Nasopharyngeal carriage of meningococci.
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Biomedical subjects
Publications and source records attributed to R Yee.
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Electrophysiologic testing is warranted in patients with the Wolff-Parkinson-White (WPW) syndrome presenting with rapid atrial fibrillation (AF) or ventricular fibrillation. Indications are less clear in patients presenting only with atrioventricular reentrant tachycardia (ART). A knowledge of propensity of this latter group to show a rapid ventricular response in the event of AF and the ability of electrophysiologic testing to reproduce the type and rate of clinical arrhythmias are relevant to this decision. The records of 126 symptomatic patients with manifest WPW syndrome were reviewed and separated into 4 groups according to presentation: group 1--AF; group 2--ART; group 3--palpitations suggesting ART; and group 4--AF and ART. All patients except those in group 3 had electrocardiographically documented clinical arrhythmias, and these arrhythmias were compared with those induced during electrophysiologic testing. The shortest RR interval during induced AF and the cycle length of induced ART correlated well with those occurring clinically (r = 0.72, p less than 0.00001), as did the cycle length of induced ART (r = 0.79, p less than 0.00001). Patients presenting with AF (65%) had a higher incidence of atrial vulnerability (48%) and sustained AF at electrophysiologic testing than those presenting with ART (16% and 5%) or undocumented palpitations (27% and 21%). Forty-one percent of patients with ART and 51% with undocumented palpitations had potentially lethal rates (shortest RR interval less than 250 ms) during induced AF. The ability to reproduce clinical arrhythmias and the frequency of rapid rates during AF induced in patients presenting with only ART or undocumented palpitations supports the recommendation for electrophysiologic testing in symptomatic patients with WPW.
An ideal approach to classification of supraventricular arrhythmias would be based on exact knowledge of the pathophysiology and mechanism of the arrhythmia. Unfortunately, the mechanism may not be apparent from electrocardiographic data or indeed may not be known after extensive invasive and non-invasive studies. Difficulties are encountered in applying and extrapolating to patients criteria that are known to exist in experimental preparations. The traditional methods of classification have used electrocardiographic features and atrial rate. Although such classifications are simple, the criteria are arbitrary and electrocardiographically similar arrhythmias may have different mechanisms. A realistic classification must incorporate both electrocardiographic description and mechanism. The classification should be such that it can readily incorporate new knowledge in an additive way without completely restructuring the classification. A classification fulfilling these requirements would begin with electrocardiographic descriptors and end with mechanism, known or unknown. For example, a tachycardia may be characterized as supraventricular, atrial rate 300, 1:1 atrioventricular relation, with atrioventricular nodal reentry mechanism. It could then be qualified by further clinical descriptors such as incessant, paroxysmal or repetitive. With this approach, the initial descriptive category will always be constant and the mechanism known or unknown. As more data are obtained in future years, the "mechanism" segment of the descriptor may be added or revised.
Invasive electrophysiologic testing and noninvasive testing were compared as methods for identifying patients with Wolff-Parkinson-White syndrome at risk for sudden death. Sixty-seven patients were studied, including nine with a history of ventricular fibrillation. Electrophysiologic testing, using the shortest interval between consecutive pre-excited beats (shortest RR interval) less than or equal to 250 ms during induced atrial fibrillation to define risk, identified seven of nine patients with previous ventricular fibrillation. The sensitivity increased to 87.5% if one patient with prior amiodarone therapy was excluded. Electrophysiologic testing had a specificity of 48.3% and a low predictive accuracy (18.9%) when using the shortest RR interval (less than or equal to 250 ms) to identify the risk for sudden death. Continuous pre-excitation after disopyramide (2 mg/kg body weight, intravenously) had a sensitivity of 71.4%, specificity of 26.1% and predictive accuracy of 12.8% for identifying patients with sudden death. Continuous pre-excitation during an exercise test identified these patients with a sensitivity of 80%, a specificity of 28.6% and a predictive accuracy of 11.8%. These noninvasive tests could also be used to predict the shortest RR interval observed during induced atrial fibrillation. Continuous pre-excitation on both tests used in combination had a sensitivity of 91.2%, a specificity of 66.7% and a predictive accuracy of 75.6% for predicting the shortest RR interval less than or equal to 250 ms. Thus, both invasive and noninvasive techniques have a good sensitivity but a low specificity for identifying patients with Wolff-Parkinson-White syndrome and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)
Although ventricular fibrillation is a well known sequel to atrial fibrillation in the Wolff-Parkinson-White syndrome, ventricular fibrillation is not generally associated with supraventricular tachycardia in the presence of enhanced atrioventricular (AV) node conduction without pre-excitation. It was hypothesized that the ventricular response during atrial fibrillation may be less in patients with enhanced AV node conduction than in their counterparts with Wolff-Parkinson-White syndrome matched for anterograde effective refractory period. Slower ventricular rates during atrial fibrillation would suggest an increased propensity for concealed conduction in the enhanced AV node conduction group than in the group with an accessory pathway. Three groups of patients aged 16 to 65 years underwent electrophysiologic testing for supraventricular tachycardia or after surgical correction of Wolff-Parkinson-White syndrome. Sixteen patients had enhanced AV node conduction, 16 had Wolff-Parkinson-White syndrome and 16 had normal AV node conduction. Patients with enhanced AV node conduction and Wolff-Parkinson-White syndrome were well matched for anterograde effective refractory period (245 +/- 22 versus 258 +/- 25 ms) and minimal cycle length, maintaining 1:1 anterograde conduction (261 +/- 21 versus 260 +/- 40). There was no difference in intervals during atrial fibrillation (average RR interval = 372 +/- 37 versus 346 +/- 66) or shortest RR interval (266 +/- 27 versus 243 +/- 51). Thus, patients with Wolff-Parkinson-White syndrome and those with enhanced AV node conduction matched for anterograde refractory period exhibit similar ventricular rates during atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)
A technique has been described for countershock in an intensive care setting using a catheter electrode in patients with recurrent ventricular tachyarrhythmias. During defibrillation or cardioversion an electrode in the superior vena cava acts as an anode and an electrode in the right ventricular apex is the cathode. This report describes the resultant changes in the hearts of four men who died with recent, large myocardial infarcts and who had received eight to 55 countershocks of 2.5-50 joules through the catheter. Mural thrombus and/or focal endothelial hemorrhage was found in three hearts at the anode site. Thrombus was seen at the cathode site in two hearts. Myocardial necrosis, secondary to the catheter, was present in only one heart which had a 2 mm rim of granulation tissue around the distal electrode. It is unlikely that this focal area of right ventricular damage would be clinically important. We conclude, therefore, that repeated countershocks delivered through the catheter system produce little myocardial damage.
When used with insight, the 12-lead electrocardiogram can provide a considerable amount of useful data in patients with the Wolff-Parkinson-White syndrome. The 12-lead electrocardiogram during tachycardia usually provides excellent clues as to the mechanism of tachycardia, with the most valuable feature being the relationship of the P wave to the QRS complex. The observation of intermittent loss of preexcitation or loss of preexcitation with late atrial extrasystoles is an indicator of a long anterograde refractory period of the accessory pathway, a clue to a benign prognosis in the event of atrial fibrillation. The preexcited morphology as assessed by the electrocardiogram can provide an accurate first approximation to accessory-pathway location using a few simple guidelines.
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The acute electrophysiologic effects of pirmenol are reported in 8 normal subjects and in 8 patients with Wolff-Parkinson-White (WPW) syndrome. Standard electrophysiologic testing was performed before and after a 50-mg intravenous bolus and a 60-minute infusion of 150 mg of pirmenol. After pirmenol administration, AH interval, atrial refractory period, atrioventricular (AV) nodal functional refractory period and Wenckebach cycle length did not change; however, sinus cycle length decreased from 743 +/- 169 to 650 +/- 133 ms (p less than 0.001), sinoatrial conduction time from 103 +/- 35 to 78 +/- 37 ms (p less than 0.05) and AV nodal effective refractory period from 308 +/- 51 to 272 +/- 23 ms (p less than 0.01). Pirmenol increased the HV interval from 43 +/- 5 to 48 +/- 6 ms (p less than 0.05) and ventricular functional refractory period from 247 +/- 21 to 260 +/- 21 ms (p less than 0.005). Anterograde effective refractory period of the accessory AV pathway increased in 4 of 6 patients with ventricular preexcitation and retrograde effective refractory period increased in all patients. Pirmenol treatment prolonged the shortest preexcited RR interval from 253 +/- 38 to 459 +/- 19 ms (p less than 0.05) and the average RR interval from 354 +/- 26 to 421 +/- 60 ms (p less than 0.01) during atrial fibrillation in all 6 patients with preexcitation. Pirmenol did not influence the inducibility or cycle length of AV reciprocating tachycardia in the patients with WPW syndrome. The pirmenol infusions were well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)
Postoperative infection rates were determined for gynecologic outpatient surgical procedures performed in a traditional operating room environment and a separate, recently opened, surgicenter within the same hospital. Infections were self-reported by attending surgeons responding to computer-generated line listings of their recent surgical procedures. Responses were obtained on 97.9% (612/625) of women having surgery in the operating room and 99.5% (629/632) of women with surgicenter procedures. The overall infection rate for reported women was 0.9% (11/1,241). The difference between operating room and surgicenter rates was not statistically significant. Postoperative infections occurred in 2.5% (3/118) of diagnostic laparoscopies with tubal lavage and 1.4% (3/214) of voluntary abortions by dilatation and evacuation and curettage (D&E&C). The five other infections were scattered among the remaining 25 procedure categories. Ten of the 11 infections were limited to the "clean-contaminated" wounds. No serious or life-threatening infections were encountered. The computer-assisted surveillance system worked well and was easily incorporated into the existing infection surveillance system. The degree of ascertainment of postoperative wound infections is unknown due to reliance on physician self-reporting. However, no patients requiring readmission for infection went unreported by the attending surgeons.
Two hundred and eight patients underwent operative therapy of supraventricular tachycardia between June 1984 and June 1986. There were 196 patients with Wolff-Parkinson-White syndrome, one with AV nodal reentry, two with atrial flutter, one with ectopic atrial tachycardia, three with paroxysmal sinus tachycardia, and five with atrial fibrillation. Map guided or direct surgery was performed in all patients except the three with atrial fibrillation. Direct surgery was generally successful with failures including one patient with Wolff-Parkinson-White syndrome, one with atrial flutter, and the three patients with paroxysmal sinus tachycardia. There was no mortality. Major complications were uncommon and included three resternotomies for bleeding, one chylopericardium. Six patients required reoperation.
In this study we sought to determine whether characteristics of ventricular-induced atrial preexcitation during reciprocating tachycardia could help differentiate atrioventricular (AV) nodal reentry from orthodromic AV reentry using an accessory pathway and to identify the site of accessory pathways in patients with Wolff-Parkinson-White syndrome. Fifty-five patients with orthodromic AV reciprocating tachycardia and 22 patients with AV nodal reentrant tachycardia were studied with standard electrophysiologic techniques. There were 24 left free wall, 23 posterior septal, seven anterior septal, and one right free wall accessory pathways. Progressively premature right ventricular complexes (V2) were introduced during reciprocating tachycardia (V1V1). The V1V1 interval during tachycardia minus the longest V1V2 at which atrial preexcitation occurred defined a preexcitation index (PI). Atrial preexcitation occurred in 49 of 55 (89%) patients with AV reentry compared with only three of 22 (14%) patients with AV nodal reentry (p less than .001). In the three patients with AV nodal reentry who demonstrated atrial preexcitation, the PI was distinct from that of the septal pathways and was in the upper range of values for left free wall pathways. The percentage of tachycardias demonstrating atrial preexcitation was not different between the free wall and septal pathways, but His bundle activation was visible at the time of atrial preexcitation in only six of 17 (35%) left free wall compared with 13 of 16 (81%) posterior septal and seven of seven (100%) anterior septal pathways (p less than .05 free wall vs posterior or anterior septal).(ABSTRACT TRUNCATED AT 250 WORDS)
During diastole, tertiary amine local anesthetic molecules may exit cardiac sodium channels quickly through the membrane if they are neutral, or more slowly through the aqueous channel pore if they are charged. Extracellular acidosis potentiates sodium channel blockade by these drugs, and drug pKa should be a potent predictor of the degree of response of drug dissociation kinetics to changes in extracellular pH. To test this hypothesis, we measured kinetics of recovery from drug-induced channel blockade in guinea pig papillary muscle exposed to lidocaine (pKa 7.86) and to W6211 (pKa 6.29) using Vmax as a measure of peak sodium current. Both compounds, which are physicochemically very similar in respects other than pKa, delayed Vmax recovery in a pH-dependent fashion. As pH was lowered from 7.9 to 6.5, the recovery time constant rose from 86 to 230 msec for lidocaine and from 53 to 154 msec for W6211. We revised an earlier kinetic scheme of drug-channel interaction to incorporate newer concepts of drug trapping and ionization within the channel, and the resulting analytic expressions fit the data well. Important implications of the new scheme are that the pKa of the drug-receptor complex may differ from the drug pKa, and that deprotonation of channel-bound charged drug molecules may be a rate-limiting process.
Many electrocardiographic criteria have been proposed for the differentiation of ventricular extrasystole and supraventricular conduction with aberrancy in atrial fibrillation but the validity of these have not been confirmed by intracardiac studies. We recorded His bundle electrograms in nineteen patients (eleven men, eight women) referred for diagnosis of abnormal QRS complexes in the context of chronic atrial fibrillation. Of 1,068 wide QRS complexes analyzed, 91% proved to be of ventricular origin. Electrocardiographic criteria which were specific for ventricular extrasystole included: left bundle branch block morphology, right bundle branch block morphology with a monophasic R in lead V1 or an RS or QS pattern in lead V6, presence of a "compensatory pause", i.e., compensatory cycle (V2-V3) longer than the average cycle length of ten normally conducted beats preceding the abnormal complex (927 +/- 317 vs 780 +/- 199, mean +/- SD in msec. p less than 0.005), frontal QRS axis of the abnormal complex directed superiorly or to the right and the presence of a "short-long" cycle sequence. Right bundle branch morphology with a triphasic R in lead V1 or QRS pattern in V6 and concordant initial vector in lead V1 or in more than one ECG leads were very specific for supraventricular conduction with aberrancy. Analysis of coupling interval and Ashman's phenomenon, i.e., the long-short cycle sequence, were not specific for supraventricular conduction with aberrancy. We conclude that in digitalis-treated patients with chronic atrial fibrillation the majority of abnormal QRS complexes are of ventricular origin. The diagnosis of ventricular extrasystole or aberrancy can be made using a single ECG lead (V1) and applying a combination of easily applied criteria.
Although supraventricular tachycardia in the Wolff-Parkinson-White (WPW) syndrome is generally due to atrioventricular reentry, the presence of the accessory pathway does not preclude other mechanisms of tachycardia. We observed AV nodal reentry in three of 95 consecutive patients (3.1%) referred for assessment of arrhythmias associated with WPW syndrome. The unique observation of spontaneous transition from atrioventricular reentry to AV nodal reentry at a similar cycle length was observed in one patient and is the subject of this report.
Recent studies have shown improved efficacy of chemotherapy in patients with advanced squamous-cell cancer of the head and neck. Our purpose was to evaluate prospectively the activity of cisplatin plus 5-fluorouracil (5FU) in 37 patients with advanced stage IV squamous-cell cancer of the head and neck. There were two groups. Group 1 consisted of 19 previously untreated patients with either T4 or N3 disease. They received 100 mg/m2 cisplatin (days 1 and 28) and 120-hour infusion of 1,000 mg/m2/24 hours 5FU (days 1 to 5 and 28 to 32). They subsequently were offered preoperative radiotherapy (RT) and surgery. Group 2 consisted of 18 previously treated patients. They received 5FU and cisplatin in the same dosage every 28 days for either recurrent or metastatic disease. It was found that in group 1 there was an 84% response rate (five complete responses (CR) and 11 partial responses (PR) ). Three of those with PR achieved a CR after RT. Seven patients have had RT plus surgery and are disease free at 8 to 27 month follow-up. Six patients (one CR, five PR) refused surgery and progressed within 4 months. In group 2 there was an 11% response rate after two cycles (two PR), three patients had a minimal response (MR, less than 50% response) and received a mean of four cycles of treatment. Three patients with stable disease received a mean of four cycles of chemotherapy until progression. Two of 11 patients who had received previous chemotherapy plus RT showed an MR; nine of these patients had shown a response to their previous chemotherapy. Only one of 14 patients who had RT plus chemotherapy had a PR, and three had MR. Of five patients who had previous surgery, only one had a PR. All five had received chemotherapy as well. It was concluded that 5FU plus cisplatin is an effective combination in previously untreated patients. In previously treated patients with recurrent disease, there is a substantially lower response rate.
The electrophysiologic effects of intravenous verapamil and propranolol were compared alone and in combination in 14 patients (aged 21 to 69 years) with paroxysmal supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) reentry utilizing a manifest (7 patients) or concealed (3 patients) accessory pathway. Four patients had AV nodal reentry. Electrophysiology studies were performed using standard techniques in the control state and after verapamil (0.15 mg/kg intravenous bolus and 0.005 mg/kg/min). The next day, studies were repeated after propranolol (0.1 mg/kg) and a combination of verapamil and propranolol. No adverse effects occurred with the drug combination. Each drug intervention prolonged anterograde functional refractory period of the AV node (control, 370 +/- 50 ms; verapamil, 446 +/- 90 ms; propranolol, 436 +/- 92, p less than 0.05), with the greatest increase occurring after the drug combination (502 +/- 103 ms, p less than 0.001). In 2 patients prolonged sinus node recovery time developed after the drug combination. Verapamil or propranolol prevented SVT induction in 7 patients (50%). However, only the drug combination prevented reinduction of sustained SVT in 6 patients. These 6 patients were treated chronically with verapamil and propranolol, with no recurrence of SVT in any patient after 2 to 26 months.
The serial changes in pacing threshold and R-wave amplitude were examined after insertion of a countershock catheter in 12 patients referred for management of recurrent ventricular tachyarrhythmias. In 6 patients, values before and immediately after catheter countershock were monitored. Pacing threshold increased (from 1.4 +/- 0.2 to 2.4 +/- 0.5 V, mean +/- standard error of the mean, p less than 0.05) while the R-wave amplitude decreased (bipolar R wave from 5.9 +/- 1.1 to 3.4 +/- 0.7 mV, p less than 0.01; unipolar R wave recorded from the distal ventricular electrode from 8.9 +/- 1.8 to 4.6 +/- 1.2 mV, p less than 0.01; and proximal ventricular electrode from 7.7 +/- 1.5 to 5.0 +/- 1.0 mV, p less than 0.01). A return to control values occurred within 10 minutes. In all patients, pacing threshold increased by 154 +/- 30% (p less than 0.001) during the first 7 days that the catheter was in place. It is concluded that catheter countershock causes an acute increase in pacing threshold and decrease in R-wave amplitude. A catheter used for countershock may not be acceptable as a backup pacing catheter.