Biosorption of trivalent chromium by free and immobilized blue green algae: kinetics and equilibrium studies.

The process of biosorption of trivalent chromium (Cr(3+)) by live culture of Spirulina platensis and the sorption potential by the dried biomass, in both free and immobilized states have been investigated for a simulated chrome liquor in the concentration range of 100-4500 ppm. Both live and dried biomass were very good biosorbents as they could remove high amounts of chromium from tannery wastewater. Polyurethane foam and sodium alginate were used as immobilizing agents and their performances compared. Biosorption kinetic data on Cr(3+) sorption onto dried biomass were analyzed using pseudo-first-and pseudo-second-order kinetic models in batch column experiments. The second-order equation was more appropriate to predict the rate of biosorption. Subsequently, the effects of height of packing & diameter of the column, concentration of blue-green algae (BGA) in varying amounts of sodium alginate, chromium concentration were studied. The results fit into both Langmuir & Freundlich isotherm models with very high regression coefficients. Furthermore, equilibrium studies using retan chrome liquor (RCL), with a chromium concentration of 1660 ppm, obtained from a tannery also showed promising results. In general, our studies indicate the efficacy of the algal species in removal of chromium from tannery wastewater.

The comparative predictive accuracy of spectral turbulence analysis and time-domain analysis for sustained monomorphic ventricular tachycardia in postinfarction patients with conduction defects.

Signal-averaged electrocardiograms obtained in 86 postinfarction patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or intraventricular conduction defect (IVCD), underwent time-domain analysis (TDA) and spectral turbulence analysis (STA) to determine which approach provided the more effective marker for patients with sustained monomorphic ventricular tachycardia. TDA parameter included the root mean square value of the last 40 ms of the vectormagnitude complex and the duration of the low amplitude signal below 40 microV. STA utilized a summation lead (X + Y + Z) and quantitated four parameters: interslice correlation mean, interslice correlation standard deviation, low slice correlation ratio, and spectral entropy. High-pass filters of 40 Hz and 25 Hz were used to study the total patient population with noise levels > or = microV and a subset of 67 patients with noise levels < or = 0.5 microV. The techniques compared their effectiveness as measured by their positive predictive values (PPV), negative predictive values (NPV), sensitivity (Sn), and specificity (Sp). In RBBB, STA was uniformly a more powerful tool utilizing either filter at both noise levels. In LBBB, STA was consistently more powerful at both noise levels at 40 Hz and, generally, more powerful at 25 Hz with isolated exceptions. In conduction defects in which QRS was > 100 ms but < 120 ms, TDA was equal to or more effective than STA, with the exception of PPV and Sp at 40 Hz at 1-microV noise level and the Sp at 0.5 microV. The addition of ejection fraction data to STA score resulted in further overall improvement in performance, but above conclusions were unchanged.

Patterns of body surface potential and ventriculograms specific to occlusion of subdivisions of the coronary arteries.

The thoracic activation map patterns, the distribution of occlusions, and the ventriculograms obtained at cardiac catheterization were examined in 166 patients with multivessel coronary disease without conduction defects or prior coronary intervention. The mean potential and ventriculographic configurations were determined for 15 groups, each formed on the basis of significant luminal occlusion (less than or equal to 90%) of an individual coronary arterial subdivision. We mathematically extracted distinctive map and wall motion patterns specific for isolated occlusion of each of the 15 major subdivisions. For these prototypes we found the following: 1) Definitive change in electrical pattern (less than 2 SD from the normal mean) occurred frequently outside the electrode sites of the standard electrocardiogram. 2) Focal akinesis systematically followed lesion site down the arterial courses; early electrical activation patterns corresponded to identifiable anatomic loss. 3) Certain paradoxes arose, for example, similar wall motion change but quite dissimilar electrical patterns from posterior descending artery occlusion of right coronary versus left circumflex origin. This technique unmasks component surface electrical patterns and ventriculographic deformities otherwise unrecognized in multisite, multivessel disease.

Relation of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction.

This study explores the relation of the presence of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction (MI). The hypothesis was that both the gross peri-infarction block pattern and subtle low-level ventricular late potentials are expressions of conduction abnormality associated with infarction. The consequent question arose whether peri-infarction block may have the same association with sustained ventricular arrhythmias that has been demonstrated in postinfarction patients with ventricular late potentials. Seventy patients with documented Q-wave MI were divided into those with (23) and those without (47) peri-infarction block. Signal-averaged electrocardiograms were obtained. Analysis of the vectormagnitude complex revealed that the total duration of that complex and the duration of terminal potential under 40 microV in the peri-infarction group exceeded that in the group without peri-infarction block (p less than 0.0001). The voltage in the last 40 ms of the vectormagnitude complex was also significantly less in the peri-infarction group (p less than 0.0005). There were 13 instances of sustained ventricular tachycardia, ventricular fibrillation or sudden death occurring subsequent to infarction not associated with the acute ischemic event, 11 of which occurred in the peri-infarction group. The significantly higher incidence of late potentials along with the significantly higher incidence of sustained ventricular arrhythmias in the peri-infarction block on the surface electrocardiogram may provide another marker for identifying persons at increased risk for these arrhythmias subsequent to MI.

Relation between the ventriculographic silhouette and topography of thoracic potential in coronary artery disease.

The body surface potential map obtained within 30 days of cardiac catheterization was examined in 180 patients with coronary artery disease. Radii to the systolic and diastolic boundaries of the right anterior oblique ventriculogram were measured at 18 degrees intervals; isointegral voltages were tabulated for early and late halves of the QRS complex at 35 definitive electrode sites. Multivariate analysis showed all ray lengths depended on all 70 voltage values. Linear transformation matrices to predict ray length from voltage distribution were calculated for a training set which was successively expanded from 80 to 160 at increments of 20 patients. Training set expansion led to a progressive decrease in the error of reproduction of the ray lengths for patients outside the training set. There is a strong relation between ventriculographic contours in patients with coronary artery disease and body surface potential values during early and late QRS complexes. Even in simplified linear formulation, the relation is detectable throughout a large population despite interindividual variations in anatomic geometry.

Thromboembolization complicating left ventricular pseudoaneurysm: serial two-dimensional and color-flow Doppler echocardiographic observations.

A left ventricular pseudoaneurysm was diagnosed by two-dimensional echocardiography and color-flow Doppler imaging, and confirmed by computerized tomography and angiocardiography, in a man with known coronary disease who had had recent recurrent systemic emboli. A thrombus within the pseudoaneurysm was visualized, and its disappearance on serial echocardiograms coincided with the occurrence of embolization to the aortic bifurcation.

Recurrent resemblance in potential topography at different instants during ventricular depolarization and repolarization. Normal conduction contrasted with left bundle branch block and paced beats.

During ventricular activation and recovery, potential distribution may be exquisitely reproduced on instantaneous maps separated in time by many milliseconds. The timing and duration of these periods of strong resemblance (absolute r = 0.80 over 142 thoracic reference sites) may provide useful insight into the underlying patterns of the spread of activation and resumption of the repolarized state. This study examined 80 normal volunteers, 35 patients with left bundle branch block (LBBB), and 41 patients with permanent pacemakers. Normal subjects showed three basic patterns of recurrent surface map resemblance: (1) positive correlation between maps in early QRS and those throughout ST-T, but with greatest focus in late ST-T; (2) negative correlation between maps in early QRS and late QRS; and (3) negative correlation between maps in late QRS and early ST-T. These findings may be hypothetically attributed to the retention or recreation of similar relationships between the anatomic distributions of resting versus active or plateau versus repolarizing cells on the endocardial and epicardial surfaces, respectively. On the other hand, patients with LBBB and pacemakers were distinctly different in the timing and frequency of sustained resemblances. In these two states, there was sustained or continuing resemblance (positive correlation) between successive maps throughout QRS and again between successive maps through ST-T. In addition, the surface map pattern found throughout ST-T consistently appeared as the negative correlate of the preceding pattern that had dominated QRS.

Anatomic localization of a single electrical source within the boundary of the human torso.

A closed prolate ellipsoid was used to approximate the surface of the Rush torso model to permit recovery of the site and orientation of known dipoles in 15 cardiac locations. Localization was found to be reasonably close, usually within 2 cm. When body surface potential maps of 37 subjects with right ventricular pacemakers were similarly treated, the discrepancy between known pacemaker site and the site of earliest activation was relatively large (mean, greater than 4 cm) and rapidly increased within the ensuing millisecond. The discrepancy not only emphasizes the wide variation in body shape and tissue distribution in living subjects, but also points to probable physical separation between stimulus site and earliest detectable activation site because of ischemia, infarction, or myocardial response to variation in current strength of the stimulus.

Use of body surface maps to identify vessel site of coronary occlusion.

Body surface mapping is more sensitive than conventional electrocardiography for various cardiac regions. In this pilot study, the authors used isoarea maps of early (the first 40 msec), late (the next 40 msec), and total (early and late, or 80 msec) QRS complex to determine the site of coronary occlusion in patients with known coronary artery disease. In the absence of conduction abnormalities or axis deviation in the 12-lead electrocardiogram, isoarea body surface map data of single-vessel disease were unremarkable; however, isoarea departure maps (ie, the average isoarea map of normal population extracted from the study group) were characteristic. Early departure isoarea maps were revealing in all three coronary artery disease groups, with a large negative potential noted over the anterior thorax, midline for the right coronary artery, left anterior in the left anterior descending artery, and further laterally for the left circumflex artery groups. The late isoarea departure map was distinct in the left circumflex artery group with positive potentials leftward, anterolaterally. Discriminant function analysis revealed a high predictive accuracy for the left anterior descending artery group. Thus, isoarea departure maps hold promise for predicting the site of coronary occlusion in this training set of patients.

A basis for determining body surface potential patterns attributable to single-site coronary arterial occlusion.

The authors focus on computational separation of the individual patterns of occlusion of the major segments of the right coronary artery. The raw patterns of occlusion throughout 15 standard subdivisions of the coronary arterial tree and body surface isoarea maps for 8 consecutive 10-msec intervals of QRS were examined in 200 patients with known coronary artery disease. Mean patterns of occlusion and of potential distribution were formed into 15 groups according to which patients showed greater than or equal to 90% occlusion of the respective segments. By diagonalization of the occlusion matrix, individual potential map patterns were obtained to represent the effect of isolated occlusion of each segment. While these patterns appeared consistent with the known anatomy of ventricular myocardial perfusion, further correlative study will be needed. The authors suggest that the use of such prototypical patterns of single-site obstruction may be helpful in forming and assessing recognition patterns in the clinical setting of multiple-site, multiple-vessel disease.

Computer-assisted learning compared with weekly seminars for teaching fundamental electrocardiography to junior medical students.

This study was designed to assess whether a self-study interactive computer program is more effective than weekly seminars for teaching fundamental skills of electrocardiographic interpretation to junior medical students. Forty-two students were assigned to the computer and 41 to the seminar group. A test was given to each participant at the beginning and end of each rotation. The computer group used a computer-assisted learning program, and the seminar group met weekly with a cardiologist to review electrocardiograms. Attendance at a minimum of 80% of the seminars or completion of 80% of the computer-assisted learning program was required for inclusion in the statistical analysis. The mean difference in test scores before and after study was 5.69 for the computer group and 4.36 for the seminar group (P less than .02 by one-tailed t-test). These results indicate that the computer group performed significantly better than the seminar group. We believe this difference to be educationally important.

Variation in the precordial QRS transition zone in normal subjects.

From body surface potential map data for 51 normal young men (with QRS axis between 0 and 90 degrees) both the spatial QRS area vector and the isoarea map of the QRS were obtained. Acting on Grant's assumption that the transition zone defined a plane perpendicular to the spatial QRS vector, we determined the angular shift in altitude and azimuth required to move the spatial vector of each individual to the position of the group mean. We then shifted the precordial map of the transition zone of each individual with the same angular correction. These resulting transition zone boundaries clustered much closer to each other, but did not move into absolute coincidence. We interpreted the nearness-to-fit to be an estimate of the degree to which the precordial QRS configurations conformed to a common simple vector or dipolar pattern.

Hyperkalemia and Wolff-Parkinson-White type preexcitation syndrome.

We have presented a well-documented case of hyperkalemia in a patient known to have Wolff-Parkinson-White type preexcitation syndrome. Increased serum potassium level appears to depress or block conduction via the accessory pathway to a greater extent than in the A-V node, i.e. the accessory pathway is more sensitive to hyperkalemia than normal A-V conduction tissue resulting in complete block of conduction in the accessory pathway.

Effect of various regimens of chronic and acute nicotine exposure on myocardial infarct size in the dog.

Smoking is a risk factor for atherosclerotic coronary heart disease, and the risk increases with increasing numbers of cigarettes smoked. The effect of cigarette smoking on the size of acute myocardial infarction (AMI) has not been evaluated. This study describes the effect of 1 component of tobacco smoke, nicotine, on the size of experimentally induced AMI in closed-chest dogs. Daily exposure to nicotine before AMI increased the volume of infarcted tissue (p less than 0.0001). Acute exposure to nicotine (with prior chronic exposure) resulted in a larger volume of infarcted tissue (p less than 0.0001). Thus, chronic, acute and post-AMI exposure to nicotine has an adverse effect on the volume of subsequent infarcted tissue, and continued exposure after AMI further enlarges infarct size.

Evaluation of the association of mitral valve prolapse in patients with Wolff-Parkinson-White type ECG and its relationship to the ventricular activation pattern.

The association of mitral valve prolapse (MVP) and Wolff-Parkinson-White (WPW) syndrome was examined using simultaneous two-dimensional and M-mode echocardiography. Twelve-lead electrocardiograms (ECGs) and two-dimensional echocardiograms (2DEs) were recorded in 24 patients with WPW. The location of the accessory pathway was predicted from the ECG as being in one of 10 possible sites correlating the delta wave polarity with epicardial mapping. Nineteen of the 24 patients had conduction via the accessory pathway and five were conducting normally during the recording of the echocardiogram. Mitral valve prolapse was found in 13 of 19 patients conducting via the accessory pathway. The only WPW patient with mitral valve prolapse during normal conduction had a chest deformity which has an independent association with mitral prolapse. No association was found between the prediction of the accessory pathway and the presence of mitral prolapse. We concluded that consideration should be given to the possibility that some patients demonstrating MVP do so as the result of the altered sequence of ventricular activation, rather than as the result of a structural abnormality.