Vagaries of acceleration dependent aberration.
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Biomedical subjects
Publications and source records attributed to S B Knoebel.
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Because decision modeling involves the construction of an explicit, mathematically describable structure of the pertinent elements of a clinical problem, the relative effectiveness of alternative approaches to care can be identified; costly procedures become apparent; new technologies can be assessed in relation to the old in terms of effectiveness and costs; the marginal benefit to be achieved by duplicative or alternative practices can be determined. All of this can be accomplished in terms of patient outcome and without the bias and self-interest of which the profession has been accused. Furthermore, if a resource allocation or reimbursement decision made in the name of cost containment eliminates or limits access to effective diagnostic or therapeutic technologies, the impact of that decision on effective care can be explicitly and quantitatively expressed through decision modeling. When such analyses are based on patient outcome, they are difficult to ignore and provide a pivotal point for discussions and eventual compromise.
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It is the thesis of this presentation that more precise diagnoses and prognostications result when clinical information is analyzed as data-sets or patterns rather than collections of discrete data. Two examples are given in support of the thesis: the classification by computer of QRS complexes in the ambulatory electrocardiogram and the prediction of risk for recurrent ventricular tachycardia. The advantages to be gained from pattern analysis are: (1) significant variables are not preselected and the data are, therefore, unbiased, and (2) nuances in clinical patterns become evident when patients are presented as data-sets. It is proposed that competent physicians undoubtedly use pattern analysis in their decision-making and that expert systems designed to simulate physician behavior might be more accurate if based in pattern analysis.
Following uncomplicated myocardial infarction patients are at varying risk for cardiovascular morbidity and mortality. In order to identify and treat high risk patients, various management approaches can be employed. We performed a decision analysis to examine the cost-effectiveness of seven alternative strategies under the assumption that prognosis is affected by both the location of anatomic obstruction and the degree of myocardial ischemia. Strategies included combinations of angiography and two theoretical diagnostic tests capable of detecting ischemia with different degrees of accuracy. The strategy associated with the lowest overall six month mortality initiated testing with the diagnostic test most sensitive for ischemia, slightly better than proceeding initially to angiography. Initial use of a test sensitive for ischemia was also considerably more cost-effective than proceeding directly to angiography. Future analyses evaluating the role of diagnostic tests in coronary artery disease should incorporate the dimension of ischemia.
The Q-T interval and apex of T wave to end of T wave (aT-eT) interval were measured by computer in four age-matched study groups at rest and during exercise to determine whether: the behavior of the aT-eT interval differs in patients with myocardial ischemia when compared with normal subjects, and the behavior of the aT-eT interval differs in subjects with true positive and false positive ST segment responses. Group I consisted of 57 normal subjects. Group II consisted of 41 symptomatic patients with documented coronary artery disease. A group of apparently healthy subjects with asymptomatic ST segment depression during exercise was divided into two additional groups: Group III, those without coronary artery disease; and Group IV, those with coronary artery disease. Subjects were excluded from the study if they had left ventricular hypertrophy or an intraventricular conduction defect or were taking digitalis or type I antiarrhythmic agents. There were no significant differences in the aT-eT interval and aT-eT/Q-T ratio among the four study groups when compared at rest; however, during exercise at similar heart rates, the aT-eT interval was significantly shorter and the aT-eT/Q-T ratio significantly smaller in Groups II and IV, the subjects with coronary artery disease, than in Group I, the normal subjects. The aT-eT interval and aT-eT/Q-T ratio measurements in Group III did not differ from those in Group I at rest or during exercise. In conclusion, the aT-eT interval and aT-eT/Q-T ratio may reflect changes in myocardial repolarization in exercise-induced ischemia and may have potential for future clinical application.
The purpose of this study was to determine whether a quantitative relationship existed between a reduction in regional myocardial blood flow, measured by radiolabeled microspheres, and the degree and type of changes in myocardial activation recorded in bipolar left ventricular subepicardial and subendocardial electrograms, in open-chest dogs following acute coronary artery occlusion. We found that the degree of regional myocardial ischemia was related quantitatively to the reduction in amplitude recorded with bipolar electrograms in the subepicardium and subendocardium, and to the increase in duration of subepicardial electrograms. Other characteristics measured in electrograms did not relate to the degree of ischemia. Despite a comparable reduction in regional myocardial blood flow, subepicardial conduction delay exceeded that recorded in the subendocardium, which often exhibited accelerated conduction.
Wall thicknesses were measured and echo densities were evaluated from the left ventricular echograms of 182 patients. The echogram was considered to reflect scar tissue when 1) either the interventricular septum, the posterior left ventricular wall or the anterior left ventricular wall was less than 7 mm thick in mid-diastole and was more echo-producing than its opposing wall or another area of the same wall in a sector scan, or 2) an area of myocardium was 30% less thick than an adjacent area within a sector scan. Myocardial scarring was diagnosed by echocardiography in 52 of the 182 patients. The echocardiographic presence or absence of scarring was confirmed in 95% (173 of 182) of cases, 34 cases by microscopic examination and 139 by surgical appearance. This study shows that M-mode echocardiography is both a sensitive and specfic method for detecting myocardial scar tissue.
A formula was derived for calculating mitral valve stroke volume (MVSV) using the rate of mitral valve (MV) opening (DE slope on the MV echogram), the vertical disease between the mitral leaflet echoes early in diastole (EE), the electrocardiographic PR interval and heart rate. The formula was tested prospectively on 80 consecutive patients from whom 95 simultaneous MV echograms and either thermodilution (45) or Fick (50) cardiac outputs were obtained. Sixteen patients were normal; 54 had coronary artery disease; three had cardiomyopathy; and seven had nonrheumatic mitral regurgitation (MR). Linear regression for stroke volume was r = 0.90, SEE +/- 6, and for cardiac output r = 0.83, SEE +/- 0.5 liter for the 73 patients without MR. The presence or absence of ventricular dyssynergy did not alter statistical findings. MVSV consistently overestimated forward stroke volume for the seven patients with MR. This study shows that the MV echogram provides an accurate, widely applicable method for calculating MVSV.
Under conditions of varying flow rates, total myocardial blood flow, measured by fractional uptake of rubidium-84, using a coincidence counting system, was compared with myocardial flow measured by microspheres (15 +/- 5 micrometer). The methods were compared, open-chested, in 47 dogs: 17 during control, ten following 5 min of ligation of left anterior descending coronary artery, five following i.v. isoproterenol, six following ligation and isoproterenol, and nine after ligation plus dipyridamole. Regional flows by Rb-84 and by either Ce-141 or Cr-51 microspheres were also compared for left ventricle, as well as for nonischemic posterior wall, which served as a reference area, and for anterior wall with ligation of left anterior descending artery in the same preparations. There were no significant differences in total or regional flow measured by the two methods, nor in the estimate of ischemic area size. The data indicate that measurement of myocardial blood flow by fractional uptake of a potassium analog is a reliable method in the presence of ischemia and drug intervention. It is suggested that the inequalities of extraction ratio that occur with differing flow rates do not invalidate fractional-uptake methods over the flow ranges examined.
Echocardiographic septal and posterior wall thicknesses and the percent change with systole were measured in 146 patients with the following diagnoses: acute myocardial infarction (40), chronic coronary artery disease (49), congestive cardiomyopathy (8), atrial septal defect (20), and no cardiac disease (29). Mean diastolic thicknesses for the groups of patients with coronary artery disease and congestive cardiomyopathy were not significantly different from normal although there were abnormal values for individual patients within each group. Mean diastolic thickness of the septum was greater than normal for the group with atrial septal defect (P less than 0.02). Wall thinning with systole was associated with acute infarction or ischemia (P less than 0.0001); decreased thickening (less than normal) commonly occurred in patients with acute myocardial infarction, chronic coronary artery disease, and congestive cardiomyopathy. Patients with atrial septal defect had normal thickening with abnormal motion. Results of this study show that 1) systolic thinning is indicative of an acute event; 2) abnormal changes in systolic wall thickening occur commonly in patients with coronary artery disease or congestive cardiomyopathy; and 3) abnormal wall motion may occur without abnormal wall thickening, as the echoes of patients with atrial septal defect indicate.
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The accuracy of a data reduction system for arrhythmia detection in identifying premature ventricular complexes was evaluated in continuous tape records of 30 patients in a coronary care unit. Computer analysis was performed with a Honeywell 316 digital computer. Threshold values for dominant complexes were automatically determined and recognition of premature ventricular complexes was based on differences in QRS configuration, timing and T wave configuration from the dominant complexes. Verification of the computer accuracy in detecting premature ventricular complexes was made with visual beat by beat inspection using a two channel strip chart recorder with simultaneous recording of the electrocardiogram and computer signal. This procedure allowed for exact beat to beat correlation and, thus, absolute determination of false positive and false negative identification. From 0.5 to 6 continuous hours of monitoring per patient (average 3.5 hours) were analyzed for a total of 105 monitoring hours. The basic cardiac rhythms noted were normal sinus rhythm, sinue arrhythmia, sinus tachycardia, demand pacemaker rhythm, atrial fibrillation and atrioventricular (A-V) dissociation with junctional rhythm. Premature ventricular complexes were evident in 28 tapes (93 percent) including 12 (43% with multifocal premature ventricular complexes and 3 (11 percent) with ventricular tachycardia. The visual count of premature ventricular complexes totaled 7,921. Of these, 7,542 (95 percent) were properly classified by the computer. The total computer count was 8.717, representing a 13 percent false positive and 5 percent false negative identification rate. The false positive identifications of premature ventricular complexes occurred during periods of 10 seconds or more of continuous noise artifact and in the presence of atrial premature complexes conducted aberrantly. When these sections of tape were excluded, the computer had a less than 2 percent false negative and 3 percent false positive rate of identification of premature ventricular complexes.
Inverted T waves due to coronary artery disease and previous myocardial infarction were observed to revert ot normal, upright position during ischemia in 38 patients. The normalization of inverted T waves was seen on the electroencephalograms of 19 patients during spontaneously occurring angina pectoris and of 11 patients when ischemia was provoked by treadmill exercise; for 8 patients, normalization occurred during the administration of isoproterenol hydrochloride and during the consequent episode of angina pectoris. The mechanism for normalization may be the algebraic sum of the extent of ST segment elevation and the amplitude of the T waves of acute ischemia plus the extent of preexisting ST segment depression and the degree of T wave inversion, to result in isoelectric ST segment and upright T wave. As with myocardial infarction, reciprocal changes may also be recorded. However, the reciprocal nature may be masked since either acute ST segment elevation of T wave inversion, or both, may not be recorded in the leads reflecting the ischemic area because of normalization.
Thirty consecutive patients with acture myocardial infarction had continuous magnetic tape recording of their stay in the coronary care unit. Analysis of the 24 hour tape recordings was implemented on a Honeywell model 316 digital computer. In the first 24 hours after admission to the coronary care unit, 12 of the 30 patients (40 percent) exhibited nonparoxysmal junctional tachycardia; in 5 the arrhythmia was not recognized by conventional monitoring techniques. For the subsequent 3 days, the incidence rate of the arrhythmia was 13 percent for the first 48 hours and 3 percent for 72 hours. Although the mortality rate in patients with nonparoxysmal junctional tachycardia was greater than in patients not demonstrating the arrhythmia (33 versus 6 percent), there was a greater percentage of patients with anterior infarction in the former group; therefore, mortality may have been related to site of infarction rather than being reflective of the arrhythmia or its associated pathophysiologic state. Of possible significance is the association of a greater degree of sinus arrhythmia with nonparoxysmal junctional tachycardia. The incidence of nonparoxysmal junctional tachycardia in this group of patients was greater than previously reported. It is possible that computer tape analysis may have provided more accurate recognition of the arrhythmia and, thus, more realistic incidence data. The association of nonparoxysmal junctional tachycardia with sinus arrhythmia could only have been recognized by computer technique. The computer system is not a diagnostic system but rather a tape review method.
Sixty-four patient with acute transmural myocardial infarction had daily echocardiograms while in the coronary care unit. Patients with previous infarction were excluded. The electrocardiographic site of infarction was anterior wall in 28, inferior wall in 33 and both anterior and inferior wall in 3 patients. Echocardiograms satisfactory for interpretation were obtained in 92 percent of cases. Abnormal left ventricular wall motion corresponding to the electrocardiographic site of infarction was seen in the echocardiogram in 84 percent of cases. Exaggerated normal motion in noninfarcted areas was seen in 30 percent. The left ventricular internal dimension correlated with clinical heart failure (P less than 0.005) and was increased in 50 percent. Abnormal mitral valve closure, which reflects increased left ventricular end-diastolic pressure, was present in 33 percent. This finding did not correlate significantly with clinical heart failure. By combining the measurements of left ventricular internal dimension and mitral valve closure, it was possible to predict hospital mortality from the echocardiograms. The results indicate that echocardiography is a useful technique in the study and management of patients with acute myocardial infarction.
Because of clinical observations suggesting that nitroglycerin may suppress premature ventricular complexes during acute ischaemia, a study was undertaken to assess the effect of nitroglycerin on the incidence of premature ventricular complexes in patients with acute myocardial infarction. Forty patients with acute myocardial infarction were studied. Twenty-six patients received 0.4 mg nitroglycerin sublingually every 4 hours for the first 24 hours after admission to the coronary care unit. The total premature ventricular complex count for the 26 patients for 15 minutes before nitroglycerin was 592, and 276 for the 15 minutes after the drug (P less than 0.005). In the remaining 14 patients on the same nitroglycerin schedule, a single electrocardiographic lead was continuously recorded on tape. During the first hour after nitroglycerin, the premature ventricular complex count decreased by 58 per cent, and the second and third hours showed a decrease from control count of 71 and 65 per cent respectively. By the end of 4 hours the ectopic count was back to control level. The data indicate that nitroglycerin may decrease the number of premature ventricular complexes for up to 3 hours in patients with acute myocardial infarction. The mechanism of action of nitroglycerin is not elucidated by this study, but the observation may be of value in further studies of specific antiarrhythmic therapy and prevention of arrhythmias in patients with coronary artery disease.