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C Kinder

Publications and source records attributed to C Kinder.

8 recordsLinked to original sources
PubMed1997

Conduction properties of the inferior vena cava-tricuspid annular isthmus in patients with typical atrial flutter.

INTRODUCTION: A functional region of slow conduction located in the inferior right atrium has been postulated to be critical to the induction and maintenance of typical human atrial flutter. We reexamined the potential role of functional conduction delay in the annular isthmus between the tricuspid valve and the inferior vena cava; it is within this region that such delays have been postulated to occur, and where interruption of conduction by radiofrequency energy application has been shown to eliminate typical flutter. METHODS AND RESULTS: Thirty patients with type I atrial flutter (30 counterclockwise, 14 clockwise) were studied. Counterclockwise and clockwise isthmus activation times adjacent and parallel to the tricuspid valve were measured during three conditions: (1) atrial pacing in sinus rhythm, (2) atrial flutter, and (3) entrainment of atrial flutter. During pacing in sinus rhythm at progressively shorter cycle lengths, both counterclockwise and clockwise isthmus activation times remained unchanged; decremental conduction prior to flutter induction or loss of capture was not observed. Counterclockwise isthmus activation time did not significantly differ during flutter (68 +/- 23 msec), inferolateral tricuspid annulus pacing (71 +/- 23 msec), or entrainment of flutter (72 +/- 23 msec). Similarly, clockwise isthmus activation times did not significantly differ between flutter (65 +/- 22 msec), proximal coronary sinus pacing (73 +/- 21 msec), or entrainment of flutter (64 +/- 15 msec). CONCLUSION: Decremental conduction is not characteristic of activation through the isthmus when activation is assessed parallel and adjacent to the tricuspid annulus. Functional slowing or conduction delay does not develop in this region during typical atrial flutter.

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PubMed1995

Adenosine-sensitive atrial tachycardia.

Limited data suggest that adenosine termination of atrial tachycardia is uncommon. To investigate further the effect of adenosine on atrial tachycardia, adenosine (6-12 mg) was administered during sustained atrial tachycardia in 17 patients. All patients underwent electrophysiological study to exclude other mechanisms of supraventricular tachycardia. Mean patient age was 51 +/- 20 years (range 18-82 years). Seven patients had no structural heart disease. The mean atrial tachycardia cycle length was 390 +/- 80 msecs (range 260-580). Sustained atrial tachycardia was induced with atrial extrastimuli in 8 patients, and was either incessant at baseline or developed spontaneously during isoproterenol infusion in 9 patients. Adenosine terminated atrial tachycardia in 3 patients (18%), transiently suppressed atrial tachycardia in 4 patients (23%), and produced AV block without affecting tachycardia cycle length in the remaining 10 patients. Adenosine sensitivity was observed in 3 of 8 patients with tachycardias initiated and terminated by atrial extrastimuli, and in 4 of 9 patients with spontaneous, but not inducible tachycardias including 3 of 4 patients with isoproterenol facilitated tachycardias. Of multiple clinical and electrophysiological variables examined as potential predictors of adenosine sensitivity, only isoproterenol facilitation of spontaneous or inducible sustained tachycardia predicted adenosine sensitivity (P = 0.02). These observations suggest that adenosine-sensitive atrial tachycardia may be more common than previously recognized. Adenosine sensitivity does not appear to be specific for tachycardia mechanism and cannot be predicted by response to pacing. Atrial tachycardias dependent on beta-adrenergic stimulation are most likely to be terminated by adenosine.

Adenosine↗
PubMed1995

Implantation of a subcutaneous lead array in combination with a transvenous defibrillation electrode via a single infraclavicular incision.

Occasional patients have excessive defibrillation energy requirements despite appropriate transvenous defibrillation lead position and modification of defibrillation waveform and configuration. Preliminary data suggest that use of subcutaneous defibrillation electrode arrays with nonthoracotomy systems is associated with a substantial reduction in defibrillation threshold. The current operative approach to subcutaneous lead array implantation involves the use of a separate left chest incision. We present two cases in which implantation of a subcutaneous lead array in combination with a transvenous defibrillation electrode was performed via a single infraclavicular incision and associated with a reduction in defibrillation threshold. Such an approach simplifies implantation and avoids the potential morbidity of the additional incision required of a left lateral chest approach.

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PubMedDate not supplied

Prognostic significance of sustained ventricular tachyarrhythmia occurring during dobutamine infusion.

The prognostic significance of a de novo sustained ventricular tachyarrhythmia occurring during a dobutamine infusion is unknown. This study was performed to determine (1) the risk of recurrent ventricular arrhythmia, (2) the safety of future dobutamine infusions, and (3) the role of electrophysiologic testing. The study population consisted of 15 patients, six with coronary artery disease, and nine with idiopathic dilated cardiomyopathy. Mean ejection fraction was 17% +/- 4.1%. The arrhythmia during the infusion was ventricular tachycardia in 13 patients and ventricular fibrillation in two patients and was not associated with preceding hemodynamic instability, electrolyte abnormality, digoxin toxicity, or antiarrhythmic drug therapy. During electrophysiologic testing, 7 of 15 patients had inducible ventricular tachycardia. All patients with inducible ventricular tachycardia were treated with either antiarrhythmic drugs, defibrillators, or ablation. Over a 12.3 +/- 5.2 month follow-up period, all 15 patients received further dobutamine treatment. Seven of 15 (47%) had a recurrent sustained ventricular tachyarrhythmia. Although three of seven recurrences occurred during a dobutamine infusion, all three of these patients had hemodynamically unstable conditions and were receiving high-dose (> 10 micrograms/kg/min) therapy at the time of recurrence. The other four recurrent arrhythmias were not associated with clear precipitating factors. Ejection fraction, origin of left ventricular dysfunction, and inducibility at baseline electrophysiologic testing did not predict arrhythmia recurrence. The de novo occurrence of a sustained ventricular tachyarrhythmia during dobutamine infusion is associated with a significant risk of arrhythmia recurrence (47%), which can occur in the presence or absence of dobutamine therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

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