Tricyclic overdose causing sustained monomorphic ventricular tachycardia.
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Adult↗
Biomedical subjects
R W Peters
Publications and source records attributed to R W Peters.
Effects of left ventricular dysfunction on the circadian variation of ventricular premature complexes in healed myocardial infarction.
Circadian variation in the onset of cardiovascular events including sudden cardiac death, myocardial infarction and ventricular arrhythmias has been described. The effect of left ventricular (LV) dysfunction on the circadian variation of ventricular premature complex (VPC) frequency was evaluated in 132 patients with frequent VPCs and reduced LV function after myocardial infarction. Patients were prospectively divided in 2 groups based on LV ejection fraction (EF) (those with LVEF less than or equal to 0.30, and those with LVEF between 0.30 and 0.45). Median hourly VPC frequencies and heart rates were compared between the 2 groups. Subgroup analyses based on treatment with beta-adrenoceptor blocking agents and on New York Heart Association functional class were also performed. In patients with LVEF greater than 0.30, a distinct circadian variation of VPCs, and the expected morning increase in VPC frequency were present. In contrast, a distinct circadian variation of VPCs was absent in patients with LVEF less than or equal to 0.30. A circadian variation of VPC frequency was also absent in patients with severe symptomatic congestive heart failure (New York Heart Association class III-IV). Treatment with beta-adrenoceptor blocking agents was associated with a loss of the circadian variation of VPC frequency. The circadian variation of heart rate was also blunted in the group treated with beta-adrenoceptor blocking agents. The proportion of subjects manifesting a positive correlation between heart rate and VPC frequency was lower in subjects with LVEF less than or equal to 0.30 (26%) than in those with LVEF greater than 0.30 (46%) (p less than 0.05). Thus, circadian variation of VPC frequency is absent in patients with severe LV dysfunction.
Adrenergic beta-Antagonists↗
Auditory filter shapes at low center frequencies in young and elderly hearing-impaired subjects.
Auditory filter shapes were measured for two groups of hearing-impaired subjects, young and elderly, matched for audiometric loss, for center frequencies (fc) of 100, 200, 400, and 800 Hz using a modified notched-noise method [B. R. Glasberg and B. C. J. Moore, Hear. Res. 47, 103-138 (1990)]. Two noise bands, each 0.4fc wide, were used; they were placed both symmetrically and asymmetrically about the signal frequency to allow the measurement of filter asymmetry. The overall noise level was either 77 or 87 dB SPL. Stimuli were delivered monaurally using Sennheiser HD424 earphones. Although auditory filters for the hearing-impaired subjects were generally broader than for normally hearing subjects [Moore et al., J. Acoust. Soc. Am. 87, 132-140 (1990)], some hearing-impaired subjects with mild losses had normal filters. The filters tended to broaden with increasing hearing loss. There were not any clear differences in filter characteristics between young and elderly hearing-impaired subjects. The signal-to-noise ratios at the outputs of the auditory filters required for threshold (K) tended to be lower than normal for the young hearing-impaired subjects, but were not significantly different from normal for the elderly hearing-impaired subjects. The lower K values for the young hearing-impaired subjects may occur because broadened auditory filters reduce the deleterious effects on signal detection of fluctuations in the noise.
Adult↗
Pitch discrimination and phase sensitivity in young and elderly subjects and its relationship to frequency selectivity.
Frequency difference limens for pure tones (DLFs) and for complex tones (DLCs) were measured for four groups of subjects: young normal hearing, young hearing impaired, elderly with near-normal hearing, and elderly hearing impaired. The auditory filters of the subjects had been measured in earlier experiments using the notched-noise method, for center frequencies (fc) of 100, 200, 400, and 800 Hz. The DLFs for both impaired groups were higher than for the young normal group at all fc's (50-4000 Hz). The DLFs at a given fc were generally only weakly correlated with the sharpness of the auditory filter at that fc, and some subjects with broad filters had near-normal DLFs at low frequencies. Some subjects in the elderly normal group had very large DLFs at low frequencies in spite of near-normal auditory filters. These results suggest a partial dissociation of frequency selectivity and frequency discrimination of pure tones. The DLCs for the two impaired groups were higher than those for the young normal group at all fundamental frequencies (fo) tested (50, 100, 200, and 400 Hz); the DLCs for the elderly normal group were intermediate. At fo = 50 Hz, DLCs for a complex tone containing only low harmonics (1-5) were markedly higher than for complex tones containing higher harmonics, for all subject groups, suggesting that pitch was conveyed largely by the higher, unresolved harmonics. For the elderly impaired group, and some subjects in the elderly normal group, DLCs were larger for a complex tone with lower harmonics (1-12) than for tones without lower harmonics (4-12 and 6-12) for fo's up to 200 Hz. Some elderly normal subjects had markedly larger-than-normal DLCs in spite of near-normal auditory filters. The DLCs tended to be larger for complexes with components added in alternating sine/cosine phase than for complexes with components added in cosine phase. Phase effects were significant for all groups, but were small for the young normal group. The results are not consistent with place-based models of the pitch perception of complex tones; rather, they suggest that pitch is at least partly determined by temporal mechanisms.
Adult↗
Detection of temporal gaps in sinusoids by elderly subjects with and without hearing loss.
Thresholds for the detection of temporal gaps in sinusoidal signals were measured as a function of frequency (100-2000 Hz) and level in 15 elderly hearing-impaired subjects and 11 elderly subjects with near-normal hearing at frequencies below 2000 Hz. The sinusoids were presented in a background noise intended to mask spectral splatter associated with the gap. In a separate experiment, auditory filter shapes and detection efficiency were estimated for the same subjects using the notched-noise method, at center frequencies of 100, 200, 400, and 800 Hz. The gap thresholds at higher signal levels were similar for the two groups of subjects at all center frequencies tested. The mean gap thresholds were slightly higher than those obtained previously from young normally hearing subjects, but this was mainly due to the results of a few subjects with large gap thresholds; the majority of the elderly subjects had gap thresholds within the normal range. Thus reduced temporal resolution does not seem to be an inevitable consequence of aging. Gap thresholds at low center frequencies tended to be positively correlated with the equivalent rectangular bandwidth (ERB) of the auditory filter, the opposite of what would be expected if the auditory filter played a role in limiting gap detection. Detection efficiency, as estimated from the notched-noise experiment, was poorer for both groups of elderly subjects than for young normal listeners, but detection efficiency was not significantly correlated with gap thresholds.
Aged↗
Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial.
BACKGROUND AND METHODS: In the Cardiac Arrhythmia Suppression Trial, designed to test the hypothesis that suppression of ventricular ectopy after a myocardial infarction reduces the incidence of sudden death, patients in whom ventricular ectopy could be suppressed with encainide, flecainide, or moricizine were randomly assigned to receive either active drug or placebo. The use of encainide and flecainide was discontinued because of excess mortality. We examined the mortality and morbidity after randomization to encainide or flecainide or their respective placebo. RESULTS: Of 1498 patients, 857 were assigned to receive encainide or its placebo (432 to active drug and 425 to placebo) and 641 were assigned to receive flecainide or its placebo (323 to active drug and 318 to placebo). After a mean follow-up of 10 months, 89 patients had died: 59 of arrhythmia (43 receiving drug vs. 16 receiving placebo; P = 0.0004), 22 of nonarrhythmic cardiac causes (17 receiving drug vs. 5 receiving placebo; P = 0.01), and 8 of noncardiac causes (3 receiving drug vs. 5 receiving placebo). Almost all cardiac deaths not due to arrhythmia were attributed to acute myocardial infarction with shock (11 patients receiving drug and 3 receiving placebo) or to chronic congestive heart failure (4 receiving drug and 2 receiving placebo). There were no differences between the patients receiving active drug and those receiving placebo in the incidence of nonlethal disqualifying ventricular tachycardia, proarrhythmia, syncope, need for a permanent pacemaker, congestive heart failure, recurrent myocardial infarction, angina, or need for coronary-artery bypass grafting or angioplasty. CONCLUSIONS: There was an excess of deaths due to arrhythmia and deaths due to shock after acute recurrent myocardial infarction in patients treated with encainide or flecainide. Nonlethal events, however, were equally distributed between the active-drug and placebo groups. The mechanisms underlying the excess mortality during treatment with encainide or flecainide remain unknown.
Actuarial Analysis↗
A recombinant fowlpox virus that expresses the VP2 antigen of infectious bursal disease virus induces protection against mortality caused by the virus.
The coding sequences of VP2 from a virulent strain, 52/70, of infectious bursal disease virus (IBDV) were excised from a cDNA clone and inserted into a fowlpox plasmid insertion vector. The resulting plasmid, pIBD 1, was used to construct a recombinant fowlpox virus, fpIBD 1, which expressed VP 2 as a beta-galactosidase fusion protein. Chickens vaccinated with fpIBD 1 at 1 and 14 days of age, were challenged at 28 days with either IBDV strain 52/70 or the highly virulent strain CS 89. These chickens were protected against mortality, but not against damage to the bursa of Fabricius. The protection achieved by the use of fpIBD 1 shows that VP 2 is a host protective antigen.
Amino Acid Sequence↗
Propranolol and the morning increase in sudden cardiac death: (the beta-blocker heart attack trial experience).
To provide insight into the protective effect of propranolol on mortality after myocardial infarction observed in the beta-Blocker Heart Attack Trial, the time of occurrence of sudden cardiac death was examined in this population. Between 5 A.M. and 11 A.M., 25 of the 56 total deaths (38%) occurred in the placebo patients compared with 11 of 45 (24%) in the propranolol patients. Excluding this period, there were nearly equal numbers of sudden cardiac deaths in the propranolol and placebo groups. This retrospective analysis suggests that beta blockade is protective during the morning hours when a surge of sympathetic activity may increase the risk of sudden cardiac death.
Adult↗
A recombinant fowlpox virus expressing the hemagglutinin-neuraminidase gene of Newcastle disease virus (NDV) protects chickens against challenge by NDV.
The hemagglutinin-neuraminidase (HN) gene from the Beaudette C strain of Newcastle disease virus (NDV) has been expressed in a recombinant fowlpox virus vector. The HN gene, under the control of the vaccinia p7.5 promoter, was inserted into a nonessential gene in the terminal inverted repeats of fowlpox virus. Expression was demonstrated in tissue culture, a protein of the correct size for fully glycosylated HN protein being recognized by an HN-specific monoclonal antibody on Western blots. When the recombinant fowlpox virus was inoculated into chickens by intravenous or wing-web routes, antibody which recognizes HN from purified NDV virions was produced. Protective immunity to NDV was generated in the chickens; at the highest dose of vaccine 100% of the chickens tested were protected against challenge with a virulent strain of NDV.
Animals↗
A fowlpox virus vaccine vector with insertion sites in the terminal repeats: demonstration of its efficacy using the fusion gene of Newcastle disease virus.
In this paper we report the development and testing of a fowlpox virus vector system. Insertion sites in non-essential regions within the terminal inverted repeats of the virus have been characterised. Foreign genes inserted into these sites are shown to be present in two copies in the resultant recombinant virus. To test the potential use of this vector as a live vaccine the fusion gene of Newcastle disease virus (NDV) has been inserted into a vaccine strain of fowlpox virus, and inoculated into chickens. The experiments demonstrate the ability of the recombinant to protect chickens against challenge by a virulent strain of NDV and to elicit the formation of anti-fusion protein antibody.
Animals↗
Prognostic value of prolonged ventricular repolarization following myocardial infarction: the BHAT experience. The BHAT Study Group.
In the Beta Blocker Heart Attack Trial (BHAT), 3837 patients were randomized to propranolol (180-240 mg/day) or placebo 5-21 days after a documented myocardial infarction and were followed in a double blind manner for a mean period of 25 months. Twelve lead electrocardiograms were routinely obtained at the time of randomization (baseline electrocardiogram) and at 12 and 24 months of follow-up. There was a positive correlation between baseline QTc interval prolongation (but not QT prolongation) and mortality and sudden death that was independent of treatment group. The data for non-sudden death and non-fatal reinfarction exhibit similar trends. We conclude that: (1) QTc prolongation identifies a high risk subset of post myocardial infarction patients. (2) The relative benefit of propranolol is similar in patients with normal and prolonged QTc.
Death, Sudden↗
Insertion of the fusion gene from Newcastle disease virus into a non-essential region in the terminal repeats of fowlpox virus and demonstration of protective immunity induced by the recombinant.
In this paper we report on the identification of non-essential genes in the terminal repeats of the avipox-virus fowlpox virus and the use of these as insertion sites in a vector system. Foreign genes inserted into these sites are shown to be present in two copies in the resultant recombinant virus. To test the potential use of this vector as a live vaccine the fusion gene of Newcastle disease virus has been inserted into a vaccine strain of fowlpox virus and inoculated into chickens. The experiments demonstrate the ability of the recombinant to protect chickens against challenge by a virulent strain of Newcastle disease virus and to elicit the formation of an anti-fusion protein antibody.
Animals↗
A comparison of the sequences of segment A of four infectious bursal disease virus strains and identification of a variable region in VP2.
The nucleotide sequences of the large open reading frame (ORF) from segment A of three European strains of infectious bursal disease virus (IBDV) have been determined using cDNA clones. This ORF of 3036 nucleotides encodes the virion proteins as a polyprotein in the following order: VP2, VP4, VP3. The nucleotide sequences determined have been compared to each other and to the published sequence of an Australian strain. The four strains are closely related, the greatest difference between two strains being 7.7% at the nucleotide level and 2.7% at the amino acid level. Comparisons show that there is a tight cluster of amino acid changes in the virion protein VP2. This variable region corresponded to the region where binding of a neutralizing monoclonal antibody has previously been mapped. A region in the centre of the segment, corresponding to the N terminal of VP4, was found to be completely conserved. Amino acid changes were spread fairly evenly through VP3 and there was no indication of a variable region as found in VP2.
Amino Acid Sequence↗
Auditory filter shapes at low center frequencies.
Auditory-filter shapes were estimated in normally hearing subjects for signal frequencies (fs) of 100, 200, 400, and 800 Hz using the notched-noise method [R. D. Patterson and I. Nimmo-Smith, J. Acoust. Soc. Am. 67, 229-245 (1980)]. Two noise bands, each 0.4fs wide, were used; they were placed both symmetrically and asymmetrically about the signal frequency to allow the measurement of filter shape and asymmetry. Two overall noise levels were used: 77 and 87 dB SPL. In deriving the shapes of the auditory filters, account was taken of the nonflat frequency response of the Sennheiser HD424 earphone, and also of the frequency-dependent attenuation produced by the middle ear. The auditory filters were asymmetric; the upper skirt was steeper than the lower skirt. The asymmetry tended to be greater at the higher noise level. The equivalent rectangular bandwidths (ERBs) of the filters at the lower noise level had average values of 36, 47, 87, and 147 Hz for values of fs of 100, 200, 400, and 800 Hz, respectively. The standard deviations of the ERBs across subjects were typically about 10% of the ERB values. The signal-to-masker ratio at the output of the auditory filter required to achieve threshold increased markedly with decreasing fs.
Adult↗
Propranolol and the morning increase in the frequency of sudden cardiac death (BHAT Study).
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Adult↗
Incidence of cardiac arrhythmias associated with mild hypokalemia induced by low-dose diuretic therapy for hypertension.
Nineteen men with mild to moderate hypertension and without a history of cardiac arrhythmias were randomized (double-blind) into groups to receive hydrochlorothiazide (HCTZ) at a dose of 25 mg/day, HCTZ at 50 mg/day, or HCTZ (25 mg) plus triamterene (50 mg) for a six-month period after a three-week (single-blind) placebo period. Serum electrolyte values were determined at baseline and at frequent intervals thereafter. Twenty-four hour ambulatory electrocardiograms were obtained at baseline and just before study termination. Mild hypokalemia (less than 3.5 mEq/L) occurred in approximately half of the patients and was unrelated to treatment group. Serious arrhythmias were infrequent, though some patients had large numbers of extra beats. The incidence of arrhythmia appeared unrelated to serum potassium concentration. We conclude that mild hypokalemia associated with low-dose diuretic therapy for hypertension is not arrhythmogenic.
Adult↗
Electrophysiologic effects of cigarette smoking in patients with and without chronic beta-blocker therapy.
After refraining from smoking for at least 8 hours, 22 adult male habitual smokers underwent baseline electrophysiologic study including atrial and ventricular burst pacing and programmed premature stimulation with single extrastimuli. After smoking 2 of their usual brand of cigarettes in rapid succession, the electrophysiologic protocol was repeated. Nicotine, catecholamine and carbon monoxide concentrations all increased significantly. Smoking increased heart rate and improved atrioventricular conduction in the 13 patients receiving chronic beta-blocker therapy (mostly for angina pectoris); increases in heart rate and improvement in atrioventricular conduction were not different statistically from those seen in patients not receiving beta-blocker therapy, suggesting the possibility of a direct effect of nicotine or other components of tobacco smoke. Ventricular refractoriness was not altered and atrial and ventricular arrhythmias were not increased by smoking. Persistent sympathomimetic actions of cigarette smoking may explain in part the failure of beta-blocking drugs to reduce cardiac mortality risk in smokers after myocardial infarction.
Adrenergic beta-Antagonists↗
Mortality in the beta blocker heart attack trial: circumstances surrounding death.
In the Beta Blocker Heart Attack Trial, a double blind, randomized, controlled study, patients taking propranolol (180 or 240 mg/day) initiated 5-21 days post myocardial infarction had 26% fewer deaths than those taking placebo over a 25 month (mean) followup. Detailed analysis of the circumstances surrounding the BHAT deaths failed to reveal any striking difference between propranolol and placebo in the type of clinical event preceding death, the incidence and type of acute and prodromal signs and symptoms, the location of death, the activity preceding death or the percentage of deaths that were sudden or instantaneous, suggesting that propranolol may exert an "across the board" effect and improve survival by a combination of mechanisms. An unexpected finding was that the protective effect of propranolol appeared to occur during the hours of 10 p.m. to 7 a.m.
Aged↗