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Biomedical subjects

A W Hamer

Publications and source records attributed to A W Hamer.

25 records · Page 2Linked to original sources
PubMed1984

Factors related to the induction of ventricular fibrillation in the normal canine heart by programmed electrical stimulation.

Programmed electrical stimulation was performed in eight normal dogs using a stimulator and endocardial electrode catheters identical to those used in human studies. The right and left ventricular apex were paced at a drive cycle length of 400 ms and, in some cases, 500 ms, with a pacing sequence of single (S1S2), double (S1S2S3) and triple (S1S2S3S4) premature impulses introduced after eight paced complexes. Pacing sequences were performed using combinations of pulse width (1, 2 and 4 ms) and current strengths of 2, 5 and 10 times diastolic threshold, and in three dogs, 15 times diastolic threshold. Twenty-two episodes of ventricular fibrillation were initiated in five dogs in 170 pacing sequences using current strengths up to 10 times diastolic threshold, and six episodes of ventricular fibrillation in the two of three remaining dogs tested at 15 times diastolic threshold. Ventricular fibrillation was reproducible on seven of nine occasions. Ventricular fibrillation was never induced by S1S2 at up to 15 times diastolic threshold; it was induced by S1S2S3 in 3 (1.8%) of 170 sequences, but only at 10 times diastolic threshold. It was induced by S1S2S3S4 in 19 (11.4%) of 167 sequences using 2 to 10 times diastolic threshold, although 20 of 28 episodes only occurred with S1S2S3S4 at 10 or more times diastolic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

The electrophysiologic basis for the use of amiodarone for treatment of cardiac arrhythmias.

The electrophysiologic basis for the use of amiodarone in the treatment of cardiac arrhythmias is outlined, with reference to studies in isolated cardiac tissues, whole animal, and human studies. Amiodarone appears to have the distinctive property of directly prolonging action potential duration (and hence refractory periods) in nearly all cardiac tissues. Independent of its effects on refractory periods, conduction may also be impaired in the His-Purkinje system, possibly due to depression of phase 0 of the action potential. Sinus node and atrial automaticity, as well as that arising from diseased Purkinje fibers, may be depressed. Normal ventricular escape pacemakers appear relatively unaffected, however. A nonspecific anti-adrenergic action may contribute to its observed effects. These electrophysiological effects are more obvious and predictable after several weeks of oral treatment than after intravenous administration, suggesting a time-dependent mechanism of action. The drug appears well suited to the prevention of enhanced automaticity in the ventricle and re-entry throughout the heart, and its frequent clinical success in a broad spectrum of cardiac arrhythmias attests to this. Unwanted side effects include sinus node depression, His-Purkinje conduction delay or block, and ventricular arrhythmias enhanced by QT prolongation. However, the frequency of clinically significant examples of unwanted arrhythmic effects appears to be acceptably low.

Action Potentials↗
PubMed1981

Disparity between the clinical and electrophysiologic effects of amiodarone in the treatment of recurrent ventricular tachyarrhythmias.

Nine patients with life-threatening ventricular arrhythmias were administered oral amiodarone over a period of months. Sustained ventricular tachycardia (VT) was induced during programmed stimulation in seven of the nine patients prior to their receiving amiodarone therapy. Despite an excellent clinical response to the drug over a period of 10 to 24 months (median 15 months), sustained VT was still able to be initiated in seven patients after 7 to 20 weeks of therapy, with multiform VT induced in several patients both before and after amiodarone. Some effects of the drug were noted, however, in that the induced VT was often slower with an increased QRS width, and right ventricular refractory periods were prolonged. Repeated ambulatory ECG monitoring in six patients showed a reduction in the frequency and complexity of spontaneous ventricular arrhythmias, but there was no consistent effect on the prematurity of the ventricular complexes. The reason for the disparity in some patients between the effects of amiodarone on the electrical initiation of VT and its clinical recurrence is unclear, but the findings suggest that the clinical efficacy of amiodarone in patients with ventricular arrhythmias may not be reliably predicted by electrophysiologic studies (EPS).

Aged↗
PubMed1980

Multiform ventricular tachycardia.

Electrophysiological studies were performed in three patients with chronic recurrent ventricular tachycardia (VT) associated with coronary artery disease. In each case the ventricular origin of the tachycardia was confirmed and induction of tachycardia by programmed stimulation suggested a re-entry mechanism. Multiple types of ventricular tachycardia were observed which differed in cycle length, QRS morphology, timing of local epicardial and endocardial ventricular electrograms and the use of the specialized conduction system for propagation. There was evidence of one or more re-entry circuits arising in or near previously infarcted areas, with features of cycle length alternation, change in exit points and variations in subsequent conduction through the myocardium and specialized conduction tissues. These findings suggest multiform VT can be due to a number of factors. A modified surgical approach is recommended for management of medically refractory VT when there is evidence of multiple types.

Adult↗