Curative transcatheter radiofrequency current ablation for atrioventricular nodal reentry tachycardia.

BACKGROUND: To evaluate the efficacy of atrioventricular nodal modification by transcatheter ablation using radiofrequency energy in preventing electrically inducible and spontaneous symptomatic atrioventricular nodal reentry tachycardia, a prospective, nonrandomized, "before-after" trial was performed. Fifty consecutive patients with recurrent spontaneous symptomatic atrioventricular nodal reentry tachycardia referred to the Massachusetts General Hospital, Boston, were recruited. METHODS: A diagnostic intracardiac electrophysiologic study was performed to define the mechanism of each patient's supraventricular tachycardia. Thereafter, selective ablation of one or more slow atrioventricular nodal pathways was attempted in 47 patients, and in three patients selective ablation of a retrograde fast atrioventricular nodal pathway was carried out. Repeated programmed cardiac stimulation was performed 30 minutes after catheter ablation therapy and, where possible, before hospital discharge to evaluate the presence of electrically inducible supraventricular tachycardia. RESULTS: Electrically inducible atrioventricular nodal reentry tachycardia was eliminated in all 50 patients. No patient developed early heart block. During a mean (+/- SD) follow-up period of 8.9 +/- 5.3 months, three patients experienced a recurrence of spontaneous atrioventricular nodal reentry tachycardia and underwent a successful second ablation procedure. Two patients required permanent pacemaker implantation, one for symptomatic first-degree atrioventricular block and one for late complete heart block. CONCLUSIONS: Catheter ablation of slow atrioventricular nodal pathways by means of radiofrequency current is a safe and effective technique for eliminating electrically inducible and spontaneous atrioventricular nodal reentry tachycardia.

Antioxidant status and lipid peroxidation in hereditary haemochromatosis.

Hereditary haemochromatosis is characterised by iron overload that may lead to tissue damage. Free iron is a potent promoter of hydroxyl radical formation that can cause increased lipid peroxidation and depletion of chain-breaking antioxidants. We have therefore assessed lipid peroxidation and antioxidant status in 15 subjects with hereditary haemochromatosis and age/sex matched controls. Subjects with haemochromatosis had increased serum iron (24.8 (19.1-30.5) vs. 17.8 (16.1-19.5) mumol/l, p = 0.021) and % saturation (51.8 (42.0-61.6) vs. 38.1 (32.8-44.0), p = 0.025). Thiobarbituric acid reactive substances (TBARS), a marker of lipid peroxidation, were increased in haemochromatosis (0.59 (0.48-0.70) vs. 0.46 (0.21-0.71) mumol/l, p = 0.045), and there were decreased levels of the chain-breaking antioxidants alpha-tocopherol (5.91 (5.17-6.60) vs. 7.24 (6.49-7.80) mumol/mmol cholesterol, p = 0.001), ascorbate (51.3 (33.7-69.0) vs. 89.1 (65.3-112.9), p = 0.013), and retinol (1.78 (1.46-2.10) vs. 2.46 (2.22-2.70) mumol/l, p = 0.001). Patients with hereditary haemochromatosis have reduced levels of antioxidant vitamins, and nutritional antioxidant supplementation may represent a novel approach to preventing tissue damage. However, the use of vitamin C may be deleterious in this setting as ascorbate can have prooxidant effects in the presence of iron overload.

Effectiveness of double bolus alteplase in the treatment of acute myocardial infarction.

Fifty-nine consecutive patients presenting within 6 hours of the onset of symptoms of an acute myocardial infarction were treated with 150 mg of soluble aspirin orally, and either 70 or 100 mg of alteplase divided into 2 intravenous bolus injections separated by 30 minutes. Dosage regimens were either 20 followed by 50 mg (group A), 50 followed by 20 mg (group B), or 50 followed by 50 mg (group C). Coronary angiography 60 minutes after the first bolus showed infarct-related coronary artery patency (Thrombolysis in Myocardial Infarction score 2 or 3) in 13 of 16 (81%) patients in group A, 12 of 17 (71%) in group B, and 10 of 11 (91%) in group C (overall patency rate at 60 minutes: 35 of 44 [80%] patients; 95% confidence interval 68 to 91%). At 90 minutes, patency rates were 15 of 20 (75%) patients in both groups A and B, and 18 of 19 (95%) in group C (overall patency rate 48 of 59 [81%] patients; 95% confidence interval 72 to 91%). Residual thrombus was identified with the 90-minute angiogram in 7 patients in group A, 5 in group B, and 3 in group C. Although there was no statistically significant difference in patency between the 3 dosage regimens at either 60 or 90 minutes there was a trend toward increased patency and more complete thrombolysis at 90 minutes in group C. No episodes of bradyarrhythmia, hypotension or cerebrovascular bleeding were observed after double bolus therapy. There were 7 episodes (12%) of reocclusion, and 3 deaths (5%) within 1-month follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

High dose nalbuphine in early acute myocardial infarction.

Twenty patients with moderate or severe pain of suspected myocardial infarction received nalbuphine 50 mg intravenously as analgesia in 2 divided doses of 30 mg and 20 mg with 10 mg metoclopramide and were observed for 2 hours. Eighteen patients received nalbuphine outside hospital. The median time from onset of pain to treatment was 73 minutes. Within 30 minutes of the drug's administration 90% of all patients reported satisfactory pain relief (grade 0 or 1). For those with definite myocardial infarction 83% reported satisfactory pain relief at 30 minutes. There were no significant adverse cardiorespiratory effects observed or serious side-effects reported. Nalbuphine is effective and safe when used in this higher dose, although no additional analgesic effect was demonstrated when compared with lower established doses used early in acute myocardial infarction.

Myocardial infarction in pregnancy.

Three cases of myocardial infarction occurring in the third trimester of pregnancy are presented. The method of delivery in each case was individualised with no maternal or fetal mortality. Each patient had significant risk factors for coronary arterial disease or thrombosis. One patient had normal coronary arteries demonstrated at coronary arteriography.

The design and performance of a 2.5-GHz telecommand link for wireless biomedical monitoring.

This paper details the implementation and operational performance of a minimum-power 2.45-GHz pulse receiver and a companion on-off keyed transmitter for use in a semi-active, duplex RF biomedical transponder. A 50-ohm microstrip stub-matched zero-bias diode detector forms the heart of a body-worn receiver that has a (CMOS baseband amplifier consuming 20 microA from +3 V and achieves a tangential sensitivity of -53 dBm. The base transmitter generates 0.5 W of peak RF output power into 50 ohms. Both linear and right-hand circularly polarized Tx-Rx antenna sets were employed in system reliability trials carried out in a hospital Coronary Care Unit. For transmitting antenna heights between 0.3 and 2.2 m above floor level, transponder interrogations were 95% reliable within the 67-m2 area of the ward, falling to an average of 46% in the surrounding rooms and corridors. Overall, the circular antenna set gave the higher reliability and lower propagation power decay index.

On the design and assessment of a 2.45 GHz radio telecommand system for remote patient monitoring.

This paper discusses the design and operational assessment of a minimum-power, 2.45 GHz portable pulse receiver and associated base transmitter comprising the interrogation link in a duplex, cross-band RF transponder designed for short-range, remote patient monitoring. A tangential receiver sensitivity of - 53 dBm was achieved using a 50 ohms microstrip stub-matched zero-bias diode detector and a CMOS baseband amplifier consuming 20 microA from + 3 V. The base transmitter generated an on-off keyed peak output of 0.5 W into 50 ohms. Both linear and right-hand circularly-polarised antennas were employed in system evaluations carried out within an operational Coronary Care Unit ward. For transmitting antenna heights of between 0.3 and 2.2 m above floor level. transponder interrogations were 95% reliable within the 82 m2 area of the ward, falling to an average of 46% in the surrounding rooms and corridors. Separating the polarisation modes, using the circular antenna set gave the higher overall reliability.

Mobile coronary care and mortality from ischaemic heart disease in a predominantly rural community.

The mobile coronary care unit based at Coleraine Hospital was called to 155 patients in the community during a six-monthly period, 74 of whom had sustained a myocardial infarction. Over the same period, 25 of 49 patients admitted via the ordinary ambulance with suspected ischaemic heart disease had sustained a myocardial infarction and received medical care significantly later than those seen by the mobile unit. A further 12 patients out of 39 with suspected ischaemic heart disease admitted by other means (the accident and emergency department or other hospital units) brought the total number of patients admitted to hospital with myocardial infarction during the study period to 111.Overall mortality from myocardial infarction was 19.8% and was significantly higher in those >/= 70 years of age. Nine patients with myocardial infarction seen by the mobile coronary care unit required early defibrillation (four outside hospital) and eight of these survived to be discharged. No patients admitted by other means required emergency defibrillation. Although no significant difference in mortality was demonstrated between those seen before or after three hours from the onset of symptoms or between patients admitted by the mobile unit or by the ordinary ambulance, a subgroup of patients below 70 years of age and seen by the mobile unit less than three hours after the onset of symptoms had the lowest mortality of 6.7%. Estimated overall mortality from ischaemic heart disease in this community over the study period was in excess of those deaths accounted for in this survey, implying a high mortality in those not admitted to hospital.

A review of direct current cardioversions for atrial arrhythmia.

UNLABELLED: The risk of arterial embolism is well recognised following Direct Current Cardioversion (DCC) for atrial fibrillation although the use of prophylactic anticoagulation remains controversial. AIM: To determine the risk of arterial embolism post-cardioversion and which factors predict successful cardioversion and maintenance of sinus rhythm. MATERIALS AND METHODS: A retrospective study was carried out of all cardioversions performed for atrial fibrillation and atrial flutter at the Waveney Hospital Ballymena, during 1989-1993. A review of medical records and electrocardiograms was carried out to assess demographic characteristics, co-existent diseases, anticoagulant status, echocardiographic features and characteristics of the arrhythmia. Embolic events in the six weeks post-cardioversion were noted. RESULTS: The study included 157 cardioversions in 109 patients. The predominant arrhythmia was atrial fibrillation (n = 108, 69%). Three of 109 patients (2.7%) experienced embolic complications, none of whom had anticoagulation prior to the procedure. No risk factors for cerebro-vascular disease or significant valvular heart disease were present. Return to sinus rhythm was achieved in 143 (91%) procedures. Increasing coarseness of atrial fibrillation was associated with a non-significant trend towards successful restoration of sinus rhythm (p = 0.18). Recurrence of the original arrhythmia was predicted by an increase in coarseness of atrial fibrillation (p < 0.05). CONCLUSIONS: These findings indicate that embolic complications can occur in patients undergoing DCC with normal echocardiographic dimensions, and that prophylactic anticoagulation should be considered in all patients. Coarseness of atrial fibrillation may be used as a guide to predict the chance of successful cardioversion and of the likelihood of maintaining sinus rhythm once this has been achieved.

Biphasic energy selection for transthoracic cardioversion of atrial fibrillation. The BEST AF Trial.

AIMS: To compare the efficacy and safety of an escalating energy protocol with a non-escalating energy protocol using an impedance compensated biphasic defibrillator for direct current cardioversion of atrial fibrillation (AF). METHODS AND RESULTS: This prospective multicentre randomised trial enrolled 380 patients (248 male, mean (SD) age 67 (10) years) with AF. Patients were randomised to either an escalating energy protocol (protocol A: 100 J, 150 J, 200 J, 200 J), or a non-escalating energy protocol (protocol B: 200 J, 200 J, 200 J). Cardioversion was performed using an impedance compensated biphasic waveform. First-shock success was significantly higher for those randomised to 200 J than 100 J (71% vs 48%; p<0.01) and for patients with a body mass index (BMI) >25 kg/m(2) (75% vs 44%; p = 0.01). In patients with a normal BMI there was no significant difference in first-shock success. There was also no significant difference between subsequent shocks or overall success. The use of a non-escalating protocol (protocol B) resulted in fewer shocks but with a higher cumulative energy. There was no difference in duration of procedure, amount of sedation administered or post-shock erythema between the groups. CONCLUSION: First-shock success was significantly higher, particularly in patients with a BMI >25 kg/m(2), when a non-escalating initial 200 J energy was selected. The overall success, duration of procedure and amount of sedation administered, however, did not differ significantly between the two protocols.

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.

Twenty year review of duodenal ulcer.

Of 31 patients (18 male and 13 female) followed up 13-29 years after diagnosis, recurrent or persistent duodenal ulcer had occurred in four. In 22 (71%) gastrointestinal symptoms persisted into adult life, although only abdominal pain was significantly more frequent than in 126 controls.

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).

Randomized comparison of enoxaparin with unfractionated heparin following fibrinolytic therapy for acute myocardial infarction.

AIMS: To compare the efficacy and safety of low molecular weight heparin with unfractionated heparin following fibrinolytic therapy for acute myocardial infarction. METHODS AND RESULTS: Three-hundred patients receiving fibrinolytic therapy following acute myocardial infarction were randomly assigned to low molecular weight heparin as enoxaparin (40 mg intravenous bolus, then 40 mg subcutaneously every 8 h, n=149) or unfractionated heparin (5000 U intravenous bolus, then 30 000 U. 24 h(-1), adjusted to an activated partial thromboplastin time 2-2.5x normal, n=151) for 4 days in conjunction with routine therapy. Clinical and therapeutic variables were analysed, in addition to use of enoxaparin or unfractionated heparin, to determine independent predictors of the 90-day composite triple end-point (death, non-fatal reinfarction, or readmission with unstable angina). The triple end-point occurred more frequently in patients receiving unfractionated heparin rather than enoxaparin (36% vs. 26%; P=0.04). Logistic regression modelling of baseline and clinical variables identified the only independent risk factors for recurrent events as left ventricular failure, hypertension, and use of unfractionated heparin rather than enoxaparin. There was no difference in major haemorrhage between those receiving enoxaparin (3%) and unfractionated heparin (4%). CONCLUSION: Use of enoxaparin compared with unfractionated heparin in patients receiving fibrinolytic therapy for acute myocardial infarction was associated with fewer recurrent cardiac events at 90 days. This benefit was independent of other important clinical and therapeutic factors.

Relation between shock-related myocardial injury and defibrillation efficacy of monophasic and biphasic shocks in a canine model.

BACKGROUND: Certain biphasic waveforms with specific time ratios of positive and negative components require less energy for successful defibrillation of the fibrillating ventricles than monophasic waveforms. However, if more efficient waveforms were also to be associated with more injurious effects on myocardial function, they might not provide a true biological advantage. This study investigates the relation between defibrillation efficacy and potential toxicity of monophasic and asymmetric, single capacitor, biphasic waveforms with equal durations of positive and negative components. METHODS AND RESULTS: The myocardial lactate extraction rate (LER) was used to measure the injurious effects on myocardial oxidative metabolism of two synchronized 35-J shocks in sinus rhythm. LER, mean arterial pressure (MAP) and, in a subset of experiments, cardiac output (CO) and coronary blood flow (CBF) were measured at baseline, 30 seconds, 60 seconds, 90 seconds, 150 seconds, 300 seconds, and 600 seconds after the shocks. In 12 dogs, three different waveforms (M 10: monophasic 10 milliseconds; BI 10: biphasic 10 milliseconds; BI 20: biphasic 20 milliseconds) were tested as series of two consecutive shocks (60 seconds apart) resulting in a total of 36 sets of data. At baseline, LER was 25 +/- 11%. After monophasic shocks, LER decreased significantly more than after biphasic shocks (LER at 150 seconds: M 10: -6 +/- 31% versus BI 10: 21 +/- 15% versus BI 20: 21 +/- 16%; M 10 versus BI 10 and M 10 versus BI 20, P < .05) and showed also a slower recovery (LER at 300 seconds: M 10: 1 +/- 24% versus BI 10: 20 +/- 11% versus BI 20: 20 +/- 15%; M 10 versus BI 10 and M 10 versus BI 20, P < .05). The maximal decrease in LER was 41 +/- 27% for M 10 compared with 18 +/- 15% for BI 10 and 15 +/- 11% for BI 20 (both, M 10 versus BI 10 and M 10 versus BI 20, P < .05). There was a similar decrease in CO and MAP, with the lowest MAP after monophasic shocks. The maximal decrease in MAP was significantly greater after M 10 compared with BI 20 (-29 +/- 15 mm Hg versus -13 +/- 11 mm Hg, P < .05). The defibrillation threshold was 18.6 +/- 8 J for M 10 compared with 11.5 +/- 4.0 J for BI 10 (P < .05) and 15.0 +/- 6.1 J for BI 20, respectively (P = NS). CONCLUSIONS: Our results suggest that these specific biphasic waveforms are associated with less injurious effects on myocardial oxidative metabolism and hemodynamic performance. Given their higher defibrillation efficacy as well, biphasic waveforms may provide important long-term benefits in patients receiving frequent shocks from implantable cardioverter-defibrillators.

Metabolic changes and mitochondrial dysfunction early following transthoracic countershock in dogs.

The mechanisms of myocardial injury and necrosis following transthoracic shocks from a direct current cardiac defibrillator were investigated in adult greyhounds. Myocardial lactate extraction became negative maximally at 1 minute, following two (mean -22% +/- SEM23) or five (-193% +/- 135) shocks and returned to baseline in 6-15 minutes. Myocardial necrosis assessed at 4 hours following the shock period was 0.05 g (+/- 0.03) after two shocks, 6.69 g (+/- 1.76) after five shocks and zero in controls. In further experiments, dogs received five or zero (dummy) shocks and mitochondria were isolated from their hearts following excision within 1 minute of receiving the final shock. Maximal oxygen consumption in right ventricular mitochondria was lower than the unshocked controls with both glutamate (66.9 +/- 9.4 nanoatoms of oxygen/mg per minute, n = 9 vs 86.6 +/- 13.6 nanoatoms/mg per minute, n = 7) and succinate (96.2 +/- 8.7 nanoatoms/mg per minute, n = 9 vs 119.5 +/- 14.4 nanoatoms/mg per minute, n = 7) as substrates. Using electron spin resonance spectroscopy, an increase in a peroxyl-free radical with g = 2.031 was detected in myocardial tissue after two internal shocks (50 joules stored energy, 0.5-minute intervals). We conclude that mitochondrial dysfunction and free-radical generation are likely contributors to cellular injury following multiple countershocks.

Ventricular pacing induced ventricular tachycardia in patients with implantable cardioverter defibrillators.

Appropriately timed noncompetitive ventricular pacing potentially may initiate ventricular tachycardia in patients prone to these arrhythmias. The combination of bradycardia pacing and stored electrograms in a currently available cardioverter defibrillator provides an opportunity to evaluate the occurrence of such pacing induced ventricular tachycardia. During a surveillance period of 18.7 +/- 11.4 months, stored electrograms documented 302 episodes of ventricular tachycardia in 77 patients. Five patients (6.5%) demonstrated 25 episodes (1-16 per patient) of ventricular tachycardia that were immediately preceded by an appropriately paced ventricular beat (8.3% of all episodes of ventricular tachycardia). All five patients had prior myocardial infarctions and a history of monomorphic ventricular tachycardia occurring both spontaneously and in response to programmed electrical stimulation. Antitachycardia pacing terminated pacing induced ventricular tachycardia in 22 episodes; in one episode antitachycardia pacing accelerated ventricular tachycardia. In two cases shock therapy was aborted for nonsustained ventricular tachycardia. We conclude that, in selected nonsustained ventricular tachycardia. We conclude that, in selected postinfarction patients with recurrent sustained monomorphic ventricular tachycardia treated with implantable cardioverter defibrillators, appropriately timed ventricular pacing may induce ventricular tachycardia.

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.