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Biomedical subjects

A A Adgey

Publications and source records attributed to A A Adgey.

At least 73 records · Page 4Linked to original sources
PubMed1994

Discriminant function analysis of body surface potential maps in acute myocardial infarction.

Using a newly developed 64-electrode portable mapping device, QRS and ST-T isointegral maps were compared in 194 control subjects and 101 patients. One hundred ninety-four control subjects (mean age, 48 years; 120 men) with no history of cardiac disease were selected randomly and mapped. One hundred one patients (mean age, 62 years; 77 men) were mapped at presentation of chest pain suggestive of first myocardial infarction (MI); all patients had classic 12-lead electrocardiographic findings--46 with anterior and 55 with inferior MI. The diagnosis was confirmed in all cases by a significant rise in serial cardiac enzymes. The mean delay between onset of chest pain to map recording was 163 minutes. Of the 101 patients, 78 were first mapped outside the hospital. Applying discriminant function analysis to the isointegral measurements made on the control subjects and on the first map of MI patients achieved a correct classification of 97% of the control subjects (189 of 194) and 72% of the anterior (33 of 46) and 76% of the inferior (42 of 55) MI groups. This preliminary study suggests that discriminant function analysis, based on isointegral maps, not only provides a method of separating control subjects from MI patients but that it can also differentiate between types of infarct. Further studies are required to improve the predictive values of discriminant function and to extend the methodology to assess both the site and size of MI.

Adult↗
PubMed1994

Assessment of ability of levcromakalim and sodium nitroprusside to reverse the cardiovascular effects of nitric oxide synthase inhibition in the anaesthetised pig.

OBJECTIVE: The aim was to test the ability of levcromakalim, a potassium channel opener, and sodium nitroprusside, a nitric oxide donor, to reverse the systemic and pulmonary vasoconstrictor actions of NG-nitro-L-arginine methyl ester (L-NAME), and thus to restore cardiac output in anaesthetised pigs. METHODS: In separate groups of pigs administration of a bolus of L-NAME (10 mg.kg-1) was followed either by no further agent (control group; n = 8) or by increasing bolus doses of levcromakalim (10, 20, and 40 micrograms.kg-1; n = 8) or by increasing infused doses of sodium nitroprusside (1, 2, and 4 micrograms.kg-1.min-1 for 15 min at each dose). The same doses of levcromakalim and sodium nitroprusside were also given to pigs (n = 6 in each group) which had been pretreated with saline rather than L-NAME. The changes in systemic and pulmonary haemodynamic indices and cardiac output as a result of each intervention were measured at each stage and compared between and within drug groups. RESULTS: In each group, the bolus of L-NAME caused increases in systemic vascular resistance, mean arterial pressure, pulmonary vascular resistance, and mean pulmonary artery pressure, and a reduction in cardiac output. These effects were significantly different from pretreatment values at 15 min, and were maintained for at least 60 min when no further agent was given. The subsequent administration of levcromakalim caused significant reductions in systemic vascular resistance and mean arterial pressure, the effects being greater than in animals that had been pretreated with saline rather than L-NAME. Pulmonary vascular resistance and mean pulmonary artery pressure were also reduced, but to a lesser degree. Cardiac output was partially but significantly restored. The subsequent administration of sodium nitroprusside caused significant reductions in systemic vascular resistance, mean arterial pressure, pulmonary vascular resistance, and mean pulmonary artery pressure. These effects were significantly greater than those in animals that had been pretreated with saline rather than L-NAME. Cardiac output was weakly, though significantly restored. CONCLUSIONS: Increased systemic vascular resistance following a bolus of L-NAME (10 mg.kg-1) is reversed by subsequent administration of levcromakalim (10-40 micrograms.kg-1) or sodium nitroprusside (1-4 micrograms.kg-1.min-1) associated with partial restoration of cardiac output. The degree to which cardiac output is restored by these two agents is limited by a concomitant reduction in preload.

Amino Acid Oxidoreductases↗
PubMed1994

Time delays to lytic therapy and outcome in 100 consecutive patients with a history suggestive of acute myocardial infarction in an area with access to a mobile coronary care unit.

Time delays to fibrinolytic treatment and outcome were assessed in 100 consecutive patients, with suggestive symptoms and electrocardiographic changes of acute myocardial infarction, admitted to the coronary care unit of this hospital. All patients admitted from out-of-hospital had access to a mobile coronary care unit. Initially, 40 patients called a general practitioner, 30 called the '999' operator, 12 called the mobile coronary care unit, 10 reported directly to the Accident and Emergency Department, seven were in-hospital and one spoke to the general practitioner's receptionist. Subsequently, 59 patients were attended by the mobile coronary care unit, 34 were admitted via the Accident and Emergency Department and seven had symptoms in-hospital. Thrombolytic therapy was initiated in 45/59 (76%) patients by the mobile coronary care unit staff and in 29/34 (85%) patients in the Accident and Emergency Department by cardiac staff. The remaining 26 patients received thrombolytic treatment in the hospital coronary care unit or cardiac department. The mean (+/- SEM) time from symptom onset to the initiation of thrombolytic therapy was 127 (+/- 11 min) for those patients treated by the mobile coronary care unit staff and for those treated in the Accident and Emergency Department was 187 (+/- 13 min) (P = 0.005). Multiple regression analysis showed significant reductions in total time delay if patients received thrombolytic therapy by the mobile coronary care unit staff out-of-hospital, when chest pain began in-hospital, or if patients had a previous myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambulances↗
PubMed1994

Comparison of the ability of nicardipine, theophylline and zaprinast to restore cardiovascular haemodynamics following inhibition of nitric oxide synthesis.

1. The use of pharmacological inhibitors of nitric oxide (NO) synthesis to treat patients with septic shock is limited by the observation that they cause a fall in cardiac output in some subjects. The aim of this work was to investigate this fall and to test whether it was reversible by subsequent administration of nicardipine, theophylline or the cyclic GMP-selective phosphodiesterase inhibitor, zaprinast (M&B 22948). 2. In pentobarbitone-anaesthetized pigs, haemodynamic indices were measured before and after intravenous administration of NG-nitro-L-arginine methyl ester (L-NAME) in a dose-response protocol (0.2-20 mg kg-1; n = 6) and as a single bolus of 10 mg kg-1 either alone or followed by increasing doses of nicardipine, theophylline or zaprinast (n = 8 in each group). 3. L-NAME caused a dose-dependent rise in systemic vascular resistance and mean systemic arterial pressure and a dose-dependent fall in cardiac output. A single bolus of L-NAME (10 mg kg-1) produced these effects within 15 min. 4. Subsequent administration of nicardipine (0.05-0.2 mg kg-1) caused complete reversal of systemic vasoconstriction and hypertension and in doing so completely restored cardiac output. Theophylline (7.5-10 mg kg-1) partially reversed the rise in systemic vascular resistance and partially restored cardiac output but the effect was small compared to that of nicardipine. Zaprinast (1-5 mg kg-1) had no significant effect on any of these variables. 5. These results suggest that reduced cardiac output following inhibition of NO synthesis is an effect of increased afterload on the heart and is reversible by nicardipine and to a lesser extent by theophylline.These findings may have potential value for those using NO synthase inhibitors to treat patients with septic shock.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1994

Transesophageal electroventilation. Optimization and improvement.

For electroventilation, short duration pulse trains (0.1 ms) were applied between two axillary pads (transchest) and compared with transesophageal electroventilation where pulses passed between the same pads to an esophageal electrode in apneic, pentobarbitone-anesthetized pigs. Significantly greater tidal volumes were produced by transesophageal electroventilation in comparison with transchest. As measured by maintained tidal volumes, duration of inspiratory air flow, peak flow, percentage hemoglobin oxygen saturation (%SaO2), and end tidal carbon dioxide concentration (ETCO2), the optimal requirements for transesophageal electroventilation were pulse frequency 40 Hz, 0.7 s duration pulses, at 60 to 100 V, pulse width 0.1 ms, with the esophageal electrode proximal to the gastroesophageal junction without producing brachial plexus stimulation. The efficiency of transesophageal electroventilation falls off rapidly following ventricular fibrillation. Thus, the application of this technique would be in respiratory arrest with maintained circulation, eg, in drug-induced respiratory depression, severe smoke inhalation, severe emphysema, high cervical cord lesion, and weaning from prolonged mechanical ventilation.

Animals↗
PubMed1994

Portable cardiac mapping assessment of acute ischaemic injury.

A portable cardiac mapping system is used to improve the accuracy of diagnosis of acute ischaemic injury outside hospital. Patients presenting chest pain suggestive of myocardial infarction (MI) were mapped by attendant medical personnel operating from a mobile coronary unit. These first MI maps were compared against average normal maps using QRS and ST-T isointegral values. Discriminant function analysis performed on the parameters achieved a sensitivity of 90% and a specificity of 96%.

Body Surface Area↗
PubMed1993

Transesophageal cardioversion.

With the use of a novel quadripolar esophageal electrode system, we have attempted 131 transesophageal cardioversions in 105 patients: 109 episodes were atrial fibrillation, 16 episodes were atrial flutter, 2 episodes were supraventricular tachycardia, and 4 episodes were ventricular tachycardia. The mean predicted transesophageal impedance (+/- SEM) of 52.6 +/- 1.1 omega was significantly lower than the mean predicted transthoracic impedance (+/- SEM) of 63.1 +/- 1.6 omega (n = 104; p < 0.01). Of the 88 patients who presented with atrial fibrillation as the initial arrhythmia, successful transesophageal cardioversion (maximal delivered transesophageal energy of 100 J in 84 patients and 200 J in 4 patients) was recorded in 70 (79.5%); transesophageal cardioversion required a mean delivered energy of 63.1 +/- 4.2 J and a mean peak current of 20.3 +/- 0.6 A. Transthoracic countershock (maximal delivered energy of 360 J) was attempted in 17 of 18 patients when the transesophageal approach had been unsuccessful; countershock was successful in 10 patients, which yielded an overall success rate of 92.0% (mean successful delivered energy [transesophageal and transthoracic] of 85.3 +/- 7.8 J). All episodes of atrial flutter, supraventricular tachycardia, and ventricular tachycardia were successfully terminated with the use of the esophagus. This esophageal electrode system permits low-energy countershock of atrial and ventricular tachyarrhythmias.

Adult↗
PubMed1993

Value of signal-averaged electrocardiography, radionuclide ventriculography, Holter monitoring and clinical variables for prediction of arrhythmic events in survivors of acute myocardial infarction in the thrombolytic era.

OBJECTIVES: This study assessed the ability of signal-averaged electrocardiography, radionuclide ventriculography and Holter electrocardiographic (ECG) monitoring and clinical variables to identify patients at risk of serious arrhythmic events after myocardial infarction in the thrombolytic era. BACKGROUND: Most studies of signal-averaged electrocardiography, radionuclide ventriculography and Holter ECG monitoring in risk stratification after myocardial infarction preceded the introduction of thrombolytic therapy. METHODS: A consecutive series of 301 survivors of myocardial infarction, 205 (68%) of whom received thrombolytic agents, underwent signal-averaged electrocardiography (1st 48 h, day 6 and discharge), Holter ECG monitoring (days 6 to 7) and radionuclide left ventriculography (days 7 to 14). Median follow-up time was 1.03 years. RESULTS: Thirteen patients (4.3%) had an arrhythmic event (sudden death in 11, sustained ventricular tachyarrhythmia in 2). The 25-Hz high pass filtered signal-averaged ECG at discharge was 64% sensitive (95% confidence intervals [CI] 36% to 92%) and 81% specific (95% CI 76% to 86%). High grade ventricular ectopic activity on the Holter ECG was only 38% sensitive (95% CI 12% to 64%) and 74% specific (95% CI 71% to 77%). Left ventricular ejection fraction < 0.4 was the best test for prediction of arrhythmic events (sensitivity 75% [95% CI 50% to 100%] and specificity 81% [95% CI 76% to 85%]). In multivariate analysis, in rank order, digoxin therapy at discharge, an abnormal 25-Hz signal-averaged ECG before discharge, absence of angina before index infarction and previous infarction were predictive of arrhythmic events. With digoxin therapy excluded, ejection fraction was an independent predictor. Discriminant analysis identified a high risk group (12% of the study patients) with an event rate of 26%. CONCLUSIONS: The signal-averaged ECG and left ventricular ejection fraction are each independently predictive of arrhythmic events after myocardial infarction, but the Holter ECG is not. A combination of clinical and investigative variables, including the signal-averaged ECG, best identifies patients at highest risk.

Aged↗
PubMed1993

Double-blind randomized trial of alteplase versus placebo in patients with chest pain at rest.

Patients who have chest pain occurring at rest are at a significant risk of myocardial infarction and or sudden death. Most trials enter patients with anginal rest pain after an initial screening period. Thus, the clinical efficacy of early thrombolytic treatment for patients with rest pain remains unproven. Eighty patients with chest pain at rest and with ECG changes of ST depression of at least 1 mm in any ECG lead, were randomized to alteplase 100 mg infused over 3 h, or placebo. Concomitantly, all patients received intravenous heparin and 300 mg of aspirin daily (unless contra-indicated). Seventy-four patients had coronary angiography (the majority within 72 h of admission) of which 73 were assessable. The patency of the ischaemia-related vessel was not significantly greater in the alteplase treated group (81% vs 78%, P = 0.82). The culprit lesion morphology tended to be more concentric in the alteplase treated group (84% vs 56%, P = 0.06) although alteplase treatment was not associated with a significant reduction in the severity of the culprit lesion stenosis. Intra-coronary thrombi were detected in 7% of patients (3% placebo, 11% alteplase, P = 0.35). The mean left ventricular ejection fraction or the alteplase-treated group was 49 +/- 3% and for the placebo-treated patients 56 +/- 3% (P = 0.05). There was no difference in the total in-hospital cardiac event rate i.e. cardiac death, myocardial infarction and coronary revascularization between patients receiving alteplase (10%, 63%, and 38%) and those receiving placebo (8%, 65%, and 30%) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1993

Lipid peroxidation and antioxidant status following thrombolytic therapy for acute myocardial infarction.

We have investigated the timescale of increased lipid peroxidation following successful early thrombolytic therapy for acute myocardial infarction and report for the first time reciprocal changes in plasma chain-breaking antioxidants. Sixty-seven patients were recruited following a first acute myocardial infarction within 6 h of the onset of symptoms and received 70 or 100 mg of recombinant tissue plasminogen activator (Actilyse) as two intravenous bolus injections 30 min apart. Serial blood samples were taken before administration of thrombolytic therapy and after 30 min, 60 min, 90 min, 6 h and 24 h. Coronary artery patency was assessed at 90 min by coronary angiography. Malondialdehyde (MDA), a marker of lipid peroxidation, and the chain-breaking antioxidants alpha-tocopherol, retinol and ascorbate were measured by high performance liquid chromatography. When the coronary artery was patent there was an early rise in plasma MDA (time 0 0.91 +/- 0.05 mumol.l-1) with levels peaking at 90 min (1.02 +/- 0.06, P < 0.05) and returning to baseline by 6 h (0.85 +/- 0.06), accompanied by reciprocal decreases in alpha-tocopherol (time 0 7.13 +/- 0.34 mumol.mmol-1 cholesterol, 90 min 6.64 +/- 0.33, P < 0.05) and retinol (time 0 1.99 +/- 0.10 mumol.l-1, 90 min 1.81 +/- 0.08, P < 0.05). Ascorbate levels did not change significantly until 24 h (time 0 29.5 +/- 4.9 mumol.l-1, 24 h 22.6 +/- 4.4, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Transoesophageal versus transchest DC cardioversion.

Attempted cardioversion via the oesophagus (transoesophageal cardioversion) was compared with the transchest approach (transchest cardioversion) in a randomized trial of 100 consecutive patients with atrial fibrillation. For the transoesophageal group, 30, 50 and 100 J were delivered via an oesophageal electrode with subsequent 200 and 360 J transchest if required. For the transchest group, 50, 100, 200 and 360 J were delivered if required. In the transoesophageal group, 36/50 (72%) of patients cardioverted using the transoesophageal route alone, and in the transchest group, 41/50 (82%) of patients cardioverted (p = NS). First shock success was similar for the transoesophageal and transchest groups: 13/50 (26%) vs. 8/50 (16%) respectively. The mean number of shocks required to achieve successful cardioversion was identical for the transoesophageal and transchest groups (2.6). However, transoesophageal cardioversion was more successful than transchest cardioversion at energies < or = 100 J (36/50 [72%], and 17/50 [34%], p < 0.05). Median total energy for successful cardioversion was lower for patients in the transoesophageal group (180 J) than the transchest group (350 J) and mean peak current at successful cardioversion was also lower for patients in the transoesophageal group (21.7 A) than the transchest group (27.3 A) (p < 0.05). No oesophageal complications occurred. Thus, using an oesophageal electrode, cardioversion can be achieved as successfully as using the transchest route. The transoesophageal approach offers a low impedance, and consequently a low-energy pathway for cardioversion.

Atrial Fibrillation↗
PubMed1993

Altered cardiac oxygen extraction, lactate production and coronary blood flow after large dose transthoracic DC countershocks.

Although problems such as hypotension and pulmonary edema complicate the use of transthoracic DC countershocks, the mechanisms are not clear. In anesthetized dogs at 1 minute after only two defibrillator shocks there was a brief rise in coronary sinus lactate, exceeding arterial concentrations. Larger rises in lactate were seen after five shocks, indicating myocardial production of lactate. By contrast in eight animals given dummy shocks the heart always extracted lactate. At 2 minutes after five shocks mean myocardial oxygen extraction (6.5 +/- 0.6 mL/100 mL/100 mL blood; n = 4; P < 0.001), and remained so until 3 minutes after shocks, without significant increase in the lipid peroxidation product malondialdehyde in coronary sinus or arterial blood. Great cardiac venous blood flow, measured by thermodilution, rose after five shocks, and the heart rate pressure product also increased at 1-2 minutes. This transient failure of oxygen extraction, in the presence of arterial normoxia, hyperemia, and increased cardiac work, is best accounted for by a central effect of countershocks on myocardial cellular respiration.

Animals↗
PubMed1992

Failure of countershock-type pulses in vitro to adversely alter mitochondrial oxidative phosphorylation.

STUDY OBJECTIVE: The aim of the study was to investigate a potential mechanism of myocardial injury after DC countershock. The effect of countershock-type electrical discharges on rabbit heart mitochondrial oxygen consumption was measured in vitro using a novel respiration cell. MEASUREMENTS AND MAIN RESULTS: Mitochondria were isolated from the hearts of adult Dutch and New Zealand White rabbits. Single rectangular shocks (voltage gradients 20 to 80 V/cm; 5 ms duration) caused no significant changes in state 3 oxygen consumption in standard incubation medium. Single and multiple defibrillator shocks (critically damped sine waveform; 5 ms duration) with peak voltage gradients of 242 to 659 V/cm similarly had no significant effect on state 3 oxygen consumption. CONCLUSION: At voltage gradients similar to and greater than those causing myocardial cell injury and necrosis, electrical discharges do not directly depress mitochondrial function. Therefore, the reduction in mitochondrial oxygen consumption observed following transthoracic shocks in vivo may invoke other mechanisms (eg, intracellular calcium influx, high circulating noradrenaline, or free radical formation in the intact heart).

Animals↗
PubMed1992

Oxidative metabolism and myocardial blood flow changes after transthoracic DC countershocks in dogs.

Changes in oxidative metabolism and myocardial blood flow were investigated in adult greyhounds following transthoracic shocks from a DC cardiac defibrillator (400 Joules stored energy, damped sine wave, 0.5 min intervals). Myocardial lactate extraction became negative maximally at 1 min, following both two (mean -24% +/- SEM24) or five (-193% +/- 148) shocks and returned to baseline by 6-15 min. Transient reductions were also observed in myocardial extraction of pyruvate and free fatty acids but not glucose. Myocardial necrosis assessed at 4 h following the shocks was 0.05 g (+/- 0.03) after two shocks, 6.5 g (+/- 1.5) after five shocks and zero in controls. Mean peak noradrenaline levels in arterial (785 +/- 319 pg.ml-1) and coronary sinus (916 +/- 313 pg.ml-1) blood at 1 min after five shocks were higher than after 0 shocks (82 +/- 33 pg.ml-1 and 201 +/- 63 pg.ml-1 respectively), P < 0.05. Great cardiac venous blood flow was measured by a thermodilution technique, with continuous infusion of 0.9% saline, before, during and after five shocks. Mean blood flow fell from 47 +/- 13 ml.min-1 to a minimum of 36 +/- 7 ml.min-1 during shocks, and then rose to 83 +/- 17 ml.min-1 at 2 min after the fifth shock (P < 0.05). Following damaging countershocks, oxidative metabolism is depressed, in keeping with a primary disturbance of mitochondrial function. These metabolic changes are not secondary to ischaemia, since an increase in blood flow in the great cardiac vein (GCV) is observed. Vasodilatation of the coronary vascular bed must occur to account for this.

Analysis of Variance↗
PubMed1992

The accuracy of decision-making of a semi-automatic defibrillator during cardiac arrest.

The accuracy of decision-making of a semi-automatic defibrillator was assessed at 57 cardiac arrests in 55 patients. The initial rhythm was ventricular fibrillation at 40 arrests and was correctly identified in 37 (sensitivity 92.5%). In the other 17 arrests initial rhythms were not ventricular fibrillation and 16 were correctly identified (specificity 94%). Continuous electrocardiographic recordings of the arrests were analysed in 8-12 s segments: of 432 segments showing ventricular fibrillation, 352 were correctly identified (sensitivity 81%); 3895 of 4139 segments showing rhythms other than ventricular fibrillation were correctly identified (specificity 94%). The percentage accuracy of detection of ventricular fibrillation varied from 0-100% (mean 91%) and for non-ventricular fibrillation from 51-100% (mean 92%). When 104 segments of ventricular fibrillation and 470 segments of non-ventricular fibrillation with cardiopulmonary resuscitation artefact were excluded from the analysis, a sensitivity of 91% and specificity of 96% were obtained. Thus the detection of cardiac arrest rhythms using a microprocessor based detection system for patients with cardiac arrest has a high sensitivity for ventricular fibrillation and specificity for non-ventricular fibrillation.

Cardiopulmonary Resuscitation↗