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Biomedical subjects

J W Mason

Publications and source records attributed to J W Mason.

At least 91 records · Page 5Linked to original sources
PubMed1986

Basic and clinical cardiac electrophysiology of encainide.

Encainide is a potent sodium channel antagonist. It dissociates slowly from blocked, repolarized channels (time constant of recovery greater than 20 seconds). It markedly slows myocardial and His Purkinje conduction in vitro, in animal models and in humans. In vitro the parent compound and its major metabolites, O-demethyl and 3-methoxy-O-demethyl encainide, have variable effects on action potential duration and refractoriness. In man the parent compound has relatively little effect on refractoriness and QT interval, but its metabolites may increase refractoriness moderately. Encainide has no significant effect on the normal sinoatrial node, and only its metabolites significantly depress atrioventricular nodal conduction and refractoriness. In models of ischemia, all of encainide's actions are more pronounced in ischemic than in normal tissue. Encainide is similar in its basic and clinical electrophysiologic profile to flecainide and lorcainide although its constellation of electrophysiologic properties is unique. It differs from quinidine, procainamide and disopyramide by slowing conduction more and affecting refractoriness less, and by absence of anticholinergic side effects.

Action Potentials↗
PubMed1986

Bereavement and catecholamines.

Urinary catecholamine output was studied in 59 middle-aged and elderly persons who were either acutely bereaved (n = 39) or threatened with the loss of a spouse (n = 20). The study was done with the hypothesis that urinary catecholamine output would be elevated among the bereaved subjects both in comparison to norms in the literature for non-stressed controls and to the group of subjects who were threatened with a loss. It was also expected that individually high measures of psychological distress would be associated with high urinary catecholamines. Twenty-four hour urinary output of norepinephrine and epinephrine was observed to be higher than normal during acute bereavement but was not associated with depression scores. No differences were found between those who had experienced an actual loss two months earlier and those who were threatened with a loss. Expected relationships between indices of psychological distress and catecholamine output were not observed. Finally, an association was found between increasing age and higher levels of urinary norepinephrine and epinephrine output among acutely bereaved subjects, suggesting that the adaptation of the sympathetic-adrenal medullary system to stress among older persons is slower.

Adaptation, Physiological↗
PubMed1986

Comparison of an implanted abdominal aortic counterpulsation device with the intraaortic balloon pump in a heart failure model.

The abdominal aortic counterpulsation device is a round pumping chamber with a valveless opening which is implanted retroperitoneally on the abdominal aorta. The Utah driver is connected to the device through an air conduit and is synchronized on the electrocardiographic signal to provide diastolic aortic augmentation. For comparison an intraaortic balloon was also driven by the Utah driver system. The abdominal aortic counterpulsation device (stroke volume = 30, 40 and 60 ml) and the intraaortic balloon pump (balloon volume = 20 ml) were tested in dogs with acute left ventricular failure. The abdominal aortic counterpulsation device was also tested in normal animals. In acute left ventricular failure the abdominal aortic counterpulsation device at a stroke volume of 30, 40 or 60 ml decreased left ventricular end-diastolic pressure by an average of 28.56 (p less than 0.001), 39.56 (p less than 0.001) and 44.14% (p less than 0.005), respectively; aortic end-diastolic pressure by 24.11 (p less than 0.001), 26.67 (p less than 0.001) and 19.57% (p less than 0.01); and aortic systolic pressure by 18.56 (p less than 0.002), 26.0 (p less than 0.001) and 22.43% (p less than 0.005). It increased cardiac index by 27.58 (p less than 0.02), 35.59 (p less than 0.005) and 43.42% (p less than 0.001) and it provided peak aortic diastolic augmentation of 64.5 (p less than 0.001), 69.78 (p less than 0.001) and 74.43% (p less than 0.001), respectively, above the control aortic end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Multicenter trial of sotalol for suppression of frequent, complex ventricular arrhythmias: a double-blind, randomized, placebo-controlled evaluation of two doses.

Sotalol is a unique beta-adrenergic blocking agent with additional actions characteristic of Vaughn-Williams class III antiarrhythmic agents in experimental models. To test the efficacy of sotalol to suppress ventricular arrhythmias, a 6 week parallel, placebo-controlled out-patient study of two doses (320 and 640 mg/day, in two divided doses) was performed in four hospitals in 56 patients with chronic premature ventricular complexes at a frequency of 30/h or more (mean +/- SE, 528 +/- 60/h) on 48 hour ambulatory electrocardiographic recording. During a placebo week, no change occurred in arrhythmia frequency (532 +/- 76/h). Subsequent sotalol therapy significantly reduced median arrhythmia frequency in patients receiving both low (n = 19) and high (n = 18) doses compared with that in patients receiving placebo (by 77 and 83%, respectively, versus 6%; p less than 0.001). Twenty-two (59%) of 37 sotalol-treated patients, 11 in each group, reached the prospectively defined criterion of efficacy (greater than or equal to 75% arrhythmia reduction) versus 2 (11%) of 19 placebo control patients (p less than 0.001). Sotalol reduced the median frequency of couplets by 94% (p less than 0.0001) and that of runs by 89% (p less than 0.0007). The electrocardiographic effects of sotalol included reductions in heart rate (by 17 to 27%) and increases in the QTc (by 6 to 9%) and PR (by 6%) intervals. Ejection fraction was unchanged. The most common adverse side effect was fatigue, but drug discontinuation was required in only three patients taking 640 mg/day. No proarrhythmic events or biochemical abnormalities were observed. In summary, sotalol displays significant antiarrhythmic activity of moderately high degree with good tolerance in doses of both 320 and 640 mg/day. Its antiarrhythmic actions are distinguished from those reported for other beta-blockers by its effects on the QTc interval and its moderately high degree of antiarrhythmic activity.

Aged↗
PubMed1986

Urinary free-cortisol levels in posttraumatic stress disorder patients.

Urinary free-cortisol levels (micrograms per day) were measured by radioimmunoassay at 2-week intervals during the course of hospitalization in the following patient groups: posttraumatic stress disorder (PTSD); major depressive disorder; bipolar I, manic; paranoid schizophrenia; and undifferentiated schizophrenia. The mean cortisol level during hospitalization was significantly lower in PTSD (33.3 +/- 3.2) than in major depressive disorder (49.6 +/- 5.9), bipolar I, manic (62.7 +/- 6.7), and undifferentiated schizophrenia (50.1 +/- 8.9), but was similar to that in paranoid schizophrenia (37.5 +/- 3.9). The same differences across groups are evident in the first sample following hospital admission. This finding of low, stable cortisol levels in PTSD patients is especially noteworthy, first because of the overt signs of anxiety and depression, which would usually be expected to accompany cortisol elevations, and second because of the concomitant chronic increase in sympathetic nervous system activity shown in prior psychophysiological studies of PTSD and reflected in marked and sustained urinary catecholamine elevations previously reported in our own PTSD sample. The findings suggest a possible role of defensive organization as a basis for the low, constricted cortisol levels in PTSD and paranoid schizophrenic patients. The data also suggest the possible usefulness of hormonal criteria as an adjunct to the clinical diagnosis of PTSD.

Bipolar Disorder↗
PubMed1986

Electrophysiologic studies in patients with ventricular tachycardia.

Invasive electrophysiologic studies are used to guide drug and non-pharmacologic therapy, including surgery, in patients with ventricular tachycardia. We discuss the indications, methods, and results of electrophysiologic studies in these patients. Both catheter and intraoperative studies are described. This approach to patients with ventricular tachycardia is contrasted to the approach using noninvasive electrocardiographic monitoring.

Anti-Arrhythmia Agents↗
PubMed1986

General concepts and mechanisms of ventricular tachycardia.

The predominant mechanism of ventricular tachycardia is thought to be reentry, although this has been proved to exist in definitely a minority of patients studied owing to technical limitations. Other mechanisms, such as spontaneous triggered automaticity, undoubtedly also cause clinical ventricular tachycardia. During electrophysiologic testing, sustained unimorphic ventricular tachycardia can be induced in the majority of patients who have this arrhythmia clinically. It is extremely rare to induce this rhythm in a patient who has not had ventricular tachyarrhythmias. Nonsustained ventricular tachycardia, repetitive ventricular responses, and pleomorphic ventricular tachycardia and ventricular fibrillation are all nonspecific responses to electrical stimulation and thus are not suitable end points for either the baseline study or serial drug testing. Although an optimal pacing protocol for all subjects does not exist, an adequate test should include pacing with multiple drive rates, at least two (and in some cases, three) extrastimuli, and more than one pacing site in the right ventricle. Isoproterenol infusion and left ventricular pacing may also be necessary in selected patients. During serial drug testing, a drug should not be considered effective if more than 15 repetitive beats are induced unless an extremely aggressive pacing protocol is used. Patients treated with drugs predicted to be effective at electrophysiologic study have a better prognosis than those treated with drugs predicted to be ineffective or those treated with drugs selected empirically.

Electrophysiology↗
PubMed1986

Results of operations for ventricular tachycardia in 105 patients.

Operations to treat ventricular tachycardia refractory to antiarrhythmic drugs were performed in 105 patients. Intraoperative epicardial activation sequence maps were completed in 83% and endocardial maps in 57%. Mapping could be used to guide 79% of operations. When no useful mapping data were obtained, patients had visually guided antiarrhythmic operations (17%) or conventional cardiac operations (4%). The most frequently performed antiarrhythmic procedures, alone or in combination, were endomyocardial resection (45%), cryothermal destruction (44%), and encircling procedures (20%). Operative mortality was 16%, including 6% from heart failure and 4% from ventricular tachycardia. Emergency operation (p = 0.002) and New York Heart Association heart failure class (p = 0.01) were independent preoperative risk factors for cardiac operative mortality in the 98 patients with coronary artery disease. At postoperative electrophysiologic study performed in 79 patients, ventricular tachycardia could not be induced in 75% of patients who had map-guided operations and 36% who had visually guided ones (p = 0.001). During follow-up of 23 +/- 21 months, results of postoperative electrophysiologic study predicted ventricular tachycardia recurrence. At 2 years the actuarial incidence of freedom from arrhythmia recurrence was 50% +/- 10% in patients with and 78% +/- 6% in patients without inducible ventricular tachycardia (p = 0.001); it was 71% +/- 5% in patients who had map-guided operations and 37% +/- 12% in patients who had visually guided ones (p = 0.004). Ventricular tachycardia recurrence was infrequent in survivors of map-guided operations; benefits of surgical treatment for ventricular tachycardia were limited by high operative mortality and frequent arrhythmia recurrence when no useful mapping data were obtained.

Actuarial Analysis↗
PubMed1985

Signal-averaged electrocardiographic late potentials in patients with ventricular fibrillation or ventricular tachycardia: correlation with clinical arrhythmia and electrophysiologic study.

High-frequency potentials measured in the terminal 40 ms of the signal-averaged QRS complex during sinus rhythm are of abnormally low amplitude in most patients with ventricular tachycardia (VT). However, less is known about high-frequency late potentials in patients with ventricular fibrillation (VF), and the relation between late potentials and arrhythmia inducibility during electrophysiologic study has not been established. Signal-averaged electrocardiography was used to measure high-frequency (more than 25 Hz) late potentials in 24 patients with spontaneous VF, 27 patients with spontaneous sustained VT, and 19 normal subjects, none of whom were receiving antiarrhythmic drugs. Late-potential amplitude in patients with VT was significantly lower than that in patients with VF (p less than 0.02). Late-potential amplitude in patients with VF was not significantly different from that in normal subjects. Ventricular arrhythmia induction was attempted during electrophysiologic study in 46 of the patients with VF or VT. Late-potential amplitude was significantly lower in 26 patients with reproducibly inducible sustained ventricular arrhythmias than in 20 without (p less than 0.001). The correlation between late-potential amplitude and arrhythmia inducibility was independent of that between late-potential amplitude and clinical arrhythmia (VT vs VF).

Action Potentials↗
PubMed1985

Treatment with oral lorcainide in patients with sustained ventricular tachycardia and fibrillation.

Fifty patients with drug-refractory (failed 7 +/- 2 other drug trials) sustained ventricular tachycardia or fibrillation were treated with oral lorcainide. Twenty-three patients underwent programmed stimulation both before and after oral lorcainide, and all 23 remained inducible, although ventricular tachycardia cycle length was prolonged and mean arterial pressure was higher. Lorcainide was discontinued in 23 patients prior to hospital discharge because of death in four patients, side effects in five patients, spontaneous clinical arrhythmia recurrence in six patients, and ventricular tachyarrhythmias induced at electrophysiologic study in eight patients. Twenty-seven patients were discharged on an average dose of 169 +/- 56 mg twice a day, including 15 in whom ventricular tachycardia remained inducible. During long-term follow-up the drug was discontinued in 15 patients; three because of side effects, three because of clinical nonfatal arrhythmia recurrence, two who selected other alternative therapy, and seven patients who died suddenly due to ventricular tachyarrhythmias. Twelve patients remain on long-term lorcainide. The actuarial 1-year chance of being arrhythmia free was 38.9%, and 1-year cardiovascular and arrhythmia survival rates were 56.8% and 60.4%, respectively. Based on our data we conclude that: In this extremely drug-resistant patient population the clinical efficacy of lorcainide is low; lorcainide should not be used empirically in such highly drug-resistant patients; persistent ventricular tachyarrhythmia inducibility at electrophysiologic study implies a poor prognosis in patients treated with oral lorcainide; the incidence of becoming noninducible during oral lorcainide therapy in highly drug-resistant patients appears low; and for patients in whom the drug seems partially beneficial it could be used in conjunction with a backup automatic implantable cardioverter/defibrillator.

Administration, Oral↗
PubMed1985

The mechanisms of ventricular tachycardia in humans determined by intraoperative recording of the electrical activation sequence.

We recorded ventricular activation sequence during ventricular tachycardia in 76 patients who underwent surgical therapy of refractory ventricular tachycardia. Ventricular tachycardia arose from a discrete site (focal origination) in 28 patients (37%) or resulted from reentry around scar (macroreentry) in 22 patients (29%). The mechanism responsible for ventricular tachycardia was not discernable in the remaining 26 patients (34%), usually because of inadequacy of activation data. We conclude: (1) although focal originating of ventricular tachycardia is common, more frequently the mechanism is either macroreentry or uncertain, as assessed by conventional recording techniques; thus, a search for the "site of earliest activation" during ventricular tachycardia frequently may fail to direct rationally the operative procedure; (2) conventional techniques for intraoperative study of electrical activation during ventricular tachycardia are inadequate.

Cardiac Pacing, Artificial↗