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V Hombach

Publications and source records attributed to V Hombach.

At least 73 records · Page 4Linked to original sources

Ca(2+)-activated K+ channels in human smooth muscle cells of coronary atherosclerotic plaques and coronary media segments.

The behavior of Ca(2+)-activated K+ channels of large conductance (BKCa) in smooth muscle cells, which were obtained from atherosclerotic plaque material (SMCP) and from media segments (SMCM) of human coronary arteries, were compared using the patch-clamp technique. Voltage-clamp protocols in cell-attached patches revealed the characteristic voltage-dependent activation of BKCa in both cell groups. Single-channel conduction as 216.4 +/- 16.7 pS (n = 6) in SMCP and 199.9 +/- 6.7 pS (n = 6) in SMCM in symmetrical 140 mM K+ solutions. Using outside-out patches, external perfusion with 500 microM tetraethylammonium ions caused a typical "flickery block" of the unitary current. The selective BKCa channel inhibitor iberiotoxin (50 nM) effectively blocked BKCa, channel activity. Comparing BKCa open-state probabilities (P0) at +80 mV in cell-attached patches, a highly significant difference between SMCP (P0 = 0.1438 +/- 0.1301; n = 15) and SMCM (P0 = 0.0093 +/- 0.0044; n = 15; Kruskal-Wallis test, p < 0.001) was found. In contrast to this finding, there was no significant difference in the open-state probability of BKCa, between SMCP (P0 = 0.542 +/- 0.0237; n = 9) and SMCM (P0 = 0.0472 +/- 0.0218; n = 10; p = n.s.) using inside-out patches. The results show an interesting difference in the behavior of large conductance Ca(2+)-activated K+ channel in SMCP compared to SMCM with a significantly higher channel activity in human smooth muscle cells obtained from coronary atherosclerotic plaque material. This finding may indicate an important functional role of BKCa channels in the development of atherosclerosis.

Calcium↗

Immunohistochemical colocalization of the terminal complex of human complement and smooth muscle cell alpha-actin in early atherosclerotic lesions.

There is substantial evidence that activated components of the complement cascade are present in atherosclerotic lesions, and it was suggested some years ago that smooth muscle cells may be an important target of complement attack by the terminal components of the cascade, C5b-9, also called the membrane attack complex. Recent in vitro studies have shown that assembly of membrane attack complex on smooth muscle cells leads to the release of monocyte chemotactic protein-1, and, if this were to occur in vivo, then it could be responsible for the recruitment of monocytes into the lesion. In this study we have investigated the localization of C5b-9 in early atherosclerotic lesions of human coronary arteries, collected from autopsies, by immunohistochemical staining, C5b-9 was found to colocalize widely with smooth muscle cell alpha-actin, but not with intact macrophages, thus supporting the hypothesis that interaction of complement with smooth muscle cells may indeed be important in atherogenesis.

Actins↗

Seasonal variations of rheological and hemostatic parameters and acute-phase reactants in young, healthy subjects.

The incidence of cardiovascular diseases is increased in winter months. Recent studies have shown seasonal changes in plasma viscosity, fibrinogen, and factor VII activity with elevated levels during winter. An increase in these factors generates a "hypercoagulable state," which may lead to a rise in cardiovascular morbidity and mortality. It has been suggested that an increase in upper respiratory infections might be the underlying cause for the raised acute-phase reactants, in particular fibrinogen, during the winter season. We investigated seasonal variations of 26 parameters, determining blood rheology and hemostasis in 16 healthy volunteers (8 men and 8 women) aged 20 to 41 years. They were seen at monthly intervals over a period of 1 year. Seasonal variation with peak fitted values in the winter months was found for plasma viscosity (P < .001 for the seasonal difference), red blood cell deformability (P < .001), whole blood viscosity (P < .001), hemoglobin (P < .001), hematocrit (P < .001), mean corpuscular volume (P = .001), platelet count (P = .01), alpha 1-glycoprotein (P < .001), fibrinogen (measured by immunonephelometry; P < .001), plasminogen activator inhibitor-1 (P = .002), LDL cholesterol (P = .003), and triglyceride levels (P < .001). HDL cholesterol (P < .001) and cortisol (P = .001) showed inverse seasonal patterns, with a maximum during summertime. No statistically significant seasonal variations were seen for red blood cell aggregation, complement factor C4, total cholesterol, ceruloplasmin, haptoglobin, white blood cell count, and plasminogen. These data do not support the hypothesis that increased morbidity and mortality from cardiovascular diseases during winter may be mainly attributable to increased synthesis of acute-phase proteins due to infections. The cause for the seasonal variations in rheological and hemostatic parameters remains unclear and should be studied in more detail.

Acute-Phase Proteins↗

Functional upregulation of the vascular endothelial growth factor receptor KDR by hypoxia.

BACKGROUND: Vascular endothelial growth factor (VEGF) is a specific endothelial mitogen and chemoattractant that has been shown to be useful for inducing therapeutic angiogenesis in ischemic myocardium and found to stimulate mitogenicity and chemotaxis of endothelial cells through the receptor tyrosine kinase KDR. Although VEGF expression is upregulated by hypoxic stimuli, regulation of KDR remained unknown under these conditions. METHODS AND RESULTS: With the use of human umbilical vein endothelial cells and transfected porcine aortic endothelial cells, KDR protein was found to be upregulated under hypoxic conditions (2% O2) in both cell types. This process of KDR upregulation was found to be reversible, was maximal after 24 hours of hypoxia, and was regulated on a posttranscriptional level. Furthermore, the susceptibility for VEGF-induced mitogenicity was enhanced under hypoxic conditions as shown by [3H]-thymidine incorporation assay. The activated state of increased VEGF function in hypoxic endothelial cells was associated with elevated tyrosine phosphorylation of KDR as demonstrated by anti-phosphotyrosine blot. CONCLUSIONS: These data indicate that hypoxia stimulates VEGF-dependent signaling not only by upregulation of VEGF ligand but also by functional upregulation of a specific signaling receptor. Therefore, these data provide evidence that the endothelium plays an active role in hypoxia-induced angiogenesis.

Animals↗

Different effects of estrogen and progesterone on experimental atherosclerosis in female versus male rabbits. Quantification of cellular proliferation by bromodeoxyuridine.

BACKGROUND: The aim of the present study was to compare the effect of estrogen and progesterone on the development of experimental atherosclerosis in female versus male rabbits to assess possible sex-specific differences. METHODS AND RESULTS: A total of 32 female and 32 male New Zealand White rabbits were ovariectomized or castrated. In addition to a 0.5% cholesterol diet, the rabbits received estradiol alone (1 mg/kg body wt [BW] per week), progesterone alone (25 mg/kg BW per week), or combined estradiol-progesterone in these dosages during 12 weeks. Ovariectomized female and castrated male rabbits served as control groups without hormone treatment. Before excision of the vessels, bromodeoxyuridine labeling was performed to determine the extent of cellular proliferation in the atherosclerotic lesions. The aortic arch was analyzed immunohistologically and morphometrically. An inhibitory effect of estrogen on intimal plaque size was found in female rabbits compared with the ovariectomized control group (0.7 +/- 0.5 versus 3.7 +/- 2.5 mm2, P < .002; proliferating cells, 3.1 +/- 1.8% versus 8.5 +/- 2.6%, P < .002). In combination with progesterone, however, estrogen was not able to reduce intimal plaque size or cellular proliferation. In contrast, estradiol in castrated male rabbits was not associated with an inhibitory effect on cellular proliferation or intimal thickening compared with controls (estrogen treatment, 7.6 +/- 2.1% proliferating cells and 2.8 +/- 1.0 mm2 neointima; control group, 7.2 +/- 2.1% cellular proliferation and 2.9 +/- 1.2 mm2 intimal thickening). CONCLUSIONS: Our data suggest that the atheroprotective effect of estrogen is probably due to a mechanism that is present in female rabbits only.

17-alpha-Hydroxyprogesterone↗

Suramin is a potent inhibitor of vascular endothelial growth factor. A contribution to the molecular basis of its antiangiogenic action.

Vascular Endothelial Growth Factor (VEGF) is a specific endothelial mitogen and an important angiogenic factor in vivo, capable of inducing therapeutic angiogenesis when administered to ischemic myocardium. Suramin, originally developed as an anti-trypanosomal agent, was recently shown to exert an antiangiogenic action. We have tested the hypothesis, whether the antiangiogenic effect of suramin may be mediated via inhibition of VEGF function. Using cultured endothelial cells and a [3H]thymidine incorporation assay we were able to show, that the action of VEGF upon mitogenicity is inhibited by suramin in a dose-dependent manner. The same was true for inhibition of VEGF-induced chemotaxis of endothelial cells. Suramin inhibited VEGF-inducible tyrosine phosphorylation of KDR as determined by in vitro kinase assay. Moreover, suramin was shown to inhibit VEGF-induced tyrosine phosphorylation of KDR in intact cells, indicating an interaction of suramin with the VEGF-receptor KDR as the cause of its inhibitory activity. The antiangiogenic effect of suramin may be mediated-at least in part-by inhibition of VEGF function. Given the feasibility of in vivo use, suramin may be a valuable tool for investigating the functional role of angiogenesis in the cardiovascular system.

Animals↗

Influence of pulse repetition frequency and high pass filter on color Doppler maps of converging flow in vitro.

Assessment of regurgitant flow by the flow convergence method is based on reading absolute velocities from color Doppler maps. Velocity overestimation by high pass filtering above 100 Hz has been reported. An extremely low filter, however, is impracticable in patients. A ratio of pulse repetition frequency (PRF)/filter of 10/1 usually results in good quality color maps as judged visually. We studied in vitro the influence of RPF and filter on the absolute velocities within color maps of the flow convergence, keeping PRF/filter at 10/1. The color maps were also compared with computerized flow simulations. Flow across different orifice plates was scanned using two different setups for each flow condition: low velocity setup (PRF 600-2500 Hz, filter 50-300 Hz) and high (PRF 1500-6000 Hz, filter 200-600 Hz). From the color maps, velocity profile curves were read along the flow center line across the flow convergence. The high velocity setup provided artefact-free color maps at a distance d = 2-4 through 8-11 mm to the orifice, the low setup at d = 6-8 through 18 mm. Within the overlapping range (d = 6-8 through 8-11 mm), the resulting curves showed no significant differences in local velocity, with a slight trend towards higher velocities with the high velocity setup (2.2-2.9%). The simulations agreed well with color Doppler except for slightly lower values at d > 10-12 mm. Changes in PRF and filter have no significant influence on the absolute velocities displayed within color maps as long as PRF/filter is kept close to 10/1.

Blood Flow Velocity↗

Increased endothelin release by cultured human smooth muscle cells from atherosclerotic coronary arteries.

OBJECTIVES: Endothelin, a 21-amino acid peptide initially purified from the medium of cultured endothelial cells, is a potent vasoconstrictor exerting its effects predominantly in a paracrine or autocrine manner. Recent data indicate that endothelin is also synthesized by cultured vascular smooth muscle cells and that endothelin is an effective stimulator of smooth muscle cell proliferation. This study aimed to investigate the endothelin release of cultured human smooth muscle cells, isolated from coronary plaques and from normal coronary tunica media, and to determine circulating endothelin concentrations in patients with coronary artery disease compared to control subjects. METHODS: Coronary plaque material was extracted by thrombendarterectomy during aorto-coronary bypass grafting (n = 19). Segments of normal coronary arteries were obtained at autopsy (n = 33). Cells were isolated by enzymatic disaggregation and identified as smooth muscle cells with antibodies against smooth muscle alpha-actin. Venous blood samples were drawn from patients with coronary artery disease undergoing cardiac catheterization (n = 32) and from control subjects (n = 38). Endothelin concentrations in culture medium and in plasma samples were measured by radioimmunoassay after Sep Pak C18 extraction. RESULTS: Cultured smooth muscle cells, isolated from coronary plaques, released a significantly (P < 0.001) higher amount of immunoreactive endothelin into the culture medium (39.2 +/- 3.9 pg/10(4) cells, mean +/- s.e.m., 31 supernatant samples) than smooth muscle cells from normal coronary tunica media (3.9 +/- 0.8 pg/10(4) cells, 28 samples). Circulating endothelin concentrations were slightly elevated (P < 0.01) in patients with coronary artery disease (3.8 +/- 0.2 pg/ml) compared to control subjects (3.0 +/- 0.2 pg/ml). CONCLUSIONS: These data suggest that the endothelin production is markedly increased in smooth muscle cells of coronary atherosclerotic plaques. The enhanced endothelin release may stimulate smooth muscle cell proliferation in a paracrine or autocrine manner and thus may contribute to the development or progression of coronary artery disease.

Cells, Cultured↗

Inhibition of the protective effect of estrogen by progesterone in experimental atherosclerosis.

The aim of the present study was to determine the effect of progesterone on the action of estrogen in the development of atherosclerosis. A total of 48 female New Zealand white (NZW) rabbits were ovariectomized. The animals were separated into 6 groups of 8 animals each and received subsequently a 0.5% cholesterol diet for 12 weeks. During this cholesterol feeding period, either estradiol (1 mg/kg body weight (BW)/week), progesterone (25 mg/kg BW/week), or combined estradiol/progesterone (in above dosages) was administered intramuscularly in each group (n = 8 each) of ovariectomized rabbits. One additional group of 8 animals received a combined estrogen/ progesterone regimen, but with progesterone at one third of the above mentioned dosage. In another 8 rabbits, progesterone was reduced to one ninth of the maximum dosage above, whereas estrogen was kept the same, at 1 mg/kg BW/week. Eight ovariectomized animals served as the control group and received no hormone treatment. After 12 weeks, the animals were sacrificed and the proximal aortic arch was removed for further histological examination. An inhibitory effect of estrogen of intimal thickening was found, in comparison to the control group (intimal area: 0.7 +/- 0.5 mm2 vs. 3.7 +/- 2.5 mm2, P < 0.01), whereas progesterone alone did not show a significant effect on intimal plaque size (intimal area: 4.0 +/- 2.3 mm2). In combination with progesterone (high dose), estrogen was not able to reduce intimal atherosclerosis (intimal area: 3.4 +/- 2.4 mm2). However, the beneficial effect of estrogen was not affected by progesterone, when this was reduced respectively to one third (intimal area: 0.8 +/- 0.7 mm2), or to one ninth of the highest dosage (intimal area: 0.6 +/- 0.4 mm2). Interestingly, these differences in atherosclerotic plaque development were observed without significant changes in plasma cholesterol concentrations by the administered hormones. In conclusion, progesterone was dose-dependently able to completely inhibit the beneficial effect of estrogen in experimental atherosclerosis, suggesting that progesterone exerts a direct inhibitory effect on the athero-protective action of estrogen. In the context of recently published data, the present work confirms the importance of the 'non-lipid-mediated', anti-atherosclerotic effect of estrogen, probably due to an interaction with six hormone receptors in vascular smooth muscle cells (VSMC).

Androgens↗

New method for accurate calculation of regurgitant flow rate based on analysis of Doppler color flow maps of the proximal flow field. Validation in a canine model of mitral regurgitation with initial application in patients.

OBJECTIVES: The purpose of this study was to develop a rational and objective method for selecting a region in the proximal flow field where the hemispheric formula for calculating regurgitant flow rates by the flow convergence technique is most accurate. BACKGROUND: A major obstacle to clinical implementation of the proximal flow convergence method is that it assumes hemispheric isovelocity contours throughout the Doppler color flow map, whereas contour shape depends critically on location in the flow field. METHODS: Twenty mitral regurgitant flow rate stages were produced in six dogs by implanting grommet orifices into the anterior mitral leaflet and varying driving pressures so that actual peak flow rate could be determined from the known effective regurgitant orifice times the orifice velocity. Because plotting flow rate calculated by using a hemispheric formula versus alias velocities produces underestimation near the orifice and overestimation far from it, this plot was fitted to a polynomial function to allow identification of an inflection point within a relatively flat intermediate zone, where factors causing overestimation and underestimation are expected to be unimportant or balanced. The accuracy of flow rate calculation by the inflection point was compared with unselective and selective averaging techniques. Clinical relevance, initial feasibility and correlation with an independent measure were tested in 13 consecutive patients with mitral regurgitation who underwent cardiac catheterization. RESULTS: 1) The accuracy of single-point calculations was improved by selecting points in the flat portion of the curve (y = 1.15x - 3.34, r = 0.87, SEE = 22.1 ml/s vs. y = 1.34x - 1.99, r = 0.71, SEE = 45.6 ml/s, p < 0.01). 2) Selective averaging of points in the flat portion of the curve further improved accuracy and decreased scatter compared with unselective averaging (y = 1.08x + 4.8, r = 0.96, SEE = 11.6 ml/s vs. y = 1.30x + 0.6, r = 0.90, SEE = 20.9 ml/s, p < 0.01). 3) The proposed algorithm for mathematically identifying the inflection point provided the best results (y = 0.96x + 4.5, r = 0.96, SEE = 9.9 ml/s), with a mean error of 1.6 +/- 9.7 ml/s vs. 11.4 +/- 11.7 ml/s for selective averaging (p < 0.01). In patients, the proposed algorithm identified an inflection point at which calculated regurgitant volume agreed best with invasive measurements (y = 1.1x - 0.61, r = 0.93, SEE = 17 ml). CONCLUSIONS: The accuracy of the proximal flow convergence method can be significantly improved by analyzing the flow field mathematically to identify the optimal isovelocity zone before using the hemispheric formula to calculate regurgitant flow rates. Because the proposed algorithm is objective, operator independent and, thus, suitable for automatization, it could provide the clinician with a powerful quantitative tool to assess valvular regurgitation.

Adult↗

QRS morphologies of the surface ECG of nonsustained ventricular tachycardias during holter monitoring compared with QRS morphologies of spontaneous sustained ventricular tachycardias.

The purpose of this study was to compare electrocardiographic (ECG) morphologies of nonsustained ventricular tachycardias (VTs) during Holter monitoring with the ECG morphology of documented, sustained, monomorphic VTs during the spontaneous event of tachycardia in 14 patients (9 with coronary artery disease), in whom a sustained, spontaneous monomorphic VT had been documented in a 12-lead ECG. All patients had a 24-hour Holter ECG without antiarrhythmic medication. Channel 1 of the Holter ECG was compared with leads V1, V2, and V3, and channel 2 with leads V4, V5, and V6. The Holter ECG of 10 patients in whom the QRS complex during sinus rhythm was similar to the QRS complex in the corresponding ECG leads was accepted for analysis. In 8 of the 10 patients, nonsustained VTs were detected during Holter monitoring. In one of these eight, the ECG morphology of at least one nonsustained VT in the Holter recordings was identical with the sustained VTs. Thus, incidences and ECG morphologies of nonsustained VTs during Holter monitoring do not correlate closely with those of spontaneous sustained monomorphic VTs. Therefore, most ventricular runs during Holter monitoring may have a mechanism different from that of spontaneous sustained VTs.

Adult↗

Influence of the mechanism of regurgitation on the quantification of mitral regurgitation by the proximal flow convergence method and the jet area method.

In 84 patients mitral regurgitation was quantified by angiography. The mechanism of regurgitation was determined by echocardiography (organic, n = 54, functional, n = 30). The radii of the proximal isovelocity surface areas in the flow convergence region for 28 and 41 cm.s-1 blood flow velocity and the area and length of the regurgitant jet were measured using colour flow Doppler imaging. The radii of the proximal isovelocity surface areas correlated more closely with the angiographic grade than the jet parameters irrespective of the mechanism of regurgitation. In more than 90% of the patients, grades I-II mitral regurgitation were correctly differentiated from grades III-IV by means of the radii of the proximal isovelocity surface areas. Using the jet parameters, the differentiation was correct in 50-90% of the patients depending on the mechanism of regurgitation. The jet area method particularly failed to identify grades III-IV organic mitral regurgitation due to a high prevalence of eccentric jets in these patients. It is concluded that the proximal flow convergence method was suitable for the quantification of mitral regurgitation irrespective of the mechanism of mitral regurgitation. On the other hand, the value of the jet area method depended largely on the regurgitation mechanism.

Adult↗

Reproducibility of left ventricular volume measurements at rest and during bicycle exercise in patients with congestive heart failure: a combined radionuclide and haemodynamic study.

A series of 14 patients with heart failure due to coronary artery disease and impaired left ventricular function underwent radionuclide ventriculography with simultaneous thermodilution measurement of cardiac output by pulmonary artery catheter on two occasions (m1, m2) separated by 6 weeks in order to determine the reproducibility of haemodynamic and left ventricular volume measurements at rest and during supine bicycle exercise. The patients were in NYHA grade II or III and had baseline left ventricular ejection fractions below 40%. Derived haemodynamic variables were calculated from the thermodilution cardiac output and from the radionuclide ejection fraction as follows: stroke volume = thermodilution cardiac output/heart rate; left ventricular end-diastolic volume = stroke volume/ejection fraction; left ventricular end-systolic volume = end-diastolic volume - stroke volume. The percentage difference (PD) between each pair of data (m1, m2) was calculated using the following formula: PD = 100% x (m2-m1)/m1. The data showed that reproducible measurements of left ventricular volume can be obtained at rest and during exercise. The mean (+/- S.D.) PD values for end-systolic volume and end-diastolic volume at rest were - 0.1 +/- 17% and - 0.2 +/- 13%, respectively. The mean PD values for end-systolic volume and end-diastolic volume during exercise were - 0.3 +/- 19% and - 0.7 +/- 15%, respectively. By contrast, the reproducibility of the pulmonary capillary wedge pressure measurements was poor, as reflected by a PD value of 14 +/- 51% for exercise pulmonary capillary pressure. Combining radionuclide ventriculography and the thermodilution measurement of cardiac output is useful for measuring left ventricular volume at rest and during exercise in patients with heart failure. This minimally invasive technique allows for a comprehensive assessment of left ventricular performance and appears to be particularly suited for assessing the effects of therapeutic interventions aimed at minimizing the progressive left ventricular enlargement in heart failure.

Adult↗

[Color Doppler echocardiography of the flow convergence region in vitro: effect of the orifice shape on proximal velocity profile].

The flow convergence method serves to determine flow across orifices (like valve leaks) by color Doppler. Both the PISA method (proximal isovelocity surface areas) and the PVP method (proximal velocity profile) were developed in vitro at circular orifice plates. Therefore, we studied the influence of a non-circular orifice shape on the color map of the flow convergence. Steady flow across orifices of the following shapes was imaged by color Doppler: Oval (6 x 2 mm), slit (12 x 1.5 mm), three-star (diameter 100, area 30 mm2), circular twin-orifice (two circular orifices diameter 2 mm at 10 mm distance from each other) and oval twin-orifice (two ovals 6 x 2 mm at 10 mm distance). As reference we imaged circular orifices with a similar opening area. The alias method was used to locate discrete velocities within the color map, and the proximal velocity profile along the flow center line was analyzed (mean of 24 subsequent images). The local velocity was plotted (y-axis) against its distance to the orifice (x-axis) providing proximal velocity profile curves. The more the orifice shape differed from circular, the more the proximal velocity profile was shifted downward: The profile proximal to the oval was not different from the reference profile proximal to the circular orifice. The profile proximal to the slit was considerably slowed, and proximal to the three-star was even slightly slower (local velocity -12 %, -23 % and -29 % at 14, 8 and 5 mm distance to the orifice). If the circular reference orifice corresponded to total flow across the twin-orifice, the proximal velocity profile of the latter was also shifted markedly downward (-20 %, -18 % and -23 % at 14, 8 and 5 mm distance to the circular twin-orifice). However, if the reference profile corresponded to flow across only one opening of the twin-orifice, the proximal velocity profile of the latter was shifted considerably upwards (+60 %, +71 % and +50 % at 14, 8, and 5 mm distance). Deviation of the orifice shape from circular leads to lower local velocities within the flow convergence; thus neglecting this orifice shape would result in underestimation of flow by the flow convergence method. However, presence of parallel neighboring flow increases the local velocities; neglecting this effect would lead to corresponding overestimation of flow.

Blood Flow Velocity↗

[Microbiological studies of a nasal positive pressure respirator with and without a humidifier system].

13 patients with obstructive sleep apnea syndrome treated with CPAP-therapy and complicating affections of the nasal and pharyngeal mucosa were enrolled in a randomized cross-over study comparing therapy with a heated humidifier (HC 100, company Fisher & Paykel) and treatment with a heat and moisture exchanger (Typ I, company Dahlhausen). We assessed the bacterial and fungal colonisation of the nasal masks of all patients. Samples of mask rinses were taken after the two treatment periods (2 weeks each) and the period without humidification in between. All microbes were found to have pathological potency. There was no significant difference in the total concentration of the microbes in the different treatment modalities. In a few cases however, gram negative bacteria were detected on the masks during humidification with a heated humidifier, but not with heat and moisture exchangers. Legionella spec. were not detectable in any of the samples. Candida albicans was the only fungus detectable. No patient had any infection of the upper or lower respiratory system associated with humidification therapy.

Adult↗

[Unmasking an exclusively retrograde accessory pathway by catecholamines].

A 52-year-old man with frequent episodes of narrow QRS complex tachycardias with rates of 150/min was admitted for electrophysiological evaluation and treatment. P waves could be seen in the ST-segment of the surface ECG during tachycardia. Atrial stimulation during electrophysiological testing was not able to induce tachycardia. During atrial stimulation, there was no evidence of conduction via an accessory pathway or of dual AV node conduction properties. Ventricular stimulation showed complete ventriculoatrial block. After intravenous administration of the catecholamine orciprenaline, single atrial extrastimuli induced an AV macro-reentrant tachycardia with a rate of 165/min. VA conduction showed the earliest retrograde atrial activation in the left anterolateral area. Thus, there was an accessory pathway which only conducted in ventriculoatrial direction and only during adrenergic stimulation. After successful radiofrequency catheter ablation, complete ventriculoatrial block was recorded even after repeat administration of orciprenaline during ventricular stimulation. This case confirms the need to administer catecholamines in every undiagnosed tachycardia during electrophysiological testing to reveal the mechanism of the tachycardia.

Adrenergic beta-Agonists↗