Dietary high-protein distiller's dried grains with solubles can fully replace soybean meal in diets for meat quails without affecting growth performance.

1. The purpose of this study was to determine the metabolisable energy of high-protein distiller's dried grains with solubles (HP-DDGS) for meat quail (Coturnix coturnix coturnix; Experiment I) and evaluate the effects of dietary levels of HP-DDGS on animal performance, carcase characteristics, meat quality, and organ weights (Experiment II).2. In Experiment 1, 96 meat quail were distributed in a completely randomised design with two treatments (reference or test diet) and six replicates of eight birds. The experimental period consisted of 5 d adaptation, followed by 5 d total excreta collection. The experimental diets consisted of a reference (control) and a test diet formulated with 800 g/kg reference diet and 200 g/kg HP-DDGS.3. In Experiment 2, 612 meat quail were distributed in a completely randomised design fed one of six dietary levels of HP-DDGS (0, 85, 170, 255, 340, or 425 g/kg) as a replacement for soybean meal. At 42 d of age, birds were slaughtered and evaluated for carcase yield, organ weights, and meat quality.4. Apparent metabolisable energy values corrected for nitrogen retention of HP-DDGS were 12.5 and 12.3 MJ/kg for males and females, respectively.5. In the starter phase (1-21 d of age), increasing dietary HP-DDGS levels had a quadratic effect on body weight (BW) (P = 0.020) and body weight gain (BWG) (P = 0.019). The maximum BW and BWG values were estimated to be achieved with 296.0 and 296.2 g/kg dietary HP-DDGS, respectively. Overall (1-42 d of age), increasing dietary HP-DDGS levels in replacement of soybean meal did not affect animal performance, carcase yield, meat quality or organ weight in meat quail.6. It was concluded that dietary HP-DDGS can fully replace soybean meal in meat quail diets without affecting growth performance, carcase yield, meat quality or organ weight.

Multivariate associates of QT dispersion in patients with acute myocardial infarction: primacy of patency status of the infarct-related artery. TEAM-3 Investigators. Third trial of Thrombolysis with Eminase in Acute Myocardial Infarction.

BACKGROUND: QT dispersion (QTd; QT interval maximum minus minimum) has been shown to reflect regional variations in ventricular repolarization and is increased in patients with life-threatening ventricular arrhythmias. METHODS: To determine correlates of QTd in patients who had had myocardial infarction (MI), 207 patients (158 men, aged 57 +/- 11 years) with acute MI who were treated with alteplase or anistreplase within 2.7 +/- 0.9 hours of symptom onset were studied. Angiograms at a median of 27 hours after thrombolysis showed reperfusion (Thrombolysis in Myocardial Infarction grade > or =2) in 184 (88%) patients. QT was measured in 10 +/- 2 leads on discharge electrocardiograms with a computerized analysis program interfaced with a digitizer. Associations of QTd with 24 variables related to patient characteristics, acute MI, angiography, interventions, and radionuclide ventriculography were evaluated by univariate and multivariate regression. RESULTS: Univariate associations with QTd (p < or = 0.10) were Thrombolysis in Myocardial Infarction flow grade 0/1 versus 2/3 (QTd = 75 +/- 33 msec vs 53 +/- 22 msec, p < 0.0001), minimal luminal diameter (p = 0.007), left ventricular ejection fraction at discharge (p = 0.007), reinfarction (p = 0.01), number of leads with ST elevation (p = 0.05), end-systolic volume at discharge (p = 0.04), time to peak creatine kinase (p = 0.06), and YST elevation (p = 0.10). Independent associates of QTd were Thrombolysis in Myocardial Infarction grade 0/1 versus 2/3 (p < 0.0001), reinfarction (p = 0.005), and ejection fraction (p = 0.02). CONCLUSIONS: Successful thrombolysis is associated with less QTd in patients after acute MI. Our results support the hypothesis that QTd after MI depends on reperfusion status, reinfarction, and left ventricular function. Reduction in QTd may be an additional mechanism by which the benefit of thrombolytic therapy is realized.

Predictive value for future arrhythmic events of fractal dimension, a measure of time clustering of ventricular premature complexes, after myocardial infarction. CAST Investigators. Cardia Arrhythmia Suppression Trial.

OBJECTIVES: Our objective was to test fractal dimension (D), a measure of clustering of ventricular premature complexes (VPCs), on entry Holter recording as a predictor of future arrhythmic death and other-cause mortality in postinfarction patients in the Cardiac Arrhythmic Suppression Trial (CAST). BACKGROUND: Nonlinear dynamic methods of signal processing are being applied in medicine to provide new insights into apparently "chaotic" biologic events, including cardiac arrhythmias. One such application is the derivation of a fractal D to describe the clustering of VPCs in time. METHODS: Baseline Holter recordings were analyzed in blinded manner for 484 patients: 237 died or had a resuscitated cardiac arrest during follow-up, and 247 matched patients had no events. Fractal D, measured in four ways, was assessed as a predictor using Cox regression. RESULTS: One measure of D (high resolution D) was a significant univariate (relative hazard ratio 0.79 per SD change, p = 0.011) and multivariate (hazard ratio 0.75, p = 0.046) predictor of arrhythmic death but not other death (univariate p = 0.95, relative hazard 0.95, p = 0.66). Fractal D was greater (VPCs less clustered) in those patients free of arrhythmic events. On subgroup analysis, the predictive value of D resided in the randomized patient group (i.e., those who showed VPC suppression during initial antiarrhythmic drug titration and were randomized to blinded therapy with active drug or placebo) (multivariate hazard ratio 0.57, p = 0.001). CONCLUSIONS: A high resolution fractal D was predictive of arrhythmic (but not nonarrhythmic) death in a large postinfarction cohort. Further study of this new signal processing approach to ambulatory electrocardiographic recording will be of interest.

Comparison of signal-averaging electrocardiographic systems using device specific criteria in 104 normal subjects.

UNLABELLED: The advent of several signal-averaged electrocardiogram (SAECG) systems for late potential (LP) assessment warrants comparisons to assess intersystem reproducibility and variability. Simultaneous SAECGs on two systems, Arrhythmia Research Technology (ART) and Marquette (MEI), were performed on 104 normal volunteers (53 males, age 44 +/- 14 years), and analyzed filtered QRS duration (TFQRS), root mean square voltage (RMS40), and low amplitude signal duration (LAS40), filtered at 40-250 Hz. The Gomes criteria (TfQRS > 114 msec, RMS40 < 20 microV and LAS40 > 38 msec) were used as criteria for LP. The data was also analyzed using the recently proposed system specific criteria for MEI (TFQRS > 120 msec, RMS40 < 20 microV and LAS40 > 38 msec). Where appropriate, statistical analysis was performed using simple linear and Spearman's rank correlation, analysis of variance, Finn's R and McNemar's test. RESULTS: The means +/- SD for ART and MEI were: TFQRS: 97.2 +/- 8.9 vs 108.2 +/- 7.2 msec (R = 0.76), RMS40: 31.8 +/- 17.8 vs 45.3 +/- 19.9 microV (R = 0.53), and LAS40: 32.2 +/- 8.4 vs 30 +/- 7.4 (R = 0.54). When the Gomes criteria were applied, the number of subjects identified by each system as abnormal were: TFQRS = 3 vs 22 (P < 0.001), RMS40 = 20 vs 8 (P = 0.004), LAS40 = 21 vs 9 (P = 0.004), TFQRS/RMS40 = 3 vs 6 (P = 0.38), TFQRS/LAS40 = 3 vs 7 (P = 0.22), RMS40/LAS40 40 = 17 vs 8 (P = 0.02), and all three criteria = 3 vs 6 (P = 0.38) for ART vs MEI, respectively. Percent agreement was 81.7% for TFQRS and 84.6% for RMS40 and LAS40 when single criteria were applied. Agreement improved when combined criteria were utilized (87.5%-95.2% for any two criteria and 95.2% for all three criteria). The intersystem agreement that was not due to chance was 0.63-0.69 for single criteria and 0.75-0.90 for combined criteria. Disagreement was highly significant for the three criteria when used singly and for RMS40 and LAS40 combined. Disagreement was not significant when TFQRS was used in combination with > or = one other criteria. When the MEI criteria were applied, there was a decrease in the number of subjects identified by the MEI system as abnormal, using the TFQRS criteria singly or in combination. Percent agreement for system specific TFQRS measurements was 94.2% for single criteria and 97.1% for combined criteria. The intersystem agreement that was not due to chance improved (88-0.94). Disagreement between system specific criteria for TFQRS was not significant (P > 0.05). CONCLUSION: Our data indicate that although there is a general correlation between ART and MEI measurements, variability is substantial, leading to significant differences when the criteria for LP are applied, especially for single parameter determinations. Thus, there is a need to establish system specific normal ranges and more accurate criteria for LP parameters.

Reduction in QT interval dispersion by successful thrombolytic therapy in acute myocardial infarction. TEAM-2 Study Investigators.

BACKGROUND: QT dispersion (QTd, equals maximal minus minimal QT interval) on a standard ECG has been shown to reflect regional variations in ventricular repolarization and is significantly greater in patients with than in those without arrhythmic events. METHODS AND RESULTS: To assess the effect of thrombolytic therapy on QTd, we studied 244 patients (196 men; mean age, 57 +/- 10 years) with acute myocardial infarction (AMI) who were treated with streptokinase (n = 115) or anistreplase (n = 129) at an average of 2.6 hours after symptom onset. Angiograms at 2.4 +/- 1 hours after thrombolytic therapy showed reperfusion (TIMI grade > or = 2) in 75% of patients. QT was measured in 10 +/- 2 leads at 9 +/- 5 days after AMI by using a computerized analysis program interfaced with a digitizer. QTd, QRSd, JT (QT minus QRS), and JT dispersion (JTd, equals maximal minus minimal JT interval) were calculated with a computer. There were significant differences in QTd (96 +/- 31, 88 +/- 25, 60 +/- 22, and 52 +/- 19 milliseconds; P < or = .0001) and in JTd (97 +/- 32, 88 +/- 31, 63 +/- 23, and 58 +/- 21 milliseconds; P = .0001) but not in QRSd (25 +/- 10, 22 +/- 7, 28 +/- 9, and 24 +/- 9 milliseconds; P = .24) among perfusion grades 0, 1, 2, and 3, respectively. Similar results were obtained comparing TIMI grades 0/1 with 2/3 and 0/1/2 with 3. Patients with left anterior descending (versus right and left circumflex) coronary artery occlusion showed significantly greater QTd (70 +/- 29 versus 59 +/- 27 milliseconds, P = .003) and JTd (74 +/- 30 versus 63 +/- 27 milliseconds, P = .004). Similarly, patients with anterior (versus inferior/lateral) AMI showed significantly greater QTd (69 +/- 30 versus 59 +/- 27 milliseconds, P = .006) and JTd (73 +/- 30 versus 63 +/- 27 milliseconds, P = .007). Results did not change when Bazett's QTc or JTc was substituted for QT or JT or when ANOVA included adjustments for age, sex, drug assignment, infarct site, infarct vessel, and number of measurable leads. On ANCOVA, the relation of QTd or JTd and perfusion grade was not influenced by heart rate. CONCLUSIONS: Successful thrombolysis is associated with less QTd and JTd in post-AMI patients. The results are equally significant when either QT or JT is used for analysis. These data support the hypothesis that QTd after AMI depends on reperfusion status as well as infarct site and size. Reduction in QTd and its corresponding risk of ventricular arrhythmia may be mechanisms of benefit of thrombolytic therapy.

Relation of reperfusion success with anistreplase or alteplase in acute myocardial infarction to body weight. The TEAM-3 investigators.

Adjustment in dose based on body size is not recommended currently for thrombolytic regimens, except for a reduction in alteplase (recombinant tissue-type plasminogen activator [rt-PA]) dose for safety reasons in patients with low body weight. It is unresolved how to dose thrombolytic agents in very heavy patients. The study objective was to assess whether patency of the infarct-related artery at 1 day after therapy with anistreplase (anisoylated plasminogen streptokinase activator complex [APSAC]) or rt-PA is adversely affected by increased body weight. Data were analyzed from a double-blind, randomized, comparative study of APSAC (30 U/5 min) versus rt-PA (100 mg/3 hours, adjusted downward for body weight < 65 kg), together with heparin and aspirin, in patients with acute myocardial infarction presenting within 4 hours of symptom onset. Coronary patency, determined at 1 day, was assessed in a blinded fashion, and patency success was correlated with body weight, divided into quintiles. In patients treated with APSAC, coronary patency rates were similar in those in the upper quintile of body weight (> 94 kg; n = 22) and in the low-normal weight group (n = 126) (86 and 90%, respectively, for perfusion grade 2/3 [p = 0.64]; and 82 and 74%, respectively, for grade 3 [p = 0.42]). In contrast, for the rt-PA group, heavy patients (n = 34) achieved significantly lower patency rates (74 vs 89% for grade 2/3 [p = 0.02]; and 59 vs 77% for grade 3 [p = 0.03]). The dose of heparin administered, adjusted to maintain a therapeutic partial thromboplastin time until the 1-day (mean 28 hours) angiogram, was greater in the heavy than in the low-normal weight group (mean +/- SE 39,680 +/- 4,818 vs 30,027 +/- 1,177 U; p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Thrombolysis-related early patency reduces ECG late potentials after acute myocardial infarction.

To assess the effects of thrombolysis and reperfusion on late potentials after myocardial infarction, 101 patients (79 men, age 63.2 +/- 10.5 years) underwent signal-averaged ECG studies at 10.7 +/- 9.2 days, with the use of a 40 to 250 Hz band-pass filter. Patients were divided into four groups: (1) 54 patients treated with thrombolytic agents at 2.8 +/- 1.1 hours, with 81% "early" patency/reperfusion (TIMI grades 2 and 3); (2) 47 patients treated conventionally with 45% "late" patency/reperfusion; (3) 56 patients with patency (TIMI grades 2 and 3); and (4) 26 patients without patency (TIMI grades 0 and 1). A late potential was present when greater than or equal to 2 of 3 defined criteria were present. There was a significant difference in the incidence of late potentials between groups 1 and 2 (22% vs 43%, respectively; p = 0.048) and between groups 3 and 4 (18% vs 50%, respectively; p = 0.006). Late potentials also tended to occur less often after "early" than after "late" patency/reperfusion (12.5% vs 25%). The odds ratio for developing a late potential was 0.39 for thrombolysis versus no thrombolysis (p less than 0.05) and 0.22 for patency/reperfusion (TIMI grades 2 and 3) versus no patency/reperfusion (TIMI grades 0 and 1) (p less than 0.05). By analysis of covariance the effects of thrombolysis on late potentials were entirely explained by reperfusion. Thus the risk of late potentials after myocardial infarction is high but is reduced by thrombolysis and reperfusion. In addition, the effectiveness of "early" reperfusion appears to be greater than that of "late" but requires further clarification.

Quantification of rate of coronary artery disease progression by a new method of angiographic analysis.

To assess the rate and variability of atherostenosis progression in patients with coronary artery disease at baseline angiography, we used a simplified quantitative method of analysis to study single angiograms in 54 patients and paired angiograms in 29 patients. All discrete lesions were identified, then traced and digitized to determine lumen diameter (LD), and summed to give the total LD; the differences in LD for paired angiograms were summed to give total stenosis change (TSC). The following results were obtained: Correlation between LD measured by our method and LD determined by the Brown/Dodge method was excellent (r = 0.99, N = 54). There also was a high correlation between interobserver (r = 0.98, N = 54) and intraobserver (r = 0.99, N = 54) findings. Short-term TSC (N = 9, angiograms paired at less than 1 week) was negligible (0.03 +/- 0.38 mm). Long-term (N = 20, angiograms paired at 0.6 to 4.3 years) total LD differed significantly from baseline total LD (4.1 +/- 2.5 mm vs 6.0 +/- 3 mm; p less than 0.001), and TSC (2.0 +/- 1.3 mm) in long-term patients differed significantly from TSC in short-term patients (p less than 0.001). These results show that true coronary disease progression occurring over 1 to 4 years can be distinguished from intraobserver, interobserver, and interstudy variability by means of a simplified method and provide approximate rates and variability of progression. These results will be useful for power calculations in therapeutic trials aimed at slowing progression. Further prospective studies with the use of this method appear indicated.

Multicenter patency trial of intravenous anistreplase compared with streptokinase in acute myocardial infarction. The TEAM-2 Study Investigators.

Thrombolytic therapy has been shown to improve clinical outcome when administered early after the onset of symptoms of acute myocardial infarction; the mechanism of benefit is believed to be reestablishment and maintenance of coronary artery patency. Anistreplase is a second generation thrombolytic agent that is easily administered and has a long duration of action. To compare anistreplase (30 units/2-5 min) and therapy with the Food and Drug Administration-approved regimen of intravenous streptokinase (1.5 million units/60 min), a randomized, double-blind, multicenter patency trial was undertaken in 370 patients less than 76 years of age with electrocardiographic ST segment elevation who could be treated within 4 hours of symptom onset. Coronary patency was determined by reading, in a blinded fashion, angiograms obtained early (90-240 minutes; mean, 140 minutes) and later (18-48 hours; mean, 28 hours) after beginning therapy. Early total patency (defined as Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion) was high after both anistreplase (132/183 = 72%) and streptokinase (129/176 = 73%) therapy, and overall patency patterns were similar, although patent arteries showed "complete" (grade 3) perfusion more often after anistreplase (83%) than streptokinase (72%) (p = 0.03). Similarly, residual coronary stenosis, determined quantitatively by a validated computer-assisted method, was slightly less in patent arteries early after anistreplase (mean stenosis diameter, 74.0%) than streptokinase (77.2%, p = 0.02). In patients with patent arteries without other early interventions, reocclusion risk within 1-2 days was defined angiographically and found to be very low (anistreplase = 1/96, streptokinase = 2/94). Average coronary perfusion grade was greater, and percent residual stenosis was less, at follow-up than on initial evaluation and did not differ between treatment groups. Enzymatic and electrocardiographic evolution was not significantly different in the two groups. Despite rapid injection, anistreplase was associated with only a small (4-5 mm Hg), transient (at 5-10 minutes) mean differential fall in blood pressure. In-hospital mortality rates were comparable for anistreplase and streptokinase (5.9%, 7.1%). Stroke occurred in one (0.5%) and three (1.6%) patients, respectively; one stroke was hemorrhagic. Other serious bleeding events and adverse experiences occurred uncommonly and with similar frequency in the two groups. Thus, for the end points of our study (patency, safety), anistreplase and streptokinase showed overall favorable and relatively comparable outcomes, with a few differences.(ABSTRACT TRUNCATED AT 400 WORDS)

Spontaneous variability in ventricular ectopic activity during chronic antiarrhythmic therapy.

Previous determinations of variability in frequency of ventricular arrhythmias have been based on repeated recordings obtained in the absence of therapy. We evaluate variability during "effective" treatment with antiarrhythmic drugs. Variability in the percent suppression of premature ventricular complexes (PVCs) was determined in 55 patients with chronic arrhythmias who underwent multiple ambulatory electrocardiographic recordings during evaluation of chronic therapy with antiarrhythmic drugs initially determined to be effective, which was defined as 70% or more reduction in total PVC frequency or 90% or more reduction in repetitive forms. During chronic therapy, total PVCs were suppressed by 92%, averaged after a logarithmic transformation step, and repetitive beats were suppressed by 88%. Variability in suppression was substantial. The one-sided 95% confidence intervals required a fall in suppression of total PVCs to 40% or less to exceed limits of spontaneous variability and of repetitive PVCs to 66% or less. Suppression declined at least once during therapy to less than 60% for total PVCs in 24 of 55 patients (44%) and to less than 80% for repetitive PVCs in 13 of 33 patients (39%); nine patients (16%) showed increases in PVC frequency at least once to levels above pretreatment baseline. Seven subgroups were analyzed for their effects on variability and loss of suppression: age, gender, disease etiology, cardiac function, baseline PVC frequency, use of beta-blockers, and class of antiarrhythmic drug. Differences in confidence bounds and loss of suppression were found to be determined in a complex way by subgroup differences in variability and in initial levels of PVC suppression. Variability was greater for patient subgroups with greater PVC frequency, beta-blocker therapy, and non-coronary artery disease. However, clinical loss of suppression was more common only in more elderly patients and those with worse cardiac function. In summary, substantial variability in arrhythmia frequency occurs during effective antiarrhythmic therapy, and the 95% confidence limits of spontaneous variability are broad and determined in a complex way. Careful consideration should be given before concluding on the basis of a single Holter test that changes (increases) in arrhythmia frequency, especially in certain subgroups, are caused by treatment failure.

Evaluation of size and dynamics of the inferior vena cava as an index of right-sided cardiac function.

To define normal criteria of size and dynamics of the inferior vena cava (IVC) and its clinical value in assessing right-sided cardiac function, 2-dimensional (2-D) and M-mode echocardiography (echo) were performed in 175 subjects, who were classified into 3 groups: group 1-80 normal subjects; group IIA--65 patients with documented right-sided cardiac disease, and group IIB--30 patients with cardiac disease but no right-sided abnormality. The IVC was adequately imaged in 175 of 185 subjects (95%). There was good correlation between M-mode and 2-D echo (r = 0.84) and long- and short-axis (r = 0.88) measurements. The IVC diameter during expiration was: group 1-9 to 28 mm (mean 18.2 +/- 4.6); group IIA--15 to 40 mm (mean 23.1 +/- 4.8) and group IIB-8-24 mm (mean 15.6 +/- 3.7). Collapsibility index (inspiratory decrease in diameter) was: group I-37 to 100% (mean 55.8 +/- 15.9); group IIA--0 to 39% (mean 13.5 +/- 10.5); and group IIB--44 to 100% (mean 60.4 +/- 13.1). A and V waves could be measured in 120 of 151 cases (79%). Both A and V waves were less than 125% of its diameter in group I. The A wave was absent in 34 patients; 30 (88%) were in atrial fibrillation. Among 8 patients with tricuspid regurgitation, 5 (63%) had V waves greater than 125%. There was no correlation between diameter or collapsibility index and age, sex, rhythm or body surface area.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-dimensional echocardiographic diagnosis of left-atrial thrombus in rheumatic heart disease. A clinicopathologic study.

Two-dimensional echocardiographic studies were performed in 293 patients with rheumatic heart disease who underwent open-heart mitral valve surgery during an 18-month period. Diagnostic confirmation of a left atrial thrombus was based on direct inspection of the left atrium during surgery and histopathologic examination. Two-dimensional echocardiographic recordings were reviewed. Of the 293 patients, 33 had left atrial thrombi by two-dimensional echocardiographic criteria. This diagnosis was confirmed at surgery and histopathologic study in 30 (specificity 98.8%). A thrombus was not found in three patients. In 21 other patients, left atrial thrombi were present but were not detected by two-dimensional echocardiography (sensitivity 58.8%). Ten of these 21 had thrombi in the left atrial cavity. In 11 patients, thrombi were located in the left atrial appendage, all of which were missed by two-dimensional echocardiography. Excluding these 11 left atrial appendage thrombi, the sensitivity of two-dimensional echocardiography for detecting left atrial cavity thrombi was 75.0%.

Two dimensional echocardiography in valvular heart disease.

From October 1, 1979 to June 30, 1980, 890 2D echocardiographic examinations were performed. Of these, 221 showed valvular lesions with predominant rheumatic aetiology. The valvular lesions encountered were pure mitral stenosis, pure mitral insufficiency, mixed mitral stenosis and insufficiency, aortic incompetence, aortic stenosis, mitral valve prolapse and left atrial thrombus. It is concluded that 2D echo imaging should in due time provide the "gold standard" for the evaluation of valvular lesions.