Aetiology of extrahepatic portal vein thrombosis.
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Female↗
Biomedical subjects
J Frederiks
Publications and source records attributed to J Frederiks.
Within-subject electrocardiographic differences at equal heart rates: role of the autonomic nervous system.
Various combinations of sympathetic and vagal tone can yield the same heart rate, while ventricular electrophysiology differs. To demonstrate this in humans, we studied healthy volunteers in the sitting position with horizontal legs. First, heart rate was increased by lowering the legs to 60 degrees and back. Thereafter, heart rate was increased by handgrip. In each subject, a leg-lowering angle was selected at which heart rate matched best with heart rate in the third handgrip minute. Thirteen subjects had a heart rate match better than 1%. Heart rate (control: 65.2+/-9.0 bpm) increased to 72.1+/-8.7 (leg lowering) and to 72.1+/-8.8 (handgrip) bpm. QRS azimuth, QRS duration, maximal T vector, T azimuth, T elevation, ST duration, QRS-T angle and QT interval differed significantly (P<0.05) between leg lowering and handgrip (QT interval 418+/-15 versus 435+/-21 ms). Also, septal dispersion of repolarization, assessed as the time difference between the apex and the end of the T wave in the V2 and V3 leads, differed significantly (V2: 96.7+/-19.3 versus 110.0+/-23.3 ms, P<0.01; V3: 88.7+/-19.3 versus 97.3+/-23.3 ms; P<0.01). Hence, leg lowering and handgrip cause different ventricular depolarization and repolarization. The hypertensive handgrip manoeuvre entails a longer QT interval and probably an increased septal dispersion of repolarization.
Adaptation, Physiological↗
The importance of high-frequency paced breathing in spectral baroreflex sensitivity assessment.
OBJECTIVE: Computation of the low-frequency (LF) blood pressure variability (BPV) to heart rate variability (HRV) transfer-index is a common method to assess baroreflex sensitivity (BRS), tacitly assuming that all LF-HRV is caused by baroreflex feedback of LF-BPV. However, respiration may also cause HRV by mechanisms not involving the baroreflex. Application of narrow-band (controlled) high-frequency breathing would keep such non-baroreflex-mediated HRV best out of the LF band. Spontaneous breathing, because of its broad-band character, might cause extra, non-baroreflex-mediated, HRV in the LF band, while paced LF breathing would even concentrate most non-baroreflex-mediated HRV in the LF band. Our study addresses the likely resulting BRS overestimation. DESIGN: We recorded HRV and BPV in 20 healthy young subjects in the sitting position. We varied the sympathovagal balance by gradual leg-lowering from horizontal till 60 degrees . At each angle the subjects performed controlled 0.10 Hz, spontaneous, and controlled 0.25 Hz respiration. RESULTS: Resting BRS values were 15.5(7.2), 13.1 (3.7), and 11.6(6.2) ms/mmHg, respectively. Both the 15/min and the free breathing values differed significantly, P< 0.01 and P= 0.04, from the 6/min breathing value. With lowered legs, the BRS values were 8.2(3.4), 8.3(2.9), and 8.3(3.4) ms/mmHg, respectively. CONCLUSION: Controlled 6/min breathing caused significant BRS overestimation under resting conditions. For the group, spontaneous respiration yielded acceptable BRS values, but individual BRS values deviated sometimes considerably. Conversely, with gravitational load, the respiratory pattern had only minor impact on BRS. Our results demonstrate that the risk of an overestimated BRS value is realistic as long as respiration is not controlled and of high-frequency.
Adult↗
Correlated neurocardiologic and fitness changes in athletes interrupting training.
PURPOSE: We studied nine male Dutch top marathon skaters during a 1-month interruption of their training schedules after their last contest in the winter to investigate a possible decline in baroreflex sensitivity. METHODS: Before and after this period, a maximal exercise test was done, and at days 0, 4, 7, 14, and 28 neurocardiologic measurement sessions--heart rate and noninvasive baroreflex sensitivity, recumbent and tilt--were performed. RESULTS: Interruption of training resulted in a significant and relevant decrease in the maximal oxygen uptake (from 65.7 +/- 5.8 to 61.6 +/- 4.7 mL O2 x kg(-1) x min(-1); P = 0.03), most likely associated with decreased competitive possibilities. Resting heart rate modestly increased (from 54.6 +/- 7.2 to 58.8 +/- 7.5 bpm), however, not significantly. Heart rate during 60 degrees tilt increased considerably (from 70.1 +/- 6.1 to 80.1 +/- 9.1 bpm; P = 0.01), possibly due to a decrease in blood volume and an increase in cardiopulmonary baroreflex gain. Arterial baroreflex sensitivity decreased significantly in the recumbent (from 13.3 +/- 5.4 to 9.8 +/- 3.8 ms x mm Hg(-1), P = 0.04), but not in the 60 degrees tilt position (from 6.7 +/- 2.0 to 6.0 +/- 2.5 ms x mm Hg(-1)). The relative decrease in baroreflex sensitivity and maximal oxygen uptake correlated significantly (r = 0.71, P = 0.02). CONCLUSIONS: In summary, our data show that correlated detrimental changes in fitness and baroreflex sensitivity are measurable in these athletes after a month of interruption of training.
Adult↗
Cardiac neural changes before vasovagal syncope.
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Heart Rate↗
Rescue PTCA Following Failed Thrombolysis and Primary PTCA: A Retrospective Study of Angiographic and Clinical Outcome.
Evidence is increasing that a patent culprit artery improves the prognosis of patients with acute myocardial infarction (AMI). Primary percutaneous transluminal coronary angioplasty (PTCA) has shown to be more effective than thrombolytic therapy alone. How effective is rescue PTCA after failed thrombolytic treatment? In a retrospective analysis, 176 consecutive patients with AMI and TIMI 0 or 1 perfusion grade were included. Patients had either rescue PTCA after failed thrombolysis (100 patients) or primary PTCA (76 patients). Angiographic data and in-hospital and 1-year outcome were analyzed. Comparison of baseline data of the two groups showed a higher proportion of long-standing angina and use of nitrates and aspirin in the primary PTCA group. Also, the delay between the onset of pain and PTCA was not significantly different, with a mean of 222 minutes for rescue PTCA and 245 minutes for primary PTCA (p = 0.52). The angiographic outcomes in the rescue PTCA group and the primary PTCA group were identical: The intervention was successful (TIMI 3 flow and residual stenosis <50%) in 86.0% and 85.5%, respectively. Complication rates of the procedure were also similar, except for bleeding complications. Blood transfusion was only needed after rescue PTCA in 3.0% versus 0.0% in primary PTCA patients. Clinical outcomes during hospital stay in terms of death rate (4.0% and 6.6%), reinfarction (6.0% and 3.9%), recurrent angina (16.0% and 11.8%), and repeat interventions were comparable, as was the first-year outcome. Failed PTCA was the most important predictor of a poor 1-year outcome; 28.0% died after failed PTCA versus 4.6% after successful PTCA (p < 0.001). In this retrospective analysis of 176 AMI patients, angiographic and clinical outcome, including a 1-year follow-up in patients who had rescue PTCA after failed thrombolysis, were of the same magnitude of patients in whom primary PTCA was performed. These findings suggest that in this subset the outcome of patients with rescue PTCA because of failed thrombolysis is good and is comparable with patients who underwent primary PTCA.
Journal Article↗
Heterogeneity of retrograde fast-pathway conduction pattern in patients with atrioventricular nodal reentry tachycardia: observations by simultaneous multisite catheter mapping of Koch's triangle.
BACKGROUND: Selective ablation of either the fast of the slow pathway resulting in cure of AV nodal reentry tachycardia (AVNRT) has led to the concept that these pathways are discrete, anatomically defined structures. We hypothesized that if a discrete retrograde fast pathway exists, it should be possible to record a single focus of early atrial activation near the apex of Koch's triangle, with sequential spread of depolarization to the rest of the atria. METHODS AND RESULTS: We evaluated 46 patients (33 women, 13 men; mean age, 45 +/- 17 years) undergoing electrophysiology study and catheter ablation for typical AVNRT. Retrograde atrial activation during AVNRT (337 +/- 43 ms) and ventricular pacing at a similar cycle length (352 +/- 51 ms) was recorded in the region of Koch's triangle with a decapolar catheter in the His bundle position, a multipolar catheter in the coronary sinus, and a deflectable quadripolar catheter along the tricuspid annulus anterior to the coronary sinus ostium. Earliest atrial activation was recorded at the apex of the triangle of Koch in 38 patients during ventricular pacing and in 43 patients during AVNRT. A broad wave front of atrial activation was recorded in 17 patients during ventricular pacing and in 26 patients during AVNRT. During AVNRT, only 2 patients had a single early site with focal and sequential activation along the tendon of Todaro. There was concordance in the pattern of atrial activation between ventricular pacing and AVNRT in only 21 of 46 patients. CONCLUSIONS: Retrograde atrial activation over the fast pathway is heterogeneous within Koch's triangle and the coronary sinus, both for the entire population and for individual patients during different modes of activation. These data do not support the concept of an anatomically discrete retrograde fast pathway.
Adult↗
An unusual cause of tachycardia-induced myopathy.
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Adult↗
Nonuniform anisotropy is responsible for age-related slowing of atrioventricular nodal reentrant tachycardia.
INTRODUCTION: AV nodal reentrant tachycardia cycle length has been shown to be longer in the elderly population. Microfibrosis associated with aging producing nonuniform anisotropic conduction or changes in membrane ionic properties could explain this finding. METHODS AND RESULTS: Forty-five patients (33 women and 12 men) with typical AV nodal reentrant tachycardia were studied to analyze the effects of age on electrophysiologic characteristics of the tachycardia using high-density catheter mapping of the triangle of Koch. We classified patients into group A (age < or = 45 years, mean [+/-SD] 32.7 +/- 8.8, n = 27) and group B (age > 45 years, mean [+/-SD] 61.1 +/- 10.2, n = 18). Retrograde atrial activation was recorded during tachycardia by means of a 2-mm decapolar catheter at the His bundle, a quadripolar catheter at the high right atrium, a multipolar catheter (6 to 10 poles) in the coronary sinus, and a deflectable quadripolar catheter at the posterior triangle of Koch. The AH interval at the AV junction as well as HA intervals at several atrial sites were measured during tachycardia. HA intervals at all atrial recording sites except in the posterior triangle of Koch were significantly longer in group B, as well as the tachycardia cycle length (362 vs 329 msec, P = 0.01). The mean AH interval was prolonged by 24 msec in group B, but this difference did not reach statistical significance. A sequential pattern of retrograde atrial activation during tachycardia was more frequently recorded in group B. CONCLUSIONS: Since the delayed activation to the atrium was heterogeneous, transverse nonuniform anisotropic conduction is a likely explanation of these age-related modifications of AV nodal reentrant tachycardia characteristics.
Adolescent↗