D J Brown

Left ventricular filling in hypertrophic cardiomyopathy. An angiographic study.

In order to study left ventricular filling in hypertrophic cardiomyopathy, left ventricular cineangiograms of 20 patients were digitised frame by frame and compared with those of 10 normal subjects. Peak left ventricular filling rate was 770+/-260 ml s-1 (mean+/-1 standard deviation), not significantly different from normal. Mitral valve opening was delayed, occurring 140+/-40 ms after time of minimum cavity area, compared with 93+/-14 msec in normals (P less than 0-01), indicating abnormal relaxation. Peak left ventricular filling rate was correlated inversely with this delay (r = 0-69, P less than 0-01), which was greater in patients with angina (155+/-27 ms) than in those without (85+/-23 ms) (P less than 0-01). The rapid filling period was also abnormally prolonged in 8 patients. End-diastolic transverse dimension was normal (5-3+/-0-7 cm) but end-systolic dimension was reduced (2-4+/-0-4 cm) (P less than 0-01) because of abnormal cavity shape. Peak rate of change of dimension during filling (18-7+/-5-3 cm s-1) was greater than normal (11-3+/-3-9 cm s-1) (P less than 0-01), and correlated with peak filling rate (r = 0-82, P less than 0-001). Thus, peak filling rate is normal in hypertrophic cardiomyopathy, but the filling pattern may be abnormal, apparently because of impaired relaxation and abnormal cavity shape rather than mechanical obstruction to inflow.

Echocardiographic features of secondary left ventricular hypertrophy.

Echocardiograms showing left ventricular cavity and mitral valve were recorded and digitised in 100 patients with secondary left ventricular hypertrophy caused by severe hypertension (23), aortic valve stenosis (21), fixed subaortic stenosis (13), and postoperative aortic stenosis (13), or regurgitation (30). Left ventricular dimension and its rate of change were determined and related to mitral valve opening. These values were compared with those from 30 patients with hypertrophic cardiomyopathy. In the patients with secondary left ventricular hypertrophy, cavity size and peak circumferential fibre shortening rate were normal. In diastole, the peak rate of increase of dimension was reduced in 56, and mitral valve opening, normally synchronous with minimum dimension, was delayed in 78, both the result of abnormal left ventricular relaxation. The septal to posterior wall thickness ratio was greater than 1-3 in 40. Values for delay in mitral valve opening were distributed bimodally in the population of patients with secondary left ventricular hypertrophy, with one subgroup in which it was normal and the other in which it was significantly delayed. The distribution of the latter, along with those of values of peak rate of dimension increase and septal to posterior wall thickness ratio were indistinguishable from those in the patients with hypertrophic cardiomyopathy. Abnormalities similar to those of hypertrophic cardiomyopathy therefore occur in patients with secondary left ventricular hypertrophy, and these echocardiographic criteria cannot separate the two conditions.

Study of left ventricular wall thickness and dimension changes using echocardiography.

The relation between transverse left ventricular cavity dimension and posterior wall thickness has been studied using digitised echocardiograms from 10 normal subjects and 63 patients with heart disease. In normal subjects, the peak systolic rate of wall thickening (4.6 ± 1-2 cm/s) is less than the peak diastolic rate of wall thinning (10.7 + 1-7 cm/s). Maximum wall thickness, minimum dimension, and mitral valve opening are synchronous, and there follows a distinct early period of rapid thinning of the wall (100 + 20 ms) which corresponds to the rapid filling period. In ischaemic heart disease the rate and duration of rapid thinning are normal, but the onset precedes mitral valve opening (by 50 + 30 ms). In hypertrophic cardiomyopathy the rate (7 4 + 4-6 cm/s) and pattern of wall thinning are more variable than normal, and closely predict the pattern of change in cavity dimension. Inflow obstruction, associated with slow and protracted increase in cavity dimension, causes the thinning period to be prolonged, but the peak rate of thinning is often not reduced to the same extent as the rate of increase in dimension. This entails reversal of septal movement. We conclude that rapid wall thinning is an intrinsic property of the left ventricular myocardium, normally associated with rapid filling, which may, however, be dissociated from filling by asynchronous relaxation or inflow obstruction, or modified by myocardial disease.

Echocardiographic assessment of left ventricular filling after mitral valve surgery.

In order to investigate the functional effects of mitral valve surgery, echocardiograms showing left ventricular dimension were recorded and digitised in 14 normal subjects and 129 patients after mitral valve surgery. Measurements were made of peak rate of increase of dimension (dD/dt) and duration of rapid filling, studies on left ventriculograms in 36 patients having shown close correlation between these values and changes in cavity volume. In 14 patients with mitral stenosis, peak dD/dt was reduced to 7-2 +/ 1-5 cm/s, and filling period prolonged to 330 +/- 65 ms, compared with normal (16-0 +/- 3-2 cm/s, and 160 +/- 50 ms, respectively), and after mitral valvotomy, these values improved significantly (10-4 +/- 2-7 cm/s and 245 +/- 55 ms). Characteristic abnormalities were found in 67 patients with mitral prostheses. Values for the Björk-Shiley (10-5 +/- 4-2 cm/s and 180 +/- 80 ms) and Hancock (10-3 +/- 3-7 cm/s, 245 +/- 80 ms) values were similar, and both superior to the Starr-Edwards (7-4 +/- 3-0 cm/s, 295 +/- 105 ms). Results after mitral valve repair in 30 cases were not significantly different from normal (14-4 +/- 5-0 cm/s, 170 +/- 50 ms). Values outside the 95 per cent confidence limits for the valve in question allowed diagnosis of value malfunction in 18 cases. The method is value in comparing different operative procedures and in following up patients after mitral valve surgery.

Regional left ventricular wall movement in hypertrophic cardiomyopathy.

Left ventriculograms of 20 patients with hypertrophic cardiomyopathy were digitised frame by frame and analysed using a contour display. Abnormalities of regional wall movement were present in 17, and included an abnormal sequence of inward movement during systole (13), regional delay in the onset of inward movement (10), and an abnormal dispersion of peak velocities (5). Diastolic wall movement was disturbed in 13, because of abnormal peak velocities in 7 and regional asynchrony in 6. Abnormal wall movement during the two isovolumic periods was rare in hypertrophic cardiomyopathy, unlike ischaemic heart disease. These disturbances may reflect underlying structural abnormalities.

Changes in left ventricular free wall thickness in patients with ischaemic heart disease.

Continuous estimates of left ventricular free wall thickness were madefrom angiograms in 10 normal subjects and 20 patients with ischaemic heart disease. The time relations and extent of changes in wall thickness were compared with those in cavity area and transverse dimension, during isovolumic relaxation. In normal subjects, there was a mean reduction in wall thickness at this time of 0-3+c0<1 cm (mean ± 1 standard deviation), but maximum rate of wall thinning occurred after mitral valve opening, during the phase of rapid ventricular filling. In 10 patients with ischaemic heart disease and regions of abnormal outward movement of endocardium during isovolumic relaxation, there was a reduction in wall thickness of 0-8±0<1 cm before mitral valve opening (P<0-001 with respect to normal), with little change during the remainder of diastole. In 4 patients with regions of inward movement of endocardium during isovolumic relaxation, there was an abnormal increase in wall thickness of 0-5±4 0-2 cm at this time (P<0-001 with respect to normal), though the wall behaved normally after mitral valve opening. In 6 patients, endocardial movement and wall thickness changes were normal. It is concluded that changes in left ventricular cavity shape occurring during isovolumic relaxation in patients with coronary artery disease result from abnormal wall thickness changes related to the presence of regional ischaemia.

Detection of abnormal left ventricular wall movement during isovolumic contraction and early relaxation. Comparison of echo- and angiocardiography.

Abnormal left ventricular wall movement during isovolumic contraction and early relaxation was assessed from simultaneous apex and echocardiograms in 50 patients with ischaemic heart disease, and compared with estimates from the corresponding digitised left ventriculograms. During isovolumic contraction, a normal angiogram was accompanied by normal apex-dimension relations in 13 out of 14 cases. In 19 cases, there was angiographic evidence of discrete outward wall movement during isovolumic contraction which was associated with abnormal apex-dimension relations in 15. During isovolumic relaxation, of 14 cases who were normal angiographically, apex-dimension relations were normal also in 11, which in 36 patients with abnormal wall movement on angiogram, apex-dimension relations were abnormal in 30. Correlation was less good between echocardiographic and angiographic estimates of left ventricular minor dimension (r = 0.75), and was absent between those of peak rates of dimension change during systole and diastole. Asynchronous onset of inward wall movement and the distribution of regional abnormalities of overall wall movement amplitude were unrelated to apex-dimension relations. The apex-dimension relation is thus a sensitive and specific means of detecting abnormalities of left ventricular wall movement during isovolumic contraction and early relaxation, unaffected by other manifestation