Trigeminocardiac reflex during temporomandibular joint arthroscopy: report of a case.
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Publications and source records attributed to R S Roberts.
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OBJECTIVES: This study was done to evaluate pacemaker therapy for severe recurrent vasovagal syncope. BACKGROUND: Nonrandomized studies have suggested that permanent pacing might help control the symptoms of recurrent vasovagal syncope. The study goal was to evaluate the effect of permanent pacemaker implantation on syncope in patients with frequently recurrent vasovagal syncope. METHODS: Patients with > or = 6 lifetime episodes of syncope and with a tilt-table test that induced syncope or presyncope, as well as a relative bradycardia, were randomized to receive a dual-chamber pacemaker or not. The pacemaker prevented bradycardia and provided high-rate pacing if a predetermined drop in heart rate occurred (rate-drop response). The primary outcome was the first recurrence of syncope. Patients also completed a detailed diary recording presyncopal episodes. RESULTS: A total of 284 patients was originally planned and a pilot study of 60 patients was initiated. At the planned first formal interim analysis of efficacy of the pilot study, an unanticipated large treatment effect was observed which fulfilled the prespecified criteria for early termination of the study. At that time, there were 54 patients enrolled, randomized evenly to no pacemaker or to pacemaker. In the no-pacemaker and pacemaker groups the mean ages were 40 and 46 years; 74% and 70% patients, respectively, were female. The baseline tilt-table test showed a slowest heart <60/min or longest heart period >1000 ms in 60% of no-pacemaker patients and 72% of pacemaker patients. There was a marked reduction in the postrandomization risk of syncope in pacemaker patients (relative risk reduction 85.4%, 95% confidence interval 59.7% to 94.7%; 2p=0.000022). CONCLUSIONS: Dual-chamber pacing with rate-drop response reduces the likelihood of syncope in patients with recurrent vasovagal syncope.
The North American Vasovagal Pacemaker Study is an ongoing multicenter randomized, clinical trial that assesses the efficacy of dual chamber pacing utilizing rate drop sensing in patients with frequent syncopal spells. Patients are eligible if they have had at least six syncopal spells and a positive tilt table test, or a recurrence of syncope within 6 months of a positive tilt test. The tilt table test must have provoked a relative bradycardia. Patients are randomized to receive a Medtronic Thera DR with rate drop sensing, or to continue on their usual therapy. All patients complete a log of their presyncopal and syncopal spells daily, and are contacted every 2 months. The primary outcome measure is the time to the first recurrence of syncope. The goal of the main study is to recruit 284 patients in 3 years with a final fourth year of follow-up; this will result in an 80% chance of detecting a 30% reduction in the risk of syncope. A pilot study is under way with the aim to recruit 60 patients over a period of 2 years with a final third year of follow-up. Recruitment began in July 1995 and 47 patients have been enrolled to date.
This study documents mortality from acute myocardial infarction (AMI), in hospital and at 1 year, for each of 3 selected 1-year periods in a stable community over a 13-year period beginning in 1979 and continuing into the thrombolytic era, to detect any changes occurring in conjunction with the introduction of new therapies. Every patient with AMI occurring in a geographically defined stable community (Hamilton, Ontario, Canada) in 3 1-year periods (1979 to 1980 [n = 816], 1986 to 1987 [n = 816], and 1991 to 1992 [n = 831]) was identified and clinically characterized by standardized criteria. Subsequent in-hospital and 1-year survival were ascertained prospectively. The 3 cohorts were similar in prognostic factors. Mean age was progressively greater over the study period from 63 years in 1979 to 1980, to 67 years in 1991 to 1992 (p = 0.02). There was no change in in-hospital mortality rates from 1979 to 1980 (17%) and 1986 to 1987 (16%). However, from 1986 to 1987 and 1991 to 1992, in-hospital mortality decreased from 16% to 9% (p < 0.001) and 1-year mortality decreased from 26% to 19% (p < 0.001). For patients who survived the hospital phase of AMI, 1-year mortality did not change and was between 11% and 12% in each of the 3 study periods. From 1986 to 1987 and 1991 to 1992, there was an increase in the use of thrombolytic therapy from 5% to 44% of patients. The acute use of aspirin increased from 30% to 88% and the acute use of beta blockers increased from 19% to 48% of patients. The observed increase in use of these agents could account for half of the actual mortality reduction observed. This prospective population-based survey demonstrates improved in-hospital survival after AMI associated with increased use of established effective therapies between 1987 and 1992. The 1-year mortality of hospital survivors of AMI was unchanged throughout the period of study, remaining at 11% to 12%.
BACKGROUND: After an acute myocardial infarction, it is important to determine the risk of a subsequent coronary event. We studied the prognostic value of myocardial ischemia detected by ambulatory electrocardiographic (ECG) monitoring in patients who had recently had an acute myocardial infarction. METHODS: Five to seven days after acute myocardial infarction, 406 patients underwent 48-hour ambulatory ECG monitoring, with submaximal exercise testing before discharge and measurement of the left ventricular ejection fraction within 28 days after infarction. Death, nonfatal myocardial infarction, and admission to the hospital because of unstable angina were the principal end points recorded during the one-year follow-up period. RESULTS: The overall incidence of myocardial ischemia detected by ambulatory ECG monitoring was 23.4 percent. The mortality rates at one year were 11.6 percent among the patients with ischemia and 3.9 percent among those without ischemia (P = 0.009); 3.9 percent among the patients with a positive exercise test, 3.0 percent among those with a negative exercise test, and 16.4 percent among those in whom an exercise test was not performed (P < 0.001); and 3.6 percent among the patients with an ejection fraction greater than 50 percent, 3.5 percent among those with an ejection fraction between 35 and 50 percent, and 18.2 percent among those with an ejection fraction below 35 percent (P = 0.001). Using multiple logistic regression, we found that no diagnostic test performed after myocardial infarction provided additional prognostic information beyond that provided by the standard clinical variables used to predict the risk of death. When nonfatal myocardial infarction and admission to the hospital because of unstable angina were also included as outcome variables, ambulatory monitoring for ischemia was the only test that contributed significantly to the model. For the patients with ischemia detected by ambulatory monitoring, as compared with those who did not have evidence of ischemia, the odds ratio was 2.3 (95 percent confidence interval, 1.2 to 4.5) for death or nonfatal myocardial infarction (P = 0.009) and 2.8 (95 percent confidence interval, 1.6 to 4.8) for death, nonfatal myocardial infarction, or admission to the hospital because of unstable angina (P < 0.001). CONCLUSIONS: Myocardial ischemia detected by ambulatory ECG monitoring is common early after acute myocardial infarction and provides prognostic information beyond that available from standard clinical information.
BACKGROUND: Heparin-induced thrombocytopenia, defined by the presence of heparin-dependent IgG antibodies, typically occurs five or more days after the start of heparin therapy and can be complicated by thrombotic events. The frequency of heparin-induced thrombocytopenia and of heparin-dependent IgG antibodies, as well as the relative risk of each in patients given low-molecular-weight heparin, is unknown. METHODS: We obtained daily platelet counts in 665 patients in a randomized, double-blind clinical trial comparing unfractionated heparin with low-molecular-weight heparin as prophylaxis after hip surgery. Heparin-induced thrombocytopenia was defined as a decrease in the platelet count below 150,000 per cubic millimeter that began five or more days after the start of heparin therapy, and a positive test for heparin-dependent IgG antibodies. We also tested a representative subgroup of 387 patients for heparin-dependent IgG antibodies regardless of their platelet counts. RESULTS: Heparin-induced thrombocytopenia occurred in 9 of 332 patients who received unfractionated heparin and in none of 333 patients who received low-molecular-weight heparin (2.7 percent vs. 0 percent; P = 0.0018). Eight of the 9 patients with heparin-induced thrombocytopenia also had one or more thrombotic events (venous in 7 and arterial in 1), as compared with 117 of 656 patients without heparin-induced thrombocytopenia (88.9 percent vs. 17.8 percent; odds ratio, 36.9; 95 percent confidence interval, 4.8 to 1638; P < 0.001). In the subgroup of 387 patients, the frequency of heparin-dependent IgG antibodies was higher among patients who received unfractionated heparin (7.8 percent, vs. 2.2 percent among patients who received low-molecular-weight heparin; P = 0.02). CONCLUSIONS: Heparin-induced thrombocytopenia, associated thrombotic events, and heparin-dependent IgG antibodies are more common in patients treated with unfractionated heparin than in those treated with low-molecular-weight heparin.
Three methods were used to combine measurements from biplane coronary views to assess restenosis following PTCA. The first 153 patients from the EMPAR trial with 118 measurable coronary stenoses were chosen for this study. The mean difference between the RAO and LAO projections used was 88 +/- 22 degrees (S.D.). There was no systematic difference in coronary dimensions between RAO and LAO views for the group. Coronary restenosis was primarily defined as loss of 50% or more of the luminal diameter gain from the procedure. The ratio of luminal loss to gain was calculated for each stenosis using (Method 1) only the lesser diameter of the two views, (Method 2) an average of the two views and, (Method 3) a calculated cross-sectional coronary lumen area. Rates of restenosis calculated in this way ranged between 36 and 44% amongst the three methods, which was not significantly different. However, individual coronary lesions might be classified as either restenosed or not by this formula, depending on which method was used to integrate the biplane coronary measurements.
OBJECTIVE: To describe the incidence and types of first Hickman catheter-related infection (HCRI) in cancer patients and to identify indicators for catheter removal. DESIGN: Retrospective cohort study. SETTING: A regional, tertiary, referral cancer center and its supportive care university teaching hospital. PATIENTS AND METHODS: A retrospective review was conducted of 316 consecutive adult oncology patients who underwent Hickman catheter placement from 1986 to 1990 at a regional oncology center. HCRI was determined on the basis of clinical information incriminating the Hickman catheter as the source of infection. Patient characteristics and data about HCRIs (exit site cellulitis, tunnel infection with concomitant exit site cellulitis, bloodstream infection, and exit site cellulitis with bloodstream infection) were abstracted from patient medical records. Subsequently, univariate and multivariate analyses for the risk of HCRI and catheter removal were completed. RESULTS: The incidence of first HCRI was 5.98 infections per 1,000 catheter days. Overall, 156 (49%) of 316 patients developed their first HCRI prior to catheter removal. The median time to HCRI was 90 days. Male gender (P = .0004) and hematologic malignancy (P = .0001) emerged as significant risk factors for HCRI in the univariate analysis. A cox model verified that male gender (P = .02) and hematologic malignancy (P = .004) were associated with an enhanced risk of HCRI. There were 35 exit site infections (23%), three infections of the tunnel and the exit site (2%), 80 bloodstream infections (51%), and another 38 bloodstream infections with concomitant exist site infections (24%). The incidence of bloodstream infection was 3.05 per 1,000 catheter days. Gram-positive pathogens outnumbered gram-negatives and fungi, with Staphylococcus epidermidis being most common. Fifty (32%) of 156 HCRIs resulted in catheter removal. Predictors of Hickman catheter removal in the univariate analysis were bloodstream infection (P = .046) and pathogen type (P = .006). Multiple regression analysis suggested that having a gram-negative (P = .014) or fungal (P = .057) pathogen was the most important factor for catheter removal. CONCLUSIONS: These data suggest that first HCRIs occur more commonly in male patients with hematologic malignancies than in patients with solid tumors. The removal of Hickman catheters in oncology patients probably is predicated on the causative pathogen, but further investigations are necessary to delineate this issue.
PURPOSE: To test the strength, at the marginal ridge, of the tunnel preparation vs the Class II traditional box preparation when restored with composite or glass ionomer (GI). MATERIALS AND METHODS: Eighty-four extracted maxillary molars stored in normal saline and thymol were randomly divided into six groups of 14 each (determined by pilot study where alpha = 0.05, beta = 0.2). Group A and C were tunnel preparations. Group B and D were traditional Class II preparations. Group E-whole tooth (negative control), and Group F-tunnel preparation unrestored (positive control). Group A and B were restored with Scotchbond 2/P-50 composite. Group C and D were restored with Ketac Fil-GI. The marginal ridge of each tooth was loaded at 0.5 mm/minute on the Instron. A loading rod produced a contact point of 1.0 mm in diameter. RESULTS: The mean compressive loads (kg) required for fracture were: (A): 42.2 +/- 11.9, (B): 53.1 +/- 10.7, (C): 52.0 +/- 10.9, (D): 23.8 +/- 8.4. (E): 79.1 +/- 16.1, (F): 27.0 +/- 10.6. A significant difference was found between whole teeth (E) and all other groups (P < 0.05). The Newman-Keuls test showed a significant difference between Class II composite (B) and tunnel composite (A) (P < 0.05), between tunnel GI (C) and tunnel composite (A) (P < 0.05) but no difference between tunnel GI (C) and Class II composite (B).
The risk of death due to cancer of the nose or lung was studied in nickel sinter plant workers during the period after they left the sintering operations. It was found that the excess risk of death from both diseases continued for many years after leaving the sinter plant. No effect of age at first exposure could be found. Possible explanations for the continued risk include an irreversible cellular change or the persistence of carcinogenic nickel compounds in the mucosa.
BACKGROUND AND PURPOSE: The Early Stroke Trial (EST) is a randomized, double-blind, placebo-controlled trial to assess the effect of monosialoganglioside GM-1 in improving recovery in patients who experienced an ischemic supratentorial stroke. METHODS: Sixteen clinical centers recruited 805 patients, of whom 792 were confirmed to be eligible. Treatment, consisting of a first dose of either 200 mg GM-1 or placebo, was initiated within 5 hours of the onset of stroke; a second dose of either 100 mg GM-1 or placebo was administered 12 hours later. Thereafter, patients received a daily injection of 100 mg GM-1 or placebo intravenously from day 2 through 10 and intramuscularly from day 11 through 21. Patients were followed up for a total of 4 months. RESULTS: Survival was similar in the two treatment groups. Improvement in neurological status, as measured by the change in Canadian Neurological Scale score between baseline and 4-month assessments, was greater in the group receiving GM-1; the observed difference between treatment groups was 0.22 (P = .06). A post hoc analysis in the subgroup of patients treated within 4 hours showed a statistically significant difference, with Canadian Neurological Scale mean improvement of 0.41 (P = .016). GM-1 use was not associated with differences in frequency, nature, or severity of adverse experiences. CONCLUSIONS: These findings suggest that GM-1 is safe in the dose and treatment schedule used and that its efficacy in ischemic stroke is greater when given soon after onset of stroke.
OBJECTIVE: To report a case of phenytoin toxicity successfully treated with multiple-dose activated charcoal. CASE SUMMARY: A 36-year-old man was first admitted with chronic phenytoin toxicity secondary to hepatitis and was treated symptomatically. His serum phenytoin concentration was 149.8 mumol/L on admission and decreased slowly over his 6-day hospitalization to 134.8 mumol/L. Upon readmission approximately 24 hours later, his phenytoin concentration was 186.7 mumol/L. Because of acute phenytoin toxicity, he was treated with multiple-dose activated charcoal. His phenytoin concentration after four doses of activated charcoal returned to the therapeutic range within 36 hours and his symptoms abated quickly, thus decreasing his hospital stay. DISCUSSION: The exact mechanism of action of multiple-dose activated charcoal to decrease serum phenytoin concentrations is unknown. Several mechanisms of action have been reported in the literature and are discussed. CONCLUSIONS: Multiple-dose activated charcoal was used successfully in treating acute phenytoin toxicity in our patient. Based on his previous admission for chronic phenytoin toxicity, his hospital stay was reduced by three days. The use of multiple-dose activated charcoal in acute phenytoin toxicity has potential therapeutic and financial implications.
OBJECTIVES: To determine the influence of timing, infarct location and thrombolytic therapy on the electrocardiographic (ECG) response to exercise testing following acute myocardial infarction. DESIGN: Maximal treadmill exercise testing was performed on postinfarction day 8 and repeated on day 90 as part of a previously reported double-blind, placebo controlled study of recombinant tissue plasminogen activator (rt-PA) in acute myocardial infarction in which left ventricular function was the primary end-point. Patients were systematically evaluated for left ventricular function, myocardial perfusion and coronary anatomy. SETTING: Ten collaborating community and academic hospitals. PATIENTS: One hundred and fifteen patients, aged 20 to 75 years, with ischemic chest pain 30 mins or longer and ST elevation on ECG. Patients with cardiogenic shock, left bundle branch block, prior aortocoronary bypass surgery, recent percutaneous transluminal coronary angioplasty or standard contraindications to thrombolytic therapy were excluded. MAIN RESULTS: The analysis is confined to the 70 patients who underwent both exercise tests without intercurrent coronary revascularization. Peak rate-pressure product was greater on day 90 than on day 8 (mean difference +/- SE 2.2 +/- 0.6 x 10(3), P = 0.001), whereas 65% of patients had 1 mm or greater of exercise-induced ST shift on day 8 compared with 47% on day 90 (P = 0.025). Patients following anterior compared with inferior infarction were more likely to have exercise-induced ST elevation (54% versus 21%, P = 0.012) but less likely to have ST depression (29% versus 63%, P = 0.017) on day 8; results were directionally similar on day 90. Treatment with rt-PA, compared with placebo, did not influence exercise performance, the ECG response to exercise or the extent of inducible ischemia on thallium scintigraphy. CONCLUSIONS: Timing and infarct location are important modifiers of the ECG response to exercise testing following myocardial infarction. Thrombolytic therapy in these uncomplicated patients did not influence inducible ischemia.
The Canadian Implantable Defibrillator Study (CIDS) is an on-going randomized multicenter clinical trial that compares implantable cardioverter-defibrillator (ICD) therapy against amiodarone in patients with prior cardiac arrest or hemodynamically unstable ventricular tachycardia. Eligible patients are equally randomized to receive or not receive an ICD as initial management. Those not receiving an ICD receive amiodarone. All patients are seen in follow-up every 6 months. The primary outcome event cluster is arrhythmic death or any other death occurring within 30 days of therapy initiation. Secondary outcomes are all-cause mortality and nonfatal occurrences of ventricular tachycardia or fibrillation. The goal of the study is to recruit 400 patients over 4 years. All patients will be followed to the end of the year. This will result in an 80% chance of detecting a reduction in arrhythmic death of 58% by ICD if such a difference in truth exists. Recruitment began in October 1990 and 184 patients have been enrolled to date.
Because there is uncertainty about the role of atherogenic and nonatherogenic risk factors for cerebral ischemia in the young, we carried out a multicenter, hospital-based, case-control study. 333 patients (15-44 years) with focal cerebral ischemia (transient ischemic attack or stroke within 8 weeks of admission) were eligible. 25 patients were excluded, according to the protocol. 308 cases were matched by age and gender to one hospital and one population control. Independent risk was shown by logistic conditional regression for migraine with aura [odds ratio (OR) = 14.8], smoking (OR = 3.7), alcohol (OR = 2.8), serum triglycerides (OR = 1.6), arrhythmias (OR = 9.5), mitral stenosis (OR = 56), coronary heart disease (OR = 4.3) and carotid stenosis or occlusion (OR = 41). Serum HDL-cholesterol had a relative protective effect (OR = 0.8). These data confirm the role of atherosclerosis and cardiac diseases as well as migraine with aura and alcohol consumption in the pathophysiology of cerebral ischemia in the young. More thorough prevention programs may contribute to earlier detection and control of all of these risk factors, but further investigations in patients with as yet unidentified risk factors are warranted because the above-mentioned factors do not account for the total risk of ischemic stroke in the young.
This article considers the implications of reporting multiple measures of efficacy in studies of patients with rheumatoid arthritis (RA). A possible solution to the problems that result is the use of a pooled index which combines the individual outcome measures. The potential advantages and disadvantages of pooled indexes are discussed in the context of clinical trials in RA.
OBJECTIVE: To evaluate therapy with aspirin plus dipyridamole in reducing restenosis after carotid endarterectomy. PATIENTS: A total of 163 patients having 175 surgical carotid endarterectomies. INTERVENTION: Eighty-three patients (90 endarterectomies) were randomly assigned to receive oral aspirin, 325 mg, plus dipyridamole, 75 mg, beginning 12 hours preoperatively, followed by a second dose administered within 8 hours after the operation, and given three times daily thereafter for 1 year. Eighty patients (85 endarterectomies) received placebo medication that was identical in appearance to the study drugs. MEASUREMENTS: After the adequacy of the surgical procedure was confirmed by intraoperative angiography, restenosis at the endarterectomy sites was evaluated using serial duplex ultrasound studies before hospital discharge and at 3-month intervals postoperatively for 1 year. RESULTS: Based on the time for developing identifiable restenosis and on efficacy analysis, greater than 50% restenosis developed in 11 operated vessels (16%) in the treated group and in 10 arteries (14%) in the placebo group, yielding an observed risk increase of 14% (95% CI, -52% to 167%; P greater than 0.2). By intention-to-treat analysis, greater than 50% restenosis developed in 16 of 90 operated vessels in treated patients and in 10 of 85 arteries in patients receiving placebo (26% for the treated group and 12% for the placebo group; P = 0.18, Mantel-Haenszel statistic), representing an observed risk increase of 110% (CI, -5% to 365%). Similar differences were observed for greater than 20% restenosis and for the comparison of patients rather than operated vessels by either intention-to-treat or efficacy analyses. CONCLUSIONS: Because therapy not only failed to reduce carotid restenosis but may have actually increased its frequency, treatment with aspirin plus dipyridamole probably has no clinically important benefit on restenosis in patients having carotid endarterectomy.
A retrospective industrial hygiene investigation was undertaken to explain the cause of a statistically significant excess lung cancer mortality observed in a subset of a large cohort of nickel workers involved in mining, smelting, and refining of nickel and copper in Ontario. The focus of this paper is to demonstrate how an industrial hygiene follow-up assessment of an epidemiologic finding can help to identify a likely cause. Polycyclic aromatic hydrocarbons (PAHs) alone or in association with particulate and gaseous contaminants (e.g., SO2) were likely the causative agents of the excess lung cancer observed among the lead welders, cranemen, and arc furnace workers of the copper refinery.