New Distribution Records of Biting Midges of the Genus Culicoides (Diptera: Ceratopogonidae) Latreille, Culicoides bergi and Culicoides baueri, in Southern Ontario, Canada.

Some species of Culicoides Latreille (Diptera: Ceratopogonidae) can be pests as well as pathogen vectors, but data on their distribution in Ontario, Canada, are sparse. Collecting this baseline data is important given ongoing, accelerated alterations in global climate patterns that may favor the establishment of some species in northern latitudes. Culicoides spp. were surveyed using UV light traps over two seasons in 2017 and 2018 at livestock farms in southern Ontario, Canada. Two Culicoides spp. not previously recorded in Canada were identified, C. bergi and C. baueri, representing new country and provincial records. Unlike some congenerics, these two species are not currently recognized as vectors of pathogens that pose a health risk to humans, livestock or wildlife in North America. However, the possibility that these Culicoides species may have recently expanded their geographic range, potentially in association with climate and/or landscape changes, warrants ongoing attention and research. Furthermore, our results provoke the question of the potential undocumented diversity of Culicoides spp. in Ontario and other parts of Canada, and whether other Culicoides spp. may be undergoing range expansion. The current and future distributions of Culicoides spp., and other potential vectors of human, agricultural, and wildlife health significance, are important to identify for proper disease risk assessment, mitigation, and management.

Natural Infections With Pigeon Paramyxovirus Serotype 1: Pathologic Changes in Eurasian Collared-Doves ( Streptopelia decaocto) and Rock Pigeons ( Columba livia) in the United States.

Pigeon paramyxovirus serotype 1 (PPMV-1) is a globally distributed, virulent member of the avian paramyxovirus serotype 1 serogroup that causes mortality in columbiformes and poultry. Following introduction into the United States in the mid-1980s, PPMV-1 rapidly spread causing numerous mortality events in Eurasian collared-doves ( Streptopelia decaocto) (ECDOs) and rock pigeons ( Columba livia) (ROPIs). The investigators reviewed pathological findings of 70 naturally infected, free-ranging columbiforms from 25 different mortality events in the United States. Immunohistochemistry targeting PPMV-1 nucleoprotein was used to determine the tissue distribution of the virus in a subset of 17 birds from 10 of the studied outbreaks. ECDOs (61 birds) and ROPIs (9 birds) were the only species in which PPMV-1-associated disease was confirmed by viral isolation and presence of histologic lesions. Acute to subacute tubulointerstitial nephritis and necrotizing pancreatitis were the most frequent histologic lesions, with immunolabeling of viral antigen in renal tubular epithelial cells and pancreatic acinar epithelium. Lymphoid depletion of bursa of Fabricius and spleen was common, but the presence of viral antigen in these organs was inconsistent among infected birds. Hepatocellular necrosis was occasionally present with immunolabeling of hypertrophic Kupffer cells, and immunopositive eosinophilic intracytoplasmic inclusion bodies were present in hepatocytes of 1 ECDO. Immunopositive lymphocytic choroiditis was present in 1 ECDO, while lymphocytic meningoencephalitis was frequent in ROPIs in absence of immunolabeling. This study demonstrates widespread presence of PPMV-1 antigen in association with histologic lesions, confirming the lethal potential of this virus in these particular bird species.

Molecular evolution of epizootic hemorrhagic disease viruses in North America based on historical isolates using motif fingerprints.

Epizootic hemorrhagic disease virus (EHDV) is an orbivirus of the Reoviridae family that has significant impact on wild and captive white-tailed deer. Although closely related to bluetongue virus that can cause disease in sheep and cattle, North American EHDV historically has not been associated with disease in cattle or sheep. Severe disease in cattle has been reported with other EHDV strains from East Asia and the Middle East. To understand the potential role of viral genetics in the epidemiology of epizootic hemorrhagic disease, a molecular characterization of North American EHDV strains from 1955 to 2012 was conducted via conventional phylogenetic analysis and a new classification approach using motif fingerprint patterns. Overall, this study indicates that the genetic make-up of EHDV populations in North America have slowly evolved over time. The data also suggested limited reassortment events between serotypes 1 and 2 and introduces a new analysis tool for more detailed sequence pattern analysis.

Host and Potential Vector Susceptibility to an Emerging Orbivirus in the United States: Epizootic Hemorrhagic Disease Virus Serotype 6.

Epizootic hemorrhagic disease viruses (EHDVs) are orbiviruses transmitted by Culicoides biting midges to domestic and wild ruminants. EHDV-1 and EHDV-2 are endemic in the United States, where epizootic hemorrhagic disease is the most significant viral disease of white-tailed deer (WTD;Odocoileus virginianus) and reports of epizootic hemorrhagic disease in cattle are increasing. In 2006, a reassortant EHDV-6 was isolated from dead WTD in Indiana and has been detected each subsequent year over a wide geographic region. Since EHDV-6 is not a historically endemic serotype in the United States, it is important to understand infection outcome in potential hosts. Specifically, we aimed to evaluate the pathogenicity of the virus in 2 primary US ruminant hosts (WTD and cattle) and the susceptibility of a confirmed US vector (Culicoides sonorensis). Five WTD and 4 cattle were inoculated with >10(6)TCID50EHDV-6 by intradermal and subcutaneous injection. All 5 WTD exhibited moderate to severe disease, and 3 died. Viremia was first detected 3 to 5 days postinfection (dpi) with surviving animals seroconverting by 10 dpi. Two of 4 inoculated cattle had detectable viremia, 5 to 10 dpi and 7 to 24 dpi, respectively. No clinical, hematologic, or pathologic abnormalities were observed. Antibodies were detected by 10 dpi in 3 of 4 cows.C. sonorensis were fed on WTD blood spiked with EHDV-6 and held for 4 to 14 days postfeeding at 25°C. From 4 to 14 days postfeeding, 19 of 171 midges were virus isolation positive and 6 of 171 had ≥10(2.7)TCID50EHDV-6. Although outcomes varied, these studies demonstrate the susceptibility of ruminant and vector hosts in the United States for this recently emerged EHDV serotype.

Demodectic mange, dermatophilosis, and other parasitic and bacterial dermatologic diseases in free-ranging white-tailed deer (Odocoileus virginianus) in the United States from 1975 to 2012.

The white-tailed deer (Odocoileus virginianus) is a common and widespread North American game species. To evaluate the incidence, clinical manifestations, demography, and pathology of bacterial and parasitic dermatologic diseases in white-tailed deer in the southeastern United States, we retrospectively evaluated white-tailed deer cases submitted to the Southeastern Cooperative Wildlife Disease Study from 1975 to 2012. Among 2569 deer examined, bacterial or parasitic dermatologic disease was diagnosed in 88 (3.4%) individuals, with Demodex spp (n = 37; 42.0%) and Dermatophilus congolensis (n = 19; 21.6%) as the most common causes. Demodicosis was significantly more common in deer older than 2 years and was most often detected in the fall; no statistically significant sex predilection was identified. Affected animals had patchy to generalized alopecia, often distributed over the head, neck, limbs, and trunk; microscopic lesions included epidermal crusts and cutaneous nodules with mild perifollicular, lymphoplasmacytic inflammation. Dermatophilosis was most common in males younger than 1 year that were often found dead. Crusting, erythema, and alopecia occurred on the face, ears, and distal extremities. Less commonly, infectious dermatologic diseases were associated with other bacteria (n = 13; 14.8%), fungi (n = 5; 5.7%), ectoparasites (chiggers, lice, mites, and ticks; n = 11; 12.5%), and larval nematodes (n = 7; 8.0%). Population-level effects of these diseases in white-tailed deer are likely minimal; however, due to their dramatic presentation, demodicosis, dermatophilosis, and other infectious skin diseases can be of concern to hunters and, in some cases, may have zoonotic potential.

Diagnostic approaches for Rift Valley fever.

Disease outbreaks caused by arthropod-borne animal viruses (arboviruses) resulting in significant livestock and economic losses world-wide appear to be increasing. Rift Valley fever (RVF) virus is an important arbovirus that causes lethal disease in cattle, camels, sheep and goats in Sub-Saharan Africa. There is concern that this virus could spread because of global warming, increased animal trade or through bioterrorism. This paper discusses the current and developing approaches to diagnosis of RVF. Diagnostic assays are available for RVF, but availability can be limited and there is a need for global harmonization. Continued improvement of standard serological and viral genome amplification approaches, including new embedded/syndromic testing, biosensor, emerging virus detection and characterization technologies is needed.

Purkinje cell heterotopy with cerebellar hypoplasia in two free-living American kestrels (Falco sparverius).

Two wild fledgling kestrels exhibited lack of motor coordination, postural reaction deficits, and abnormal propioception. At necropsy, the cerebellum and brainstem were markedly underdeveloped. Microscopically, there was Purkinje cells heterotopy, abnormal circuitry, and hypoplasia with defective foliation. Heterotopic neurons were identified as immature Purkinje cells by their size, location, immunoreactivity for calbindin D-28 K, and ultrastructural features. The authors suggest that this cerebellar abnormality was likely due to a disruption of molecular mechanisms that dictate Purkinje cell migration, placement, and maturation in early embryonic development. The etiology of this condition remains undetermined. Congenital central nervous system disorders have rarely been reported in birds.

Segmental configuration and putative origin of the reassortant orbivirus, epizootic hemorrhagic disease virus serotype 6, strain Indiana.

In 2006, an exotic reassortant orbivirus, epizootic hemorrhagic disease virus serotype 6 (EHDV-6) [strain (Indiana)], was first detected in the United States. To characterize the reassortment configuration of this virus and to conclusively determine the parental virus of each RNA segment, the complete genome of EHDV-6 (Indiana) was sequenced, in addition to the genomes of representative EHDV-6 and EHDV-2 isolates. Based on genomic comparisons to all other EHDV serotypes, we determined that EHDV-6 (Indiana) originated from a reassortment event between the Australian prototype strain of EHDV-6 (CSIRO 753) and the North American topotype of EHDV-2 (Alberta). Additionally, phylogenetic analysis of all EHDV-6 (Indiana) isolates detected in the United States from 2006 to 2010 suggests that the virus may be undergoing continual reassortment with EHDV-2 (Alberta). In 2010, EHDV-6 (CSIRO 753) was detected in Guadeloupe, demonstrating that the parental virus of the reassortment event is circulating in the Caribbean.

Aspergillus fumigatus infection of an automatic internal cardiac defibrillator.

We report a patient without immune compromise with infection of an automatic internal cardiac defibrillator patch due to Aspergillus fumigatus presenting 8 years after implantation. The mechanism of infection was unknown, but symptoms began 1 month after laser uvulopalatopharyngoplasty was performed for sleep apnea. The patches were surgically removed and the patient was treated sequentially with amphotericin B and itraconazole. He remains without evidence of infection 12 months after the completion of therapy.

Clinical pharmacology of intravenous enoximone: pharmacodynamics and pharmacokinetics in patients with heart failure.

Twenty-one patients with heart failure (New York Heart Association [NYHA] class II to IV) received a 24-hour infusion of enoximone followed by a 12-hour washout period. Patients were randomly assigned to one of four treatment groups. Groups I to III received an 0.5 mg/kg bolus, followed by a maintenance infusion of 2.5, 5.0, or 10.0 micrograms/kg/min. Group IV patients received a maintenance infusion of 5.0 micrograms/kg/min without a loading dose. Serial assessment of hemodynamics, plasma levels of enoximone and enoximone sulfoxide, and ventricular ectopy were performed. Enoximone produced a clinically significant increase in cardiac index, and a decrease in mean pulmonary artery wedge pressure and systemic vascular resistance in all groups. Enoximone mildly increased heart rate, and had a minimal effect on mean arterial pressure. There was no statistically significant change in ventricular ectopy during the infusion. Significant hemodynamic improvement was noted at even the lowest infusion rate, and did not increase in linear fashion at higher infusion rates. In patients who did not receive an initial loading bolus of 0.5 mg/kg, the increase in cardiac index was delayed by approximately 1 hour. Plasma concentrations of both enoximone and its major metabolite continued to rise throughout the 24-hour infusion in group III (10.0 micrograms/kg/min), rather than reaching steady state as predicted by the terminal exponential half-lives of these compounds. This is suggestive of nonlinear pharmacokinetics and indicates a potential for excessive accumulation of enoximone and its metabolite during prolonged infusion. These findings may have important implications in guiding the intravenous administration of enoximone.(ABSTRACT TRUNCATED AT 250 WORDS)

Disposition kinetics of orally administered enoximone in patients with moderate to severe heart failure.

Enoximone is a phosphodiesterase inhibitor, which has been studied extensively for use in the management of patients with moderate-to-severe heart failure. The authors have studied the absorption and disposition kinetics of enoximone and its primary metabolite, enoximone sulfoxide, after both single oral doses of enoximone and at steady-state after short-term chronic oral therapy. A total of ten patients (two female, eight male) with moderate-to-severe heart failure (NYHA class II-IV) were enrolled into the study after giving written informed consent. The plasma levels of enoximone sulfoxide were greater than those of enoximone at all sampling times. The peak enoximone sulfoxide plasma concentrations ranged from 3.5 to 17.3 times the peak enoximone plasma levels for individual patients. The average steady-state plasma concentrations for enoximone were 115 +/- 40 ng/mL and 190 +/- 78 ng/mL for 50 mg every 8 hours and 100 mg every 8 hours dosage regimens, respectively. The absorption and disposition kinetics of enoximone were found to be significantly variable between patients. The authors also evaluated the relationship between dose administered and steady-state plasma levels as well as the relationship between the observed and predicted steady-state plasma levels. The authors found a linear relationship between the dose that was administered and the accrued plasma levels, as well as a good correlation between the predicted and observed steady-state levels. Although these data confirm previous reports that the sulfide metabolite of enoximone accumulates extensively in the plasma during oral therapy, reaching levels much higher than those of enoximone, these data do not support previous suggestions that the disposition of enoximone is nonlinear.

Comparison of pre- and postoperative conduction patterns in patients surgically cured of atrioventricular node reentrant tachycardia.

Patients with atrioventricular (AV) node reentrant tachycardia characteristically have short and constant retrograde His-atrium conduction times (H2A2 intervals) during the introduction of ventricular extrastimuli. It has therefore been suggested that the tachycardia circuit involves retrograde conduction up an accessory pathway located in perinodal tissue. If the mechanism of surgical cure of AV node reentrant tachycardia is interruption of this accessory pathway, postoperative changes in retrograde conduction would be expected. Thirteen patients with drug-refractory AV node reentrant tachycardia underwent surgery. Preoperatively, H2A2 intervals were short and constant. During AV node reentrant tachycardia, earliest atrial activation was seen near the His bundle and was 0 to 25 ms before ventricular activation in all patients except one. Surgery consisted of dissection of right atrial septal and anterior inputs to the AV node and central fibrous body. Postoperatively, the H2A2 interval remained short and constant compared with preoperative values although it was slightly prolonged (74 +/- 18 versus 61 +/- 21 ms, p less than 0.005). Twelve of the 13 patients are free of tachycardia after 28 +/- 13 months and no patient has had evidence of AV node block. Thus, surgical cure of AV node reentrant tachycardia is highly successful; however, there is no reason to postulate an accessory pathway or use of perinodal tissue as part of the tachycardia circuit and the mechanism of surgical success remains obscure.

Pharmacodynamics of enoximone during intravenous infusion.

Twenty-one patients with heart failure (NYHA class II-IV) received a 24-hour infusion of enoximone, followed by a 12-hour washout period. Patients were randomly assigned to one of four treatment groups. Groups I-III received a 0.5 mg/kg bolus, followed by a maintenance infusion of 2.5, 5.0 or 10.0 micrograms/kg/minute. Group IV patients received a maintenance infusion of 5.0 micrograms/kg/minute without the bolus. Serial assessments of haemodynamics, plasma levels of enoximone and enoximone sulphoxide, and ventricular ectopy were performed. Enoximone produced a significant increase in cardiac index (28.1-46.7%) and a decrease in mean pulmonary artery wedge pressure (6.4-35.7%) and systemic vascular resistance (34.7-78.9%). Enoximone had minimal effect on heart rate and blood pressure. In patients who did not receive an initial bolus of 0.5 mg/kg, haemodynamic changes were delayed by approximately 1 hour. Significant haemodynamic improvement was noted at even the lowest infusion rate and did not increase in linear fashion at higher infusion rates. During infusion of enoximone at 10.0 micrograms/kg/minute, both enoximone and its sulphoxide accumulated non-linearly and did not achieve a steady state. No significant adverse effects were noted in these patients. Enoximone infusion at rates greater than 5.0 micrograms/kg/minute may confer minimal additional haemodynamic benefit, while resulting in significant accumulation of enoximone and enoximone sulphoxide. Ventricular ectopy did not increase significantly in most patients.

Effect of duration of ventricular fibrillation on defibrillation efficacy in humans.

The currently available automatic implantable cardioverter-defibrillator has proven highly successful for termination of ventricular tachycardia and fibrillation. Newer devices, however, permit lower energy shocks to be delivered initially and longer episodes of arrhythmia to occur before shocks are delivered. These changes may result in longer durations of arrhythmia before successful termination. Little is known about the effects of the duration of ventricular fibrillation on the efficacy of defibrillating shocks. In this study, we examined the efficacy of defibrillating shocks in 22 patients undergoing automatic implantable cardioverter-defibrillator implantation or generator change. Defibrillating shocks ranging from 300 to 600 V (5.9-24.2 J) were delivered in matched pairs after 5 and 15 seconds of ventricular fibrillation. For the 300-V shocks (5.9 J), defibrillation was accomplished in 82% of patients when the shocks were given after 5 seconds of ventricular fibrillation and in only 45% of patients when the shocks were delivered after 15 seconds (p less than 0.01). At higher energies, there was no difference in the efficacy of defibrillation shocks delivered after 5 compared with 15 seconds of ventricular fibrillation. The postshock aortic, systolic, and diastolic blood pressures were significantly lower when the shocks were given after 15 seconds of ventricular fibrillation than after only 5 seconds. We conclude that the duration of ventricular fibrillation affects defibrillation efficacy especially at energies that are relatively low compared with maximal device outputs and that longer episodes of ventricular fibrillation cause more postshock hemodynamic depression. These observations have implications for defibrillation threshold testing at the time of device implantation and for the design and programming of future automatic implantable antitachycardia devices.

Long-term outcome with the automatic implantable cardioverter-defibrillator.

The automatic implantable cardioverter-defibrillator was implanted in 270 patients because of life-threatening arrhythmias over a 7 year period. There was a history of sustained ventricular tachycardia or fibrillation, or both, in 96% of these patients, 80% had one or more prior cardiac arrests and 78% had coronary artery disease as their underlying diagnosis. The average ejection fraction was 34%, and 96% of these patients had had an average of 3.4 antiarrhythmic drug failures per patient before defibrillator implantation. There were four perioperative deaths and eight patients had generator infection or generator erosion, or both, during the perioperative period or during long-term follow-up. Concomitant antiarrhythmic drug therapy was given to 69% of patients. Shocks from the device were given to 58% of patients. and 20% received "problematic" shocks. The device was removed from 16 patients during long-term follow-up for a variety of reasons. There were 7 sudden cardiac deaths and 30 nonsudden cardiac deaths, 18 of which were secondary to congestive heart failure. The actuarial incidence of sudden death, total cardiac death and total mortality from all causes was 1%, 7% and 8%, respectively, at 1 year, and 4%, 24% and 26% at 5 years. The automatic implantable cardioverter-defibrillator nearly eliminates sudden death over a long-term follow-up period in a high risk group of patients. It has an acceptable rate of complications or problems, or both, and most late deaths in these patients are nonsudden and of cardiovascular origin.

Improved low energy defibrillation efficacy in man with the use of a biphasic truncated exponential waveform.

The standard implantable defibrillator waveform is a truncated exponential of approximately 6 msec duration. This study compares the defibrillation efficacy of a standard monophasic truncated exponential to a biphasic 12 msec truncated exponential waveform in 21 patients undergoing automatic implantable cardioverter defibrillator (AICD) surgery. For the biphasic waveform, the polarity was reversed and remaining capacitor voltage was attenuated by 75% after 6 msec. Two hundred thirty episodes of VF were induced with 115 "matched pairs" of monophasic and biphasic waveforms of identical initial capacitor voltages given over a range from 70 to 600 V (0.35 to 25.7 joules). The biphasic waveform was superior to the monophasic waveform (p less than 0.006), especially for "low energy" defibrillation. For initial voltages less than 200 V, the percent successful defibrillation was 28% for the monophasic waveform versus 64% for the biphasic waveform and from 200 to 290 V (energies less than 6.4 joules) it was 45% versus 69%. There was no difference in the two waveforms in time to the first QRS complex or in the blood pressure following defibrillation. This study shows that a 12 msec biphasic truncated exponential is superior to a 6 msec monophasic waveform for defibrillation in man, especially at energies less than 6.4 joules. The waveform can be achieved in an implanted device without any increase in capacitor size or in battery energy consumption.

Clinical experience with sotalol in patients with drug-refractory ventricular arrhythmias.

Sixty-five patients with symptomatic, drug-refractory, sustained ventricular tachycardia or fibrillation were treated with oral sotalol (80 to 480 mg twice daily). Sotalol was withdrawn in 11 patients because of continued inducibility of ventricular tachycardia at the time of follow-up electrophysiologic study. Therefore, the clinical effectiveness of sotalol could be evaluated in 54 patients followed up for 11.5 +/- 6 months (range 0.2 to 25). The actuarial incidence of successful sotalol therapy was 54 +/- 13% at 6 months and 47 +/- 13% at 12 months. In 39 patients who underwent electrophysiologic testing while receiving oral sotalol, the drug prevented the reinduction of ventricular tachycardia/fibrillation in 8 (20%). During follow-up study, arrhythmia recurred in 1 (17%) of 6 patients whose ventricular tachycardia was noninducible with oral sotalol and in 8 (44%) of 18 with inducible tachycardia but who were continued on oral sotalol therapy. Adverse effects were noted in 28 patients (42%), requiring drug withdrawal in 13 (22%) and dose reduction after hospital discharge in 10 (15%). Exacerbation of ventricular arrhythmia occurred in six patients (9%), one of whom had associated hypokalemia. Sotalol is frequently useful in the control of intractable, life-threatening ventricular arrhythmias, and its efficacy appears to be predicted by programmed stimulation. However, there is a high rate of limiting side effects, which precludes its use in a large number of patients, and a substantial risk of arrhythmia exacerbation.

Transvenous catheter ablation of extranodal accessory pathways.

Twelve patients with an accessory pathway and recurrent symptomatic reciprocating tachycardia or atrial fibrillation, or both, underwent attempted transvenous catheter ablation of the accessory pathway. In one patient with a small right coronary artery, the pathway was along the right free wall. In 11 patients, the pathway was located at or within 15 mm of the coronary sinus os. For these patients, a quadripolar electrode catheter was placed in the coronary sinus and positioned, if possible, so that the proximal pair of electrodes straddled the pathway. For those patients with a pathway greater than 5 mm within the coronary sinus, the most proximal electrode was placed at the os. This proximal pair of electrodes was connected to the cathodal output of a defibrillator with an anterior chest wall patch serving as the current sink. Two shocks were then delivered for a cumulative energy of 500 to 600 J (stored energy). Among the eight patients with a pathway at or within 5 mm of the coronary sinus os, conduction over the pathway was abolished in five and modified in one. Among the four patients with a pathway farther from the os (10 to 15 mm) and along the right free wall, pathway conduction was modified only in two. Rupture of the coronary sinus did not occur in any patient. There were no serious complications. Minor damage surrounding the area of ablation was seen at the time of surgical division of the accessory pathway in two of five patients with unsuccessful ablation who subsequently underwent surgery.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of catheter-delivered electrical discharges near the tricuspid anulus in dogs.

The possibility of using electrical discharges to ablate right free wall accessory pathways by delivering a series of catheter shocks near the tricuspid anulus was assessed in a canine model. Before the shock, the amplitudes of the atrial and ventricular electrograms recorded from the distal electrodes were compared (A/V ratio), and the atrial pacing threshold was determined. To assess effects on function and arrhythmogenicity, right heart pressures were measured and programmed ventricular stimulation was performed before the shock and prior to sacrifice 7 to 10 days after the shock. Nine dogs received a total of 24 discharges at varying energies (50 to 400 J). Nonsustained ventricular tachycardia occurred with 13 shocks (62%) and transient atrioventricular block with 9 shocks (43%). There was no worsening in cardiac or valvular function as determined by right heart pressure measurements or right ventriculography. Programmed ventricular stimulation performed before the shocks and repeated before sacrifice failed to induce ventricular arrhythmias. The endocardial lesion produced by the shock was roughly circular and its area correlated with both the magnitude of the shock as well as the atrial pacing threshold. Transmural necrosis always occurred at the anulus when the A/V ratio was between 1.00 and 1.50 and preshock atrial pacing threshold suggested adequate wall contact (less than 1.5 mA). There was mild inflammation of the adventitia of the right coronary artery near two discharge sites (both 200 J) and inflammation of the media near one discharge site (400 J); no intimal involvement was seen.(ABSTRACT TRUNCATED AT 250 WORDS)