Search PubMed⌕ Search

Biomedical subjects

S Rasmussen

Publications and source records attributed to S Rasmussen.

At least 253 records · Page 14Linked to original sources
PubMed1977

Choreoathetosis during phenytoin treatment.

A patient with symptomatic epilepsy receiving only phenytoin developed choreoathetosis and orofacial dyskinesias. These movement disorders disappeared when the drug was stopped and reappeared when the patient was challenged. Throughout the period of treatment, concentrations of phenytoin in serum were consistently low within the therapeutic range. Interfering symptoms from the cardiovascular system and the absence of some classic symptoms of phenytoin intoxication (nystagmus and dysarthria) contributed to delay the diagnosis. The patient died in hospital and autopsy of the brain showed rather localized encephalomalacies of corpus striatum. The pathogenic action of phenytoin and the role of preexisting brain lesions are discussed. Phenytoin must be suspected as the cause, when patients on this drug present with uncontrolllable epilepsy or neurological or mental deterioration.

Aged↗
PubMed1977

Systolic thickening and thinning of the septum and posterior wall in patients with coronary artery disease, congestive cardiomyopathy, and atrial septal defect.

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.

Acute Disease↗
PubMed1977

Delayed hypersensitivity and borderline essential hypertension.

By means of the leucocyte migration technique, it has been demonstrated that the migration indices from 19 patients suffering from borderline essential hypertension are significantly different from those of 19 normal persons. These results support the view that delayed hypersensitivity directed against arterial wall components is a possible pathogenetic factor in patients suffering from essential hypertension.

Antigens↗
PubMed1976

[A blood filter].

Explore the source record for details and available documents.

Blood Preservation↗
PubMed1976

Role of echocardiography in patients with coronary artery disease.

Impaired left ventricular performance, one of the hallmarks of coronary artery disease, can be detected by echocardiography in various ways. One of these approaches is the recording of abnormal wall motion. Because of the way in which the left ventricle can be examined echocardiographically, this technique has the capability of detecting regional wall abnormalities. In fact echocardiography is probably the most sensitive technique available, including even contrast ventriculography, for the detection of akinetic, hypokinetic or dyskinetic wall segments. With increasing experience it is apparent that more areas of the left ventricle can be examined echocardiographically than had previously been thought possible. Newer techniques include directing the ultrasonic beam not only through the body of the left ventricle but also toward the apical portion of the ventricle near the vicinity of the papillary muscles. In addition the true anterior left ventricular wall can be examined by moving the transducer laterally away from the left sternal border. Yet another approach utilizes a subxiphoid position for the transducer while the ultrasonic beam is directed through the medial portion of the septum and posterolateral wall of the left ventricle. M-mode scanning techniques together with recently developed cross-sectional echocardiographic instruments give great promise of improved detection of abnormalities of ventricular shape, especially the presence of aneurysms. The cross-sectional approach makes it possible to examine the left ventricular apex, an area virtually impossible to record with M-mode echocardiography. Recording of left ventricular dimensions and abnormal mitral valve motion may help in assessing overall left ventricular performance. A dilated left ventricular dimension in the vicinity of the mitral valve seems to be an ominous finding both in patients with acute myocardial infarction and in patients with chronic coronary disease being considered for possible surgery. Another echocardiographic sign of abnormal ventricular performance is altered closure of the mitral valve, which reflects a significantly elevated left ventricular diastolic pressure. These echocardiographic techniques are still in the investigational stages and are more technically difficult than the usual echocardiographic applications. However, the preliminary data are encouraging and make us hopeful that echocardiography will prove to be an important tool in the overall evaluation of the left ventricle in patients with coronary artery disease.

Coronary Disease↗
PubMed1976

Computer detection of premature ventricular complexes: a modified approach.

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.

Arrhythmias, Cardiac↗
PubMed1976

Renal and intrarenal blood flow distribution in swine during severe exercise.

It is known that a compensatory reduction and diversion of renal flow occurs in severe exercise in humans but not in dogs. We investigated this in miniature swine by measuring changes in total renal blood flow (TRF) and intra-renal blood flow (IRBF) distribution with tracer microspheres (15 +/- 5 mum) at rest and during steady-state exercise at 4.8-7.2 kph and 0% grade, and during severe exercise at 4.8-7.2 kph and 10% grade. We measured heart rate and cardiac output (Q) via implanted probes. TRF was determined as a percent of Q and as ml/100 g per min. IRBF was determined for the outer cortex, inner cortex, outer medulla, and inner medulla. Our results show that renal blood flow is significantly (P less than 0.05) reduced in pigs with exercise. Steady-state exercise reduced flow to about 66% of control and severe exercise reduced renal flow to 30% of control. IRBF was unchanged throughout. These results show that the exercising pig augments blood flow to skeletal muscle by reducing blood flow to kidneys, a response known to occur in man.

Animals↗
PubMed1975

Nonparoxysmal junctional tachycardia in acute myocardial infarction: computer-assisted detection.

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.

Analog-Digital Conversion↗
PubMed1975

Echocardiography in acute myocardial infarction.

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.

Acute Disease↗
PubMed1975

Nitroglycerin and premature ventricular complexes in 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.

Administration, Oral↗