Surface potential contribution from discrete elements of ventricular wall: A closed chest,postmortem-documented prospective study

Isopotential distribution maps were recorded before and after infarction in five dogs with an induced lesion in the circumflex branch of the left coronary artery and in five dogs with an occlusion created in the ventral interventricular branch by a closed chest catheter technique. Maps of “lost” potential distribution, derived by subtracting time-equivalent postinfarction maps from the dog's original or base-line maps, proved to be remarkably consistent in their configuration with respect to the location of the myocardial lesion. Even when the small, discrete infarctions, documented by histochemical postmortem examination, went undetected by conventional vector and scalar cardiography, the “difference” technique not only verified the presence of the lesion, but also served to predict its location.     

Electrocardiographic changes in cerebrovascular hemorrhage

The electrocardiographic abnormalities found in localized cerebrovascular hemorrhage which have been documented by computerized tomography (CT) scans are described. Frontal lobe hemorrhages are associated especially with the electrocardiographic abnormalities of QT prolongation and neurogenic T waves. Brain stem hemorrhage seems to be associated with noncardiogenic pulmonary edema, and sudden development of atrial fibrillation. It is proposed that the cause of ECG abnormalities in association with lesions in the vincinity of area 13 on the orbital surface of the frontal lobe, or around the circle of Willis, results from alterations in sympathetic and parasympathetic tone mediated by fibers from the orbito-frontal area to the heart via the stellate ganglia.     

Cigarette smoking,physical activity,and alcohol consumption: Relationship to blood lipids and lipoproteins in premenopausal females

A total of 164 premenopausal female subjects were randomly selected for evaluation from a much larger pool of volunteers. The relationships between blood lipid and lipoprotein levels as dependent variables and cigarette smoking, physical activity, and alcohol consumption were determined from partial regression coefficients. A lower HDL-C level (10.1 mg/dL) was seen in smokers v nonsmokers. For each ounce of alcohol consumed, HDL-C level was higher by 2.8 mg/dL, and greater physical activity was associated with a higher HDL-C level of 8.6 mg/dL. An analysis of covariance with covariance adjustments for age and body fat revealed that smokers who regularly exercise or consume alcohol had significantly lower HDL-C levels than nonsmokers with similar habits. Subjects who both exercise and consume alcohol demonstrated higher HDL-C levels than those who indulge in one or the other separately. Results suggest that cigarette smoking may attenuate the effects of chronic exercise or alcohol consumption, or of both, to raise HDL-C levels. Also, chronic exercise and alcohol consumption may exert an additive effect, raising HDL-C level.     

Predicting adverse events in patients undergoing hepatectomy—validation of preoperative nomogram and risk score

Background/Purpose

Much research exists on preoperative measures of postoperative mortality in the surgical treatment of liver malignancies, but little on morbidity, a more common outcome. This study aims (i) to validate the published calculations as acceptable measures of postoperative mortality and (ii) to assess the value of these published measures in predicting postoperative morbidity.

Surface recording of electrical activity from the region of the bundle of His

In 16 dogs, by appropriate filtering and digital averaging on a PDP-9 computer, we were able to enhance the detection of electrical activity of interest in the P-R segment of the electrocardiogram. In instances (1) when such activity in the surface record coincided temporally with the internal recording from the bundle of His area, (2) when, with atrioventricular nodal block, the electrical activity of interest continued to be associated with the internally recorded His bundle deflection and not with atrial activity, and (3) when, with production of transmission delay between the bundle of His and the ventricle, the surface signal of interest continued to be associated with the internal His bundle deflection, a common signal source was considered likely. In certain instances the surface signal of interest in the P-R segment occurred well after the internally recorded His bundle deflection but about 15 msec before the earliest evidence of ventricular activity. In these instances, when the tests cited were applied and the blip of interest was associated with ventricular activity, the origin of the blip was thought to be in the region of the bundle branches.In the 16 animals studied, one or more pieces of the evidence described were present to localize the origin of the signal. In seven animals, the signal was thought to originate from the bundle of His, in six from the region of the bundle branches and in three from both the bundle of His and bundle branches.     

The determination of the human ventricular gradient from body surface potential map data

We have analyzed the Wilson ventricular gradient in terms of body surface potential maps and of the reduction of such surface patterns to equivalent dipoles or vectors. While the ventricular gradient traditionally was treated as first a scalar, then a vector concept, we found that the three entities (QRS area, T area, QRST area) did not reduce to vectors with a common location. However, conventional vector addition (QRST area = QRS area + T area) did precisely apply. Further we found considerable more-than-vector or extra-dipolar information remaining for all three entities after removal of the dipole effect. This suggests that maps of these entities should be considered the boundaries of complex electrical fields rather than simple surface effects of vectors.     

The influence of electrode placement in the reconstruction and analysis of body surface potential maps from limited thoracic arrays

Despite their capacity to indicate abnormality outside the scope of routine electrocardiography body surface maps remain extensive, time-consuming research procedures. By contrast, a 35-electrode grid which sums precordial ST segment deviations has received wide attention as a clinical monitor of acute myocardial infarction. First, this study examined the feasibility of recovering essential data from a small electrode array to construct maps equal to those obtained from a much larger array. Such a small-array technique would offer economy, easy application, plus the comprehensiveness and clinical correlation of the large system. Second, the relationships between map, small-array and a 35-component equivalent multipolar generator were explored for a transformation system which both expands the small-array data to map displays and reduces such data to non-redundant waveforms. Comparisions were made between direct maps and those derived from two 35-electrode sets in normal subjects and patients with myocardial infarction or cardiomyopathy. Electrode placement did not conform to the conventional rectangular grid; for one, the electrodes encircled the thorax symmetrically; in the other they were statistically selected for signal information content. We found 1) symmetrical electrode placement and analytic reconstruction of maps from multipolar lead components consistently reproduced known maps well (.91 correlation, 120 microvolts error); but 2) empirical electrode placement and statistical prediction of known maps averaged .99 correlation and 20 microvolts error for the normal training population and .97 and 60 microvolts for the abnormal test sample. Worsening occurred when placement and prediction methods were mixed; however, maps reconstructed by the empirical-statistical approach reduced to a reasonable approximation of equivalent generator scalar leads     

Comparative metabolic effects of acetate and dichloroacetate infusion in the anesthetized dog

The comparative effects of acetate (10 mmol/h/kg) and dichloroacetate (DCA) (1 mmol/h/kg and 10 mmol/h/kg) on acid-base and intermediary metabolism were assessed using the fasted anesthetized dog, undergoing controlled ventilation, as a metabolic model. Infusion of acetate resulted in a marked metabolic alkalemia and a decline in PaO2, while DCA had minimal effects on acid-base state and oxygen consumption. Serum glucose decreased with both DCA and acetate infusion, although only significantly with the latter. At infusion rates of 10 mmol/h/kg, acetate caused marked decreases, while DCA caused marked increases, in serum potassium and phosphorus. Acetate and DCA also had opposing effects on lactate and citrate levels, the former caused increases and the latter decreases in both metabolites. Pyruvate levels decreased similarly in response to both infusates. Acetoacetate and beta-hydroxybutyrate levels increased significantly with both acetate and DCA infusions; however, the increases were much greater with acetate than with DCA infusion. Blood alanine levels decreased significantly during the infusion of both acetate and DCA, whereas, free fatty acids tended to increase with acetate infusion, remained unchanged with low dose DCA and fell significantly with high dose DCA. Plasma insulin levels were sustained during acetate infusion, but fell abruptly with termination of infusion. In contrast, insulin levels fell markedly with DCA infusion and remained depressed throughout the infusion and recovery periods. Blood levels of acetate and DCA rose markedly during infusion; however, while acetate levels decreased nearly to control values during the recovery period, DCA levels remained elevated.(ABSTRACT TRUNCATED AT 250 WORDS)