Treatment with esmolol of ventricular fibrillation unresponsive to lidocaine and procainamide.
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Biomedical subjects
Publications and source records attributed to R W Koster.
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The current mode of administration of recombinant tissue-type plasminogen activator (rt-PA) in acute myocardial infarction is rather complex, although the rationale for the different components of this scheme is not clearly established. We compared pharmacokinetics of a continuous infusion of 38.5 MU of Burroughs Wellcome t-PA (duteplase) over 90 minutes in nine patients (phase I) with a scheme including a 0.04 MU/kg bolus, a 60-minute 0.36 MU/kg lytic infusion and a 180-minute 0.21 MU/kg maintenance infusion in 15 patients with acute myocardial infarction (Phase II). t-PA activity and antigen were fitted in a one-compartment model from which model-dependent and model-independent parameters were derived. Clearance of t-PA activity was 1020 +/- 465 (mean +/- SD) ml/min in phase I and 1359 +/- 590 ml/min in phase II. Clearance of t-PA antigen was 666 +/- 230 ml/min in phase I and 704 +/- 199 ml/min in phase II. Clearance of activity was significantly (p less than 0.01) higher than of antigen. Clearance and steady-state plasma levels showed a large interindividual variability (coefficient of variation, 56.4%), but this was significantly reduced by dosing by weight (coefficient of variation, 28.9%; p = 0.031). A 10% bolus in phase II shortened the time to reach 75% and 90% of the steady-state plasma level by 4 and 5 minutes, respectively, not significantly different from phase I. A simulation study showed that a bolus should be approximately 15% of the lytic dose to achieve a maximal level in the shortest period.
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We studied the localization of pain in the acute phase of myocardial infarction in comparison with localization in non-cardiac chest pain. Myocardial infarction patients could not be differentiated from patients with non-cardiac chest pain in localization of pain on mid-chest, left side of the chest and left arm. However, myocardial infarction patients reported pain on the right side of the chest and in the right arm twice as often as non-cardiac chest pain patients. Results are similar when patients indicated the localization of the pain symptoms on attending the Emergency Coronary Care Unit, or when asked five days later. Pain symptoms on the right side of the chest and the right arm differentiate better between myocardial infarction and non-cardiac chest pain than the 'classical' symptom pattern.
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The clinical course of the first six weeks after discharge after consultation was studied in 527 patient contacts in 460 patients who were evaluated for acute cardiac symptoms in a six-month period at the acute cardiac care facility 'Eerste Harthulp' in the Academic Medical Centre. Analysis revealed that the initial diagnosis of acute ischaemia (261 cases) was correct in 118 (45%) and the initial diagnosis of arrhythmia (114 cases) in 92 (81%). In 220 patients there was no cardiac history; in those instances the initial diagnosis of acute ischaemia was confirmed in only 40% but the initial diagnosis of arrhythmia in 78%. Three patients died within six weeks after evaluation and 28 patients were admitted within that period. Patients without cardiac history and without a clear cardiac diagnosis consulted their general practitioner moderately frequently in the first six weeks and used specialist care only rarely.
This study was designed to examine the relationships between dose of Wellcome two-chain recombinant tissue type-plasminogen activator (BW rt-PA) and coronary patency and fibrinolytic parameters in acute myocardial infarction (AMI). In an open randomized study, patients with AMI (determined by ECG) and symptoms of less than 4 h duration without contraindications for fibrinolytic therapy were treated with rt-PA in nominal doses of 20 (7.7 MU), 50 (14.8-29.6 MU) or 100 mg (29.6-48.2 MU) administered over 90 min followed by intravenous heparin. Coronary patency was determined by coronary arteriography of the infarct-related artery and haematological parameters (fibrinogen, plasminogen, alpha 2-antiplasmin and fibrin(ogen) degradation products) measured at 90 min. Coronary patency increased in a dose-related manner to 53% (95% C.I. 37-69%) in the 100 mg/90 min group. Logistic regression demonstrated a relationship between dose (in MU kg-1) and coronary patency. Fibrinogen at 90 m was reduced to 74 (61.5-86.4%) of the pooled plasma standard in the nominal 100 mg group. Patients with a higher predose fibrinogen had higher reductions of fibrinogen. Serious bleeding occurred in three (3%) patients, and no intracranial bleeds were reported. BW rt-PA produces dose-related patency of the coronary arteries with moderate, dose-related reduction in fibrinogen.
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The effects of prophylactic lidocaine hydrochloride on early ventricular fibrillation and death in patients with suspected acute myocardial infarction were investigated in an overview of 14 randomized trials. During follow-up intervals of one to four hours in the trials of intramuscular lidocaine infusion (6961 patients) and 24 to 48 hours in the trials of intravenous lidocaine injection (2194 patients), a total of 103 cases of ventricular fibrillation and 137 deaths were recorded. Overall, allocation to lidocaine was associated with a reduction in the odds of ventricular fibrillation of about one third, with a 95% confidence interval that ranged from a 3% to a 56% reduction. There was no evidence of any beneficial effect on early mortality; indeed, the odds of early death were about one third greater among patients allocated lidocaine, though this difference was not statistically significant (95% confidence interval, 2% reduction to 95% increase). Because of the small numbers of reported events, the short follow-up periods, and the unavailability of data for some specific causes of death, even an overview of all the trial results does not provide good evidence as to whether prophylactic lidocaine is likely to be helpful or harmful. To answer this question reliably, future trials will need to involve large numbers of patients and prolonged follow-up.
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A personal computer-based data management system for the cardiac catheterization laboratory is described. This is a cooperative effort on the part of the Dutch academic hospitals, through the Interuniversity Cardiology Institute, to put in place a more uniform structure for data collection and reporting in the context of cooperative studies. The major design criteria included the necessity that the system provide a clear and present benefit to the users in terms of their day-to-day work. This requires a practical data entry package together with a full reporting capability, including management tools for supervision of the catheterization laboratory in general. Ancillary activities include quantitative analysis of ventriculograms and an elementary statistics package with graphics. To facilitate supportability of the system, commercially available packages for data base management, text processing, and communications have been used to advantage. After a prototype test phase involving two centers, five other centers have been equipped with similar systems and used successfully in the majority.
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In a randomized controlled study examining the value of an intramuscular injection of lidocaine in the prehospitalization phase of suspected acute myocardial infarction, paramedics used an automatic injector to administer 400 mg of the drug into the patient's deltoid muscle before transport to the hospital. In a 33-month period, 7026 patients with acute chest pain were seen. Of the 6024 patients randomized (2987 to the lidocaine group and 3037 to the control group), 1935 (32 per cent) proved to have an acute myocardial infarction. In the entire 60-minute period of observation by continuous electrocardiography, primary ventricular fibrillation was observed in 8 treated and 17 control patients (P = 0.08). However, from 15 minutes after randomization onward, when plasma lidocaine levels were in the therapeutic range, only 2 cases of ventricular fibrillation occurred in the treated group, as compared with 12 in the control group (P less than 0.01). Ventricular tachycardia terminated a mean of 10 minutes after injection in six of nine lidocaine-treated patients with acute myocardial infarction but in none of five control patients with infarction (P less than 0.02). Mean plasma lidocaine levels were 3 micrograms per milliliter 11 to 20 minutes after injection in 369 consecutive patients. In 65 patients, levels were below 2 micrograms per milliliter, and in 15 patients, levels were above 6 micrograms per milliliter. Side effects were rare and did not contribute to mortality. We conclude that intramuscular lidocaine may be useful if given by a paramedic, another person, or the patient himself when acute myocardial infarction is suspected outside the hospital.
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Ventricular fibrillation (VF) and transient arrhythmias after defibrillation were analyzed from the recordings of 28 patients containing at least one episode of ventricular fibrillation. An R-on-T extrasystole initiated VF in 60% of the episodes. Other initiating factors were a late premature beat (24%), stable ventricular tachycardia (VT) (7%), accelerating idioventricular rhythm (5%) and cardioversion of VT (5%) with a sinusoidal waveform. After the initiating beat, in most cases, evidence was found of a transient ventricular tachycardia which then deteriorated into VF. With a stable VT this may occur after a long time; in the case of apolymorphic VT (with changing amplitude) it generally occurred within 30 s. The main transient arrhythmias generated by circulatory arrest during VF and by the defibrillation shock were: total arrest, total AV-block and/or bradycardia. The combination of a longer duration of VF and a high energy level generally resulted in an increase in the duration of these arrhythmias (P less than 0.01, N = 30). Comparison of episodes of VT and VF recorded in a single patient also shows that arrhythmias are more unfavourable and of longer duration after VF than after VT. These data emphasize fast defibrillation, initially with stored energy levels less than 250J.
Transdermally delivered nitroglycerin (TTS-NTG) through a rate-controlling membrane yields stable blood levels for 24 h. We studied the effect of TTS-NTG (25 mg per 10 cm2) on exercise induced angina in 10 patients with stable angina pectoris, all in NYHA class III, who were not under treatment with other cardiac drugs. In a pre-study exercise test, all patients had angina pectoris and more than one mm ST depression. The study was placebo controlled and double blind with a randomized cross-over. Exercise tests were carried out on a treadmill according to the Bruce-protocol, 12 to 16 h after administration of TTS-NTG or of an identical placebo. After a 48 h wash-out period, the procedure was repeated after application of a plaster with the alternative content. A significant improvement was seen on TTS nitroglycerin compared with placebo in the total duration of exercise (7.2 +/- 3.6 min (mean +/- SD) vs 6.2 +/- 3.8 min; P less than 0.002). In 7 patients, the time to onset of angina was extended by TTS nitroglycerin. Maximal ST depression (lead V4 and V6) was significantly lower on TTS nitroglycerin (1.85 +/- 1 mm) compared with placebo (2.2 +/- 1 mm; P less than 0.05). It is concluded that 12 to 16 h after administration, transdermally delivered nitroglycerin improves exercise capacity and reduces maximal ST depression in patients with stable angina.
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