Howard J. Zeft

Conversion of Supraventricular Tachycardias with Atrial Stimulation Evidence for Re-entry Mechanisms

Atrial stimulation at rates less than the atrial rate was effective in terminating junctional tachycardia and atrial flutter in two patients. Analysis of the stimulus response in the patient with junctional tachycardia defined an atrial excitable and refractory period and a critical interval, the first 12 milliseconds of the excitable period, during which atrial stimulation terminated the tachycardia. The termination of atrial flutter appeared to occur simultaneously with capture of the atrial rate by the slower atrial stimulus. Atrial fibrillation did not occur. These observations suggest that a variety of tachycardias are supported by re-entry mechanisms and that the response to atrial stimulation may be useful in recognizing and treating such arrhythmias.

Right atrial stimulation in the treatment of atrial flutter.

Abstract The use of right atrial stimulation in the treatment of atrial flutter was evaluated in 10 patients. Atrial flutter was present in these patients from 6 to 96 hr before the procedure. Eigh...

Natural history of experimental coronary occlusion in pigs: A serial cineangiographic study☆☆☆

Abstract In order to evaluate, in vivo, the serial changes of the coronary arteries and the development of collateral circulation during the course of a gradual coronary occlusion, 32 farm pigs were studied with serial selective coronary cineangiograms following placement of an Ameroid constrictor on the left anterior descending coronary artery. Delaved clearance of contrast medium and poststenotic dilatation of the constricted artery appeared by the second to third day; complete occlusion on the sixth to seventh day. Demonstrable collateral vessels developed in most of the surviving animals by the sixth to seventh day. These channels increased in size and number in the subsequent 4 to 5 weeks so that the left anterior descending artery distal to the constrictor again became completely opacified through the collateral channels. In 16 animals that survived longer than 6 days, major collateral channels perfusing the distal portion of the obstructed artery arose proximal to the constrictor in 8, from the left circumflex artery in 11, and from the right coronary artery in 13. Despite the development of such collateral circulation, massive myocardial infarction developed indicating that the rapidity and/or extent of the collateralization was inadequate to prevent myocardial death. These findings also provide the basic information needed for using this preparation as the model for studies of myocardial infarction.

Termination of Paroxysmal Junctional Tachycardia by Right Ventricular Stimulation

This report documents the use of right ventricular stimulation in the termination of a rapid junctional tachycardia. The tachycardia developed in the background setting of heart block and bradycardia. Right ventricular stimulation was effective at 94/min, a rate considerably slower than that of the tachycardia. Analysis of pacemaker stimuli during the tachycardia defined ventricular refractory and excitable periods. Within the ventricular excitable period there was a critical time interval during which stimulation produced premature ventricular depolarization and abrupt termination of the tachycardia. These findings support the hypothesis that junctional tachycardias in the absence of the Wolf-Parkinson-White syndrome may be sustained by reentry mechanisms. Moreover, right ventricular stimulation may be a valuable therapeutic adjunct in the treatment of such tachycardias.

Increased Survival with Prophylactic Quinidine After Experimental Myocardial Infarction

Experimental myocardial infarction was produced in 60 farm pigs by gradual coronary occlusion with an Ameroid constrictor placed around the left anterior descending coronary artery. Twenty animals were treated with 10 mg/kg/6 hr of quinidine, 10 with 5 mg/kg/6 hr, and 10 with 2.5 mg/kg/6 hr for a total period of 72 hours. Twenty animals served as controls. Serum quinidine levels were measured at 6-hour intervals. Significantly increased survival, when compared to controls, were observed in those animals treated with 5 and 10 mg/kg/6 hr of quinidine, but not in those receiving 2.5 mg/kg/6 hr. Under the described experimental conditions, designed to cause a reproducible, consistent infarction, quinidine treatment in nontoxic and well-tolerated doses significantly increased survival. Furthermore, there is a dose level below which this effect is lost. Whether the results of this study are applicable to man in preventing sudden death is unknown.

Pulmonary Air Embolism During Insertion of a Permanent Transvenous Cardiac Pacemaker

In two patients pulmonary air embolism was a complication of the implantation of a permanent transvenous cardiac pacemaker. One of these patients, in whom air embolism was documented by cinefluorograms, is described in detail. Cinefluorograms demonstrated air in the right ventricle and main pulmonary artery with clear visualization of the opening and closing of the pulmonary valve. Both patients were treated conservatively by use of the left lateral decubitus position and administration of oxygen. The pathophysiology, hazards, and therapy of this complication are reviewed. Massive pulmonary air embolism is potentially fatal, and special care with regard to insertion of the electrode catheter should be taken in order to prevent it.

Postpericardiotomy syndrome in a patient with a retained foreign body

Abstract A patient is described in whom the postpericardiotomy syndrome developed secondary to a gunshot wound to the chest with the retained missile in close proximity to the pericardium. Steroid therapy produced a prompt and sustained clinical remission. The literature is reviewed, and it is suggested that retained foreign bodies in or near the pericardium are still another precipitating cause of the postpericardiotomy syndrome. Possible etiologic mechanisms, the role of corticosteroids in therapy, and indications for surgery are discussed.

Propranolol in the Long-Term Treatment of Angina Pectoris.

Excerpt There is increasing evidence that propranolol hydrochloride, a beta-adrenergic receptor blocking agent, may be a useful adjunct in the treatment of angina pectoris. The effect of this agent...

Prophylaxis versus treatment of acetylstrophanthidin intoxication

Abstract Treatment and pretreatment of acetylstrophanthidin-induced ventricular tachycardia was studied in awake pigs. The pharmacologic agents employed were diphenylhydantoin and 2 beta-adrenergic blocking agents, MJ 1999 and propranolol. These agents when administered intravenously at the onset of the arrhythmia significantly shortened the duration of acetylstrophanthidin-induced ventricular tachycardia. Pretreatment with diphenylhydantoin in doses ranging from 5 to 30 mg. per kilogram failed to increase acetylstrophanthidin intoxicating doses. Pretreatment with MJ 1999 and propranolol, likewise, showed no prophylactic effect on acetylstrophanthidin intoxication. Animals pretreated with MJ 1999 had a shorter duration of tachycardia, whereas animals pretreated with propranolol exhibited a high mortality rate. This increased mortality rate from propranolol pretreatment possibly resulted from more profound blockade of beta receptors or severe myocardial depression. These findings indicate that diphenylhydantoin and beta-adrenergic blocking drugs, agents which are effective in the acute therapy of digitalis arrhythmias, do not protect against acetylstrophanthidin toxicity in awake pigs. MJ 1999, previously considered specific for catecholamine-induced arrhythmias, was found to antagonize acetylstrophanthidin toxicity by decreasing the duration of ventricular tachycardia. The high mortality rate with propranolol pretreatment may be relevant to clinical situations where digitalization is undertaken in patients receiving certain beta blocking agents.