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Biomedical subjects

Y Myreng

Publications and source records attributed to Y Myreng.

14 recordsLinked to original sources
PubMed1992

Intravenous injection of Albunex microspheres causes thromboxane mediated pulmonary hypertension in pigs, but not in monkeys or rabbits.

Intravenous injection of the ultrasound contrast agent Albunex (manufactured by Nycomed AS, Oslo, Norway; 400 million air-filled albumin microspheres per ml, mean diameter 4 +/- 1 microns) caused a dose-dependent increase of mean pulmonary arterial pressure in nine pigs. The highest dose (0.014 +/- 0.002 ml kg-1) increased mean pulmonary arterial pressure from 17 +/- 1 mmHg to 42 +/- 3 mmHg and decreased mean systemic arterial pressure from 111 +/- 9 to 93 +/- 12 mmHg. The pressure responses began 22 +/- 1 s after particle injection, and reached maximum after 51 +/- 3 s. No changes in mean pulmonary arterial pressure or mean systemic arterial pressure were observed after Albunex injections during treatment with indomethacin (10 mg kg-1 + 5 mg kg-1 h-1 i.v., n = 6) or the thromboxane A2 receptor antagonist HN-11500 (10 mg kg-1 + 5 mg kg-1 h-1 i.v., n = 3). No Doppler enhancement could be detected in a carotid artery following injection of 0.12 ml kg-1 Albunex during indomethacin treatment. In five rabbits, Albunex caused Doppler enhancement in a carotid artery, and 0.48 ml kg-1 did not affect mean pulmonary arterial pressure or other haemodynamic parameters in five rabbits or in three cynomolgus monkeys. The pressure response in pigs may be explained by release of thromboxane A2 from the pulmonary intravascular macrophages during phagocytosis of the microspheres. This response to Albunex was totally absent in rabbits and monkeys.

Albumins↗
PubMed1990

Reproducibility of echocardiographic estimates of the area of stenosed aortic valves using the continuity equation.

Interobserver variability in echocardiographic estimates of the area of stenosed aortic valves was assessed in 30 consecutive patients. Using the continuity equation, two independent observers calculated the area of stenosis from separate recordings of the diameter of the aortic orifice and the velocity time integral in the left ventricular outflow tract and in the stenotic jet. No significant difference between the observers was noted for any measurement. With respect to the area of stenosis, a high correlation between the observers was found (r = 0.92, P less than 0.001) and the regression line was close to the line of identity. The 95% limits of agreement were less than +/- 0.3 cm2. No discrepancy between the observers was found in the assessment of cases for aortic stenosis less than 0.8 cm2. Regression analyses showed good interobserver agreement also for the diameter of the orifice, the velocity time integrals, and the mean pressure gradient (r greater than 0.90, P less than 0.001). The greatest variability was noted for the diameter of the aortic orifice (95% limits of agreement +/- 1.4 cm2). We conclude that echocardiography enables reproducible estimates of the orificial area of stenosed aortic valves. Changes greater than 0.3 cm2 can be detected with a confidence probability of 95%. The greatest source of error is the measurement of the diameter of the outflow tract at the basal attachments of the aortic leaflets.

Adult↗
PubMed1990

Left ventricular filling at elevated diastolic pressures: relationship between transmitral Doppler flow velocities and atrial contribution.

The relationship between transmitral Doppler blood flow velocities and atrial contribution to left ventricular (LV) filling was investigated in seven open-chest dogs. At LV filling pressures greater than 15 to 20 mm Hg, LV volume approaches a maximum. Thus we hypothesized that when LV pressure before the onset of atrial systole exceeds this level, the atrial contribution would decrease and the ratio between peak early (E) and atrial-induced (A) mitral velocities would increase. Atrial contribution was measured as LV diameter increase during atrial contraction expressed as a percentage of the total LV diameter change during diastole (sonomicrometry). When left ventricular end-diastolic pressure (LVEDP) was progressively increased from 10 +/- 1 (mean +/- standard deviation) to 28 +/- 3 mm Hg by intravenous saline solution, the atrial contribution decreased from 34 +/- 14% to 8 +/- 10% (p less than 0.001). Concomitantly the A velocity decreased from 39 +/- 7 to 24 +/- 8 cm.sec-1 (p less than 0.01), and the E/A ratio increased from 1.8 +/- 0.3 to 3.6 +/- 1.5 (p less than 0.001). The E/A ratio and the atrial contribution were constant until LVEDP exceeded 17 to 20 mm Hg, at which level marked changes in both parameters were noted. Thus when LV filling pressure was increased, the E/A ratio increased, indicating a filling shift towards early diastole. The reduced atrial contribution during increased preload was explained by the curvilinear shape of the LV pressure-volume curve. At markedly elevated filling pressures, near-maximum LV diameter was achieved before atrial contraction; hence the atrial contribution decreased and the E/A ratio increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Assessment of left ventricular relaxation by Doppler echocardiography. Comparison of isovolumic relaxation time and transmitral flow velocities with time constant of isovolumic relaxation.

Isovolumic relaxation time (IVRT) and events of early transmitral flow measured by Doppler echocardiography were validated against the time constant of left ventricular relaxation (tau) in open-chest dogs. During increased inotropy (by isoproterenol infusion) at constant preload, enhancement of relaxation was indicated by a decrease in tau from 48 +/- 12 (mean +/- SD) to 33 +/- 5 msec (p = 0.04) with a concomitant decrease in IVRT from 74 +/- 18 to 38 +/- 8 msec (p = 0.03). During decreased inotropy (by propranolol infusion) at constant preload, slowing of relaxation was indicated by an increase in tau from 40 +/- 8 to 51 +/- 13 msec (p = 0.02) with a concomitant increase in IVRT from 71 +/- 15 to 83 +/- 21 msec (p less than 0.05). A significant correlation between changes in tau and changes in IVRT was found (r = 0.66, p less than 0.001). In contrast, when left ventricular end-diastolic pressure was increased from 7 +/- 2 to 24 +/- 4 mm Hg at constant inotropy, tau increased from 47 +/- 14 to 64 +/- 25 msec (p = 0.03), whereas no change in IVRT was observed (76 +/- 19 and 71 +/- 19 msec, respectively). Aortic pressure was not significantly changed during any intervention, and heart rate was kept constant by pacing. Peak early transmitral velocity was unchanged by propranolol but increased during isoproterenol and saline infusion (p less than 0.001 and p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effects of verapamil on left ventricular relaxation and filling dynamics in coronary artery disease: a study by pulsed Doppler echocardiography.

The effect of verapamil on left ventricular diastolic function in coronary artery disease was assessed by Doppler echocardiography of transmitral flow velocities in 20 patients. At baseline, isovolumic relaxation time was prolonged compared with that in 18 age-matched normal subjects (95 +/- 13 msec versus 74 +/- 12 msec, p less than 0.001), but decreased to 80 +/- 14 msec (p less than 0.001) after treatment. The ratio between early and atrial-induced transmitral velocities (E/A-ratio) at baseline was lower in patients than in normal subjects (1.1 +/- 0.2 versus 1.4 +/- 0.3, p = 0.01), as was the filling fraction of the first third of diastole (43% +/- 5% versus 50% +/- 4%, p less than 0.001). Verapamil treatment increased the E/A-ratio to 1.3 +/- 0.4 (p less than 0.001) and filling fraction to 45% +/- 4% (p = 0.055) because of increased early filling. No change in systolic performance or heart rate was observed. Thus, coronary artery disease was associated with retarded relaxation and impairment of early filling. However, verapamil treatment enhanced relaxation and induced a filling shift toward early diastole, which indicated improved diastolic performance. The changes probably reflected reduced myocardial ischemia.

Adult↗
PubMed1989

Age-dependency of left ventricular filling dynamics and relaxation as assessed by pulsed Doppler echocardiography.

Left ventricular diastolic function was assessed from transmitral flow velocity curves as measured by Doppler echocardiography in healthy individuals aged 21-69 years, each decade comprising 12 subjects. By ageing, progressive changes in the various filling parameters were observed. When comparing the youngest and oldest age groups, the ratio between peak velocities in early and late diastole decreased from 2.0 +/- 0.3 to 1.2 +/- 0.3 (P less than 0.001). The filling fraction of first third of diastole decreased from 54 +/- 5% to 45 +/- 4% (P less than 0.001). Isovolumic relaxation time increased from 61 +/- 11 ms to 77 +/- 12 ms (P less than 0.01). Correlation coefficients of velocity ratio, filling fraction and isovolumic relaxation time vs. age were r = -0.71 (P less than 0.001), r = -0.56 (P less than 0.001) and r = 0.44 (P less than 0.001), respectively. When isovolumic relaxation time and age were used together in multivariate regression analysis, only age was an independent predictor of velocity ratio and filling fraction. Stroke volume, peak velocity in left ventricular outflow tract, heart rate and systolic blood pressure were similar in all age groups. Thus, velocity ratio and filling fraction indicated a relative filling shift towards late diastole by ageing and were more sensitive than systolic parameters in reflecting age-related changes in cardiac function. The changes could be explained neither by delayed relaxation nor by change in systolic parameters. When using Doppler echocardiography for evaluation of left ventricular filling, age-matching of reference groups is necessary.

Adult↗
PubMed1988

Effects of beta-adrenergic blockade on left ventricular relaxation and filling dynamics in coronary artery disease: a pulsed Doppler echocardiographic study.

Left ventricular (LV) filling as assessed by Doppler transmitral flow velocity measurements was studied in 20 male patients with coronary artery disease (CAD) and in 18 normal individuals. Stroke volume, blood pressure and heart rate in the two groups were not significantly different. Compared to normals, the ratio between early and atrial-induced peak velocities was significantly lower in the patients (1.2 +/- 0.3 vs. 1.40 +/- 0.3, P = 0.01), as was the fraction of transmitral filling during the first 1/3 of diastole (45 +/- 7% vs. 50 +/- 4%, P less than 0.001). Isovolumic relaxation time (IV R) was 96 +/- 13 ms in patients vs. 74 +/- 12 ms in normals (P less than 0.001). The CAD patients were treated with atenolol for 13-24 days. The velocity ratio increased by 30% (P less than 0.001) due to a 12% increase in early (P = 0.004) and an 11% decrease in atrial-induced peak velocities (P = 0.01). Filling fraction and deceleration rate of early inflow both increased by 22% (P less than 0.001). IV R decreased by 8% (P = 0.01). After atenolol treatment, heart rate and blood pressure decreased by 23% and 10% (P less than 0.001), respectively, whereas stroke volume increased by 14% (P less than 0.001). Thus, CAD was associated with Doppler indices of retarded LV filling and myocardial relaxation. After atenolol treatment, significant increases in velocity ratio and filling fraction indicated a shift of filling from late towards early diastole, suggesting improved diastolic function. However, different factors related to beta-adrenergic blockade may have contributed to the observed changes.

Adrenergic beta-Antagonists↗
PubMed1988

Acute phase reactants and complement activation in patients with acute myocardial infarction.

The acute phase proteins, C-reactive protein (CRP), orosomucoid, alpha 1-antitrypsin and haptoglobin, the native complement components C3 and C4, activation products of C3, and the terminal SC5b-9 complement complex were quantified in samples obtained on admittance and on days 1, 2, 3 and 6 in 21 patients with non-complicated acute myocardial infarction (AMI) and in 22 controls. For all proteins peak and median concentrations were higher in the AMI group than in the controls, but the difference was significant only for CRP and orosomucoid. Median CRP concentration was 46 mg/l in the AMI group and 2.5 in the control group. The corresponding orosomucoid concentrations were 1.6 and 1.2 g/l. There was no correlation between the concentration of CRP in peripheral blood and the degree of complement activation. Furthermore, no correlation was observed between complement activation and the size of infarction. The present study cannot demonstrate that the increased concentrations of CRP and other acute phase reactants observed in patients with AMI, are associated with systemic fluid-phase complement activation. Furthermore, the complement activation previously shown locally in infarcted myocardium cannot be demonstrated systemically in non-complicated AMI.

Acute-Phase Proteins↗
PubMed1987

Reproducibility of cardiac stroke volume estimated by Doppler echocardiography.

Doppler echocardiography was used to measure cardiac stroke volume in 10 patients with coronary artery disease who were treated with cardioactive drugs. Stroke volume estimates were determined at the aortic orifice by multiplying area by systolic velocity integral measured both from the suprasternal and the apical approach. Recordings were done independently by 2 experienced observers on the same day and repeated once after 1 to 21 days. Analysis of variance showed that no systematic differences were introduced by the 2 observers and Doppler approaches or by measuring on different days. The coefficient of variation between any pair of measurements in each patient was 9%. This variability is probably a result of the method or spontaneous fluctuations of the stroke volume and not of the varying recording conditions. The ultrasonic method detects day-to-day changes of cardiac stroke volume larger than 20% with a probability greater than 0.95.

Adult↗