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Biomedical subjects

D S Cannom

Publications and source records attributed to D S Cannom.

At least 55 records · Page 3Linked to original sources
PubMed1983

Control of sudden recurrent arrhythmic deaths: role of amiodarone.

Patients resuscitated after out-of-hospital cardiac arrest have electrical instability of the myocardium, with 30% to 40% propensity for recurrent arrest in the first year. About 85% to 90% of such patients have complex ventricular ectopy and runs of ventricular tachycardia; in 70% to 80%, ventricular tachycardia or fibrillation are inducible by programmed electrical stimulation. The attempt to control recurrent cardiac arrest using these parameters and conventional antiarrhythmic drugs has yielded conflicting or variable results. Amiodarone was therefore studied in 40 consecutive patients (with previous cardiac arrests) in whom conventional antiarrhythmic therapy had proved ineffective or was not tolerated. The mean ejection fraction of the group was 0.29 +/- 0.12. At a mean follow-up of 16 months (range 5 to 40 months) six patients had died, three from heart failure, one from liver failure (not drug induced), and two from sudden (presumably arrhythmic) death. Late occurrences of arrhythmia were found in two patients (complicated by digitalis intoxication in one). Ambulatory ECG recordings showed that amiodarone had a potent suppressant effect on ventricular ectopy and runs of VT, but electrophysiologic studies demonstrated that it did not inhibit inducible VT/VF in greater than 65% despite an excellent clinical outcome. Limiting adverse reaction was seen in only one patient; other relatively minor side effects occurred in 10% to 15% of patients receiving maintenance therapy. Our data provide further evidence for the effectiveness of amiodarone in life-threatening ventricular arrhythmias, with a potential for the prolongation of survival in patients resuscitated after out-of-hospital cardiac arrests.

Amiodarone↗
PubMed1983

Orthogonal electrogram sensing.

Intracardiac electrogram sensing is the afferent limb of demand pacing systems. Under- and over-sensing at the ventricular level has been demonstrated in almost 50% of implanted unipolar pulse generators, and atrial electrogram sensing problems are more common. A unique dedicated sensor employing noncontacting and circumferentially placed orthogonal electrodes was tested at both the atrial and ventricular levels. Electrograms demonstrated voltages similar to those recorded from contacting electrodes, but with complete far-field rejection of signals from the opposite chamber. Orthogonal electrograms allowed for activation sequencing and capture verification as well.

Electric Conductivity↗
PubMed1983

Orthogonal ventricular electrogram sensing.

Inappropriate demand pacing is most commonly due to improper ventricular electrogram sensing. Filters and programmable sensitivities improve electrogram sensing of conducted beats, but paced electrograms cannot be sensed by conventional unipolar or bipolar systems. A permanent pacing lead with a standard tip electrode and three orthogonal 0.8 mm2 sensing electrodes located circumferentially 2 cm proximal to the pacing tip was tested in 22 patients. The tip electrode was placed in the right ventricular apex in standard pacing position. Orthogonal electrodes were not in contact with ventricular myocardium. Orthogonal ventricular electrograms from 54 electrode pairs were compared with unipolar tip electrograms during conducted rhythms and paced beats. Tip ventricular electrograms averaged 12.8 mV with 3.04 mVT waves. Orthogonally recorded ventricular electrograms during conducted beats averaged 8.86 mV with T waves of 1.57 mV. During pacing, tip ventricular electrograms were obscured by the stimulus artifact and repolarization events. Orthogonal ventricular electrograms, however, demonstrated small discrete stimuli of 1.99 mV followed by discrete ventricular electrograms of 9.19 mV and T waves of 1.9 mV. Orthogonal ventricular electrograms compared favorably with contacting tip electrograms during conducted beats and provided a redundant sensing capability. During pacing, orthogonal ventricular electrograms allowed the capability for capture verification. A new pacing catheter allows for improved ventricular electrogram sensing and capture verification.

Arrhythmias, Cardiac↗
PubMed1983

Amiodarone in refractory life-threatening ventricular arrhythmias.

Ninety-six patients with life-threatening ventricular arrhythmias refractory to two or more conventional agents were treated with amiodarone and followed for 6 to 40 months (mean, 15 months). Currently, 75 are alive and well. Seven patients died from nonarrhythmic and five from arrhythmic causes. Nonfatal arrhythmias recurred in four patients, one with early and three with late onset. Intolerable side effects occurred in five patients but heart failure was not aggravated by the drug. On 24-hour Holter recordings done before and serially during therapy in 72 patients, amiodarone eliminated episodes of ventricular tachycardia and complex ectopy and reduced total ectopic beat counts by 90% or more in all but 4 patients. In contrast, ventricular tachycardia inducible by programmed electrical stimulation was suppressed in only 50% of patients, but failure of such suppression did not compromise an excellent clinical outcome. Thus, amiodarone is highly effective in the prophylaxis of recurrent refractory life-threatening ventricular arrhythmias.

Acute Disease↗
PubMed1981

A new orthogonal lead for P synchronous pacing.

P synchronous pacing has long been identified as advantageous for patients with atrioventricular conduction defects and intact sinus node function. Prior endocavitary systems have been infrequently employed, because of unreliable P wave sensing from standard ring electrodes in the atrium or the requirement for a second atrial sensing lead. A single endocardial lead employing a unipolar ventricular stimulating electrode and an orthogonal P wave sensing design was developed and tested in 22 patients undergoing electrophysiologic study or pacemaker implantation. Thirteen centimeters from the stimulating tip of a standard permanent pacing lead, three or four electrodes with a surface area of one millimeter squared, equidistant from the tip, were placed circumferentially about the catheter. With the catheter tip normally placed in the right ventricular apex, atrial sensing electrodes were positioned in the mid-high lateral right atrium, adjacent to, but not affixed to, the right atrial wall. Bipolar orthogonal leads X and Y were obtained. In 22 patients, during sinus rhythm, atrial electrogram voltages in the X axis of 2.47 plus or minus 1.6 millivolts and 2.32 plus or minus 1.6 millivolts in the Y axis were recorded. QRS voltages of 0.078 millivolts and 0.073 millivolts, respectively, allowed dramatic ability to discriminate P from QRS complexes (P/QRS equals 32/1). There was no change in QRS or unipolar ventricular pacing. A single catheter designed for P synchronous pacing employing circumferentially placed atrial sensing electrodes has demonstrated unique atrial sensing voltages with excellent QRS signal rejection.

Cardiac Catheterization↗
PubMed1980

Initial ventricular activation in left-sided intraventricular conduction defects.

Nine patients with ECG evidence of rate-related left bundle branch block (LBBB) were studied using His bundle electrograms, electrograms from the right ventricular (RV) apex and vectorcardiograms recorded as heart rate was increased to produce LBBB. In five patients, when LBBB occurred, initially normal septal activation reversed and the HV intervals increased 10-30 msec, while the H-RVA interval did not change (group 1). Four patients had initially normal QRS duration (90-100 msec) but reversed septal activation (group 2). When LBBB developed there was no shift in either the HV interval or H-RVA interval. Only the QRS complex itself widened to distinguish these patients from group 1. These studies defined ventricular septal activation in normal conduction and in complete LBBB (group 1) and incomplete LBBB (group 2). The conduction patterns of group 1 and 2 patients are similar but are both markedly different from normal.

Adult↗
PubMed1978

Relations between ventricular refractoriness and regional myocardial blood flow after acute coronary occlusion.

Myocardial ischemia has been associated with dispersion of ventricular refractory periods and this dispersion has been related to the ventricular arrhythmias seen with coronary occlusion. This study relates the degree of change in measured ventricular refractory period with the degree of regional myocardial blood flow abnormality after coronary occlusion. When regional myocardial blood flow is less than 70% of that of nonischemic areas, refractory periods are significantly (P less than 0.001) shortened. The greatest change in refractory periods occurs in areas with a regional myocardial blood flow that is 21 to 40% of that of nonischemic areas. Marked (less than 20%) and minimal (61 to 80%) reductions in regional myocardial blood flow are associated with less, but still significant, shortening of ventricular refractory periods. Thus dispersion of refractoriness can be related to the inhomogeneity of regional myocardial blood flow after acute coronary occlusion. Interventions designed to salvage ischemic myocardium by increasing regional myocardial blood flow may affect dispersion of ventricular refractory periods in complex and divergent ways.

Acute Disease↗
PubMed1976

The short- and long-term prognosis of patients with transmural and nontransmural myocardial infarction.

To compare the long-term prognosis in patients surviving transmural with patients surviving nontransmural myocardial infarctions, the records of 188 consecutive patients with clinical histories and enzyme elevations consistent with acute infarction were reviewed. According to standard electrocardiographic criteria the patients were divided into two groups: 148 with transmural myocardial infarction (group 1) and 40 with nontransmural myocardial infarction (group 2). Of the patients who survived hospitalization, follow-up data were obtained on 119 of 124 patients in group 1 and 36 of 37 patients in group 2 at a mean follow-up period of 36 months. In group 2, the patients had a high incidence of sudden death after discharge (33 per cent in group 2 versus 15 per cent in group 1, p less than 0.02) as well as a significantly higher incidence of death from all cardiac causes (41.6 per cent in group 2 versus 24.3 per cent in group 1, p less than 0.05). Furthermore, the patients in group 2 still alive at the end of the follow-up period had an increased incidence of angina pectoris and of recurrent infarction. The data suggest that patients with nontransmural myocardial infarction carry a particularly guarded prognosis.

Connecticut↗
PubMed1976

Echocardiographic diagnosis of large fungal verruca attached to mitral valve.

In a patient with endocarditis due to Candida tropicalis echocardiograms from mitral valve vegetations were found to mimic the typical pattern of a left atrial myxoma. A mass was shown occupying the mitral orifice posterior to the anterior mitral leaflet; densities also appeared in the left atrium. Though these echocardiographic findings were consistent with the diagnosis of a left atrial myxoma, there were other distinctive differential diagnostic features. Other diagnostic possibilities must, therefore, be considered in the interpretation of echocardiograms which suggest left atrial tumour.

Candida↗
PubMed1975

A demonstration of differential refractoriness within a single fascicle of the human ventricular specialized conduction system.

In 15 patients with left bundle branch block (LBBB), atrial (A), His bundle (H), and ventricular (V) electrograms were recorded. Successively more premature atrial depolarizations were introduced via a catheter in the right antrium. In eight patients, the ventricular specialized conducting system (VSCS) was the most refractory portion of the entire atrioventricular conducting system (AVCS) and A-V conduction, which had been occurring via the right bundle branch (RBB), failed below the His bundle as the effective refractory period (ERP) of the VSCS was reached. In two of these eight patients, after the ERP of the VSCS was exceeded, further shortening of the H1-H2 interval (by 40 to 50 msec.) resulted in an unexpected resumption of A-V conduction, but with markedly prolonged H-V intervals (160 to 230 msec.). This demonstrates that differential refractoriness exists within the RBB of these patients. A zone of maximal refractoriness was initially encountered within the RBB when the premature impulse first blocked below the His bundle. In relative terms, this zone was distal to a more proximal area of the RBB where, with further shortening of the H1-H2 interval, sufficient conduction delay occurred to permit recovery of excitability distally and the resumption of A-V conduction.

Atrioventricular Node↗
PubMed1975

Electrophysiologic studies in the denervated transplanted human heart. II. Response to norepinephrine, isoproterenol and propranolol.

Five patients who had received a transplanted human heart 1 to 3 years previously were studied to determine the effects of norepinephrine, isoproterenol and propranolol on the atrioventricular (A-V) conduction system. Using the His bundle technique, atrial, His bundle and ventricular electrograms were recorded, and central aortic pressure was monitored during the administration of these drugs. Norepinephrine was given by continuous infusion to four patients in doses ranging from 4 to 8 mug/min, with the systolic arterial pressure increasing by an average of 72 mm Hg. Concomitantly, there was an average increase in the rate of the donor atrium of 32 beats/min, and a reflex slowing of the recipient atrium of 23 beats/min. The A-H interval shortened by an average of 27 msec. Isoproterenol dose-response curves were performed in three patients, with the maximal dose being 5.2 mug by intravenous bolus infusion. The rate of the donor atrium increased by an average of 40 beats/min, and that of the recipient atrium by 18 beats/min. The A-H time shortened by an average of 25 msec, with a drop in systolic blood pressure averaging 23 mm Hg. Propranolol (7 mg intravenously) was given to three patients and the peak doses of norepinephrine and isoproterenol were again infused. Beta adrenergic blockade was achieved at this dose of propranolol since there was only a minimal increase in the donor atrial rate after infusion of the drug. The A-H interval was not altered by catecholamine infusion after achievement of beta blockade. However, the levels of systolic hypertension noted after infusion of norepinephrine was not altered by propranolol. The denervated transplanted human heart appears to respond normally to norepinephrine and isoproterenol, and the electrophysiologic effects of these agents are blocked by propranolol. Extensive investigative work in the denervated canine model has demonstrated the presence of the alpha and beta cardiovascular receptors. Although the automonic nervous system is important in cardiac performance, this work is the first validation in man that (1) the functional integrity of the beta receptor is maintained even when the autonomic nerves are absent, and (2) the intrinsic properties of the sinus and atrioventricular nodes are the keystone in stabilizing cardiac electrophysiology after denervation.

Atrioventricular Node↗
PubMed1975

Effect of digoxin on atioventricular conduction. Studies in patients with and without cardiac autonomic innervation.

The effect of digoxin on atrioventricular (a-v) conduction was compared in five patients with an intact cardiac autonomic nervous system (Group I) and seven patients who had undergone cardiac transplantation (Group II), in whom we have previously shown the transplanted heart to be completely denervated. Small decreases in the atrial effective refractory period (ERP) (from 262 plus or minus 12 to 254 plus or minus 11 msec) and atrial functional refractory period (FRP) (from 304 plus or minus 12 msec) were observed in Group I patients after digoxin, but these changes were not significant. However, significant increases in the A-V nodal ERP (from 315 plus or minus 18 msec to 351 plus or minus 17 msec, P less than 0.05), and A-V nodal FRP (from 426 plus or minus 42 to 460 plus or minus 46 msec, P less than 0.01) were produced by digoxin and were unrelated to changes in cycle length. In Group II patients with denervated hearts, changes in atrial ERP (from 246 plus or minus 4 to 243 plus or minus 6 during spontaneous sinus rhythm; from 204 plus or minus 10 to 216 plus or minus 8 msec during atrial pacing) and atrial FRP (from 311 plus or minus 12 to 316 plus or minus 11 msec during spontaneous sinus rhythm; from 254 plus or minus 12 to 260 plus or minus 10 msec during atrial pacing) were not significant. However, in contrast to the Group I patients, the digoxin-induced changes in A-V nodal ERP (from 280 plus or minus 22 to 297 plus or minus 18 msec during atrial pacing) and FRP (from 368 plus or minus 18 to 377 plus or minus 18 msec during spontaneous sinus rhythm; from 334 plus or minus 13 to 346 plus or minus 16 msec during atrial pacing) were also statistically insignificant. Our results demonstrate that the electrophysiologic effects of digoxin on atrioventricular conduction in man are most marked in the atrioventricular node and are dependent on cardiac innervation

Adult↗