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Biomedical subjects

C R Webb

Publications and source records attributed to C R Webb.

At least 19 recordsLinked to original sources
PubMed1995

Risk factors for the development of specific noncardiovascular adverse effects associated with amiodarone.

Noncardiovascular adverse effects associated with amiodarone result in substantial morbidity. Adverse effects involving the skin, liver, thyroid, and lungs have been reported in as many as 57%, 55%, 11%, and 13% of patients, respectively. Although risk factors for some amiodarone-induced adverse effects have been identified, risk factors for these specific side effects have not been systematically evaluated. Therefore, risk factors for development of amiodarone-induced dermatologic, hepatic, thyroid, or pulmonary adverse effects were identified using univariate analysis in 44 patients receiving the drug for supraventricular or ventricular arrhythmias (mean duration of therapy 99.5 +/- 110.8 weeks). Dermatologic side effects occurred in 4 (9.1%) patients. Patients who experienced dermatologic side effects were younger than patients who did not (mean age, 48.3 +/- 15.8 years versus 60.1 +/- 9.5 years, respectively; P = .03). Patients younger than 60 years of age were more likely to develop photosensitivity or blue-gray skin discoloration than those aged 60 or older (P = .05). Hepatic adverse effects occurred in 3 (6.8%) patients. Left ventricular ejection fraction was lower in those who developed hepatic adverse effects than in those who did not (15.0 +/- 4.0% versus 39.1 +/- 13.9%, P = .005). Adverse thyroid effects occurred in 6 (13.6%) patients; and pulmonary fibrosis occurred in 2 (4.5%) patients. No specific risk factors for adverse thyroid effects or pulmonary fibrosis were revealed. In conclusion, age less than 60 may be a risk factor for amiodarone-induced dermatologic adverse effects, whereas severely depressed left ventricular ejection fraction may be a risk factor for hepatic side effects associated with amiodarone.

Adult↗
PubMed1995

Proarrhythmic effects of intravenous vasopressors.

OBJECTIVE: To review the electrophysiologic properties and the in vitro, ex vivo, animal, and human data regarding proarrhythmic effects of intravenous vasopressors. DATA SOURCES: A comprehensive (MEDLINE) search (1960-1994) was conducted for dopamine, epinephrine, norepinephrine, phenylephrine, and methoxamine. STUDY SELECTION: In vitro and ex vivo studies and investigations performed in animals or humans reporting electrophysiologic and/or proarrhythmic effects of the above intravenous vasopressors were selected. A comprehensive search of all human studies involving these agents was conducted to reveal any proarrhythmic effects that may have been reported. In addition, case reports of proarrhythmic effects associated with these agents were reviewed. DATA EXTRACTION: Data regarding electrophysiologic and proarrhythmic effects of these agents were extracted from in vitro, ex vivo, animal, and human studies. Because few studies with the specific purpose of investigating proarrhythmic effects of vasopressors have been performed in humans, all studies involving these drugs for evaluation of hemodynamic effects, clinical efficacy, or other endpoints in humans were reviewed. In addition, data were extracted from case reports of proarrhythmic effects associated with these agents. DATA SYNTHESIS: Dopamine increases automaticity in Purkinje fibers and has a biphasic effect on action-potential duration. Dopamine has caused both atrial and ventricular tachyarrhythmias in animals. Human data have revealed dose-related sinus tachycardia, with few reports of clinically significant ventricular arrhythmias. Epinephrine shortens sinus cycle length, increases atrial and ventricular automaticity, promotes atrioventricular nodal conduction, and decreases ventricular effective refractory period (ERP). It is well known to induce ventricular fibrillation and decrease the ventricular fibrillation threshold (VFT) in ex vivo models as well as intact animals. In humans, epinephrine may cause dose-related sinus tachycardia, supraventricular arrhythmias, or, more commonly, ventricular arrhythmias. Norepinephrine increases automaticity of the sinoatrial node, atria, and ventricles; promotes atrioventricular nodal conduction; and decreases ventricular ERP. In vitro/ex vivo and animal data have shown that norepinephrine significantly decreases VFT. Although electrophysiologic studies suggest that norepinephrine may be proarrhythmic, few supporting data exist in humans. Phenylephrine demonstrates differential electrophysiologic effects in atrial and ventricular tissue. Most data suggest that phenylephrine causes prolongation of the ventricular ERP. Rather than being proarrhythmic, phenylephrine may be protective against arrhythmias. The drug elevates VFT in dogs. In humans, phenylephrine effectively terminates supraventricular tachycardias and may be protective against ventricular arrhythmias. Like phenylephrine, methoxamine elevates the repetitive extrasystolic, atrial, and ventricular fibrillatory thresholds. Methoxamine also may have antiarrhythmic effects because of alpha-receptor stimulation and reflex vagal activity. Despite the relatively low risk of arrhythmogenicity associated with intravenous vasopressors, patients should be monitored for potential proarrhythmic effects and appropriate action taken as necessary. Critically ill patients often have concurrent conditions, electrolyte disturbances, and underlying arrhythmias that predispose them to a higher risk of vasopressor proarrhythmic effects. CONCLUSIONS: Controlled data supporting the proarrhythmic potential of intravenous vasopressors in humans are lacking. Sinus tachycardia, asymptomatic ventricular ectopic activity, and other ventricular or supraventricular arrhythmias have been reported in association with dopamine and epinephrine. Phenylephrine and methoxamine have been associated with sinus bradycardia, but otherwise may be antiarrhythmic. Intravenous vasopressors appear relatively safe w

Animals↗
PubMed1994

Social and physical factors in the referral of people with traumatic brain injuries to rehabilitation.

Using standardized data abstracted from a representative sample of hospitals in north-central Alabama, we analyze significant social and physical factors in acute care discharge referral patterns for 756 people with traumatic brain injury (TBI). When a Physical Medicine and Rehabilitation specialist is involved in the referral, patients receive more formal rehabilitation care following discharge, even after controlling for the relevant social and physical characteristics of the patient. Other significant variables predicting the level of rehabilitation care include presence of injury-related complications, abnormal computed tomography scan, longer length of acute care stay, being unmarried, older, and having an unintentional injury. Patients not seen by rehabilitation medicine specialists and/or those whose injuries provide less clinical evidence (implying greater uncertainty of diagnosis) are less likely to be referred to more formal rehabilitation. Thus, social and demographic factors may be significant in referral patterns when diagnostic uncertainty is present. Results suggest the importance of increasing availability of rehabilitation medicine consultation for TBI patients, while informing acute care providers about formal rehabilitation as a management option.

Adult↗
PubMed1991

A perception of the rural health situation in central Texas: we need regionalization.

Central Texas, considered representative of the state, has experienced closure of many of its rural hospitals and the loss of many practicing physicians in rural areas. The reasons for these losses are complex. One important reason is that rural hospitals and physicians do not compete successfully against urban hospitals and their specialty staffs. We suggest that rural practice areas can be made attractive to physicians and that rural communities can be provided access to health care through a system of regionalization. Rural and urban physicians can collaborate in providing health care by using rural health clinics and small hospitals centered on urban referral hospitals that serve as the hub for each system.

Hospital Planning↗
PubMed1990

[Electrophysiologic study in 42 cases of unexplained syncope].

Forty two patients with unexplained syncope underwent intracardiac electrophysiologic study to identify the cause of syncope and to select appropriate therapy. Electrophysiologic abnormalities were demonstrated in 26 patients (62%): sustained ventricular tachycardia in 7 patients (27%) of the abnormal group. His-Purkinje system dysfunction in 4 (15.4%), atrioventricular nodal dysfunction in 4 (15.4%), atrioventricular nodal reentrant supraventricular tachycardia in 2 (7.7%), atrial flutter in 1 (3.8%), sinoatrial nodal dysfunction in 2 (7.7%), carotid sinus hypersensitivity in 3 (11.5%) and hypervagotonia in 3 (11.5%). The results of this study suggest that electrophysiologic study should be considered in patients with unexplained syncope. Electrophysiologic study in an effective method for approaching the diagnosis and improving management of unexplained syncope.

Adult↗
PubMed1988

Frequency and significance of cardiac arrhythmias in chronic obstructive lung disease.

Ambulatory electrocardiograms obtained in 69 patients enrolled in the nocturnal oxygen therapy trial group were examined for frequency and significance of arrhythmias in patients with stable chronic obstructive lung disease. Ventricular premature beats occurred in 83 percent, ventricular bigeminy in 68 percent, paired ventricular premature beats in 61 percent, and nonsustained ventricular tachycardia in 22 percent of the patients. Supraventricular tachycardia occurred in 69 percent. Repetitive ventricular arrhythmia occurred in 64 percent of the patients, and was significantly more frequent in men and in patients with edema or elevated PCO2. Ventricular premature beats greater or equal to 25 per hour occurred in 35 percent of the patients. Univariate and multivariate Cox proportional hazards analysis showed that a history of coronary heart disease, increased sinus heart rate and decreased maximum work load (measured by maximal treadmill exercise test)--but not arrhythmias--were predictors of death.

Aged↗
PubMed1987

Risks and complications of clinical cardiac electrophysiologic studies: a prospective analysis of 1,000 consecutive patients.

The complications of clinical cardiac electrophysiologic studies were prospectively evaluated in 1,000 consecutive patients studied in one laboratory with an unaltered protocol to better assess the risks of this procedure. There were 728 men and the mean age of the entire group was 58 years (range 16 to 84). Coronary artery disease was the most common type of heart disease (56%) and 200 patients had no identifiable organic heart disease. The indication for study was a ventricular tachyarrhythmia or cardiac arrest in 582 patients. Each patient underwent an initial (baseline) study and 444 patients underwent serial drug studies (2.7/patient). There was one death during these studies. Other major complications included arterial injury (0.4%), thrombophlebitis (0.6%), systemic arterial embolism (0.1%), pulmonary embolism (0.3%) and cardiac perforation (0.2%). Significant arrhythmic complications included catheter-induced permanent complete atrioventricular (AV) block in 1 patient, nonclinical atrial fibrillation that required therapy in 10 patients and severe proarrhythmic events in 12 (3%) of 397 patients undergoing drug studies for ventricular tachyarrhythmias. Cardioversion was required for termination of ventricular tachyarrhythmias in 179 baseline studies (53% of patients with inducible arrhythmia), and in an additional 35 patients, cardioversion was required at least once during follow-up studies. Although clinical cardiac electrophysiologic studies are associated with complications, the risks are small and acceptable.

Arrhythmias, Cardiac↗
PubMed1986

Flecainide: steady state electrophysiologic effects in patients with remote myocardial infarction and inducible sustained ventricular arrhythmia.

The effect of flecainide in 24 patients with inducible sustained ventricular arrhythmia and a history of remote myocardial infarction was determined. Flecainide was administered in oral doses individually adjusted to suppress all spontaneous ventricular tachycardia and 80% of ventricular premature complexes on 24 hour ambulatory (Holter) electrocardiography. Antiarrhythmic therapy, as assessed by Holter monitoring, was adequate in 20 (83%) of the study patients at a mean dose of 144 +/- 28 mg every 12 hours; the mean plasma flecainide level was 583 +/- 329 ng/ml. In 18 patients, the mean sinus cycle length, sinus node recovery time and atrial, atrioventricular nodal and ventricular refractory periods were unchanged. The AH interval increased by 15 +/- 15%, the HV interval by 35 +/- 32% and the QRS duration by 24 +/- 21%. Toxicity or failure to suppress ventricular premature complexes and ventricular tachycardia by Holter monitoring precluded electrophysiologic study with flecainide in four patients; two patients refused electrophysiologic study with flecainide for nonmedical reasons. Ventricular tachycardia was not inducible in 4 (22%) of 18 patients receiving flecainide. Sustained arrhythmia remained inducible in 14 patients (78%) despite evidence of antiarrhythmic efficacy on Holter monitoring, but the rate of the induced ventricular tachycardia was slower and symptoms were alleviated during ventricular tachycardia in 10 (56%) of 18 patients. The 4 patients who had no inducible ventricular tachycardia with flecainide, and the 10 patients who had inducible ventricular tachycardia with a longer cycle length and alleviation of their symptoms, have been followed up as outpatients for 16 +/- 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Myocardial infarction.

When a diagnosis of infarction or ischemia is considered, the diagnostic value is greatly amplified by comparison of serial ECGs, particularly when at least one is recorded during chest pain and another immediately after a therapeutic maneuver. Daily evaluation of serial ECGs, with a consistent standardization technique and lead placement, is essential to determine the evolution of MI and to evaluate changes indicating that new cardiac regions might be jeopardized by acute ischemia.

Electrocardiography↗
PubMed1985

Efficacy of combination therapy with mexiletine and a type IA agent for inducible ventricular tachyarrhythmias secondary to coronary artery disease.

The efficacy of combination therapy using a type IA agent (quinidine or procainamide) and a type IB agent (mexiletine) in suppressing inducible sustained ventricular tachyarrhythmias was studied in 23 patients undergoing serial drug testing with programmed stimulation. All patients had coronary artery disease (CAD) with previous myocardial infarction and abnormal left ventricular function (mean ejection fraction 35%). Fifty-five percent of the patients presented with syncope or cardiac arrest. In 19 patients therapy had failed during empiric trials of 1 to 3 antiarrhythmic agents. All 23 patients had inducible sustained ventricular tachyarrhythmias (18 had uniform morphology sustained ventricular tachycardia (VT) and 5 had ventricular fibrillation [VF]) during control electrophysiologic study, and therapy had failed with a type IA agent and mexiletine alone. The combination therapy of mexiletine and the type IA agent prevented induction of any ventricular tachyarrhythmias in 8 of 23 patients. In 15 patients, the combination significantly prolonged the tachycardia cycle length and reduced the symptoms associated with the induced arrhythmia. Patients more likely to respond to the combination had shorter cycle lengths and polymorphic configuration of the control-induced arrhythmia. The increased efficacy of the combination therapy could not be attributed to higher plasma drug levels for the combination, as there was no significant difference in plasma levels for each drug when given alone or in combination. Thus, the increased efficacy most likely reflects a synergistic electropharmacologic effect of the 2 agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Antiarrhythmic drug efficacy for ventricular tachyarrhythmias associated with coronary artery disease as assessed by electrophysiologic studies.

The efficacy and proarrhythmic potential of antiarrhythmic agents were evaluated. Programmed ventricular stimulation was performed in 160 consecutive patients with coronary artery disease during a baseline study and 432 subsequent drug studies. The tachyarrhythmias induced during baseline studies were sustained ventricular tachycardia (121 patients), ventricular fibrillation (16 patients), and symptomatic nonsustained ventricular tachycardia (23 patients). Regimens were completely successful if fewer than 6 repetitive ventricular responses were inducible during therapy and partially successful if no more than 15 repetitive ventricular responses were inducible. Procainamide and quinidine were the most successful single agents, with overall success rates of 24% and 35%, respectively. Either procainamide or quinidine combined with mexiletine was the most successful combination (overall success of 23%). Each anti-arrhythmic regimen showed a proarrhythmic potential. The incidence of proarrhythmic effects ranged from 4 to 13%, with no significant difference between regimens. In 13% of patients at least 1 regimen produced a proarrhythmic effect. Patients treated with an antiarrhythmic regimen that prevented induction of arrhythmia had significantly fewer arrhythmia recurrences than patients treated with a regimen that failed to prevent it. In conclusion, identification of an effective drug regimen is possible in 38% of patients with lethal ventricular arrhythmias, proarrhythmic effects occur in a significant number of patients during electrophysiologic testing of antiarrhythmic regimens, and the clinical outcome in patients in whom ventricular arrhythmias are not inducible with ventricular stimulation have a better prognosis than those in whom arrhythmias continue to be inducible on therapy.

Adult↗
PubMed1985

Usefulness of electrophysiologic testing in evaluation of amiodarone therapy for sustained ventricular tachyarrhythmias associated with coronary heart disease.

The prognostic importance of electrophysiologic studies in patients with sustained ventricular tachyarrhythmias treated with amiodarone was prospectively studied in 100 consecutive patients. Sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) was inducible in all patients before amiodarone therapy. After amiodarone administration 2 groups of patients were identified. In group 1 patients the ventricular tachyarrhythmia was no longer inducible and in group 2 patients the arrhythmia remained inducible. In group 1, no recurrent arrhythmia occurred during a follow-up of 18 +/- 10 months. In group 2, 38 of 80 patients (48%) had arrhythmia recurrence during a follow-up of 12 +/- 9 months. The difference between group 1 and 2 could not be explained by clinical variables, amiodarone doses or plasma concentrations, or electrocardiographic variables. In patients in whom cardiovascular collapse or other severe symptoms where noted during electrophysiologic study after amiodarone treatment, recurrences caused sudden death (n = 12). However, in patients in whom the induced arrhythmia produced moderate symptoms, the recurrent arrhythmia was nonfatal VT (n = 26). Electrophysiologic testing provides clinical guidance and predicts prognosis in patients treated with amiodarone as it does for the evaluation of other antiarrhythmic agents.

Adult↗
PubMed1985

The clinical electrophysiology of intravenous indecainide.

The electrophysiologic effects of indecainide, a new class IC antiarrhythmic agent, were assessed in 10 patients with left ventricular dysfunction and inducible sustained ventricular tachycardia. Indecainide was administered intravenously in a dose of 60 to 90 mg/kg at a rate of 12.5 to 15 micrograms/kg/min. Indecainide had no effect on sinus node function or atrial and ventricular effective refractory periods. The AH (106 +/- 13 vs 130 +/- 24 msec, p less than 0.002) and HV (57 +/- 7 vs 73 +/- 19 msec, p less than 0.001) intervals were significantly increased. The QRS duration increased (102 +/- 9 vs 120 +/- 13 msec, p less than 0.001); however, the JT duration did not change. Induction of ventricular tachycardia was prevented in 1 of 10 patients. In the remaining nine patients, the ventricular tachycardia cycle length was significantly prolonged (248 +/- 47 vs 320 +/- 71 msec, p less than 0.001). Indecainide significantly depressed intracardiac conduction at several sites.

Adult↗
PubMed1985

Limitations of failure of procainamide during electrophysiologic testing to predict response to other medical therapy.

To determine whether failure of procainamide to prevent initiation of ventricular tachyarrhythmias during electrophysiologic testing predicted failure of other antiarrhythmic regimens, 81 consecutive patients with coronary artery disease whose ventricular tachyarrhythmias remained inducible during procainamide administration were studied. Overall, 26 (12%) of 216 subsequent drug studies were successful and at least one effective drug regimen was identified in 22 (27%) of the 81 patients. Drug success was significantly related to the arrhythmia induced at baseline study; 7% of drug studies were successful in patients with sustained ventricular tachycardia, 24% in patients with ventricular fibrillation, and 29% in patients with nonsustained ventricular tachycardia. An effective drug regimen was found in 11 (19%) of 59 patients with sustained ventricular tachycardia, 4 (50%) of 8 patients with ventricular fibrillation and 7 (50%) of 14 patients with nonsustained ventricular tachycardia. In patients with sustained ventricular tachycardia, failure of procainamide to suppress the arrhythmia correlated with failure of other agents used singly but not in combination. This study supports the view that when procainamide fails to prevent initiation of the arrhythmia in patients with inducible sustained ventricular tachycardia it is unlikely that other individual standard agents will be effective. However, combination regimens may suppress the arrhythmia and should be evaluated. In patients with nonsustained ventricular tachycardia, all agents should be evaluated because failure to respond to procainamide does not predict subsequent responses to other agents either alone or in combination.

Adult↗
PubMed1985

Electrophysiologic testing in patients at high risk for sudden cardiac death. I. Nonsustained ventricular tachycardia and abnormal ventricular function.

Nonsustained ventricular tachycardia, although usually asymptomatic, is associated with a high risk of sudden cardiac death in patients with depressed left ventricular function. To test the vulnerability of such patients to symptomatic and potentially life-threatening arrhythmias, complete electrophysiologic studies were performed in 58 patients with clinically documented nonsustained ventricular tachycardia (greater than or equal to three complexes but less than 15 seconds of self-terminating ventricular tachycardia by 24 hour ambulatory electrocardiographic [Holter] or telemetric monitoring) and abnormal left ventricular function (ejection fraction less than 50% by radionuclide angiography). All patients had nonsustained ventricular tachycardia in the absence of antiarrhythmic drugs, acute ischemia, long QT syndrome, recent infarction or electrolyte abnormalities. The stimulation protocol for each patient included the introduction of single, double and triple ventricular extrastimuli at three cycle lengths (sinus, 600 and 450 ms) and two right ventricular sites (apex and outflow tract). A sustained ventricular tachyarrhythmia was induced in 23 patients (40%) and a nonsustained ventricular tachycardia in 14 patients (24%). Induction of sustained tachycardia correlated with the presence of akinesia or aneurysm, or both, by radionuclide angiography, but not with ejection fraction or presence or absence of coronary artery disease. These results indicate that: 1) patients with clinical nonsustained ventricular tachycardia and chronic left ventricular dysfunction have a high incidence of inducible sustained ventricular tachycardia or ventricular fibrillation; and 2) electrophysiologic testing may allow further substratification of risk of sudden cardiac death in high risk patients with nonsustained ventricular tachycardia.

Adult↗