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GT Wetzel

Publications and source records attributed to GT Wetzel.

2 recordsLinked to original sources

Neonatal bradycardia.

Heart rate monitoring has become a ubiquitous part of fetal and neonatal assessment, and has made detection of bradycardia in the fetal and neonatal periods a frequent occurrence. Evaluation of a fetus or neonate with bradycardia requires an understanding of the mechanisms of bradycardia as well as the cardiac and non-cardiac causes of bradycardia. The mechanisms of bradycardia include sinus bradycardia, abnormalities of sinus node function and abnormalities of atrioventricular conduction. In the instances where sinus bradycardia is pathologic, it usually results from non-cardiac disease. Sinus node dysfunction is rare early in life but can arise from surgical interventions, congenital heart disease, or endovascular manipulations. Abnormalities of atrioventricular conduction have a similar etiology but are more common than sinus node disease. Atrioventricular nodal disease can also result from maternal collagen vascular disease, even in the absence of symptoms in the mother. In these cases, epidemiological issues such as heart block in subsequent pregnancies and the maternal risk of developing symptomatic collagen vascular disease become important. The approach to treatment and long-term prognosis for bradycardia in the neonate is highly dependent on the underlying etiology and on the presence of concurrent factors such as structural heart disease.

Journal Article↗

Age-Dependent Changes in the Effects of Amiodarone on Rabbit Cardiac Myocyte Contractions.

BACKGROUND: Intravenous amiodarone has increasingly been used to control life-threatening atrial and ventricular arrhythmias. In addition to its four antiarrhythmic properties, amiodarone may have complex effects on intracellular Ca(2+) stores and myocyte contractility. METHODS AND RESULTS: Contraction amplitude was recorded for cardiac ventricular myocytes isolated from neonatal and adult rabbits. Sarcoplasmic reticulum (SR) Ca(2+) stores were loaded to steady-state levels by a train of eight electric field stimulations. The SR Ca(2+) load was quantified by recording the contraction amplitude resulting from the complete depletion of SR Ca(2+) stores by exposing the cell to a 1-second pulse of 10 mmol/L caffeine. After the cells were exposed to 1 µmol/L amiodarone for 10 minutes, electrically stimulated contraction amplitudes significantly decreased in both adult and neonatal cells. Caffeine-induced cell contraction amplitudes were not affected by amiodarone in adult ventricular myocytes. By contrast, amiodarone markedly inhibited caffeine-induced contractions in neonatal ventricular myocytes. The inhibitory effect of amiodarone on the caffeine-induced contractions was not replicated by Ca(2+) channel blockade with diltiazem. CONCLUSIONS: Amiodarone markedly inhibits caffeine-induced contraction in neonatal myocytes but has no significant effect on adult myocytes. Ca(2+) influx through amiodarone-sensitive Ca(2+) channels may play a primary role in maintaining SR Ca(2+) stores in neonatal heart.

Journal Article↗