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Biomedical subjects

G K Feld

Publications and source records attributed to G K Feld.

49 records · Page 3Linked to original sources
PubMed1989

Effect of thyroid replacement therapy on the frequency of benign atrial and ventricular arrhythmias.

Whether thyroid replacement therapy can trigger cardiac arrhythmias in patients with hypothyroidism is not known. In this prospective study, 24 h ambulatory electrocardiographic (ECG) monitoring was used to assess the frequency of atrial and ventricular premature beats in 25 patients with hypothyroidism (5 men and 20 women, aged 56 +/- 3 years) before and 3.5 +/- 0.5 months (mean +/- SEM) after thyroid replacement therapy. Plasma thyroid-stimulating hormone was 73.6 +/- 12.3 and 3.1 +/- 0.6 microU/ml and free thyroxine index was 2.4 +/- 0.4 and 9.8 +/- 0.9 micrograms/100 ml at baseline and after thyroid replacement therapy, respectively. The frequency of ventricular premature beats was not affected by thyroid replacement therapy (from 273 +/- 221 at baseline to 352 +/- 235 beats/24 h after therapy), even in patients with frequent baseline arrhythmias. In contrast, the frequency of atrial premature beats was slightly increased after thyroid replacement therapy (from 47 +/- 17 to 279 +/- 197 beats/24 h), largely as a result of changes seen in three patients. No patient developed new onset of sustained ventricular or supraventricular arrhythmias. Average, basal and maximal heart rates during ECG monitoring increased significantly after thyroid replacement therapy (average 72 +/- 2 to 80 +/- 2; basal 64 +/- 2 to 70 +/- 2; maximal 114 +/- 3 to 130 +/- 3 beats/min, respectively, p less than 0.001). In conclusion, thyroid replacement therapy is safe in patients with common benign cardiac arrhythmias, and does not trigger an increase in arrhythmia frequency except in rare patients with baseline atrial premature beats. It is, however, associated with an increase in basal, average and maximal heart rates.

Adult↗
PubMed1988

Anomalous origin of the circumflex coronary artery in association with the right superior septal artery.

The presence of anomalous coronary arteries is observed infrequently during routine coronary angiography. However, their identification is crucial to the management of the patient with associated coronary artery disease. A case is described in which concomitant anomalous origin of the circumflex coronary artery from the right coronary artery, and a right superior septal coronary artery with a separate ostium occurred in association with severe three-vessel coronary artery disease requiring bypass graft surgery. Clues to the presence of the anomalous vessels were (1) their visualization during left ventriculography and (2) their presence or absence during injection of the normally originating vessels. This particular association of anomalous vessels was previously unreported.

Coronary Angiography↗
PubMed1988

Clinical and electrophysiologic effects of amiodarone in patients with atrial fibrillation complicating the Wolff-Parkinson-White syndrome.

The clinical and electrophysiologic effects of oral amiodarone were evaluated in 10 patients with a history of spontaneous atrial fibrillation and a rapid ventricular response, complicating the Wolff-Parkinson-White syndrome. Five patients developed ventricular fibrillation during an episode of atrial fibrillation. Seven patients underwent electrophysiology study and arrhythmia induction, both before and during chronic amiodarone treatment. During a mean 30 months of follow-up (range 8 to 59 months), no recurrences of atrial fibrillation or ventricular fibrillation were noted. One patient had recurrent supraventricular tachycardia and underwent surgery. One had serious and five had minor side effects. Arrhythmia suppression was associated with prolongation of the anterograde accessory pathway (+38%, p less than 0.01) and atrial (+34%, p less than 0.01) effective refractory periods. Amiodarone also slowed the ventricular response to induced atrial fibrillation, prolonging the mean (+90%, p less than 0.01) and minimum (+104%, p = 0.01) R-R intervals. Thus, amiodarone is a safe and effective alternative for arrhythmia prevention if surgery is inadvisable or is not desired by the patient.

Adult↗
PubMed1988

Effects of N-acetylprocainamide and recainam in the pharmacologic conversion and suppression of experimental canine atrial flutter: significance of changes in refractoriness and conduction.

The electrophysiologic determinants of the pharmacologic conversion and the prevention of atrial flutter are poorly defined. This study investigated the effects of pharmacologically induced changes in atrial conduction velocity and refractoriness, in the conversion and suppression of atrial flutter induced in the open-chest anesthetized dog by intercaval crush and rapid atrial pacing. The effects of an intravenous infusion of the new class III antiarrhythmic drug N-acetylprocainamide (30 mg/kg over 15 min) and the class Ic antiarrhythmic drug recainam (10 mg/kg over 20 min followed by 10 mg/kg/h) were evaluated. N-acetylprocainamide restored sinus rhythm in 10 of 15 (66%) dogs, while recainam converted only 2 of 10 (20%). N-acetylprocainamide prevented reinduction in 3 (20%), while recainam was effective in none. In the atria, N-acetylprocainamide induced significant increases in effective refractory period (+27%, p less than 0.01), functional refractory period (+22%, p less than 0.01), and in atrial flutter cycle length (+13%, p less than 0.01). Recainam increased effective refractory period (+28%, p less than 0.01), functional refractory period (+20%, p less than 0.01), conduction time at atrial paced cycle length of 150 msec (+70%, p less than 0.01) and atrial flutter cycle length (+56%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acecainide↗
PubMed1987

Hemodynamic and electrophysiologic effects of combined infusion of lidocaine and propafenone in humans.

The hemodynamic and electrophysiologic effect of a combined intravenous infusion of lidocaine (100 mg bolus followed by 2 mg/min infusion) and propafenone (1 or 2 mg/kg) in patients with a history of ventricular arrhythmia was studied. Lidocaine infusion alone significantly increased the mean pulmonary artery (+28%) and pulmonary capillary wedge (+17%) pressure, with no effect on cardiac index. Lidocaine alone produced no consistent change in any measured electrophysiologic parameter, except slight QTc shortening (-2%, P less than .05). Propafenone alone, particularly at the higher dose (2 mg/kg), produced significant increases in mean blood pressure (+14%), right atrial pressure (+78%), pulmonary artery pressure (+50%), pulmonary capillary wedge pressure (+65%), systemic vascular resistance (+29%), and pulmonary vascular resistance (+61%) and a decrease in cardiac index (-12%). Significant prolongation of PR (+9%), AH (+29%), and HV (+23%) intervals, atrial functional refractory period (+12%), ventricular effective (+7%) and functional (+6%) refractory period, and Wenckebach cycle length (+13%) also occurred after the administration of propafenone alone. Only the effects on atrioventricular (AV) node were observed at the lower dose of propafenone (1 mg/kg). Combined infusion of lidocaine with propafenone produced a mild, statistically insignificant additional negative inotropic effect but reversed the prolongation in atrial and ventricular refractoriness produced by propafenone alone. Thus, the data show that lidocaine attenuates certain electrophysiologic effects of propafenone, which might alter its antiarrhythmic efficacy, while producing mild additive negative inotropic effects that may be of hemodynamic significance.

Adult↗
PubMed1986

Pharmacologic conversion and suppression of experimental canine atrial flutter: differing effects of d-sotalol, quinidine, and lidocaine and significance of changes in refractoriness and conduction.

The electrophysiologic determinants of conversion and the prevention of atrial flutter are poorly defined. This issue was therefore investigated by evaluating the effects of the new class III antiarrhythmic drug d-sotalol and the class I antiarrhythmic drugs quinidine and lidocaine. Atrial flutter was reproducibly induced in the open-chest anesthetized dog with intercaval crush and rapid atrial pacing. In this preparation, intravenous d-sotalol restored sinus rhythm in 14 of 15 (93%) dogs, whereas quinidine converted nine of 15 (60%) and lidocaine two of 10 (20%). d-Sotalol prevented reinduction in eight (53%), whereas quinidine was effective in four (27%) and lidocaine in none (0%). In the atria, d-sotalol induced significant increases in effective refractory period (+32%; p less than .01), functional refractory period (+30%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+9%; p less than .05), and atrial flutter cycle length (+8%; p less than .01). Quinidine increased effective refractory period (+40%; p less than .01), functional refractory period (+27%; p less than .01), conduction time at sinus cycle length (+13%; p less than .01), conduction time at an atrial paced cycle length of 150 msec (+18%; p less than .01), and atrial flutter cycle length (+31%; p less than .01). Lidocaine decreased functional refractory period (-6%; p less than .05) while lengthening the atrial flutter cycle length (+13%; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Postinfectious glomerulonephritis in a renal allograft associated with a mycotic aneurysm of a coronary artery.

Postinfectious glomerulonephritis is well known to occur after various infections but is rare in renal allografts, perhaps as a result of immunosuppressive therapy. This report describes a 47-year-old man who, seven years after receiving a cadaveric renal transplant, had biopsy-proved crescentic glomerulonephritis presenting with gross hematuria and rapidly progressive renal failure. The patient underwent cardiac surgery to define an abnormal structure shown on echocardiography, and a mycotic aneurysm of the left circumflex artery was discovered. Such aneurysms are uncommon and rarely diagnosed during life. This case appears to be the first report of glomerulonephritis associated with a mycotic aneurysm of a coronary artery and one of the few reports of postinfectious glomerulonephritis in a renal allograft.

Aneurysm, Infected↗
PubMed1984

Electrophysiologic basis for the suppression by amiodarone of orthodromic supraventricular tachycardias complicating pre-excitation syndromes.

Ten patients with refractory recurrent supraventricular tachycardia were found by electrophysiologic study to have bypass tracts and orthodromic atrioventricular reentrant tachycardia. All had failed to respond to conventional antiarrhythmic therapy and were therefore treated with oral amiodarone (1,600 to 2,000 mg/day for 2 weeks, then 800 to 1,200 mg/day for another 2 weeks with subsequent 200 to 600 mg/day maintenance doses). During or after the fourth week of therapy, electrophysiologic study was repeated. In 9 of 10 patients, supraventricular tachycardia could not be reinduced by programmed stimulation. In the remaining patient, nonsustained supraventricular tachycardia (greater than 10 beats, lasting less than 30 seconds) with a slower basic cycle length than that during the control period was provoked. Significant increases in the effective refractory period of the accessory pathway in both the anterograde (+26%, p less than 0.05) and retrograde (+40%, p less than 0.02) directions were noted, the magnitude of change being independent of the control effective refractory period. There were also significant increases in the effective refractory period of the right atrium (+24%, p less than 0.01) and the right ventricle (+15%, p less than 0.01) during long-term therapy with amiodarone. Over a mean follow-up period of 20 months, symptomatic control of the arrhythmia occurred in all patients; in only one patient treatment with amiodarone could not be continued because of side effects. These data establish the electrophysiologic basis for the effectiveness of amiodarone in the prophylactic control of refractory paroxysmal supraventricular tachycardia complicating the bypass tract syndromes.

Adult↗
PubMed1976

Direct chronotropic and dromotropic actions of contrast media: ineffectiveness of atropine in the prevention of bradyarrhythmias and conduction disturbances.

Methyl glucamine sodium diatrizoate (Renografin 76) was directly infused into the isolated arteries to the sino-atrial and atrioventricular nodes of anesthetized dogs, causing a dose-related inhibition of sino-atrial nodal automaticity and atrioventricular nodal conductivity; these effects were not attenuated by autonomic blockade or cervical vagotomy. The important negative chronotropic and dramatropic effects of contrast media used for coronary angiography are direct actions and cannot be effectively blocked by premedication with atropine.

Animals↗
PubMed1975

The choleretic effect of iodipamide.

It is well established that a number of organic anions are excreted by the liver into bile in association with a marked increase in bile flow. Previous studies have shown that iodipamide (3,3'-(adipoyl-diimino)bis[2,4,6-triiodobenzoic acid]), the radiographic contrast material used for intravenous cholangiography, is a potent choleretic. Experiments were performed in unanesthetized dogs to determine if the increased bile flow produced by iodipamide is canalicular or ductular in origin, to quantitate the choleresis associated with iodipamide and taurocholate excretion, and to correlate these findings with the results of in vitro studies in which the osmotic activities of iodipamide and taurocholate in both isotonic saline and bile were determined. The plasma erythritol clearance increase linearly with the excretion of iodipamide, indicating that iodipamide stimulates canalicular bile flow. The choleretic potency of iodipamide (22 ml/mmol) is approximately 3 times that of taurocholate (7.8 ml/mmol), yet the osmotic activity of iodipamide in bile (1.5 mosmol/mmol) is only twice as great as that of taurocholate in bile (0.8 mosmol/mmol). It therefore appears that, per unit of effective osmotic solute secreted, iodipamide carries more water into the bile canaliculi than does taurocholate.

Animals↗
PubMed1975

Biliary excretion of iodipamide.

Conflicting data have been reported concerning the optimum dose and rate of administration of iodipamide required to obtain maximum radiographic opacification of the biliary tree during intravenous cholangiography. Experiments were performed in dogs to determine the effect of plasma concentration on the excretion and concentration of iodipamide in the bile and urine during a steady state of infusion and excretion. The data indicate that a hyperbolic relation exists between the plasma concentration and both the biliary concentration and the total biliary excretion. A mathematical expression of these relations is presented. At low plasma concentrations, iodipamide was not excreted in the urine. However, at high plasma concentrations, urinary excretion increased sharply. It appears that a biliary concentration of iodipamide sufficient to achieve adequate radiographic visualization of the biliary tree can be obtained without significant renal excretion by constant infusion of iodipamide at an appropriate rate in dogs. Stepwise increase in the infusion rate until adequate radiographic visualization is obtained may be the best method for performing intravenous cholangiography to obtain visualization with the least amount of iodipamide in order to minimize toxicity.

Animals↗
PubMedDate not supplied

Catheter ablation for the treatment of atrial tachycardia.

Radiofrequency (RF) catheter ablation has revolutionized the treatment of supraventricular tachycardia, particularly those caused by atrioventricular nodal reentry and Wolff-Parkinson-White syndrome. Recently, RF catheter ablation has also been used to treat atrial flutter (AFL), focal automatic atrial tachycardia, and intra-atrial reentrant tachycardia. Typical AFL is caused by reentry in the right atrium, with an area of slow conduction in the isthmus between the inferior vena cava and tricuspid valve annulus. Ablation of exit sites from the isthmus near the coronary sinus ostium, or the isthmus itself, may cure AFL in the majority of patients. Intra-atrial reentrant tachycardia also has an area of slow conduction where application of RF energy is curative in most patients. In this arrhythmia, which is particularly common after congenital heart disease surgery, the reentrant circuit may occur in the right or left atrium. Focal automatic atrial tachycardia is probably caused by abnormal automaticity and, although it may arise from the right or left atrium, is easily ablated in most patients. Thus, RF catheter ablation is a highly effective alternative to pharmacologic therapy for treating atrial tachycardia, and it is likely to be increasingly used as curative therapy in the future.

Adult↗