Search PubMed⌕ Search

Biomedical subjects

B Lown

Publications and source records attributed to B Lown.

At least 127 records · Page 7Linked to original sources
PubMed1983

Unrecognized organic mental disorders in survivors of cardiac arrest.

Long-term survivors of cardiac arrest may suffer from mild cerebral impairment manifested primarily by personality changes and behavioral symptoms that can be mistaken for emotional responses to illness. The authors report six cases that illustrate the clinical problem of differentiating depression from organic brain dysfunction in this population. The diagnosis is facilitated by observation over time and by information from the spouse on baseline and current function. Chronicity, dysinhibition, apathy, and disturbances of judgment and insight indicate cerebral dysfunction. The accurate diagnosis of cerebral impairment after cardiac arrest is essential to the rehabilitation process.

Adult↗
PubMed1982

Effects of prostacyclin (PGI2) on vulnerability to ventricular fibrillation in the normal and ischemic canine heart.

Prostacyclin (PGI2) has been shown to have a number of beneficial effects on the cardiovascular system. However, its effects on ventricular electrical properties remain unexplored. We studied the effects of this naturally occurring humoral agent on ventricular vulnerability in the normal heart and in two models of myocardial ischemia: coronary artery occlusion and release and ergonovine-induced coronary vasoconstriction. Prostacyclin lowered the vulnerable period threshold in the normal animal. PGI2 had no effect on ventricular vulnerability when the blood pressure was controlled with phenylephrine and was not protective during either occlusion or release. However, when blood pressure was controlled, PGI2 did not reverse the vasoconstrictor and profibrillatory effects of ergonovine.

Animals↗
PubMed1982

Tocainide for refractory symptomatic ventricular arrhythmias.

Tocainide, an oral form of lidocaine, was employed in 120 patients with recurrent malignant ventricular arrhythmia refractory to conventional antiarrhythmic drugs. After discontinuation of all antiarrhythmic agents, patients underwent control studies including 48 hours of ambulatory electrocardiographic monitoring and maximal symptom-limited exercise testing. One hundred patients had frequent as well as repetitive ventricular premature beats whereas in 20 patients, because of infrequency of ectopic activity, invasive electrophysiologic studies were carried out to provoke a repetitive ventricular response. Tocainide therapy was begun at 1,200 mg daily and increased to 2,400 mg daily guided by drug efficacy and the occurrence of adverse effects. After 48 hours of treatment with a fixed dose, drug action was evaluated by repeat monitoring and exercise stress testing or electrophysiologic testing. Fifty-five patients (46 percent) responded to tocainide. The average daily dose of drug and peak blood levels were equivalent in responders and nonresponders. Adverse effects occurred in 42 patients (35 percent) and were primarily related to the central nervous system. Lidocaine predicted the response to tocainide in 78 percent of patients. Thirty-four patients were continued on long-term maintenance therapy. After an average follow-up period of 16 months (range 2 to 39), treatment with the drug was discontinued in nine patients. The remaining 25 patients have had no adverse effects and no recurrence of ventricular arrhythmia.

Adult↗
PubMed1982

Use of radionuclide ventriculography for assessment of changes in myocardial performance induced by disopyramide phosphate.

Disopyramide phosphate may precipitate heart failure in susceptible patients with cardiomegaly. To identify those at risk, gated radionuclide ventriculography (RVG) was performed in two groups. Eleven patients without evidence of structural heart disease constituted group 1, and 12 with impaired ventricular function made up group 2. RVG was carried out before and 2 hours after administration of a single 300-mg dose of disopyramide orally. After disopyramide mean left ventricular ejection fraction (EF) decreased in the 12 patients in group 2 (35% to 26%) (p less than 0.01); depression of function was most pronounced in regions with the poorest baseline value. Of the 11 patients in group 1 (mean EF 60%), EF was reduced after disopyramide in only one. Serum levels of drugs were comparable in patients in both groups (3.1 vs. 3.7 micrograms/ml). We conclude that (1) patients with left ventricular dysfunction are particularly susceptible to the depressant effects of disopyramide; (2) RVG is a sensitive technique for detecting disopyramide-induced changes in ventricular performance; and (3) RVG before and shortly after a dose of disopyramide orally may help to identify those patients at high risk.

Adolescent↗
PubMed1982

Pindolol for ventricular arrhythmia.

The role of pindolol in treating ventricular arrhythmia was studied in 43 patients with this disorder. Of these patients, 23 had coronary heart disease, 5 had valvular disease, and 15 had no demonstrable heart disease. patients underwent acute drug testing with 20 mg pindolol (phase 1) followed by maintenance therapy (phase 2) for 3 days (20 to 80 mg daily). Efficacy during both phases was evaluated by ambulatory monitoring and treadmill exercise testing. During acute drug testing, 50% of te patients responded. A concordant response between acute drug testing and phase 2 monitoring was seen in 81% (p less than 0.005) of patients and between acute drug testing and phase 2 exercise testing in 88% (p less than 0.005). Arrhythmia was suppressed during the phase 2 exercise test in 53% of patients; these included 80% of the patients without heart disease and 50% of those with coronary heart disease (not significant). During phase 2 monitoring, 60% of patients without heart disease responded vs. 25% with coronary heart disease (not significant). Side effects occurred in 12 patients (28%). These included congestive heart failure (3 patients); fatigue, lightheadedness, and insomnia (2 patients each); nausea, tremor, urinary retention, and bronchospasm (1 patient each); and aggravation of arrhythmia (7 patients). It is concluded that although pindolol alone is marginally effective for treating ventricular arrhythmia in patients with coronary heart disease, it appears to be more valuable in those without heart disease, especially when arrhythmia is provided by exercise. Acute drug testing proved highly predictive of the results with maintenance therapy and is a valuable rapid-screening procedure for identifying potential responders to pindolol.

Adult↗
PubMed1982

Influence of the autonomic nervous system on coronary blood flow during partial stenosis.

Partial coronary stenosis produces cyclical changes in coronary blood flow (CBF) which are the result of spontaneous aggregation and disaggregation of platelet plugs at the site of occlusion. The possible influence of the autonomic nervous system on this phenomenon has not been hitherto determined. The present study was performed in 20 chloralose-anesthetized dogs in which the effects of bilateral vagotomy and stellectomy were examined during partial stenosis of the left circumflex coronary artery. Vagotomy reduced the frequency of CBF oscillations from 11.5 +/- 2.1 to 5.0 +/- 2.1 cycles/hr (p less than 0.05). The magnitude of the flow changes was reduced from 13.8 +/- 4.0 to 9.7 +/- 3.0 ml/min (NS). Bilateral cervical stellectomy reduced the frequency of CBF changes from 7.8 +/- 2.7 to 3.7 +/- 1.3 cycles/hr (p less than 0.025) and their magnitude from 10.6 +/- 2.5 to 5.6 +/- 1.8 ml/min (P less than 0.05). In five dogs in which cyclical CBF changes were reduced or abolished by decentralizing the stellate ganglia, electrical stimulation of the main body of the left ganglion evoked or enhanced the oscillations in two dogs, had no distinct effect in two dogs, and elicited no response in one dog. A 5-minute infusion of 0.5 microgram/kg/min and 0.75 microgram/kg/min epinephrine (four dogs) provoked the CBF changes in all animals for a period of 5 to 10 minutes. Blockade of muscarinic receptors by 0.2 mg/kg atropine resulted in a significant attenuation of flow changes, which may at least in part have been due to a direct effect of atropine on platelets. We conclude that cardiac sympathetic tone significantly influences the CBF pattern during critical coronary stenosis. While the afferent limb of the vagus may in part mediate this effect via a reflex increase of adrenal medullary catecholamines, the role of the efferent vagus awaits further clarification.

Animals↗
PubMed1982

Management of patients at high risk of sudden death.

Patients who experience malignant ventricular arrhythmias (i.e., ventricular fibrillation or ventricular tachycardia with syncope or with hemodynamic compromise) are at high risk of sudden death. Such patients can now be protected from recurrent arrhythmias by the use of conventional and experimental drugs. Drug therapy must be individualized, and this requires a system of testing to expedite the selection of the most efficacious and least toxic agent. In 85% of these patients, the frequency and advanced grades of ventricular premature beats exposed either by Holter monitoring or by maximal exercise stress testing provide an adequate target for assessing drug action. Only 15% of patients require invasive electrophysiologic studies to guide antiarrhythmic therapy. In 10% of instances, antiarrhythmic drugs cause aggravation of arrhythmias. When drug therapy is individualized, an effective program can be achieved for 80%, with less than a 3% incidence of sudden death annually.

Anti-Arrhythmia Agents↗
PubMed1982

Effects of sulfinpyrazone on ventricular vulnerability in the normal and the ischemic heart.

The effects of sulfinpyrazone were studied in 33 chloralose-anesthetized dogs. Ventricular fibrillation thresholds, mid diastolic thresholds and duration of the effective refractory period were determined in the normal heart after intravenous administration of sulfinpyrazone, 30 mg/kg body weight. The drug significantly raised the ventricular fibrillation threshold by 24 percent and the mid diastolic threshold by 36 percent and prolonged the effective refractory period by seven percent. The influence of sulfinpyrazone during acute myocardial ischemia was evaluated before and during a 10 minute occlusion of the left anterior descending coronary artery and after abrupt release of the occlusion. Although the drug afforded significant protection during coronary occlusion, it had no effect on the ventricular fibrillation threshold after reperfusion. Because potent cardiocardiac reflexes are elicited during ischemia, the influence of sulfinpyrazone on the ventricular fibrillation threshold was studied during norepinephrine infusion. Sulfinpyrazone attenuated the reduction of the ventricular fibrillation threshold during sympathetic humoral stimulation. Its effect was additive to beta adrenergic blockade with practolol and membrane stabilization with lidocaine. This investigation suggests that sulfinpyrazone exerts significant effects on ventricular vulnerability of both the normal and the ischemic myocardium. Further studies are needed to elucidate its precise mechanism of action.

Animals↗
PubMed1982

Long-term survival of patients with malignant ventricular arrhythmia treated with antiarrhythmic drugs.

The protective effect of antiarrhythmic agents for patients with malignant ventricular arrhythmia (defined as noninfarction ventricular fibrillation or sustained hemodynamically compromising ventricular tachycardia) remains uncertain. We have analyzed survival among 123 such patients (98 males, 25 females, average age 53.6 years) dependent on the abolition of antiarrhythmic drugs of salvos of ventricular tachycardia and R-on-T ventricular premature beats (Lown grades 4B and 5). Over an average follow-up of 29.6 months there were 35 deaths (11.2 percent annual mortality rate) of whom 23 patients succumbed suddenly (8.2 percent annual mortality rate). Among 98 patients in whom antiarrhythmic drugs abolished grades 4B and 5 ventricular premature beats, only 6 sudden deaths occurred for a 2.3 percent annual mortality rate. Of the 25 patients in whom advanced ventricular premature beats were not controlled, 17 died suddenly. Seventy-nine patients had left ventricular studies suitable for analysis. Among 44 patients with left ventricular dysfunction, control of ventricular premature beats was a critical element predicting survival. The annual sudden death rate for the 12 noncontrolled patients with left ventricular dysfunction was 41 percent contrasting with only 3.1 percent for the 32 patients with similar abnormalities in ventricular function in whom advanced ventricular premature beats were abolished. It is concluded that antiarrhythmic drugs can protect against the recurrence of life-threatening arrhythmias in patients who have manifest ventricular fibrillation or ventricular tachycardia and that abolition of certain advanced grades of ventricular premature beats provides an effective therapeutic objective.

Adult↗
PubMed1982

Clinical management of ventricular arrhythmias.

Ventricular arrhythmias are associated with a high risk of sudden cardiac death. Thus, a sense of urgency attends the issue of identifying and treating susceptible patients in advance of the catastrophic event. Expeditious selection of the most appropriate and least toxic drugs for each patient at risk can be accomplished in more than 80% of cases with an inexpensive noninvasive approach.

Arrhythmias, Cardiac↗
PubMed1982

Experimental studies of psychophysiological factors in sudden cardiac death.

Earlier research in the field of sudden cardiac death is reviewed. Such studies have largely oriented towards the provocation of myocardial injury and asystole in normal animals. However, such investigations constitute an inadequate model to describe the clinical appearance of sudden death, where underlying coronary disease is often present and the precipitating event is usually ventricular fibrillation rather than asystole. This report describes a series of studies designed to investigate the processes underlying cardiac vulnerability and the influence upon it of various psychological stresses. It is concluded that the primary mediator of ventricular vulnerability is the sympathetic nervous system. The efferent vagus appears to exert some protective influence against arrhythmias due to adrenergic stimulation. An appropriate clinical strategy for the treatment of malignant arrhythmias would therefore involve attempts to decrease cardiac sympathetic drive whilst at the same time enhancing vagal tone. Treatments are described which aim to bring this situation about by the use of clonidine, morphine sulphate, l-tryptophan and tyrosine. The use of neurochemical agents in this context appears promising.

Animals↗
PubMed1982

Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs.

Antiarrhythmic drugs may aggravate or even induce ventricular arrhythmias. This type of adverse reaction is becoming more prevalent as the use of antiarrhythmic agents becomes more widespread. In a retrospective analysis of antiarrhythmic drug action, a worsening of arrhythmia was observed in 80 of 722 (11.1%) antiarrhythmic drug tests in 53 of 155 patients being treated for ventricular tachyarrhythmias. Aggravation of arrhythmias was defined by occurrence of a fourfold increase in the frequency of ventricular premature complexes, a 10-fold increase in repetitive forms, or the first emergence of sustained ventricular tachycardia coincident with time course of action of the particular drug under study. Such aggravation was noted with each of nine drugs tested: quinidine, procainamide, disopyramide, propranolol, metoprolol, aprindine, mexiletine, tocainide and pindolol. The frequency of this complication for a specific drug ranged from 5.9-15.8%. Blood drug concentrations were consistently in the therapeutic range. A study of the variability of ventricular arrhythmia during 48-hour Holter monitoring and exercise stress testing in no instance showed arrhythmia enhancement commensurate with that defining aggravation. Our data suggest that this potentially serious complication is not readily predictable and requires a systematic approach to antiarrhythmic drug testing before a patient is prescribed a long-range maintenance program.

Adolescent↗