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Biomedical subjects

B Lown

Publications and source records attributed to B Lown.

At least 163 records · Page 9Linked to original sources

Episodic drug treatment in the management of paroxysmal arrhythmias.

The use of maintenance medication in the treatment of episodic cardiac arrhythmia is often complicated by problems of patient compliance with therapy and adverse side effects. Furthermore, repeated hospitalizations and cardioversions are both costly and inconvenient. A method of intermittent drug therapy is described in which antiarrhythmic medication is taken only at the onset of an episode of arrhythmia. This approach was effective in terminating both supraventricular and ventricular arrhythmias in 24 of 32 patients and obviated the need for hospitalization and further treatment. In cases in which maintenance therapy was required because of the frequent occurrence of arrhythmia, periodic drug therapy was still of value in the treatment of breakthrough episodes. The use of intermittent drug therapy is a safe and effective approach to the management of episodic cardiac arrhythmia and, in addition, results in significant financial saving.

Adolescent↗

Protective effect of verapamil on vulnerability to ventricular fibrillation during myocardial ischaemia and reperfusion.

The effects of verapamil on vulnerability to ventricular fibrillation were studied in 55 chloralose-anaesthetised dogs. Ventricular fibrillation threshold was measured before and during a 10 min period of left anterior descending coronary artery occlusion and following abrupt release of occlusion. The action of intravenous verapamil (0.01 mg.kg-1.min-1, following a 0.1 mg.kg-1 bolus) on vulnerability to fibrillation was examined before and during coronary artery occlusion and reperfusion. While the infusion of verapamil did not alter the ventricular fibrillation threshold in the nonischaemic myocardium, the vulnerable period threshold was raised and the incidence of spontaneous ventricular fibrillation was reduced both after coronary artery occlusion and release. Since cardiocardiac sympathetic reflexes are elicited in response to coronary artery occlusion, the effect of verapamil on vulnerability during left stellate ganglion stimulation and during noradrenaline infusion was investigated. Verapamil completely prevented the reduction in vulnerable period threshold during sympathetic nerve stimulation or noradrenaline infusion. This study suggests that the antifibrillatory action of verapamil during coronary artery occlusion may be, in part, related to antagonism of enhanced adrenergic input to the heart, while the mechanism of protection during reperfusion is as yet uncertain.

Adrenergic Fibers↗

Ventricular premature beats and coronary risk factors.

Of 10,119 men aged 35 to 57 years studied in the Multiple Risk Factor Intervention Trial (MRFIT), ventricular premature beats (VPBs) were more frequent among the 112 men who reported having previously had a myocardial infarction (MI) (22.3%) as well as among the 143 men with a history of diabetes mellitus (13.3%) than among the remaining 9864 (7.6%). There was no demonstrable association between VPBs and cholesterol or blood pressure levels, either overall or in various age groups. There was, however, a strongly positive relationship between VPBs and age (p less than 0.001). A positive association between VPBs and smoking was present which was statistically significant overall (risk ratio = 1.21, 95% confidence limits from 1.03 to 1.43), as well as in the age groups 35 to 39 years (1.74, 1.13 to 2.68) and 55 to 57 years (1.50, 1.01 to 2.22). This association, if confirmed, raises the question of whether VPBs offer a mechanism for the increased morbidity and mortality from coronary heart diseases among cigarette smokers compared with nonsmokers.

Adult↗

Ethmozin, a new antiarrhythmic drug for suppressing ventricular premature complexes.

Ethmozin, a phenothiazine derivative, is an antiarrhythmic drug synthesized in the USSR. Preliminary data suggest that it is effective against a diversity of ectopic arrhythmias. The present study, carried out in the USSR, was designed to assess efficacy and patient tolerance of this new drug. Thirty-seven patients with chronic, persistent, frequent and symptomatic ventricular premature complexes (VPCs) were studied. VPCs were exposed by means of 24-hour ambulatory monitoring and exercise stress testing. Two drug schedules were used. Group 1, consisting of 11 patients, received 225 mg/day of ethmozin, while group 2, consisting of 26 patients, received 600 mg/day. Acute drug testing with a single large dose of ethmozin was followed by multiple dosing for a minimum of 4 days. Placebo was given in a single-blind fashion only to responders. Only two patients in group 1 had a significant reduction in VPCs as evaluated by both monitoring and exercise testing. Fourteen patients in group 2 (54%) showed striking suppression of VPCs. Mild and transiet effects were encountered in only four of the 37 patients. We conclude that ethmozin appears to be a well-tolerated, relatively effective agent for controlling VPCs.

Action Potentials↗

Psychophysiologic factors in sudden cardiac death.

Sudden cardiac death due to ventricular fibrillation is the leading cause of fatality in the industrially developed world. A considerable body of evidence indicates that the higher nervous system modifies electrical activity of the heart and may trigger sudden death. The evidence for increased risk for ventricular fibrillation due to psychophysiologic factors is supported predominantly by animal studies, but increasing evidence is forthcoming from human studies. The involvement of psychiatrists, psychologists, and cardiologists in a multidisciplinary approach to managing patients at risk for sudden death from ventricular fibrillation is yielding significant insights and prolonging their lives.

Animals↗

Digitalis drugs and vulnerability to ventricular fibrillation.

The effect of acetylstrophanthidine (AS), a rapid-acting digitalis-like agent, on the ventricular fibrillation (VF) threshold was examined in normal and denervated chloralose-anesthetized dogs. In neurally intact dogs an intravenous bolus of AS (0.075 mg/kg) increased the VF threshold up to a maximum 50% (P less than 0.01) within 30 min after injection. The augmented VF threshold following intravenous administration of AS was not altered by vagotomy. Bilateral stellectomy in vagotomized dogs, as well as carotid sinus and aortic arch denervations, however, prevented the AS induced increase in VF threshold. In neurally intact dogs beta-adrenergic blockade with propranolol (0.25 mg/kg) precluded AS effects. These data suggest that the increase in the VF threshold resulting from AS administration in the normal canine ventricle is due to withdrawal of sympathetic tone mediated via the baroreceptor reflex. The direct effect of AS on the myocardium is to decrease the VF threshold.

Adrenergic beta-Antagonists↗

Continuous monitoring for ventricular arrhythmias during exercise tests.

Exercise stress testing is being increasingly used to verify exercise-induced arrhythmia and to aid in assessing antiarrhythmic drug efficacy. The true prevalence of ventricular arrhythmia during exercise testing is underestimated by means other than continuous monitoring. We compared the yield of ventricular premature beats (VPBs) between a continuous recording system ("trendscription") and intermittent monitoring among 39 patients undergoing a total of 50 consecutive exercise studies. By intermittent monitoring, 22 (44%) of 50 of the exercise tests demonstrated VPBs; with trendscription, 31 (62%) exhibited such arrhythmia. Most striking, however, was a sixfold increase in the disclosure of complex and repetitive forms of VPBs (56 vs nine episodes). Thus, this form of monitoring presents a cost-efficient, on-line method that allows concentration on the patient during exercise as well as clear recording of all arrhythmic events.

Anti-Arrhythmia Agents↗

Effect of nitroglycerin on vulnerability to ventricular fibrillation during myocardial ischemia and reperfusion.

The effect of nitroglycerin on vulnerability to ventricular fibrillation was examined in 44 chloralose-anesthetized dogs. In 19 animals ventricular fibrillation threshold was measured before and during a 10 minute period of occlusion of the left anterior descending coronary artery followed by abrupt release of occlusion. Fibrillation threshold was determined using the single stimulus and train of stimuli methods. The influence of nitroglycerin on vulnerability was assessed with and without prevention of the drug's hypotensive effect by intravenous injection of phenylephrine. In the nonischemic myocardium, infusion of nitroglycerin alone or in combination with phenylephrine did not alter the ventricular fibrillation threshold. However, during both coronary occlusion and reperfusion, administration of nitroglycerin alone afforded partial protection against vulnerability to ventricular fibrillation. Nearly complete protection was imparted by combined administration of nitroglycerin and phenylephrine. The incidence of spontaneous ventricular fibrillation during reperfusion was significantly reduced by combined administration of nitroglycerin and phenylephrine. It is concluded that infusion of nitroglycerin decreases susceptibility to ventricular fibrillation during both acute myocardial ischemia and reperfusion and that this beneficial action is substantially enhanced when the drug's hypotensive effect is prevented.

Animals↗

Central serotonergic agents raise the repetitive extrasystole threshold of the vulnerable period of the canine ventricular myocardium.

Systemic administration of three central serotonergic agents, melatonin, 5-methoxytryptophol, and 6-chloro-2-(1-piperazinyl)-pyrazine (MK-212), produced significant increases in the threshold of the vulnerable period for repetitive electrical activity in the canine cardiac ventricle. MK-212 was effective despite bilateral vagotomy. The specific serotonin antagonist, metergoline, blocked the effect of MK-212 on the threshold. An increase in central serotonergic activity may inhibit the flow of arrhythmogenic sympathetic nerve traffic from the brain to the heart.

Animals↗