Biomedical subjects

J E Hubbard

Publications and source records attributed to J E Hubbard.

21 records · Page 2Linked to original sources

PubMedDate not supplied

A prospective analysis of the incidence and risk factors associated with junctional ectopic tachycardia following surgery for congenital heart disease.

This study was designed to evaluate the incidence and risk factors associated with the occurrence of junctional ectopic tachycardia (JET) in patients after congenital heart surgery. We prospectively analyzed cardiac rhythm status in 336 consecutive patients undergoing surgery for congenital heart disease at our institution during a 1-year period. The incidence of JET was 8% (27/336). Repairs with the highest incidence of JET were arterial switch operation (3/13, 23%), atrioventricular (AV) canal repair (4/19, 21%), and Norwood repair (2/10, 20%). Compared to patients with no arrhythmias, patients with JET were more likely to be younger (2.75 +/- 2.44 vs 5.38 +/- 7.25 years, p < 0.01), have had longer cardiopulmonary bypass times (126 +/- 50 vs 85 +/- 73, p < 0.01), and have a higher inotrope score (6.26 +/- 7.55 vs 2.41 +/- 8.11, p < 0.01). By multivariate analysis, ischemic time was the only factor associated with JET [odds ratio, 1.01 (confidence interval, 1.005-1.02); p = 0.0014). The presence of JET did not correlate with electrolyte abnormalities. JET is not necessarily related to surgery near the His bundle or hypomagnesemia. Longer ischemic time is the best predictor of JET. Patients undergoing arterial switch operation, AV canal repair, and Norwood repair are at highest risk of postoperative JET and should be considered for prophylactic therapy.

Adolescent↗

PubMedDate not supplied

Autonomic changes and heart rate variability in children with neurocardiac syncope.

This study evaluated resting autonomic function and autonomic responses to head-up tilt-table testing in children who experienced neurocardiac syncope to determine whether predictable differences existed between these patients and normal volunteers. Neurocardiac syncope is a common cause of syncope in children. The mechanism, though related to abnormalities in autonomic function, has not been fully elucidated, particularly in pediatric patients. This study evaluated resting autonomic tone using noninvasive autonomic function tests (i.e., Valsalva, handgrip, and deep breathing) and 24-hour heart rate variability (HRV). In addition, heart rate and blood pressure were evaluated during head-up tilt examination. Values from patients who experienced neurocardiac syncope were compared to those from age-matched normal volunteers. No significant differences were noted during noninvasive testing. Some time domain HRV variables demonstrated a trend toward significant difference (p < 0.10). Tilt testing data were significantly different in sinus beat to sinus beat (RR) intervals between controls and syncope patients at 2, 5, and 10 minutes after tilting. In addition, significant differences were noted in RR interval and the standard deviation of RR interval 1 or 2 minutes prior to syncope when compared to controls at 5 and 10 minutes after tilting. Children with syncope exhibited abnormalities during tilt testing indicating an increased sympathetic or decreased parasympathetic tone, particularly prior to syncope. Some measures of HRV might constitute noninvasive parameters that correlate with the positive tilt table test.

Adolescent↗

PubMedDate not supplied

Tolerance development to the arousal effects of nicotine.

To determine if repeated daily doses of nicotine induces tolerance to both its EEG and behavioral activating effects, rats implanted with sets of bipolar cortical elecrodes and carotid cannulae received intracarotid injections of either (1) 6 daily doses of nicotine (as tartrate, 30 mug/kg) (Group 1) or (2) 3 daily doses of saline followed by 4 days of nicotine (Group 2). From an exercise-induced resting state, nicotine produced immediate EEG and behavioral arousal, both of which disappeared in Group 1 by Day 6. Saline administered to Group 2 rats produced little or no response but subsequent nicotine resulted in responses similar to those produced by Group 1 animals. It is concluded that tolerance development to nicotine activation is reflected not only in behavior, but also in the EEG.

Animals↗