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Biomedical subjects

B F Hoffman

Publications and source records attributed to B F Hoffman.

At least 127 records · Page 7Linked to original sources
PubMed1976

Ventricular paired pacing to control rapid ventricular heart rate following open heart surgery. Observations on ectopic automaticity. Report of a case in a four-month-old patient.

An unusual case is presented in which an atrioventricular (A-V) junctional tachycardia at a rate of 285 beats/min developed in the immediate postoperative period following surgical repair (a Mustard procedure) of transposition of the great vessels in a four-month-old infant. With that heart rate the systolic blood pressure bacame 35-40 mm Hg and urinary output ceased. Ventricular paired pacing was employed successfully to halve the mechanically effective ventricular rate. This resulted in a clinically effective blood pressure and return of normal urinary output. The clinical course of the A-V junctional tachycardia, plus its response to several interventions, suggested that the mechanism of the A-V junctional tachycardia was automatic rather than re-entrant. The study demonstrates that ventricular paired pacing for the control of cardiac arrhythmias is a useful clinical technique in selected cases.

Atrioventricular Node↗
PubMed1976

Intraoperative recording of the His bundle electrogram in man. An assessment of its precision.

To estimate the effect of distance between the electrode and the signal source on the amplitude of the His bundle electrogram (HBE) recorded during open heart surgery, a specially designed probe, containing six pairs of closely spaced (1 mm) electrodes was placed on the endocardial surface of the right atrium such that each electrode pair was parallel to the course of the His bundle. The amplitude of the HBE recorded through electrodes closest to the His bundle ranged from 0.76 to 2.44 mV, at 1mm from 0.38 to 1.13 mV, at 2mm from 0.27 to 0.86 mV, and at 3 mm from 0.2 to 0.44 mV. Maximal amplitude of HBE decreased by 57% at 1mm, 73% at 2 mm, and 82% at 3mm. The percent decrease was initially rapid, then declined more slowly at distances greater than 1 mm, resembling in form data obtained previously in animal studies by different techniques. Since the maximum HBE was greater than 1.0 mV in nine of 11 patients, and equal to or greater than 1.0 mV in only two of 11 patients at 1 mm, and less than 1.0 mV in all patients 2.0 mm from the maximal HBE, the anatomic location of the His bundle can be estimated from HBE amplitude. Intracardiac electrograms, recorded through closely spaced bipolar electrodes during open heart surgery, afford clinically useful precision in locating the specialized conduction tissue of the heart.

Adolescent↗
PubMed1976

Electrophysiologic properties and response to pharmacologic agents of fibers from diseased human atria.

We used standard microelectrode techniques to record action potentials of human right atrial fibers obtained during cardiac surgery, and correlated these potentials with clinical and preoperative ECG data. Human atrial fibers were classified as follows: Group A (ten patients) had a maximum diastolic potential (MDP) of -71.4 +/- 5.1mV (mean +/- SD), and action potentials that were primarily fast responses. These atria were normal or slightly dilated. In group B (12 patients) MDP was 50.3 +/- 5.7 mV; action potentials were slow responses and the atria were moderately to markedly dilated. Atrial arrhythmias occurred in four group B and no group A patients. The ECG revealed a signficant difference (P less than 0.005) in P wave duration: group A, 89 +/- 3.0 msec; group B, 111 +/- 6.0 msec. Verapamil, 0.1 mg/L, markedly depressed only the action potential plateau of group A. Procainamide 1-100 mg/L had equivalent effects on fibers of both groups A and B, effects which were small at dosages of less than 40 mg/L. Procainamide did not depress slow response automaticity, but verapamil (0.1-1 mg/L) did.

Action Potentials↗
PubMed1976

Effects of pulsatile and nonpulsatile coronary perfusion on performance of the canine left ventricle.

This study compares the effect of pulsatile (Group C, Fib/P) and nonpulsatile (Group B, Fib/NP) coronary perfusion on myocardial performance during 2 hours of normothermic ventricular fibrillation. Group A (BH/NP), used as a base-line observation, consisted of 2 hours of nonpulsatile coronary perfusion in beating hearts. The assessment of ventricular performance included diastolic ventricular compliance, myocardial oxygen consumption and lactate extraction, regional myocardial blood flow, and histology. After 120 minutes of ventricular fibrillation, Group C showed normal ventricular diastolic compliance as compared to a 50 per cent decrease in Group B (p less than 0.01). Myocardial oxygen consumption was not significantly different from that in Group B. Because of a 70 per cent increase in oxygen extraction above Group B (p less than 0.05), total left ventricular myocardial blood flow was reduced (103 +/- 23 versus 260 +/- 36 ml. per 100 Gm. per minute, p less than 0.05) and had near-constant resistance. Lactate extraction was significantly greater and more stable as compared to Group B (9.28 +/- 1.33 versus 1.8 +/- 1.08, p less than 0.05). Left ventricular endocardial/epicardial flow ratio was greater in Group C (1.21 +/- 0.08 versus 1.06 +/- 0.06, p less than 0.05). Minimal subendocardial histologic changes were present as compared to the marked patchy subendocardial ischemic changes seen in Group B. The results demonstrate that the addition of pulsatile flow to coronary perfusion minimized the deleterious effects of prolonged ventricular fibrillation on myocardial performance.

Animals↗
PubMed1975

Electrophysiology and pharmacology of cardiac arrhythmias. III. The causes and treatment of cardiac arrhythmias. Part B.

Studies on the electrophysiologic mechanisms responsible for disturbances of cardiac rate, rhythm, and conduction, and studies on the actions and mechanisms of action of antiarrhythmic and other drugs, permit the development of an apparently reasonable approach to treatment of cardiac arrhythmias. Some of the rules derived from an appreciation of cardiac electrophysiology are generally applicable. Others appear to require further testing. There are many discrepancies between what can be predicted or expected and what happens; these discrepancies result from many factors. It is likely that cardiac disease in humans has effects on the electrical activity of cardiac cells which have not been reproduced in the laboratory. It is likely, also, that disease modifies the response of cardiac cells to drugs in ways that have not yet been discovered. Nevertheless, some progress has been made and further experiment and thought may provide both better understanding and new and better therapeutic agents.

Arrhythmias, Cardiac↗
PubMed1975

Electrophysiology and pharmacology of cardiac arrhythmias. VIII. Cardiac effects of diphenylhydantoin. B.

DPH is highly effective against both atrial and ventricular arrhythmias resulting from digitalis toxicity and should be considered one of the primary antiarrhythmic drugs in this clinical situation. Clinical studies have indicated that DPH, for the most part, is effective against atrial arrhythmias and not markedly effective against ventricular arrhythmias associated with acute or chronic cardiac disease. For the latter ventricular arrhythmias, DPH is usually considered only after other antiarrhythmic drug therapy has failed. Studies on the mechanisms responsible for the antiarrhythmic effects of DPH are, as yet, inconclusive, There is good evidence that its actions differ from those of the commonly used drugs with local anesthetic effects. The extent to which it exerts direct effects on the heart which are therapeutically relevant remains to be demonstrated; further, there is solid evidence that its effects on the central nervous system may be of prime importance in its antiarrhythmic efficacy.

Action Potentials↗
PubMed1975

Electrophysiology and pharmacology of cardiac arrhythmias. VI. Cardiac effects of verapamil.

It is clear from clinical and experimental data that have been reported thus far that verapamil is highly effective in the therapy of cardiac arrhythmias, and that it acts by a different mechanism than most of the commonly used antiarrhythmic drugs. The available clinical data indicate that on intravenous administration verapamil is as good as and perhaps superior to quinidine, procainamide and propranolol for the therapy of many atrial arrhythmias. Unfortunately the extent to which it is useful as longterm prophylaxis has not yet been reported, nor has its toxicity during protracted oral administration. The effects of verapamil on cardiac action potentials clearly indicate that it modifies the slow response to a much greater extent than the fast response. Studies of cardiac tissues from diseased human atria have indicated that slow response action potentials occur frequently. It is possible that such action potentials are responsible for the reentrant and automatic arrhythmias which occur in association with clinical cardiac disease. Whether the efficacy of verapamil in the therapy of atrial arrhythmias is primarily due to abolishing slow response activity in diseased atrial tissues or to suppression of propagation through the atrioventricular node is uncertain. However, it is likely that the therapeutic action of the drug may result from altered propagation of an arrhythmia through the atrioventricular junction as well as from the effects of the drug on diseased atrial and ventricular tissues.

Action Potentials↗
PubMed1975

Effects of AY-22,241 (Actodigin) on electrical and mechanical activity of cardiac tissues.

AY-22,241 (Actodigin) is a new rapid-acting semisynthetic cardiotonic steroid. In experiments on contractility of cat papillary muscle, Actodigin (2 times 10(-7) to 4 times 10(-6) M) produced a dose-dependent positive inotropic effect, a marked increase in the maximum rate of force development, and no change in resting tension. Electrophysiologic studies performed with microelectrode techniques on isolated Purkinje fibers superfused with Tyrode solution, revealed dose-dependent decreases in resting membrane potential, action potential amplitude and duration, and the maximum rate of rise of phase 0 (Vmax). Purkinje fibers superfused with extracorporeally circulated blood from a donor dog receiving 0.075 mg/kg/min Actodigin showed small decreases in resting membrane potential preceding the onset of donor premature ventricular contractions. Progressive decreases in resting membrane potential, action potential amplitude and duration, and Vmax accompanied donor ventricular tachycardia. All effects were rapidly reversible, and compared to ouabain, equi-inotropic concentrations of Actodigin caused significantly less electrophysiologic toxicity.

Animals↗