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Biomedical subjects

B Lown

Publications and source records attributed to B Lown.

At least 199 records · Page 11Linked to original sources
PubMed1977

Neural and psychologic mechanisms and the problem of sudden cardiac death.

Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.

Animals↗
PubMed1977

Management of patients with malignant ventricular arrhythmias.

The patient with recurrent malignant ventricular arrhythmias (ventricular fibrillation or ventricular tachycardia with syncope) presents a complex therapeutic problem. To examine this problem, a study was made of 43 consecutive patients with such arrhythmias (mean age 54 years for the 33 men and 43 years for the 10 women). Arrhythmias were not precipitated by either remediable clinical conditions or acute myocardial infarction. The population was divided into two nonrandomized groups based on the type of therapeutic intervention employed. The 26 patients in Group 1 (20 with ventricular fibrillation, 6 with ventricular tachycardia) were subjected to a systematic attempt to select two independently effective antiarrhythmic drugs. Acute drug testing was followed by drug usage over 48 to 72 hours with drug efficacy determined with use of ambulatory monitoring and exercise stress. The 17 patients in Group 2 (10 with ventricular fibrillation, 7 with ventricular tachycardia) received standard antiarrhythmic therapy based on clinical factors and "therapeutic" blood drug concentrations. Twenty-four of 26 patients in Group 1 (92 percent) demonstrated control of arrhythmias and are alive at a mean follow-up period of 17 months. Of 121 drug tests, 47 (39 percent) were effective, 58 (48 percent) were ineffective and 16 (13 percent) provoked major adverse effects. The most effective combination of drugs involved a beta adrenergic blocking agent, a cardiac glycoside and quinidine. Ten of 17 patients in Group 2 (59 percent) have died after a mean follow-up period of 14.8 months. Elements of a successful management program are outlined.

Adult↗
PubMed1977

Ventricular premature beats and anatomically defined coronary heart disease.

Ambulatory 24 hour electrocardiographic monitoring was performed in 124 patients before cardiac catheterization and coronary angiography. Ventricular premature beats were demonstrated in 83% of all patients. Ectopic activity persisted for at least 3 of the 24 hours in 75% of the 84 patients with coronary heart disease, 61% of 28 with other heart disease and in 24% of 12 normal subjects. The prevalence and grade of ventricular premature beats were increased in the 57 patients with multivessel disease compared with values in the 27 patients with one vessel disease (P less than 0.01). Findings in the latter group did not differ from those of normal subjects. The presence of elevated left ventricular end-diastolic pressure of asynergy was associated with increased ventricular ectopy. Of 15 patients having both asynergy and elevated left ventricular end=diastolic pressure (more than 19 mm Hg), 40% had paroxysms of ventricular tachycardia and 67% had coupled beats; these findings were present in 6 and 12%, respectively, of the 34 patients without asynergy or pressure abnormality (P less than 0.005). Repeat monitoring performed in 65 patients demonstrated greater reproducibility of advanced grades of ventricular premature beats among those with the most severe lesions. For the individual patient the prevalence and grade of ventricular ectopy may not always correlate with the severity of coronary artery disease or degree of left ventricular dysfunction.

Adult↗
PubMed1977

Effect of a digitalis drug on ventricular premature beats.

To determine the efficacy of digitalis drugs in suppressing ventricular ectopic activity, 142 patients with frequent (greater than 1 per minute) ventricular premature beats underwent acetyl strophanthidin tolerance testing. In 65 patients (46 per cent), frequency and grade were reduced during testing. In 37 (26 per cent), the ectopic activity remained unaltered; frequency increased during testing in the remaining 40 patients (28 per cent). In the group with a suppressive effect, ventricular premature beats decreased by 82 per cent, with complete abolition of arrhythmias in 46 per cent. The three groups were not distinguishable clinically by either the type or the extent of heart disease. The antiarrhythmic action of acetyl strophanthidin did not appear to depend upon its positive inotropic action. In some patients it appears to be due to an indirect reduction of Purkinje-fiber automaticity resulting from enhanced vagus-nerve activity that thereby lessens adrenergic tone on the heart.

Adolescent↗
PubMed1977

Verbal conditioning of angina pectoris during exercise testing.

A 40 year old man with far advanced coronary heart disease consistently experienced pain and exhibited marked S-T segment depression after 44 crossings during a Master two-step test. When the number of times traversed was miscounted so that he exercised less, the pain occurred at the precise count of 44 and he showed the same marked degree of S-T depression. However, when the count was accurate, he had neither pain nor S-T segment deviation at the reduced exercise level. The possible basis for verbal conditioning provoking angina pectoris is explored.

Adult↗
PubMed1977

Acute blood pressure elevation and ventricular fibrillation threshold during coronary occlusion and reperfusion in the dog.

The effect of acute elevation of arterial blood pressure on the ventricular fibrillation threshold was examined in 19 closed chest dogs anesthetized with chloralose during 10 minutes of occlusion followed by abrupt reperfusion of the left anterior descending coronary artery. Ventricular fibrillation threshold was determined using two methods of electrical testing: sequential R/T pulsing and the train of stimuli method. Blood pressure was increased with an intravenous injection of the alpha adrenergic stimulator phenylephrine. Acute hypertension significantly diminished the enhanced vulnerability associated with coronary occlusion. After denervation of the carotid sinus and aortic arch baroreceptors, elevation of blood pressure failed to affect vulnerability during occlusion. In both intact and denervated animals, the predisposition to ventricular fibrillation after reperfusion was unchanged by the increase in blood pressure. It is suggested that withdrawal of sympathetic tone mediated by the baroreceptor reflex is the basis for the protection against ventricular fibrillation resulting from elevation of blood pressure. The failure of acute hypertension to alter vulnerability during reperfusion suggests that the predisposition to ventricular fibrillation during reperfusion is due to mechanisms other than those operating during coronary occlusion.

Animals↗
PubMed1977

Effect of stellectomy and vagotomy on ventricular refractoriness in dogs.

The influence of tonic sympathetic and parasympathetic nervous system activity on ventricular refractory period duration was studied in 13 mongrel dogs. Strength-interval curves were obtained from the apex of the right ventricular endocardium with a transvenous bipolar catheter. The effects of sympathetic activity were assessed by unilateral and bilateral stellectomies and tonic vagal effects were studied by inducing cholinergic blockade with atropine (0.2 mg/kg) and by sectioning the cervical vagi bilaterally. Right stellectomy shifted the strength-interval curve 3-5 msec earlier (P less than 0.005). In contrast, left stellectomy shifted the strength-interval curve 4-7 msec later (P less than 0.001). Thus, right and left unilateral stellectomy produced opposite effects. However, when the contralateral ganglion was removed, right and left stellectomy produced qualitatively similar effects, increasing refractoriness. The net effect of bilateral stellectomy was to shift the strength-interval curve 8-10 msec later (P less than 0.001) and this was primarily dependent on left stellectomy. Blockade of vagal efferent activity with atropine shifted the strength-interval curve 3-6 msec earlier (P = .001). Removal of vagal afferent activity by vagotomy during atropine blockade shifted the strength-interval curve 2-3 msec earlier (P = 0.03). It is concluded that both stellate ganglia exert qualitatively similar effects on cardiac refractoriness; however, the left ganglion dominates and unilateral right stellectomy produces a paradoxical decrease in refractoriness. The sympathetic effects are tonically antagonized by vagal activity.

Animals↗
PubMed1976

Acute oral testing for determining antiarrhythmic drug efficacy. I. Quinidine.

Acute oral drug testing with quinidine was used in 18 patients with high grade ventricular arrhythmia. This method involves administering a single large dose of the antiarrhythmic agent, monitoring heart rhythm by means of programmed trendscription and determining blood drug levels at selected intervals. After quinidine was given in a dose of 0.6 g, 10 patients had a positive response, defined as a 50% or greater reduction in ventricular premature beats and abolition of repetitive ectopic beats. Drug action began a mean of 88 minutes after administration, and the mean peak blood quinidine level was 3.2+/-0.5 (standard error) mug/ml. Four patients had a paradoxic increase in arrhythmia. In nine patients the response to acute drug testing was compared with the response to maintenance quinidine therapy with doses of 1.2 and 1.8 g/day. The presence of arrhythmia was assessed with 24 hour ambulatory monitoring and exercise stress testing. With both techniques, seven of nine patients showed results concordant with those of acute testing. Disparity in results of the two methods of drug administration was explained by the serum concentration of quinidine. Acute oral drug testing provides a new approach for determining expeditiously whether quinidine is effective or hazardous in an individual patient.

Administration, Oral↗
PubMed1976

Ventricular electrical instability in the conscious dog: effects of psychologic stress and beta adrenergic blockade.

The effect of psychologic stress on cardiac vulnerability was examined in 10 conscious dogs. The repetitive extrasystole threshold was employed as a measure of susceptibility to ventricular fibrillation. Instrumental aversive conditioning constituted a stressful environment. The repetitive extrasystole threshold decreased by nearly 50 percent during 3 days in which the animals were exposed to the stressful environment. When Tolamolol hydrochloride, a cardioselective beta adrenoceptor blocking agent, was administered before a stress session, the repetitive extrasystole threshold was unaltered from the control value. Thus, stress-evoked changes in cardiac vulnerability are mediated through the sympathetic nervous system.

Action Potentials↗
PubMed1976

Basis for recurring ventricular fibrillation in the absence of coronary heart disease and its management.

A 39-year-old man twice experienced ventricular fibrillation and exhibited numerous ventricular premature beats. Coronary arteries were normal, and no impaired cardiac function was found upon catheterization. Evidence was adduced that the ventricular premature beats were related to higher nervous activity. The patient had serious psychiatric problems; the ventricular premature beats were provoked by psychophysiologic stress, increased during REM sleep, were reduced by meditation, and were controlled by beta-adrenergic blockade, phenytoin and digitalization. We conclude that psychologic and neurophysiologic factors may predispose to life-threatening cardiac arrhythmia in the absence of organic heart disease. Effective management of the recurrent ventricular arrhythmia involved; acute drug testing for assessing antiarrhythmic efficacy; use of programmed trendscription to provide on-line information on drug action; a treatment program involving more than one agent; and use of measures to reduce sympathetic nervous activity.

Adult↗
PubMed1976

Nitrous oxide as an analgesic in acute myocardial infarction.

Nitrous oxide in a concentration of 35% has been shown to ameliorate the pain of acute myocardial infarction. This conclusion was reached on the basis of a double-blind study in 69 patients and a clinical study in an additional 42 patients. The use of nitrous oxide was not accompanied by hemodynamic changes or significant adverse reactions.

Acute Disease↗
PubMed1976

Effect of vagus nerve stimulation upon excitability of the canine ventricle. Role of sympathetic-parasympathetic interactions.

The effect of vagus nerve stimulation on ventricular excitability was studied in 28 dogs under various conditions of adrenergic neural tone. Strength-interval curves were delineated from the apex of the right ventricular endocardium with a transvenous bipolar catheter. Vagus nerve stimulation in both closed chest and open chest dogs shifted the strength-interval curve 6 to 8 msec later into electrical diastole (P less than 0.001). Left stellate ganglion stimulation shifted the strength-interval curve 9 to 11 msec earlier into diastole (P less than 0.001). The effect of simultaneous left stellate ganglion and vagus nerve stimulation was not significantly different from that of left stellate ganglion stimulation alone. The influence of vagus nerve stimulation on the strength-interval curve under basal conditions was abolished by acute beta adrenergic blockade with propranolol. It is concluded that vagus nerve stimulation affects ventricular excitability as well as vulnerability by opposing the effects of sympathetic neural tone.

Adrenergic beta-Antagonists↗