Intravenous sedation for cardiac procedures can be administered safely and cost-effectively by non-anesthesia personnel

Aims Primary: to determine the safety and efficacy of intravenous sedation for cardiac procedures administered by non-anesthesia personnel. Secondary: to assess cost effectiveness of such sedation. Methods Anesthesiologists trained non-anesthesia personnel, and established our sedation protocol, which was then used in 9,558 patients who had cardiac procedures with sedation by non-anesthesia personnel, recorded on a computerized database. Most sedation used was midazolam (MID) and morphine (MOR). Complications and problems were derived from the database and quality assurance committee records. Doses were based on desired level of sedation and procedure duration; highest dose used: MID 78 mg, MOR 84 mg. Results Data included catheterization (n = 3,819) and transesophageal echo procedures (n = 260); and overall electrophysiology (n = 5,479) and selected subsets. There were complications or problems in only 9 patients (0.1%), a strong safety statement. There were 3 deaths in electrophysiology related procedures, 2 deaths in catheterization related procedures, all in very sick patients and not definitely related to sedation; 4 others developed clinical instability (hives, hypotension and heart failure—all with no sequellae), 2 of which needed reversal medications. Three patients (<0.03%) proved difficult to sedate, and their procedures were completed with help from the anesthesia department; by protocol this was not a complication. A total of $5,365,691 was saved during the last decade on cardiac procedures performed with conscious sedation. Conclusion Non-anesthesia personnel can administer intravenous sedation for cardiac procedures in cardiac settings, with safety and cost-effectiveness demonstrated over many years. Anesthesia services are still appropriate for selected cases. Supported by: Department of Medicine Resident Research Elective Program.     

Histopathological correlation of ablation lesions guided by noncontact mapping in a patient with peripartum cardiomyopathy and ventricular tachycardia

A patient with peripartum cardiomyopathy developed a nearly incessant nonsustained VT. Guided by a noncontact mapping system, the tachycardia was mapped to the mid-septum of the right ventricle and ablated. Despite transient success, the tachycardia recurred and the patient subsequently died of multiorgan failure. Histopathological correlation of the ablation site revealed a nontransmural lesion that may have contributed to the failure of the ablation.     

Comparison of left ventricular cryolesions created by liquid nitrogen and nitrous oxide.

OBJECTIVES. This study was designed to compare the cryosurgical lesions produced by liquid nitrogen (-196 degrees C) and nitrous oxide (-76 degrees C). BACKGROUND. Cryosurgical ablation is a useful method of arrhythmia surgery, but information on the dimensions of cardiac lesions produced by modifying cryoprobe temperature is limited. METHODS. We compared the dimensions, volumes and electrophysiologic effects of cryolesions created by a liquid nitrogen cryoprobe (Group I) and a nitrous oxide cryoprobe (Group II) on the left ventricular myocardium in the beating canine heart. Exposure time was compared at 1, 2, 3 and 4 min. In each of 18 dogs, two to four lesions were created on the left ventricle and analyzed: 35 lesions created with use of the nitrous oxide cryoprobe and 30 lesions created with the liquid nitrogen cryoprobe. Lesions were measured at the time of induced death 6 weeks postoperatively and assessed by tissue staining with the Masson trichrome technique. RESULTS. The volumes (mm3) of the cryolesions created by the liquid nitrogen cryoprobe were significantly larger (p < 0.05) than those of lesions created by nitrous oxide: 826 +/- 163 versus 493 +/- 197 at 1 min; 1,101 +/- 327 versus 666 +/- 185 at 2 min; 1,356 +/- 318 versus 787 +/- 258 at 3 min and 1,735 +/- 534 versus 923 +/- 376 at 4 min. CONCLUSIONS. Decreasing the temperature of the cryoprobe by using liquid nitrogen increases the volume of the lesions. Programmed electrical stimulation before and 6 weeks after cryoablation indicated no arrhythmogenicity.     

Identification of a novel selD homolog from Eukaryotes, Bacteria, and Archaea: Is there an autoregulatory mechanism in selenocysteine metabolism?

Escherichia coli selenophosphate synthetase (SPS, the selD gene product) catalyzes the production of monoselenophosphate, the selenium donor compound required for synthesis of selenocysteine (Sec) and seleno-tRNAs. We report the molecular cloning of human and mouse homologs of the selD gene, designated Sps2, which contains an in-frame TGA codon at a site corresponding to the enzyme’s putative active site. These sequences allow the identification of selD gene homologs in the genomes of the bacterium Haemophilus influenzae and the archaeon Methanococcus jannaschii, which had been previously misinterpreted due to their in-frame TGA codon. Sps2 mRNA levels are elevated in organs previously implicated in the synthesis of selenoproteins and in active sites of blood cell development. In addition, we show that Sps2 mRNA is up-regulated upon activation of T lymphocytes and have mapped the Sps2 gene to mouse chromosome 7. Using the mouse gene isolated from the hematopoietic cell line FDCPmixA4, we devised a construct for protein expression that results in the insertion of a FLAG tag sequence at the N terminus of the SPS2 protein. This strategy allowed us to document the readthrough of the in-frame TGA codon and the incorporation of ⁷⁵Se into SPS2. These results suggest the existence of an autoregulatory mechanism involving the incorporation of Sec into SPS2 that might be relevant to blood cell biology. This mechanism is likely to have been present in ancient life forms and conserved in a variety of living organisms from all domains of life.     

Rapid suppression of spontaneous ventricular arrhythmias during oral amiodarone loading.

OBJECTIVE: To determine the time course of effects of amiodarone during an oral loading period. DESIGN: A prospective, nonrandomized study. SETTING: Arrhythmia referral center at a university hospital. PATIENTS: Fifty patients with refractory sustained ventricular tachycardia (n = 44) or ventricular fibrillation (n = 6) and frequent (greater than or equal to 30/h) ventricular premature complexes. INTERVENTION: Oral amiodarone, 1200 mg/d for 14 days and 400 mg/d thereafter. MEASUREMENTS: Ambulatory electrocardiographic monitorings, 12-lead electrocardiograms, and amiodarone blood levels on days 3, 5, 7, 9, 11, 13, and 28. RESULTS: Dramatic reductions of ventricular arrhythmias were noted during the first 72 hours of the therapy. Average ventricular premature complexes/h, couplets/h, and nonsustained ventricular tachycardias/24 h were 524 +/- 1224/h, 16 +/- 61/h, and 167 +/- 611/24 h, respectively, at baseline, and reduced to 140 +/- 243/h, 11 +/- 50/h, and 33 +/- 117/24 h, respectively, on day 3 (P less than 0.05 for all). Subsequent reductions of ventricular arrhythmias from day 3 to day 13 were more gradual but were still significant (P less than 0.05). A significant reduction of ventricular arrhythmias (greater than or equal to 70% reduction of ventricular premature complexes and greater than or equal to 90% reduction of nonsustained ventricular tachycardias) was noted in 50% of patients on day 3, in 65% on day 7, and in 83% on day 13. Prolongation of the QT interval exhibited a similar time course. There were no further differences in reduction of ventricular premature complexes or QT intervals between day 13 and day 28. CONCLUSIONS: Oral amiodarone given in loading doses produces rapid and dramatic reductions in spontaneous ventricular arrhythmias within 72 hours. Subsequent reductions of spontaneous arrhythmia were gradual and less dramatic.     

Antigenic and nucleotide characterization of a herpesvirus isolated from Pacific harbor seals (Phoca vitulina richardsii)

Summary.  This report describes the antigenic and nucleotide characterization of a herpes-like virus that has been isolated from the adrenal tissues of neonatal Pacific harbor seals. Infection with this virus has been previously implicated as a major cause of death of animals undergoing rehabilitation. Comparison and phylogenetic analysis of sequenced fragments of the DNA polymerase, glycoprotein B and glycoprotein D genes, and immunofluorescence assay using herpesvirus-specific monoclonal antibodies, demonstrated close similarity of the Pacific harbor seal herpesvirus to European isolates of phocid herpesvirus-1 (PHV-1) and other α-herpesviruses affecting terrestrial carnivores. Received June 22, 1997 Accepted May 16, 1998     

I-123 MIBG imaging and heart rate variability analysis to predict the need for an implantable cardioverter defibrillator

BACKGROUND: Iodine 123 metaiodobenzylguanidine (MIBG) imaging and heart rate variability (HRV) analysis were compared in patients with an implantable cardioverter defibrillator (ICD) who did and did not receive defibrillator discharges. Although the ICD has been shown to abort potentially fatal ventricular arrhythmias, identification of patients who most benefit from this device remains difficult. As the autonomic nervous system has been implicated in the genesis of these arrhythmias, we undertook a pilot study to evaluate local myocardial sympathetic innervation with the use of I-123 MIBG myocardial imaging, as well as central autonomic tone with the use of HRV, in patients with implantable defibrillators. Test results were correlated with the occurrence of ICD discharges. METHODS AND RESULTS: Seventeen patients with previously implanted defibrillators were studied. Of these, 10 had at least 1 appropriate device discharge for ventricular tachyarrhythmias, whereas 7 had no discharge. Patients with a discharge had a significantly lower I-123 MIBG heart-mediastinal tracer uptake ratio, higher I-123 MIBG defect scores, more extensive sympathetic denervation, and significantly reduced values for several HRV parameters, particularly those in the frequency domain. When combined, the I-123 MIBG heart-mediastinal ratio and HRV 5-minute low-frequency variables were highly predictive of defibrillator discharges. All patients with a heart-mediastinal ratio lower than 1.54 and 5-minute low frequency lower than 443 ms(2) had an ICD discharge (4/4), whereas no patient with an uptake ratio greater than 1.54 and 5-minute low frequency greater than 443 ms(2) did (0/3, P =.03). CONCLUSIONS: Cardiac autonomic assessment using a combination of myocardial scintigraphic and neurophysiologic techniques may help select patients who would most benefit from an implantable defibrillator by identifying those at increased risk for potentially fatal arrhythmias.     

Synthesis of some quaternary ammonium alkylating agents and their effects on soman-inhibited acetylcholinesterase

A number of compounds were synthesized and tested for their ability to realkylate the phosphonate anion of "aged", soman-inhibited acetylcholinesterase. None were found able to do so, but two of the compounds in particular, [2-(4-pyridyl)ethyl]diethylmethylammonium iodide (6) and its 2-isomer 7, proved able to slow the rate of aging significantly.     

Evaluation of end points of serial drug testing in patients with sustained ventricular tachycardia after healing of acute myocardial infarction

Serial electrophysiologic drug testing was used to guide antiarrhythmic therapy in a consecutive series of 150 patients with clinical sustained ventricular tachycardia (VT) or cardiac arrest and inducible monomorphic VT. All patients had coronary artery disease and a history of myocardial infarction. For patients with clinical sustained VT, drug responders and partial drug responders (VT slowed by drug to rate <150 beats/min, with systolic blood pressure ≥90 mm Hg) had similar total mortality rates (2-year actuarial survival 100% and 94%, P = NS), which were statistically different from that or patients with drug inefficacy (2-year survival 67%). Partial drug responders had high arrhythmia recurrence rates, similar to those of patients with drug inefficacy. For cardiac arrest survivors, the results of electrophysiologically guided drug testing did not predict prognosis. Patients with a change in mode or VT induction during antiarrhythmic therapy had a favorable prognosis (no deaths during follow-up).