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Biomedical subjects

J A Reiffel

Publications and source records attributed to J A Reiffel.

15 recordsLinked to original sources
PubMed1979

A previously unrecognized drug interaction between quinidine and digoxin.

Following the development of digoxin radioimmunoassay, we noted that serum digoxin concentrations appeared to rise in patients given quinidine. To further evaluate this important possible interaction between digoxin and quinidine, charts from 863 cardiology patients were reviewed. Ninety two patients received both drugs after having been on digoxin alone; 38 were ineligible for the study because of insufficient data and 27 were excluded because of changing renal function and/or concomitant antiarrhythmic drug therapy, leaving 27. Serum digoxin increased in 25 of the 27 study patients (93%) during quinidine therapy; mean serum digoxin rose from 1.4 ng/ml before quinidine to 3.2 ng/ml during quinidine. Anorexia, nausea and/or vomiting developed in 16 patients (59%) during quinidine therapy, but disappeared in all 10 patients in whom digoxin alone was reduced in dose, suggesting that digoxin had a causative role in the appearance of these symptoms although they developed only after quinidine had begun. Three of thirteen patients with only atrial arrhythmias on digoxin prior to quinidine developed new ventricular premature depolarizations (VPD) after starting quinidine; two of these three as well as four patients with prior VPDs developed new ventricular tachycardia, ventricular fibrillation, asystole, or sudden death. When starting quinidine in patients who are taking digoxin, the clinical course, ECG and serum digoxin should be followed closely.

Adult↗
PubMed1979

Effects of digoxin on sinus nodal function before and after vagal blockade in patients with sinus nodal dysfunction: a clue to the mechanisms of the action of digitalis on the sinus node.

To increase the limited knowledge of the effects of digitalis on sinus nodal function in patients with sinus nodal dysfunction and to initiate an investigation into the mechanisms underlying its effects, 34 patients with sinus nodal dysfunction were studied. Twenty patients underwent determination of sinus cycle length, estimated sinoatrial conduction time and maximal corrected sinus recovery time before and after the administration of 0.75 mg of intravenous digoxin. For the group, sinus cycle length did not change, sinoatrial conduction time increased insignificantly and maximal corrected sinus recovery time shortened; however, individual variation occurred. The effects of acute digitalization appeared to predict the effects of chronic digitalis administration on sinus nodal function in the eight patients who subsequently continued to take digoxin. Fourteen patients received digoxin after vagal blockade with atropine. After vagal blockade, digoxin lengthened sinus cycle length, sinoatrial conduction time and maximal corrected sinus recovery time. The effects of digoxin administered after atropine could be antiadrenergic, direct, or both, and are opposite to those induced by atropine alone. Because these effects are similar to those of vagotonia yet are not apparent when the vagi are unblocked, digoxin may have direct excitatory, adrenergic or previously unrecognized vagolytic effects on sinus nodal function in man and their manifestation may be dependent on heart rate or autonomic tone.

Adult↗
PubMed1979

Sick sinus syndrome.

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Anti-Arrhythmia Agents↗
PubMed1979

Enhanced cardiac effect of digoxin during quinidine treatment.

Quinidine causes an increase in the serum digoxin concentration. Three patients were studied to determine if the increase in serum concentration is paralleled by an increase in the cardiac effect of digoxin. Each patient's clinical condition and serum digoxin concentration were stable when quinidine administration was begun. In all three patients, serum digoxin concentrations increased significantly after beginning quinidine, and decreased when quinidine was discontinued. While taking quinidine, all three patients had ECG findings that suggested enhanced digitalis effect and one patient had clinical evidence of an increased hemodynamic effect. These effects paralleled the increases in serum digoxin concentration. Our findings suggest that the increase in serum digoxin concentration, which occurs after beginning quinidine, is associated with an increase in the effect of digoxin on the heart.

Aged↗
PubMed1978

Interaction between quinidine and digoxin.

The serum digoxin concentration increased in 25 of 27 study patients (93%), and the mean serum digoxin concentration rose from 1.4 ng/ml to 3.2 ng/ml during quinidine therapy. Anorexia, nausea, or vomiting developed in 16 patients (59%) but disappeared in all ten patients for whom the digoxin dose alone was reduced, suggesting that digoxin excess caused these symptoms. Ventricular premature depolarizations developed in three patients after starting quinidine therapy; ventricular tachycardia developed in one patient, and another died suddenly. When starting quinidine therapy in patients who are taking digoxin, the clinical course, ECG, and serum digoxin level should be followed closely.

Aged↗
PubMed1978

Direct current cardioversion. Effect on creatine kinase, lactic dehydrogenase and myocardial isoenzymes.

Creatine kinase (CK), lactic dehydrogenase (LDH), and more recently their isoenzyme determinations (CK-MB and LDH1) have been useful adjuncts in verification of myocardial injury. To determine whether DC cardioversion affects these serum enzyme levels, we recorded total CK, total LDH, CK-MB, and LDH1 levels serially during 24 hours following elective DC cardioversion in 18 patients without cardiac ischemia. New postcardioversion elevations in total CK and total LDH levels were small and occasional: CK (one of 18 patients), LDH (four of 18 patients). Elevations of CK-MB or LDH1 following cardioversion did not develop in any of the patients. Therefore, new CK-MB or LDH1 elevations associated with arrhythmias must result from myocardial damage to DC cardioversion.

Acute Disease↗
PubMed1978

Pure anterior conduction delay: a variant "fascicular" defect.

Based upon electrocardiographic studies of conduction disturbances, the human intraventricular conduction system has been considered trifascicular: a right bundle and a bidivisional left bundle. Right bundle branch block, left anterior hemiblock, and left posterior hemiblock have been described. Microscopic and endocardial mapping studies, however, do not demonstrate a corresponding anatomical basis of this useful functional concept. Atrial premature beats in our two cases resulted in ventricular aberrancy which strongly suggests an additional form of a functional conduction delay. Such delay is manifest as a narrow QRS with anterior displacement in the horizontal plane but no axis shift in the frontal plane. This aberrancy is important to recognize because it can mimic the ECG findings of true posterior myocardial infraction. We do not postulate, however, a specific fascicle of the left bundle as the anatomic substrate for this recently recognized effect.

Adult↗
PubMed1977

Case studies: Simultaneous intermittent intraatrial and intraventricular conduction defects mimicking trifascicular conduction delay.

Both intermittent rate related left bundle branch block and intermittent rate related trifascicular conduction delay (left bundle branch block with marked H-V interval prolongation) have been previously described. However intermittent rate related intraatrial block with left bundle branch block has not. No only does the case presented herein reveal intermittent rate related intraatrial block with left bundle branch block, but also PR prolongation secondary to the intraatrial block. This combination mimicked intermittent trifascicular conduction delay. Electrophysiological testing allowed differentiation of this pseudotrifascicular defect from true trifascicular conduction delay.

Arrhythmia, Sinus↗
PubMed1975

Diagnosis of acute myocardial infarction. Relative efficiency of serum enzyme and isoenzyme measurements.

Total serum enzyme activity for creatine phosphokinase (CPK), alpha-hydroxybutyric dehydrogenase (HBDH), lactic dehydrogenase (LDH), and serum glutamic oxaloacetic transaminase (SGOT), as well as the isoenzymes of CPK and LDH, were measured on admission and for ten subsequent days in 100 patients admitted consecutively to a coronary care unit. On discharge, patients were classified by a cardiologist as either having or not having suffered an acute myocardial infarction (MI) on the basis of clinical and electrocardiographic criteria--without knowledge of the enzyme studies. The combined use of CPK and LDH isoenzyme levels provided the greatest laboratory discrimination between the two clinical groups (MI vs non-MI). The routine use of HBDH and SGOT levels can be abandoned in the setting of a coronary care unit if CPK and LDH isoenzyme assays are available.

Acute Disease↗
PubMed1975

"Paradoxical" prolongation of sinus nodal recovery time after atropine in the sick sinus syndrome.

A case of symptomatic sick sinus syndrome is presented with confirmation of sinus nodal dysfunction established by functional testing. The validity of such provocative testing and the criteria for abnormality are discussed. A newly recognized, seemingly "paradoxical" and potentially detrimental effect of atropine noted in this patient is examined. Despite an increase in sinus rate and an improvement in sinoatrial conduction time after administration of atropine, a markedly prolonged sinus recovery time after rapid atrial pacing occurred, and atrial quiescence for more than 10 seconds was seen. Possible electrophysiologic mechanisms for this phenomenon, such as decreased atriosinus entrance block, concealed sinoatrial reentry or enhanced intranodal depolarization, are discussed and potential clinic correlates are made.

Arrhythmia, Sinus↗