Bernard Lown

Bio: Bernard Lown is an academic researcher from Harvard University. The author has contributed to research in topics: Ventricular fibrillation & Ventricular tachycardia. The author has an hindex of 73, co-authored 330 publications receiving 20320 citations. Previous affiliations of Bernard Lown include Georgetown University & Boston University.

Approaches to Sudden Death from Coronary Heart Disease

Abstract: Sudden cardiac death (SCD) continues unabated. Coronary care units, while effective in lowering hospital mortality, cannot significantly reduce SCD which occurs primarily outside the hospital and accounts for the majority of deaths from coronary heart disease (CHD). In view of the frequent precipitous nature of SCD, only a program which identifies and protects the victim prior to the event can hope to be successful in preventing the majority of SCD. Since it is likely that SCD is due to an arrhythmia, drug prophylaxis might prove effective. In view of the toxicity of currently available agents, it is mandatory to preselect a population at highest risk before embarking on a drug trial. Ventricular premature beats (VPB) may identify subjects susceptible to SCD. Epidemiologic and physiologic information on VPB is reviewed, and proposals are made for studies designed to establish the usefulness of VPB as a risk factor for SCD.

Neural activity and ventricular fibrillation.

Abstract: Ventricular fibrillation is the likely mechanism for sudden death and the leading cause of fatality among patients with coronary heart disease. In this country alone, ventricular fibrillation claim...

New method for terminating cardiac arrhythmias. Use of synchronized capacitor discharge.

Abstract: THE ECTOPIC TACHYCARDIAS are currently treated by either vagal stimulation or drugs. The 3 most effective drugs are quinidine, procainamide hydrochloride, and the digitalis glycosides. When the ectopic mechanism drives the ventricles at rates above 160 per minute, cardiac output falls and coronary blood flow is compromised. This is most likely to occur with ventricular tachycardia which constitutes a serious cardiac emergency requiring immediate treatment. Frequently, however, the arrhythmia cannot be terminated promptly. Reversion with drugs generally involves a time-consuming biologic titration. Since it is impossible in any one patient to predict either the effective or the toxic dose, small increments of antiarrhythmic drugs are given at frequent intervals until a therapeutic end point is reached. The interval between doses is determined by the gravity of the patient's illness as well as by the rapidity of action of the particular agent. It may thus take minutes, days, or even weeks

Aggravation and provocation of ventricular arrhythmias by antiarrhythmic drugs.

Abstract: 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.

The Coronary Care Unit: New Perspectives and Directions

Abstract: In the past two decades there have been momentous advances in the care of patients with cardiovascular ailments. Yet, mortality from coronary-artery disease has remained unaffected. Year after year myocardial infarction and its complications exact the highest toll of any single disease. 1 In large metropolitan hospitals, the death rate from this condition 30 years ago ranged from 30% to 40% and remains unaltered today. Certain facts are forcing reevaluation of the problem. Peak mortality occurs at the very onset of myocardial infarction and then recedes almost exponentially, with 65% of deaths occurring in the initial three days and 85% during the first week of attack. Arrhythmias probably account for 40% of deaths. Of these about two thirds are due to ventricular fibrillation and one third to bradycardia, heart block, and asystole. 2 It is well established that these electrical catastrophes are usually not due to irreversible cardiac damage. On

Dabigatran versus warfarin in patients with atrial fibrillation

Abstract: Background Warfarin reduces the risk of stroke in patients with atrial fibrillation but increases the risk of hemorrhage and is difficult to use. Dabigatran is a new oral direct thrombin inhibitor. Methods In this noninferiority trial, we randomly assigned 18,113 patients who had atrial fibrillation and a risk of stroke to receive, in a blinded fashion, fixed doses of dabigatran — 110 mg or 150 mg twice daily — or, in an unblinded fashion, adjusted-dose warfarin. The median duration of the follow-up period was 2.0 years. The primary outcome was stroke or systemic embolism. Results Rates of the primary outcome were 1.69% per year in the warfarin group, as compared with 1.53% per year in the group that received 110 mg of dabigatran (relative risk with dabigatran, 0.91; 95% confidence interval [CI], 0.74 to 1.11; P<0.001 for noninferiority) and 1.11% per year in the group that received 150 mg of dabigatran (relative risk, 0.66; 95% CI, 0.53 to 0.82; P<0.001 for superiority). The rate of major bleeding was 3.36% per year in the warfarin group, as compared with 2.71% per year in the group receiving 110 mg of dabigatran (P = 0.003) and 3.11% per year in the group receiving 150 mg of dabigatran (P = 0.31). The rate of hemorrhagic stroke was 0.38% per year in the warfarin group, as compared with 0.12% per year with 110 mg of dabigatran (P<0.001) and 0.10% per year with 150 mg of dabigatran (P<0.001). The mortality rate was 4.13% per year in the warfarin group, as compared with 3.75% per year with 110 mg of dabigatran (P = 0.13) and 3.64% per year with 150 mg of dabigatran (P = 0.051). Conclusions In patients with atrial fibrillation, dabigatran given at a dose of 110 mg was associated with rates of stroke and systemic embolism that were similar to those associated with warfarin, as well as lower rates of major hemorrhage. Dabigatran administered at a dose of 150 mg, as compared with warfarin, was associated with lower rates of stroke and systemic embolism but similar rates of major hemorrhage. (ClinicalTrials.gov number, NCT00262600.)

Decreased heart rate variability and its association with increased mortality after acute myocardial infarction

Abstract: A high degree of heart rate (HR) variability is found in compensated hearts with good function, whereas HR variability can be decreased with severe coronary artery disease, congestive heart failure, aging and diabetic neuropathy. To test the hypothesis that HR variability is a predictor of long-term survival after acute myocardial infarction (AMI), the Holter tapes of 808 patients who survived AMI were analyzed. Heart rate variability was defined as the standard deviation of all normal RR intervals in a 24-hour continuous electrocardiogram recording made 11 +/- 3 days after AMI. In all patients demographic, clinical and laboratory variables were measured at baseline. Mean follow-up time was 31 months. Of all Holter variables measured, HR variability had the strongest univariate correlation with mortality. The relative risk of mortality was 5.3 times higher in the group with HR variability of less than 50 ms than the group with HR variability of more than 100 ms. HR variability remained a significant predictor of mortality after adjusting for clinical, demographic, other Holter features and ejection fraction. A hypothesis to explain this finding is that decreased HR variability correlates with increased sympathetic or decreased vagal tone, which may predispose to ventricular fibrillation.

Cardiovascular neural regulation explored in the frequency domain.

Abstract: A consistent link appears to exist between predominance of vagal or sympathetic activity and predominance of HF or LF oscillations, respectively: RR variability contains both of these rhythms, and their relative powers appear to subserve a reciprocal relation like that commonly found in sympathovagal balance. In this respect, it is our opinion that rhythms and neural components always interact, just like flexor and extensor tones or excitatory and inhibitory cardiovascular reflexes, and that it is misleading to separately consider vagal and sympathetic modulations of heart rate. In humans and experimental animals, functional states likely to be accompanied by an increased sympathetic activity are characterized by a shift of the LF-HF balance in favor of the LF component; the opposite occurs during presumed increases in vagal activity. In addition, LF oscillation evaluated from SAP variability appears to be a convenient marker of the sympathetic modulation of vasomotor activity. Although based on indirect markers, the exploration in the frequency domain of cardiovascular neural regulation might disclose a unitary vision hard to reach through the assemblage of more specific but fragmented pieces of information.