Douglas Cameron

Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons

The ability of isoproterenol to induce symptoms and laboratory findings of a vasodepressor reaction was tested in 48 patients, ages 17 to 74, divided into 4 groups according to the reason for their referral. Group 1 comprised 12 patients with vasodepressor syncope, group 2 had 8 patients with syncope of unknown origin, group 3 included 11 patients with syncope due to seizures in 2 and ventricular tachycardia in 9, group 4 had 17 patients with various arrhythmias not associated with syncope. Isoproterenol boluses were administered starting at 2 micrograms and increased in 2-micrograms steps to a maximum of 8 micrograms at 0 degree and +60 degrees. The responses at 0 degrees were all normal. At +60 degrees a vasodepressor reaction consisting of syncope or near syncope, hypotension and bradycardia was produced by isoproterenol (mean dose 6.0 +/- 0.26 micrograms) in 8 patients from group 1 (66.6%), 4 from group 2 (50%), 0 from group 3 and 4 from group 4 (23.5%). Three of the 4 patients in group 4 had a remote history of classic vasodepressor syncope. The overall sensitivity and specificity of the test were 73 and 85%, respectively, while the predictive accuracy of a test with positive or negative outcome were 69 and 89%, respectively. Muscarinic receptor blockade with atropine in 4 patients prevented isoproterenol-induced bradycardia but not hypotension or symptoms of fainting. Beta-adrenergic receptor blockade with propranolol inhibited all aspects of the isoproterenol-induced faint. Thus, the administration of isoproterenol during a passive upright tilt may identify persons who suffer from or are prone to a vasodepressor reaction.

Vagal techniques for termination of paroxysmal supraventricular tachycardia

Maneuvers that reflexly increase vagal tone were deployed to terminate the tachycardia in 68 consecutive patients with paroxysmal supraventricular tachycardia. The order and success rate of the protocol was as follows: 57 episodes were terminated with carotid sinus pressure alone or after pretreatment with edrophonium, 5 were terminated with the Valsalva maneuvers and 6 were terminated with phenylephrine. Potency testing showed that phenylephrine evoked the greatest increase in vagal tone. All cases demonstrated slowing of tachycardia ranging from 40 to 220 ms +/- standard error of the mean (mean 79.0 +/- 3.8 ms) followed by abrupt termination. Pauses after termination ranged from 900 to 3,300 ms (mean 1,683.8 +/- 66.6) with 54 patients showing pauses of 2,000 ms or less. Termination was highly reproducible showing an overall success of 148 (92 percent) of 160 trials among 22 selected cases. The extent of increased vagal tone needed to terminate paroxysmal supraventricular tachycardia was raised by augmented sympathetic tone (infusion of isoproterenol) and decreased by reduced sympathetic tone (pretreatment with propranolol). Thus, paroxysmal supraventricular tachycardia can be rapidly, safety and consistently terminated by maneuvers that reflexly increase vagal tone.

Reflex mechanisms responsible for early spontaneous termination of paroxysmal supraventricular tachycardia

The incidence and possible mechanism of early spontaneous termination of paroxysmal supraventricular tachycardia was studied in 20 consecutive patients. Episodes of induced tachycardia that terminated spontaneously within the 1st minute after initiation were included. Tachycardias ending spontaneously were associated with a reproducible course of hypotension at the onset followed by blood pressure recovery above control levels and termination. Spontaneous termination of tachycardias occurred within the A-V node 18 to 45 seconds (mean +/- standard error of the mean 27.9 +/- 5.3) after their onset. In the supine position (0 degrees) 9 (45 percent) of 20 patients showed spontaneous termination in 36 (16 percent) of 219 episodes of tachycardia. In the head-dependent position (-20 degrees) only 1 (8 percent) of 13 patients manifested spontaneous termination in 2 (4 percent) of 54 episodes. In the head up position (+60 degrees) only 1 (6 percent) of 18 patients exhibited termination in 2 (2 percent) of 102 episodes. After partial cholinergic blockade with intravenous hyoscine butylbromide, 20 mg, or atropine, 0.6 mg, none of five patients showed spontaneous termination in 25 episodes. After beta adrenergic blockade with 10 mg of propranolol intravenously, none of 16 patients showed spontaneous termination in 87 episodes of tachycardia. We conclude that the initial hypotension during tachycardia evokes a sympathetic response that increases blood pressure and this increase in turn causes a rise in vagal tone that breaks the tachycardia.

Modulation of an idioventricular rhythm by vagal tone

A 28 year old man with a stable permanent idioventricular rhythm of 80 to 85 beats/min, with all the characteristics of a pacemaker, is described. This pacemaker was slowed by maneuvers that enhanced vagal tone, including carotid sinus massage, the postrelease phase of the Valsalva maneuver and phenylephrine. The pacemaker was also slowed by a cholinesterase inhibitor (edrophonium hydrochloride) and accelerated by a muscarinic receptor blocking drug (hyoscine butylbromide). The actions of these maneuvers and agents were independent of sympathetic tone as propranolol pretreatment did not alter their effects. Similarly, propranolol did not affect the pacemaker rate. The pacemaker was not dependent on a slow inward current because verapamil did not affect its rate. The pacemaker accelerated in response to increased sympathetic tone induced by exercise and upright tilting and to the adrenergic agonist isoproterenol. The pacemaker was localized to the high posterior septal region of the left ventricle underneath the mitral valve. This report describes in a man an idioventicular pacemaker that is innervated by sympathetic and vagal fibers and responsive to alterations in tone of both limbs of the autonomic nervous system. It offers the first clear proof that a ventricular pacemaker can be innervated and controlled by the vagus nerve and provides its location.

Duration of Discharge of Neuromuscular Incapacitating Device and Inappropriate Implantable Cardioverter-Defibrillator Detections

Neuromuscular-incapacitating devices (NID) are being used increasingly worldwide by law-enforcement authorities to restrain violent behavior.1 Electrical noise-related, inappropriate detection by implantable cardioverter-defibrillator (ICD) has been documented.2,3 Detection of NID discharge by ICD has been described,4,5 but the effects of duration of NID discharge and ICD detection and therapy have not been established. The authors hypothesized that a longer duration of NID energy might lead to shocks from the defibrillator.4nnWith the approval of the animal care committee of our institution, we tested this hypothesis in a pig implanted with Medtronic 7275 GEM III DR ICD. The method used for performing the experiment in a pig model has been described previously. …

Radiofrequency catheter ablation of a posteroseptal accessory pathway along the morphologic tricuspid valve in a patient with congenitally corrected transposition of the great arteries and complete atrioventricular block.

We report a patient with Congenitally Corrected Transposition of the Great Arteries, complete atrioventricular block and a posteroseptal accessory pathway across the morphologic tricuspid valve. Ablation of the accessory pathway was performed for her symptomatic palpitations.

Inappropriate therapy from a defibrillator complicating transcoronary ablation of septal hypertrophy in a patient with hypertrophic obstructive cardiomyopathy.

This case report describes a patient with obstructive hypertrophic cardiomyopathy who received therapy inappropriately from his implanted defibrillator, subsequent to transcoronary alcohol ablation for septal hypertrophy (TASH). Widening of the intracardiac electrogram postablation resulted in “double counting” of the intrinsic ventricular electrogram by the device and inappropriate tachycardia detection. (PACE 2004; 27:677–680)

Continuous On‐Line Beat‐to‐Beat Analysis of AV Conduction Time

A simple analog circuit is described which is capable of measuring on a beat‐to‐beat basis P‐R, R‐P, P‐P, and R‐R intervals during sinus rhythm and paroxysmal supra ventricular tachycardia. In addition the circuit will emit a pulse when the consecutively alternating P and R wave sequence is interrupted thereby signalling a trigger problem or a change in rhythm. The operation of the device requires proper P and R wave sensing and provides outputs which are linear over a range of rates which are applicable to the human heart.

Atrial overdrive pacing and incidence of heart failure-related adverse events in permanently paced patients.

BackgroundAtrial overdrive pacing algorithms may be effective in preventing or suppressing atrial fibrillation (AF). However, the maintenance of a heart rate incessantly faster than spontaneous could induce left ventricular (LV) dysfunction and promote heart failure (HF) on the long term.ObjectiveThis post hoc analysis examined the effects of a new overdrive algorithm on the incidence of HF-related adverse events in 411 patients enrolled in the ADOPT-A trial.Materials and methodsThe AF Suppression™ algorithm was randomly programmed ON in 209 patients (treatment group) versus OFF in 202 patients (control group). The incidence of HF-related adverse events and HF-related deaths over a 6-month follow-up was compared between the two groups. Patients with versus without HF-related clinical events were also compared to each other within each group.ResultsThere were eight HF-related adverse clinical events (3.8%) in the treatment group and 11 (5.4%) in the control group, including four HF-related deaths (1.9 vs. 2.0%) in each group during follow-up. Baseline NYHA functional class in patients with versus without HF-related adverse events was 1.4u2009±u20090.5 versus 1.5u2009±u20090.7 in the control, and 1.5u2009±u20090.8 versus 1.5u2009±u20090.6 in the treatment group. LV ejection fraction (EF) was 49u2009±u20097% in patients with, versus 57u2009±u200912% in patients without HF-related adverse events, in the control group, and 43u2009±u200914% in patients with, versus 56u2009±u200913% in patients without HF-related adverse events, in the treatment group. LVEF was lowest and similar in both groups among patients who died from HF (35u2009±u200910% in the control and 38u2009±u200927% in the treatment group).ConclusionsIn ADOPT-A, HF-related clinical events and deaths were related to LV dysfunction and not to atrial pacing overdriven by the AF suppression algorithm.

On Line (Real Time) Quantitative Measurement of Premature Ventricular Beats

A real time system for graphically displaying premature ventricular beat trends is described. The system consists of analog detector circuits coupled to a Fortran based software program for premature ventricular beat processing. The software program runs four independent channels and has three available analysis modes: a “counting” mode which provides a running total of counts to date; an “averaging” mode which displays average number of events overtime, and a “ratio” mode which provides an output reflecting changes in the ratio of premature ventricular beats to all beats. Various scale factors can be applied to accommodate differing background states. The systems strengths lie in its simplicity, accuracy, and simultaneous analog display of both the original ECG signal as well as the derived quantitative data.