[Electrophysiological effects of disopyramide on the specialized cardiac conduction system in man (author's transl)].
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Biomedical subjects
Publications and source records attributed to V Hombach.
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Theoretically there should be two possibilities of recording His-Bundle potentials from the body surface. Extensive amplifying and signal averaging can improve the signal to noise ratio of the His-Bundle potential. Random noise can be filtered and the periodic signal of the His bundle can be selected. On the other hand improvement of the noninvasive leading conditions could be achieved by positioning of the recording electrodes close to the structure to be investigated and by direction of the surface leading according to the anatomical axis of the bundle of His. For this purpose these new oesophagosternal and oesophagoapical leadings have been developed. The different oesophageal electrode is placed nar the upper cava-right atrial border close to the heart. The indifferent electrode is situated at the xiphisternum or at the apex of the heart. The direction of this lead is close to the direction of the anatomical axis of the His-Bundle. By this means a positive wave within the PR-segment can be registered, which we have called the "HP-wave". In a total of 17 patients these bipolar oesophageal leads were employed, in 12 cases simultaneously with the intracardiac HBE as a reference method. At rest the peak of the HP wave correlated to the maximal amplitude of the intracardiac His spike in more than 90% of patients. 4 patients were investigated by atrial pacing, in 3 cases this correlation could be found, too. Apparently the true His bundle signal can be obtained from the body surface by this new leading system. For improvement of the surface His bundle recordings, we reflect the combination of our noninvasive oseophageal lead with a modified signal averaging system with lesser amplication of the original signal.
The semitendinosus muscle of the dog is supplied by two separate arteries and drained by two corresponding veins. In the muscles used in this study no blood entering via the distal artery was found to leave via the proximal vein during perfusion through both arteries (orthograde perfusion). Therefore, collateral flow (CF) could be determined as proximal venous outflow during occlusion of the proximal artery. During orthograde perfusion total blood flow averaged 12 ml x min-1 x 100 g-1 at rest and 58.4 ml x min-1 x 100 g-1 during exercise. CF was found to average 6.2 ml x min-1 x 100 g-1 at rest and increased to 9.2 ml x min-1 x 100 g-1 during exercise. CF was sufficient to cover the metabolic demand of resting muscle. During exercise the O2-uptake (VO2) of the distal muscle portion was increased 13.4 fold in comparison to a 3.1 fold increase in the proximal muscle portion. The average contractile power decreased by 46%. Additional infusion of adenosine into the distal artery resulted in an increase of CF to 11.4 ml x min-1 x 100 g-1 and of orthograde flow to 71 ml x min-1 x 100 g-1. The average contractile power of the muscle increased by 13%. Both orthograde flow and CF were found to decrease with increasing muscle load. But this decrease was significantly more pronounced in the case of CF especially at a lower range of loads. It is concluded that after acute occlusion of orthograde flow, CF is limited by the number, the size and the dilatory capacity of precapillary network vessels. Furthermore, CF is influenced considerably by changes of extravascular support.
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In isolated, blood perfused, supramaximally stimulated, isotonically working gastrocnemii of dogs lactic acid (LA) output and O2-consumption (V O2) were measured according to the Fick principle. Simultaneously concentration of muscle tissue was determined at rest and at different times during exercise. In one series of experiments metabolic alkalosis was induced by infusions of THAM of Na bicarbonate. As a result arterial pH increased to about 7.5 and standard [HCO3-1] to 31-35 mmol per 1. In another group of experiments metabolic acidosis was induced by HCl infusions. In these experiments pH decreased to 7.0-7.1 and standard [HO301] to 8-11 mmol per 1. During the first 3-4 min after the onset of exercise LA concentration of muscle tissue rose to 18-19 mumol per g wet weight in both series of experiments. During acidosis the highest average values for LA release from the muscle were about 1.1 mumoles per g per minute. During alkalosis LA permeation rate was nearly three times as high. As a consequence of increased rate of permeation, LA concentration of muscle tissue decreased more rapidly in alkalosis than in acidosis. In both series of experiments work per time and VO2 were practically equal during the first 5-6 min of exercise. Thereafter work per time and VO2 decreased more rapidly in acidosis than in alkalosis, a result which probably is due to higher LA concentration in muscle at this time in acidosis. It is concluded that LA permeation rate across muscle cell membrane is increased by high extracellular HCO3- concentration in combination with low H+ activity and vice versa.
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High resolution electrocardiography (HRECG) recordings have already shown an increased beat-to-beat microvariability of the QRS duration of the terminal QRS in patients with a history of ventricular tachycardia (VT). The purpose of this study is to detect QRS-duration microvariability with magnetocardiographic (MCG) recordings in normals, patients with coronary heart disease (CHD), patients with a history of myocardial infarction (MI), and VT patients. QRS microvariability is calculated as the variance of time-shifts of single beats respectively to the average of all beats. The average over all channels of the MCG is performed. QRS microvariability was evaluated from 55-channel MCG in 15 normal persons, in 12 patients with CHD, in 13 patients with MI, and in 10 patients with VT. We found a significantly higher microvariability in patients with MI compared to normals. The highest microvariability was found in VT patients.
Parameterization of the ST-segment is used as a tool for risk stratification for patients to suffer from ventricular tachycardia. This parameterization is performed in terms of Principal Component Analysis (PCA) applied on multichannel magnetocardiographic (MCG) recordings. 55-channel MCG was recorded from 14 normal persons, 10 patients with CHD, 14 patients with MI, and six patients with VT. We found a significantly (p < 0.05) lower PCA-score in patients with MI compared to normals. The lowest PCA-score was found in VT patients. Significant differences can be found between VT patients and normals and also between VT patients and CHD patients.
Modelling the electromagnetic properties of the thorax in magnetocardiographic (MCG) studies is usually performed by the Boundary Element Method (BEM). Magnetic Resonance Imaging (MRI) scans are generally used as the basis for extracting the coordinates for BEM. As MRI is a (time) expensive technique and scanners have a high use demand, in this work a strategy is presented that reduces the costs and the need for additional MRI images. This strategy is based on the use of low resolution and incomplete MRI image sets of the thorax.
BACKGROUND: Restenosis after coronary angioplasty is considered to be caused mainly by increased migration and proliferation of smooth muscle cells (SMC). The concept of local, site-specific delivery of pharmacologic therapies has opened the door for new, high-dose drug regimes. METHODS AND RESULTS: SMC were isolated by enzymatic disaggregation with collagenase/elastase from human coronary plaque tissue of 29 patients (pSMC) and post mortem from the coronary media of 33 corpses (mSMC). Endothelial cells were isolated from human umbilical veins by enzymatic disaggregation with collagenase/dispase. By positive reaction with antibodies against smooth muscle alpha-actin and von Willebrand factor cells were identified as SMC or endothelial cells. In proliferation studies 5-150 micrograms/ml diltiazem was added to the culture media of pSMC, mSMC and endothelial cells. After 5 days there was a significant dose-dependent inhibition of cell proliferation (for pSMC with > 50 micrograms/ml, for mSMC with > 25 micrograms/ml, and for endothelial cells with > 5 micrograms/ml). In migration studies the effect of 5-150 micrograms/ml diltiazem on the velocity of migration of pSMC was investigated over a period of 48 h. Administration of diltiazem at concentrations of 100 and 150 micrograms/ml caused a significant inhibition of the migration of pSMC. The cytoskeletal components smooth muscle alpha-actin, vimentin, and alpha-tubulin of pSMC and the expression of von Willebrand factor of endothelial cells were investigated after an incubation period of 5 days with 50 and 150 micrograms/ml diltiazem. In the transfilter coculture model the effect of 50 micrograms/ml diltiazem on mSMC was investigated after mechanical injury of cocultured endothelial cells. Administration of diltiazem at a concentration of 50 micrograms/ml inhibited the development of a neointimal proliferate in the transfilter coculture model significantly (P < 0.001). CONCLUSIONS: A high dose of diltiazem inhibited the migratory and proliferative activities of coronary SMC significantly. In further experimental studies the effect of locally applied high doses of diltiazem on postangioplasty restenosis should be elucidated.
BACKGROUND: Because of the beneficial effects of estrogen, premenopausal women are normally protected against coronary heart disease (CHD) and are at lower risk for myocardial infarction; consequently, CHD occurs very rarely in menstrually active women. Given this background, the aim of the present study was to test the hypothesis that decreased concentrations of estrogen are associated with CHD in premenopausal women. METHODS: Fourteen premenopausal women with CHD were investigated and compared with a healthy control group comparable for age and cardiovascular risk factors. Relevant characteristics of patients and controls were assessed: age, blood pressure, body mass index, total cholesterol and high-density lipoprotein cholesterol, triglycerides, former pregnancies, ovariectomy and related surgical interventions, smoking history and former use of oral contraceptives. To ensure the premenopausal status of the participants, the regularity of the menstrual cycle and the follicle-stimulating hormone concentrations were also assessed. Plasma estradiol and progesterone and urine estrone concentrations (24 h urine collection) were measured at day 6 after estimated ovulation to assess the relative increase in plasma estradiol and progesterone during the second half of the menstrual cycle. RESULTS: Compared with the control group, premenopausal women with CHD had significantly lower concentrations of plasma estradiol (408.9 +/- 141 pmol/l and 287.8 +/- 109 pmol/l respectively; P = 0.0228) and total estrogen (2061 +/- 693 pg/mumol creatinine and 1607 +/- 448 pg/mumol creatinine respectively; P = 0.025) in the urine. However, the progesterone concentrations were not significantly different between the groups. These findings might be explained by a partial ovarian dysfunction, as the patient group had a significantly higher number of tubal sterilizations (eight compared with one). CONCLUSION: Our data provide support for the hypothesis that decreased concentrations of estradiol might be an additional pathogenetic factor for the development of CHD in menstrually active premenopausal women.