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Biomedical subjects

P R Reid

Publications and source records attributed to P R Reid.

At least 19 recordsLinked to original sources

The automatic implantable cardioverter-defibrillator. Long-term clinical experience and outcome at a hospital without an open-heart surgery program.

From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.

Adult

Characterization of refractory period extension by transcardiac shock.

BACKGROUND: To better understand the refractory period extension (RPE) produced by transcardiac shocks and its possible role in defibrillation, we measured RPE under various experimental conditions. METHODS AND RESULTS: Using ventricular pacing in pentobarbital-anesthetized dogs, we characterized RPE in relation to the anatomic site of pacing, the local voltage gradient (LVG) produced by the shocks at the pacing site, and the pacing rate and pacing current used to make the measurements. We also determined if RPE persisted into the next refractory period after the shock and measured RPE at the end of 30-second episodes of acute ischemia to the pacing site, which were caused by occluding the left anterior descending artery. Each anatomic site tested showed RPE, which increased sharply with increasing LVG at lower levels but less sharply at higher LVG. The RPE versus LVG was approximated with an exponential curve that had an exponential constant of about 5-6 V/cm. At faster pacing rates, RPE occurred earlier in the refractory period but was unchanged when expressed as a percent increase of refractory period. RPE did not vary with the pacing current and was present only in the refractory period during which the shock was delivered. The RPE was not significantly altered by acute ischemia. These results show that transcardiac shocks selectively extend the refractory period of tissue proportional to the LVG and the timing of the shock in the refractory period. They are consistent with the concept that RPE prevents depolarization from tissue directly excited by a shock from propagating to tissue that was refractory to that same shock. CONCLUSIONS: The insensitivity of RPE to short ischemic episodes and the presence of RPE at increased activation rates suggest that RPE might exist under conditions of fibrillation and be a major determinant of the success or failure of defibrillation.

Acute Disease

Dietary intake methodology. II. USDA's Nutrient Data Base for Nationwide Dietary Intake Surveys.

The U.S. Department of Agriculture's (USDA) Nutrient Data Base for Nationwide Dietary Intake Surveys is specifically organized and maintained to analyze data from nationwide dietary surveys within the federal government's National Nutrition Monitoring System. These surveys include the Nationwide Food Consumption Survey and the Continuing Survey of Food Intakes by Individuals conducted by USDA, and the National Health and Nutrition Examination Survey conducted by the Department of Health and Human Services (DHHS). Each public release of the data base covers one or more specific surveys. The data base contains data for energy and 28 components for over 5000 food items. Data are based on the latest information from USDAs National Nutrient Data Bank, the computer-based system used to update USDAs standard reference on food composition, Agriculture Handbook No. 8. An automated system is also used to update the survey nutrient data base with new information released from the Nutrient Data Bank. This system includes three supplementary data sets (primary nutrient data set, recipe file, and table of nutrient retention factors) and a computer program for calculating nutrient content of mixed food items based on nutrient content of their ingredients. Updates are performed at the beginning of new surveys to incorporate the most up-to-date nutrient values.

Agriculture

Ventricular refractory period extension caused by defibrillation shocks.

In pentobarbital-anesthetized dogs, transcardiac shocks of up to 30 J or pacing stimuli were delivered to myocardial tissue at different times in the electrical cycle. When delivered midway or later into electrical systole, shocks, but not pacing stimuli, greatly extended the refractory period as determined by left ventricular pacing. There was a positive correlation between both the shock energy and timing and the amount of delay. A 30-J shock given 10 msec before the end of the refractory period extended the refractory period by 63 +/- 15 msec (p less than 0.001), whereas the same shock given 40 msec earlier produced only 25 +/- 10 msec (p less than 0.001) of extension. By comparison, a 5-J shock given at those times produced 36 +/- 18 (p less than 0.005) and 10 +/- 8 msec (p less than 0.001) of extension, respectively. When delivered early into electrical systole, both a pacing stimulus and a shock had no substantial effect on the tissue refractory period. Because the tissue that is late in electrical systole would otherwise be the first to repolarize if no shock were given, the selective refractory period extension may create a period after the shock during which no tissue is repolarized to a level sufficient for wavefront propagation. Thus, the energy- and time-dependent refractory period extension may help explain the mechanism by which ventricular defibrillation occurs during transcardiac shocks.

Animals

Comparison of acebutolol and propranolol therapy for ventricular arrhythmias.

The effects of acebutolol, a new investigational cardioselective beta blocker, and propranolol on ventricular arrhythmias were compared in 14 patients with more than 30 premature ventricular contractions (PVCs) per hour. Each patient served as their own control, receiving both drugs and placebo in random sequence and in double-blind fashion, with an intervening one-week, drug-free period. Each drug was given for a two-month period, the maximum acebutolol dosage reaching 600 mg tid and the maximum propranolol dosage 80 mg tid. Seventy-two-hour ambulatory electrocardiographic monitoring assessed arrhythmia frequency for each study period. Mean PVC counts did not significantly differ during the two control periods. Acebutolol decreased mean PVC count by 65% (P less than .02), with eight patients exhibiting a 70% or greater decrease. Only three patients exhibited a similar decline with propranolol. The incidence of PVCs was not significantly decreased by propranolol. Acebutolol reduced the number of couplets by 70% (P less than .04), whereas propranolol did not significantly affect couplets. At the dosage of 600 mg tid, acebutolol was well tolerated, effectively suppressed total PVCs and couplets, and appeared to be more effective than propranolol administered at 80 mg tid.

Acebutolol

Quantitative determination of trinitroglycerin in human plasma.

We developed a simplified method for quantitative measurement of trinitroglycerin in human plasma using hexane extraction and analysis by gas-liquid chromatography with electron-capture detection. This assay was linear from 0.5-60 ng/ml. Sensitivity and reproducibility were +/- 0.5 ng/ml. We used this assay to evaluate the pharmacodynamics of trinitroglycerin in 14 patients. Maximum plasma levels were similar with trinitroglycerin given by constant intravenous infusion (1.6 +/- 0.4 ng/ml (SEM)), transcutaneously (2.3 +/- 0.6 ng/ml), or sublingually (1.6 +/- 0.6 ng/ml). Despite similar levels and hemodynamic responses after intravenous trinitroglycerin, the dose range was wide (37.5-175 microg/min, n = 5), emphasizing the need to individualize therapy. In normal volunteers on no other drugs, the plasma level time course followed changes in heart rate better than blood pressure changes. Use of the trinitroglycerin assay may enhance optimization of trinitroglycerin therapy when administered by different methods.

Angina Pectoris

Digoxin -- quinidine interaction.

A patient with chronic paroxysmal atrial fibrillation, receiving maintenance doses of digoxin, was admitted for addition of quinidine therapy. With stable serum digoxin levels, the institution of oral quinidine sulfate resulted in a rise in the serum digoxin level in less than 24 hours. The serum digoxin concentration increased more than threefold before digoxin was discontinued. The rise and fall of the digoxin serum concentration appeared to correlate directly with an increase and decrease in the PR interval. With the reinstitution of digoxin at lower doses, apparently stable therapeutic levels of both digoxin and quinidine were achieved. However, discontinuation of quinidine alone was followed by a prompt fall in the serum digoxin level. This study demonstrates that quinidine produces a significant increase in the serum digoxin level. The increased digoxin concentration appears to correlate with enhanced electrophysiologic effects of digoxin and emphasizes the caution required when these two drugs are used simultaneously.

Atrial Fibrillation

The repetitive ventricular response in man. A predictor of sudden death.

We examined the value of cardiac pacing for assessing ventricular electrical instability and for predicting ventricular tachycardia and sudden death in 50 patients with refractory symptomatic ventricular tachycardia, 12 normal patients, and 48 survivors of a recent myocardial infarction. The repetitive ventricular response (two or more ventricular premature beats produced by a single ventricular pacing stimulus during control of heart rate with atrial pacing) was absent in all 12 normal patients but was present in 44 of the 50 patients (88 per cent) with recurrent ventricular tachycardia (P less than 0.001). Of the 48 survivors of myocardial infarction, 19 had repetitive ventricular responses. During the next 12 months 15 of these patients (79 per cent) had symptomatic ventricular tachycardia or sudden death, or both, as compared with four of 29 patients (14 per cent) who did not have repetitive ventricular responses (P less than 0.001). The repetitive ventricular response identifies patients with life-threatening ventricular instability, but it is still an investigational technic that should be used only with due precautions.

Adult

Lidocaine kinetics predicted by indocyanine green clearance.

To evaluate the importance of hepatic blood flow in lidocaine kinetics, we compared indocyanine green clearance, an estimate of hepatic plasma flow, to lidocaine clearance in 26 patients, half with and half without congestive heart failure, who received a lidocaine infusion for 24 hours as clinically indicated. The results demonstrated that patients with congestive heart failure had significantly higher steady-state lidocaine levels (6.8 +/- 3.6(S.D.) vs. 2.9 +/- 0.9 microgram per milliliter, P less than 0.005) and reduced lidocaine clearance (3.8 +/- 1.4 vs. 10.9 +/- 3.1 ml per minute per kilogram, P less than 0.005) than patients without heart failure. Potentially subtherapeutic or toxic lidocaine levels were found in 10 patients. The regression line (y = 0.3 + 1.07 x) relating clearance of lidocaine to that of indocyanine green was linear (r = 0.95, P less than 0.001). Since indocyanine green clearance can be determined rapidly and noninvasively, it offers the potential of predicting lidocaine dosage requirements with avoidance of toxicity or suboptimum therapy.

Aged

Prolongation of cardiac conduction times by intravenous aprindine in man.

The acute electrophysiologic effects of intravenous aprindine were evaluated in 48 patients to assess the effect on conduction times and refractoriness in patients with severe cardiac disease and arrhythmias. The patients had not responded to conventional antiarrhythmic medications or had been unable to tolerate effective doses of conventional medications because of side effects. Eleven patients had an abnormal H-V interval, 9 had prolonged QRS duration and 22 had evidence of severe left ventricular dysfunction. Aprindine prolonged conduction transiently in the atria, the atrioventricular (A-V) node, the His-Purkinje system and the ventricles. The refractory times of the atria, the A-V node and the ventricles increased insignificantly, both functionally and statistically. Atrioventricular block did not develop in any patient, and side effects were minor. Thus, aprindine can be safely administered intravenously (10 to 15 mg/min) to severely ill patients with arrhythmias that are refractory to other medications even in the presence of underlying conduction system and myocardial disease.

Adult

Suppression of the repetitive ventricular response: an index of long-term antiarrhythmic effectiveness of aprindine for ventricular tachycardia in man.

The repetitive ventricular response, defined as the production of two or more ventricular premature complexes in response to a single ventricular pacing stimulus, is common in patients with serious ventricular arrhythmias. Twenty-seven patients with refractory ventricular tachycardia were studied to determine whether acute suppression of the repetitive ventricular response by aprindine predicts long-term effectiveness of this agent. Twenty-three of the 27 patients had the repetitive ventricular response before intravenous administration of aprindine, whereas only 6 had the response after aprindine. All patients were maintained on a regimen of oral aprindine and evaluated repeatedly for a mean of 12 months. Twenty of the 21 patients who had no repetitive ventricular response after intravenous aprindine manifested clinical improvement compared with only 1 of the 6 in whom the repetitive response was present after aprindine (P less than 0.0005). Aprindine is a useful agent in refractory ventricular tachycardia, and the absence of the repetitive ventricular response after its intravenous administration predicts long-term clinical responsiveness to the oral form.

Administration, Oral

Mitral-valve prolapse syndrome and recurrent ventricular tachyarrhythmias: a malignant variant refractory to conventional drug therapy.

Of 60 patients referred for management of drug-refractory ventricular tachyarrhythmias, 10 (17%) had mitral-valve prolapse. These 10 patients ranged in age from 19 to 70 years (mean, 47 years); seven were women. All 10 had recurrent ventricular tachycardia, while four had a history of ventricular fibrillation. Nine patients were refractory to propranolol in combination with one or more of the standard antiarrhythmic agents. All showed improvement with aprindine therapy. The results show that refractory malignant ventricular prolapse syndrome; patients with mitral-valve prolapse account for a rather high percentage of those patients referred with recurrent drug-refractory ventricular tachyarrhythmias; in patients with unexplained ventricular arrhythmias, mitral-valve prolapse should be considered; and aprindine may be effective for ventricular tachyarrhythmias associated with mitral-valve prolapse.

Adult

Aprindine hepatitis.

We have seen two patients whose hepatitis was due to the administration of aprindine, a new antiarrhythmic agent. In both patients evidence of hepatitis appeared within 3 weeks of initiating aprindine therapy and resolved rapidly when the drug was withdrawn. The reintroduction of aprindine in one patient was associated with the reappearance of hepatitis, which resolved despite continued administration of the drug.

Aprindine

Acute mental status changes caused by propranolol.

A 74-year-old woman with mild dementia became disoriented and developed paranoid delusions when treated with low-dose propranolol. There was no evidence of cardiovascular instability, and the symptoms resolved within a week. Rechallenge with propranolol led to a recurrence of mental status changes.

Aged

Suppression of refractory arrhythmias by aprindine in patients with the Wolff-Parkinson-White syndrome.

Four patients with supraventricular tachycardia associated with the Wolff-Parkinson-White syndrome were refractory to conventional pharmacological therapy and received aprindine hydrochloride intravenously and orally. Electrophysiological studies disclosed that intravenous aprindine caused increased refractoriness and slowed conduction in the atria, atrioventricular node, ventricles, and accessory pathway. The ability to induce supraventricular tachycardia with timed atrial and ventricular premature stimuli was totally abolished in all 4 patients after intravenous aprindine. Oral aprindine therapy, twice daily thereafter, provided symptomatic relief of the supraventricular tachycardia without significant side effects. Aprindine is useful in the management of supraventricular tachycardia associated with Wolff-Parkinson-White and may offer significant advantages over currently available therapy.

Administration, Oral