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Biomedical subjects

C van Eyll

Publications and source records attributed to C van Eyll.

26 records · Page 2Linked to original sources
PubMed1984

Early changes in sodium and water balances in patients with acute myocardial infarction: relationship to haemodynamics and creatine kinase.

The changes in sodium and water balances during the first 4 days after an uncomplicated transmural myocardial infarction (MI) were determined in forty patients. The sodium balance was positive 4 days after MI in 80% of the patients but negative in 20%. Neither in anterior (n = 23) nor in inferior (n = 17) MI were rank correlations found between the haemodynamic parameters (cardiac index, mean arterial pressure, mean right atrial or pulmonary capillary pressures, right or left ventricular work indices) and sodium balance. However, the sodium balances correlated with the total creatine kinase (CK) release in anterior MI after 1 day (r = 0.60; P less than 0.002) and after 4 days (r = 0.65; P less than 0.001) but not in inferior MI. Furthermore, in anterior and inferior MI matched for their CK release, the sodium handling was different both after 1 day (-70 in anterior v. +44 mmol (24 h)-1 in inferior MI; P less than 0.001) and after 4 days (-36 v. +147 mmol (72 h)-1; P less than 0.01), a difference unexplained by differences in medical management or in sodium intake. Finally, sodium balance correlated with the changes in left ventricular stroke work index (LVSWI) observed during this period (r = 0.48, P less than 0.001), LVSWI being more stable when sodium balance was more positive. In conclusion, sodium balance after uncomplicated acute MI is related to MI location, to the size of anterior MI, and cannot be predicted from initial haemodynamics. Finally, the relation between LVSWI stability and positive sodium balance suggests that arbitrary sodium restrictions or diuretics might be deleterious to the haemodynamics after uncomplicated myocardial infarction.

Adult↗
PubMed1984

Assessment of regional left ventricular relaxation in patients with coronary artery disease: importance of geometric factors and changes in wall thickness.

To assess local myocardial relaxation abnormalities in patients with coronary artery disease, local myocardial left ventricular wall stress was computed in nine normal subjects and in 22 patients with coronary artery disease. In normal left ventricles, the rate of decrease in isovolumic local stress was not significantly different from the rate of decrease in isovolumic pressure, and the residual wall stress at the end of isovolumic relaxation was uniformly low. In patients with coronary artery disease, the residual wall stress was increased both in infarcted areas and in non-infarcted areas perfused by stenosed arteries (43 +/- 31 and 30 +/- 19 kdyne/cm2, respectively, vs 9 +/- 5 kdyne/cm2 in normal areas; p less than .001). The rate of decrease in local stress in infarcted areas paralleled the rate of decrease in pressure (48 vs 49 msec; NS), but in ischemic areas the rate of decrease in stress was significantly slower than the rate of decrease in pressure (69 +/- 35 vs 48 +/- 15 msec; p less than .05). It is concluded that in patients with coronary artery disease, indexes based only on the analysis of decreases in isovolumic pressure underestimate the severity of local impairments in relaxation rate and cannot be used to predict the level of residual diastolic wall stress.

Adult↗
PubMed1983

Force-velocity-length relations in hypertrophic cardiomyopathy: evidence of normal or depressed myocardial contractility.

To assess myocardial contractility in patients with hypertrophic cardiomyopathy (HC), force-velocity-length relations were analyzed during left ventricular (LV) ejection. LV pressure, volume and wall stress data in 15 patients with HC were analyzed and compared with values from 32 normal subjects. Patients with HC had a greater LV mass than did normal subjects (272 versus 96 g/m2, p less than 0.001), elevated LV end-diastolic pressure (17.5 versus 9.8 mm Hg, p less than 0.01) and impaired LV relaxation compared with those of normal subjects. Patients with HC also had a greater ejection fraction (84 +/- 7 versus 74 +/- 8%, p less than 0.01) and mean velocity of shortening than did normal subjects. However, in patients with HC, end-systolic stress (60 +/- 29 versus 187 +/- 61 kdyne/cm2, p less than 0.001) was significantly lower. End-systolic volume and stress data were linearly related in normal subjects (r = 0.88), and values from patients with HC fell either within the lowest part of the 95% confidence interval of this normal relation or outside it in the zone of depressed contractility (11 patients with HC). In addition, the slopes of the relations between end-systolic wall stress and ejection fraction or mean velocity of shortening were abnormal in patients with HC; the slope of the stress-volume trajectory during late ejection was also depressed in 12 patients with HC (average slope 2.6 versus 5.5 kdyne/cm5/m2, p less than 0.001). Thus, there is no evidence of a hypercontractile state in patients with HC; their high values of ejection phase indexes may be explained by a reduction in myocardial afterload.

Adolescent↗
PubMed1978

Significance of pulmonary input impedance in right ventricular performance.

Right ventricular adaptation to changes in pulmonary input impedance was studied in open-chest dogs. When identical increases in pulmonary vascular resistance are imposed by two different manoeuvres (lung inflation and clamping of the left pulmonary artery), external power and pressure-time integral of the right ventricle at similar filling pressure are always greater during clamping than during inflation. Further studies demonstrate that, at equal increases in pulmonary input impedance modulus at 0 Hz, the clamping produces a greater change in the sum of the first three harmonics of impedance than the inflation (respectively +77% and -10% vs control modulus; -82% and +8% vs control phase). These impedance changes could explain the different behaviour of the right ventricle either by better matching of the ventricular internal impedance or by functional modification of the outflow tract.

Animals↗