Dermatitis caused by radio-frequency electromagnetic radiation.
Explore the source record for details and available documents.
Abdomen↗
Biomedical subjects
M J De Jongste
Publications and source records attributed to M J De Jongste.
Coronary blood flow dynamics during transcutaneous electrical nerve stimulation for stable angina pectoris associated with severe narrowing of one major coronary artery.
To study the effect of transcutaneous electrical nerve stimulation (TENS) on coronary vasomotion, patients with New York Heart Association class III angina pectoris and significant single-vessel left coronary artery disease and who were also scheduled for elective percutaneous transluminal coronary angioplasty, were allocated to a study group (precordial actual TENS, n = 10) and a control group (precordial simulated TENS, n = 5, and TENS on the back, n = 3). Coronary volumetric flow was assessed in the stenotic and nonstenotic coronary artery before and after neurostimulation. The diameter (in millimeters) of the stenotic coronary artery was reduced in the study group after actual TENS (from 2.73 +/- 0.55 by 0.12 +/- 0.11; p = 0.008). In the nonstenotic coronary artery, the diameter increased in the study group (from 2.64 +/- 0.43 by 0.24 +/- 0.15; p = 0.01). In both the stenotic and nonstenotic coronary arteries, no effect was shown on the average peak velocity (centimeters per second) in the study group. The coronary volumetric flow (milliliters per minute) was reduced in the stenotic artery of the study group (from 62 +/- 18 by 8 +/- 7; p = 0.007). In the nonstenotic coronary artery, volumetric flow increased in the study group (from 57 +/- 18 by 11 +/- 10; p = 0.007). In the control group, simulated TENS and TENS on the back had no effect on the diameter of the artery, average peak velocity, or volumetric flow. In addition, in all patients, TENS had no effect on the total volumetric flow of the left coronary artery and hemodynamic variables during the study period. This observation suggests that TENS modulates regional coronary vasomotion in patients with coronary artery disease.
Aged↗
[Early ruling out of myocardial ischemic damage by means of new biochemical markers].
Explore the source record for details and available documents.
Biomarkers↗
Refractory angina pectoris in end-stage coronary artery disease: evolving therapeutic concepts.
Refractory angina pectoris in coronary artery disease is defined as the persistence of severe anginal symptoms despite maximal conventional antianginal combination therapy. Further, the option to use an invasive revascularization procedure such as percutaneous coronary balloon angioplasty or aortocoronary bypass grafting must be excluded on the basis of a recent coronary angiogram. This coronary syndrome, which represents end-stage coronary artery disease, is characterized by severe coronary insufficiency but only moderately impaired left ventricular function. Almost all patients demonstrated severe coronary triple-vessel disease with diffuse coronary atherosclerosis, had had one or more myocardial infarctions, and had undergone aortocoronary bypass grafting (70% of cases). We present three new approaches with antiischemic properties: long-term intermittent urokinase therapy, transcutaneous and spinal cord electrical nerve stimulation, and transmyocardial laser revascularization.
Aged↗
Neuroanatomy of cardiac activity-regulating circuitry: a transneuronal retrograde viral labelling study in the rat.
The anatomy of cardiac activity-regulating circuitry was studied with retrograde transneuronal viral labelling after pseudorabies virus injections into different parts of the rat heart. Transection of the spinal cord at Th1 was used to reveal selectively the parasympathetic neuronal networks. Virus-labelled sympathetic preganglionic cells were found in the Th1-Th7 thoracic intermediolateral cell groups, with some additional infections at Th8-Th11 after inoculations of the ventricular myocardium. After ventricular injections the thoracic spinal labelling pattern was bilateral and after right atrial infection it was contralateral. Approximately 20% of the parasympathetic preganglionic cells were located in the dorsal motor vagus nucleus; the rest occupied positions in the peri-ambiguus area ventrolateral to the nucleus ambiguus. Here and in the ventrolateral reticular formation myocardiotopy was found. Supraspinal transneuronal infections were bilateral, showed no apparent side dominance and were found in the nucleus of the solitary tract, the area postrema, the raphe nuclei, the A5 group, the parabrachial region, the periaqueductal grey, the hypothalamus, the amygdala and the cortex, in particular the anterior cingulate, the frontal, prelimbic, infralimbic and insular cortices. Spinal transections at Th1 reduced the number of labelled cells, gave a right side labelling dominance and affected the infection patterns in the ventrolateral reticular area, the raphe nuclei, the periaqueductal grey matter, the perifornical and retrochiasmatic area and the rostral parts of the insular cortex. The latter structures are linked selectively to the sympathetic innervation of the heart. The anatomical and functional aspects of these findings are discussed in relation to the autonomic control of heart activity.
Animals↗
Transneuronal viral labelling of rat heart left ventricle controlling pathways.
Retrograde transneuronal viral labelling and immunocytochemical methods were used for revealing neuronal networks controlling the left ventricle myocardium of the rat heart. After injections of 1 microliter pseudorabies virus solution (3 x 10(6) PFU ml-1) into the left ventricle, infected orthosympathetic preganglionic cells were found in the intermediolateral cell groups of the first 6 thoracic spinal segments. Preganglionic parasympathetic neurones were seen both in the nucleus ambiguus/retro-ambiguus area and the dorsal motor vagus nucleus. Large numbers of infected projecting interneurones were found in the rostral, caudal and medial parts of the ventral medulla oblongata, the Kölliker-Fuse nucleus and catecholaminergic cell group A5 and in the paraventricular hypothalamic nucleus.
Animals↗
Analysis of the morphology of the unipolar endocardial paced evoked response.
In a retrospective study we analyzed the unipolar endocardial evoked response signal (ERS) of 103 patients prior to pacemaker implantation. The objective of this study was to give a complete description of the ERS morphology and to evaluate influences on this morphology of both various electrode characteristics and pacing rate. In addition, spontaneous endocardial signals were studied. The results demonstrate that acute leads had both higher R wave and T wave amplitudes and a faster downslope of the T wave. In the acute leads those with porous titanium carbon coated tips showed a more pronounced T wave. Pacing rate influences the R wave amplitude and the stimulus to T wave interval. Both stimulus to maximum and stimulus to minimum T wave interval show an exponential correlation with the stimulus interval. The interval between maximum and minimum of the T wave and the absolute amplitude of T wave are not influenced by rate. Although there were significant correlations of the spontaneous endocardial signal with the ERS, the predictive value of the spontaneous signal for the ERS morphology is low. Prospective studies will be necessary to confirm the findings in this study.
Aged↗
Orthodromic pacemaker circus movement tachycardia.
We report on the case of a 33-year-old woman with sick sinus syndrome who had an orthodromic pacemaker circus movement tachycardia (PCMT), with antegrade atrioventricular (AV) conduction and a retrograde pathway by means of a DDD (AV universal) pacemaker. This PCMT was provoked and sustained by premature ventricular contraction-synchronous atrial stimulation (PVC-SAS), which is a new feature for the prevention of antidromic PCMTs. The conditions for occurrence of this tachycardia were: PVC-SAS; atrial undersensing; first degree AV block. Recommendations for prevention of this pacemaker-mediated tachycardia are given.
Adult↗
Rate stabilization by right ventricular pacing in patients with atrial fibrillation.
A recent study of de Jongste has demonstrated the lengthening of short R-R intervals in patients with atrial fibrillation by right ventricular pacing. We have further analyzed the data from this study and specifically looked at the effect of right ventricular pacing on the R-R interval instability and heart rate. At the cost of only a slight increase in mean heart rate, a major reduction of the R-R interval instability can be obtained by right ventricular pacing. Based on these findings, we have developed and evaluated an automatic pacing rate algorithm, which continuously varies the stimulation rate in order to stabilize the otherwise irregular rhythm in patients with atrial fibrillation.
Atrial Fibrillation↗