Assessment of left ventricular filling by echocardiography in normal subjects and in subjects with coronary artery disease and with asymmetric septal hypertrophy

• Published in: Acta cardiologica Vol. 34; no. 1; p. 11
• Main Authors: Decoodt, P, Mathey, D, Swan, H J
• Format: Journal Article
• Language: English
• Published: England 1979
• Subjects: Adult; Aged; Cardiac Volume; Cardiomegaly - physiopathology; Compliance; Coronary Disease - physiopathology; Echocardiography - methods; Female; Heart Ventricles - physiopathology; Humans; Male; Middle Aged; Myocardial Contraction; Ventricular Function
• ISSN: 0001-5385

To examine the time course of left ventricular filling, a computerized analysis of echocardiograms was performed in 16 normal subjects, 10 patients with coronary artery disease (CAD) but no cardiac enlargement and 7 patients with asymmetric septal hypertrophy (ASH). After hand-controlled digitization of the echocardiogram, a plot of the left ventricular diameter time-curve demonstrated separate phases of rapid filling, slow filling and atrial contribution. The left ventricular diameter at end-systole and at the end of the three diastolic phases was determined by pattern analysis of the diameter-time curve. On analysis of successive beats in the normals, the coefficient of variation for each of these four values of the left ventricular diameter was less than +/- 5%. Between CAD, ASH and normals there was no significant difference in left ventricular end-diastolic diameter, nor in the extent and percentage of diameter shortening during systole. In contrast, abnormalities of the filling pattern were found in CAD and ASH. The maximal rate of diameter lengthening was not different in CAD (13.0 vs 13.7 cm/sec in normals, N.S.) but decreased in ASH (9.3 cm/sec, p less than .01). The percentage of diameter lengthening occurring in the rapid filling phase was decreased in both patient groups (55% in CAD and ASH vs 73% in normals, p less than .001). The slow filling phase did not contribute to more diameter lengthening (13% in CAD and 17% in ASH vs 12% in normals, N.S.). In CAD and ASH, the atrial contribution was markedly increased (33% in CAD and 28% in ASH, vs 15% in normals, p less than .001), and there was a higher rate of diameter lengthening during the atrial contraction (7.6 cm/sec in CAD, p less than .001 and 5.7 cm/sec in ASH, p less than .01, vs 3.1 cm/sec in normals). In conclusion, after computer processing, noninvasive measurements of the left ventricular diameter allows to identify a typical filling pattern in patients with CAD and ASH, consistent with an abnormal compliance of the left ventricle and a compensatory increased atrial contribution.