusion arrhythmias and a possible role for antiadhesive pharmacological substances.

OBJECTIVES: It is known that neutrophilic leukocytes contribute to cellular damage in the course of cardiac ischemia/reperfusion. A role in arrhythmogenesis, although controversial, has been ascribed in some studies to the leukocytes, but investigations evaluating possible beneficial effects of inhibitors of neutrophil adhesion or transmigration are still missing. METHODS: Isolated spontaneously beating rabbit hearts, perfused with saline solution at constant pressure according to the Langendorff technique, were treated with 15 min infusion of autologous neutrophils. 10 min after the start of this infusion the hearts were submitted to coronary occlusion (LAD) for 30 min followed by 30 min reperfusion. Four experimental groups were investigated: (1) saline-perfused control hearts, (2) leukocyte-perfused hearts, (3) leukocyte-perfused hearts treated with RGDS peptide, (4) leukocyte-perfused hearts treated with chondroitin sulfate C. In all experiments epicardial potential mapping was carried out (256 unipolar leads). At the end of each experiment the hearts were prepared for histology and after staining leukocyte accumulation in the ischemic zone, in the border zone and in the non-ischemic area was evaluated. RESULTS: In leukocyte-perfused hearts submitted to ischemia/reperfusion we found a somewhat enhanced arrhythmogenesis, enhanced ST-segment deviation, and a 2-3-fold increase in leukocyte accumulation in the ischemic and border zone as compared to the non-ischemic tissue as well as increased dispersion of epicardial potential duration especially during reperfusion. These changes and the leukocyte accumulation could be suppressed by treatment with RGDS and to a somewhat lesser extent with chondroitin sulfate C. In addition, arrhythmogenesis could be reduced but not completely suppressed by that treatment. CONCLUSIONS: From these results we conclude that: (a) leukocytes exert an aggravating effect in arrhythmogenesis during ischemia/reperfusion, (b) the arrhythmogenic substrate for this effect may consist of an enhanced dispersion of potential duration and (c) that inhibition of leukocyte accumulation can at least partially reduce arrhythmogenesis and may be of therapeutic interest as an additional treatment.

Animals↗
PubMed1994

Frequency-dependent effects of propafenone decrease with duration of ventricular tachycardia in isolated guinea pig hearts.

Na+ channel blockers terminate tachyarrhythmias primarily by rate-dependent effects. The purpose of this study was to investigate the use-dependent effects of propafenone in isolated guinea pig and rabbit hearts perfused by the method of Langendorff. In the presence of propafenone (0.3 microM) during ventricular pacing, an abrupt decrease of the pacing cycle length (220 ms to 120 ms) slowed the intraventricular conduction with a transient peak QRS prolongation of 33.8 +/- 2.0% after 5.7 +/- 0.5 s (P < 0.01) which subsequently decreased to a steady state of 14.0 +/- 2.5% after 38.0 +/- 5.5 s (mean +/- S.E.M.; n = 10; P < 0.01). The ventricular effective refractory period was significantly prolonged if evaluated by a train of 10 basic stimuli (S1) (interstimulus interval: 120 ms) followed by a premature stimulus (S2). However, when the train of basic stimuli was increased the effective refractory period diminished progressively. An initial increase in total activation time vanished with continued rapid ventricular stimulation. These effects may be explained by a shortening of the action potential during high rates resulting in a decreased binding of propafenone to Na+ channels.

Action Potentials↗
PubMed1994

A new synthetic antiarrhythmic peptide reduces dispersion of epicardial activation recovery interval and diminishes alterations of epicardial activation patterns induced by regional ischemia. A mapping study.

Common antiarrhythmic agents affect ionic membrane channels and thereby alter cellular electrical activity. Since this accounts for the proarrhythmic effects as well we tried to find new substances with different profiles of actions. A new antiarrhythmic peptide, H2N-Gly-Ala-Gly-4 Hyp-Pro-Tyr-CONH2 (AAP 10), was synthetized using the Fmoc-strategy. This peptide was analyzed for its electrophysiological profile of action in normal isolated rabbit hearts perfused according to the Langendorff technique either under control conditions or after induction of a regional ischemia. For this purpose 256 channel epicardial mapping was employed allowing the determination of the timepoints of activation at each electrode thus identifying the origins of epicardial activation (socalled breakthrough-points, BTP). Epicardial spread of activation was then described mathematically by activation vectors which gave direction and velocity of the epicardial activation wave at each electrode. Single heart beats were analyzed under control conditions and under treatment with AAP 10 or under regional ischemia with or without AAP 10-pretreatment (10(-8) mol/l). We calculated the percentage of similar vectors (VEC) with unaltered direction (deviation < or = 5 degrees) and the percentage of identical breakthroughpoints (deviation < or = 1 mm) compared to control conditions. In addition, apparent epicardial velocities, total activation time of a given region and activation-recovery interval (ARI) as well as dispersion of ARI (i.e. standard deviation of ARI) and distribution of ARI were analyzed. Under control conditions treatment with AAP 10 (10(-10) to 3 x 10(-7) mol/l) led to a significant decrease in ARI-dispersion without alteration of any of the other parameters under investigation. Left ventricular regional ischemia resulted in a marked alteration of the activation patterns (a significant decrease in vectorfield- and breakthroughpoint-similarity) which could be significantly inhibited by pretreatment with AAP 10. In addition, we found that AAP 10 depressed the increase in ARI-dispersion during the first minutes of ischemia and accelerated normalization of ARI-dispersion during reperfusion. In additional experiments, it could be shown that AAP 10 did not alter action potential duration, maximum dU/dt, amplitude or resting membrane potential of isolated guinea pig muscles using a common intracellular action potential recording technique.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Cryopreservation of veins as an alternative to autografts in coronary by-pass grafting.

Cryopreserved venous segments could be used as allografts in coronary by-pass surgery in patients with limited availability of venous or arterial conduits for autologous grafting. After primarily disappointing clinical results it was the aim of these experiments to improve freezing procedure and incubation media in order to maintain most of the functional integrity of the biological material after cryopreservation, and thus to contribute to the essential prerequisites for a successful implantation. Freshly prepared segments of human saphenous vein were cryopreserved: 1) using various computer-assisted freezing programs with definite cooling rates and seeding temperatures; 2) after incubation in media consisting of RPMI 1640 and cryoprotective agents in different combinations and concentrations. The veins were stored at -196 degrees C, thawed quickly and analyzed in an in vitro perfusion system. The degree of vitality of the vein segments was assessed by measuring vasoconstriction after application of Norepinephrine and Serotonine and vasodilatation following release of endothelium-derived relaxing factor (EDRF) after perfusion with Acetylcholine. Our results show that the preservation of vascular smooth muscle can be maintained only by: 1) equilibrating the vein in RPMI 1640 with 2.2 M Glycerol and 1.6 M Ethylene-Glycol and 2) preventing an increase of temperature during the crystallization in the cooling process. The results clearly demonstrate the maintainance of vitality in vein segments after an appropriate freezing and equilibration process with specific cryoprotective agents. The data obtained in the study could serve as the basis for a better longterm prognosis of transplanted cryopreserved venous allografts.

Acetylcholine↗
PubMed1993

Propranolol unmasks class III like electrophysiological properties of norepinephrine.

Isolated perfused spontaneously beating rabbit hearts were treated with increasing concentrations of norepinephrine (0.01, 0.1, 0.5 mumol/l) either alone or in presence of propranolol (0.1 mumol/l). For analysis of the epicardial activation and repolarization process and epicardial mapping (256 unipolar leads) was performed. For each electrode the activation and repolarization time was determined. From these data the "breakthrough-points" (BTP) of epicardial activation were determined. At each electrode an activation vector (VEC) was calculated giving direction and velocity of the local excitation wave. The beat similarity of various heart beats (under NE) compared to control was evaluated by determination of the percentage of identical BTP and of similar VEC (deviation < or = 5 degrees). Moreover at each electrode the local activation recovery interval (ARI) and its standard deviation (of 256 leads, dispersion, DISP) were determined. Norepinephrine alone (0.01, 0.1, 0.5 mumol/l) led to an increase in left ventricular pressure, heart rate and DISP with concomitant frequency dependent reduction in ARI, and to changes in the epicardial activation pattern (reduction in BTP, VEC). We found that in the presence of propranolol (0.1 mumol/l) norepinephrine prolonged ARI and reduced ARI-dispersion. This effect was not due to changes in heart rate. The disturbing effects on the activation pattern were diminished. These effects could be prevented by pretreatment with 1 mumol/l prazosin. From these results we conclude, that norepinephrine prolongs the relative action potential duration via stimulation of alpha 1-adrenoceptor and enhances cellular coupling.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1993

Beneficial effect of amrinone on the size of acute regional ischemia in isolated rabbit hearts.

The effect of inotropes on myocardial ischemia is difficult to predict because they may influence the determinants of myocardial O2 demand and O2 supply differently. Several PDE-inhibitors have been reported to possess antiischemic properties related to their hemodynamic and O2-sparing effects. To assess whether PDE-inhibitors also possess direct cardioprotective properties, the effects of amrinone (2.5 x 10(-5) mol/L) in comparison to isoproterenol (5 x 10(-9) mol/L) and ouabain (1.5 x 10(-7) mol/L) were studied in isolated rabbit hearts perfused according to Langendorff at a constant pressure (70 cmH2O) and electrically driven at a constant pacing rate. Regional ischemia was induced by coronary artery ligation and quantified by epicardial NADH fluorescence. All substances significantly increased the actively developed left ventricular pressure to a similar extent (+20%) (P < 0.05). Coronary flow was significantly decreased by ouabain (-15%) and significantly increased by isoproterenol (+25%) and particularly by amrinone (+50%) (P < 0.05). Neither ouabain nor isoproterenol significantly changed the intensity or the distribution pattern of NADH fluorescence, whereas the size of the ischemic zone was significantly reduced by amrinone (-25%) (P < 0.05). The PDE-inhibitor amrinone was shown to possess a direct cardioprotective effect by improving myocardial perfusion and O2 supply in isolated rabbit hearts.

Amrinone↗
PubMed1993

Comparative study on the proarrhythmic effects of some antiarrhythmic agents.

BACKGROUND: A main side effect of antiarrhythmic drug therapy is the tendency of these drugs to promote arrhythmia within the therapeutic concentration range, i.e., the proarrhythmic activity of these drugs. However, a model for in vitro assessment, quantification, and comparison of proarrhythmic drug activities was still lacking, and only sparse data were available. METHODS AND RESULTS: To analyze the arrhythmogenic risk of common antiarrhythmic drugs in a quantitative and comparative manner, isolated perfused rabbit hearts were treated with increasing concentrations of antiarrhythmic drugs corresponding to low, medium, and high therapeutic concentrations. For analysis of the epicardial activation process, an epicardial mapping (256 unipolar leads) was performed. For each electrode, the activation time was determined. From these data, the origins of epicardial activation ("breakthrough points" [BTP]) were determined. At each electrode, an activation vector (VEC) was calculated giving direction and velocity of the local excitation wave. The beat similarity of various heartbeats (under treatment) compared with control was evaluated by determination of the percentage of identical BTPs (deviation < or = 1 mm) and of similar VECs (deviation < or = 5 degrees). BTP and VEC were reduced by all antiarrhythmic agents tested (propafenone = flecainide > quinidine > ajmaline > procainamide > disopyramide > mexiletine = lidocaine > sotalol), indicating a more or less pronounced disturbance of the epicardial activation process. Treatment with propafenone, quinidine, and disopyramide and to a lesser extent sotalol prolonged the activation-recovery interval (ARI). ARI dispersion was greatly enhanced by flecainide and was reduced by sotalol. In addition, it could be shown that propranolol is able to reduce the proarrhythmic action of flecainide. This effect seemed to be due to a reduction of the flecainide-induced increase in ARI dispersion. CONCLUSIONS: From the results of our study, we propose the following rank order of the arrhythmogenic risk: flecainide > propafenone > quinidine > ajmaline > disopyramide > procainamide > mexiletine, lidocaine > sotalol. Moreover, we conclude that propranolol given additionally may be helpful in reducing the proarrhythmic risk of flecainide.

Animals↗
PubMed1992

Celiprolol exerts microvascular dilatation by activation of beta 2-adrenoceptors.

In order to clarify the question whether the beta 1-selective adrenoceptor antagonist celiprolol possesses vasodilating properties, isolated vascular networks were perfused with increasing concentrations of celiprolol (in a cumulative manner) ranging from 10(-8) to 10(-4) mol/l. The study was carried out using the isolated mesenteric vascular bed of the guinea pig mesenterium coli. Vascular diameters of four different vascular regions [vessels classified as G1 (585 +/- 30 microns), G2 (403 +/- 25 microns), G3 (282 +/- 27 microns) and G4 (197 +/- 13 microns)] were assessed by means of microscopic videoangiometry. Perfusion with celiprolol resulted in concentration dependent vasodilation which was more pronounced in G3 and G4 vessels. In addition, cumulative concentration-response curves were determined from responses obtained in the presence of 10(-8), 10(-7), 10(-6) and 10(-4) mol/l ICI 118,551 (a highly selective adrenoceptor antagonist). In the presence of ICI 118,551 at concentrations greater than or equal to 10(-6) mol/l, no celiprolol response could be observed. Lower concentrations of ICI 118,551 shifted the celiprolol concentration-response curve to the right in a concentration-dependent manner. Therefore, it is concluded (a) that celiprolol has a vasodilating effect, (b) that this vasodilation is produced by stimulation of beta 2-adrenoceptors and (c) that the vasodilating effect is more pronounced in smaller than in larger vessels (G3, G4 vs G1, G2).

Adrenergic beta-Antagonists↗
PubMed1991

Endothelial function and contractility of human vena saphena magna prepared for aortocoronary bypass grafting.

The aim of this study was to examine whether contractility and endothelial function of the human saphenous vein prepared for aortocoronary bypass grafting are altered by the surgical technique, e.g. cannulation and gentle distension of the vessel. Two segments (2 cm length each) of native vena saphena magna and 2 segments (2 cm length each) of the same vessel prepared for coronary bypass grafting were taken for further experimentation. After ligation of all side branches the segments were cannulated and arranged in two systems (with two segments each) in a serial manner (system I: prepared vessel followed by a native segment; system II: native vessel followed by a prepared segment) and perfused with Tyrode's solution at a constant flow rate of 20 ml/min (PO2 = 45 mmHg). Pressure gradient was measured continuously over each segment as a function of the vessel's radius according to the Hagen-Poiseuille equation. Endothelial and smooth muscle function was checked by perfusion with increasing concentrations of acetylcholine (ACH) to provoke the release of endothelium-derived relaxing factor (EDRF) (ACH; 0.3, 1, 3, 10, 30 mumol/L) after precontraction of the vessels with 1 mumol/L norepinephrine (NE). This showed normal contractility and ACH-induced relaxation in the native vessels but a reduced contractile response and a total lack of ACH-EDRF-induced relaxation in the prepared vessels. Perfusion with 5-hydroxytrytamine (5-HT) (0.25, 0.5, 1, 10 mumol/L for 10 min each concentration) resulted in marked constriction of all vessels with preserved contractility which could be completely prevented by pretreatment with the 5-HT2-receptor antagonist ketanserine (20 mumol/L).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1990

Nifedipine antagonizes ouabain-induced ST-segment changes and derangement of epicardial activation pattern in isolated rabbit hearts.

Isolated rabbit hearts, perfused according to the Langendorff technique were treated with 0.2 mumol/l ouabain or with a combination of 0.2 mumol/l ouabain and 3 nmol/l nifedipine. In a second series of experiments, a combination of 0.2 mumol/l ouabain with 0.2 mumol/l nitroglycerin was examined. Under this treatment, coronary flow and left ventricular pressure were continuously measured and, furthermore, the epicardial potential distribution was mapped with high temporal (4 kHz/channel) and spatial resolution (256 electrodes, arranged in 4 plates with 64 electrodes each, 8 x 8 matrix with 1 mm mesh size). Ouabain led to the expected positive inotropy of 10%, but also to a decrease in coronary flow of 15%. Besides these changes a nearly generalized ST-segment elevation could be observed. Moreover, the epicardial activation pattern was disturbed by changes in the location of epicardial breakthrough-points. Concomitantly, the epicardial activation vector field was deranged. Under the additional influence of nifedipine, coronary flow was reduced by only 5%, whereas the positive inotropic effect remained unchanged. The epicardial ST-elevation was diminished significantly and there was no derangement in the process of epicardial activation. Nitroglycerin led to an increase in relative coronary flow comparable to that observed under nifedipine but did not antagonize the disturbances of the process of activation by ouabain and only partially inhibited ST-elevation. Hence, it is concluded that ouabain already provokes coronary vasoconstriction in therapeutic concentrations leading to ST-elevation and prearrhythmic changes in the process of excitation. These changes could be diminished by additional treatment with nifedipine, but not with nitroglycerin.

Animals↗
PubMed1989

The potential of epicardial activation mapping in isolated hearts for the assessment of arrhythmogenic and antiarrhythmic drug activity.

In isolated rabbit hearts perfused according to the Langendorff technique, the pathway and time course of the epicardial activation process were studied by means of computer-assisted epicardial potential mapping, using a matrix of 256 unipolar AgCl electrodes (1 mm spatial and 0.25 msec temporal resolution). Activation time of each electrode was calculated (point of time of fastest negative intrinsic deflection). From the activation times of the surrounding electrodes, the direction and velocity of activation for each electrode were calculated, thereby allowing construction of an epicardial vector field. Furthermore, breakthrough points (BTPs) were determined as the earliest activated electrodes in a given region. Vector-field orientation and BTP localization were compared under different conditions during perfusion with Tyrode's solution or during drug treatment. Thereby, we determined the similarity of the vector fields (two vectors were considered to be identical if not differing by more than 5 degrees) and the percentage of BTPs with changed localization, referred to the total number of BTPs. For verification of the method we treated the hearts with ouabain (0.2 mumol/l) and observed progressive decline in vector-field similarity from 32% down to 14%, resulting in arrhythmia. Concomitantly, the percentage of BTPs with identical localization decreased from 81% to 50%. These changes could be reversed by additive treatment with 10 nmol/1 verapamil. From these results we conclude that arrhythmia is preceded by a state of deteriorated epicardial activation pattern (prearrhythmia), which can be quantitatively evaluated and used for detection of preventive antiarrhythmic drug action.

Animals↗
PubMed1989

A new endothelium-dependent vasoconstricting factor (EDCF) in pig coronary artery.

In order to investigate the influence of the endothelium on hypoxia-induced vasospasms we examined vascular tone after reduction of the oxygen supply, dependent on endothelial function. Therefore, after ligation of all side branches, vessel segments of porcine or human right coronary arteries or of rabbit abdominal aorta, prepared either with or without endothelium, were cannulated, perfused with Tyrode's solution and arranged in a serial manner (system I: endothelium-denuded vessel followed by a normal segment; system II: normal vessel followed by an endothelium-denuded segment). The pressure gradient over each segment was continuously measured as a function of vessel radius. After 2 h equilibration the oxygen concentration in the perfusion and superfusion solutions was lowered (reduction from 'control' = 95% O2/5% CO2 to 'hypoxia' = 95% N2/5% CO2) leading to a marked long-lasting vasoconstriction in those endothelium-denuded vessel segments which were mounted distal to a normal vessel with an intact endothelium, whereas the other vessels did not change their tone. This hypoxic contraction could be inhibited by pretreatment with either 1 mumol l-1 dexamethasone or quinacrine or indomethacine. From these results it is concluded that endothelium releases a vasoconstricting factor (EDCF) under hypoxic conditions probably dependent on phospholipase A2 and cyclooxygenase. This EDCF may be of pathophysiological importance by inducing or aggravating hypoxic vasospasms.

Animals↗
PubMed1988

A new method for analysing the geometry and timecourse of epicardial potential spreading.

A 256 unipolar electrode matrix fixed at the surface of an isolated rabbit heart was connected to a PC system via an amplifying and analog/digital converting frontend computer. This system allows measurement of 256 electrodes within 100 microseconds with a sampling rate of 0.25 ms. The data are displayed on a PC system either on-line as common ECG-recordings or off-line in projection on a two-dimensional model of the heart surface. Thereby, it is possible to visualize the epicardial potential spreading in a slow-motion presentation on a high resolution computer graphic. The samples are displayed sequentially and can be delayed by choice. This method allows the determination of the origin ("break-through-points") of the epicardial excitation and an analysis of the potential spreading. The electrodes are arranged in four grids with 64 electrodes each at an interelectrode distance of 1 mm. Thereby, it is possible to evaluate the direction of the epicardial excitation wave and the local state of epicardial activation. Furthermore, it is possible to demonstrate irregular pacemakers or re-entry circuits. The method seems to be helpful in analysis of cardiac arrhythmogenesis and mode of action of anti-arrhythmic agents.

Analog-Digital Conversion↗