To determine whether left ventricular (L V) filling dynamics may be influenced by the type of LV morphologi- cal adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (1RT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis ofh/r ratio (h/r). Subgroup 1:16 patients with normal hjr, < 0-42, (five patients with increased L V mass index, > 129-2g m~2, and 11 patients with normal LV mass index, < 129-2 gm~2). Subgroup 2: 14 patients with increased h/r, >0-42, (nine patients with increased LV mass index, > 129-2 gm~2 and five patients with normal L Vmass index, < 129-2gm~2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR. In comparison with the control group, early LV filling was clearly impaired in Subgroup 2, as indicated by the decrease in E ('52±0-12cms'1, P<0-01 vs normals), by the slower deceleration of early flow (112-8 ± 13-8 ms, P < 0001 vs normals) and by the compensatory increase in A and A/E ratio (54 ±01 cms'1, /><001 and 1 08 ± 0-29, ?<0001 respectively vs normals). In Subgroup 1 the minor impairment in early L Vfilling was reflected by the 'normal' valuesfor E and DHT (64 ±0-1 cms~', NS, 97-2 ± 22-4 ms, NS, respectively vs normals), in a state of increased CO, as well as by the increase in A and A/E ratio (58 ±013 cms'1 ,?<001, 0-91 ±0-23, P<001, respectively vs normals). These findings indicate that: (I) in hypertensive patients early L Vfilling dynamics are not uniform but vary in relation to h/r, irrespective of changes in L V mass; (2) early L Vfilling, expressed as E and DHT, is clearly impaired in patients with increased h/r, whereas it is only mildly affected in those with normal h/r; (3) atrial contribution to LV overall filling, expressed as A and A/E is increased in both hypertensive subgroups.
Different patterns of left ventricular filling in arterial hypertension
MELONI, LUIGI;MERCURO, GIUSEPPE;
1990-01-01
Abstract
To determine whether left ventricular (L V) filling dynamics may be influenced by the type of LV morphologi- cal adaptation to arterial hypertension, pulsed Doppler mitral flow velocity recordings were performed in 30 hypertensive patients and in 18 normotensive subjects matched for age, body surface and heart rate. Peak early (E) and late (A) mitral flow velocity, A/E ratio (A/E), time to peak E (TP), acceleration (AHT) and deceleration half-time (DHT) of early mitral flow and isovolumic relaxation time (1RT) were measured. Compared with the control group, hypertensive patients showed prolonged IRT and DHT, increased A and A/E, whereas TP, AHT and E were unchanged. Hypertensive patients were classified into two subgroups on the basis ofh/r ratio (h/r). Subgroup 1:16 patients with normal hjr, < 0-42, (five patients with increased L V mass index, > 129-2g m~2, and 11 patients with normal LV mass index, < 129-2 gm~2). Subgroup 2: 14 patients with increased h/r, >0-42, (nine patients with increased LV mass index, > 129-2 gm~2 and five patients with normal L Vmass index, < 129-2gm~2). In Subgroup 1 the cardiac output (CO) was increased and the total peripheral resistance (TPR) was unchanged in comparison with the control group. In Subgroup 2 the opposite haemodynamic profile was detected: normal CO and increased TPR. In comparison with the control group, early LV filling was clearly impaired in Subgroup 2, as indicated by the decrease in E ('52±0-12cms'1, P<0-01 vs normals), by the slower deceleration of early flow (112-8 ± 13-8 ms, P < 0001 vs normals) and by the compensatory increase in A and A/E ratio (54 ±01 cms'1, /><001 and 1 08 ± 0-29, ?<0001 respectively vs normals). In Subgroup 1 the minor impairment in early L Vfilling was reflected by the 'normal' valuesfor E and DHT (64 ±0-1 cms~', NS, 97-2 ± 22-4 ms, NS, respectively vs normals), in a state of increased CO, as well as by the increase in A and A/E ratio (58 ±013 cms'1 ,?<001, 0-91 ±0-23, P<001, respectively vs normals). These findings indicate that: (I) in hypertensive patients early L Vfilling dynamics are not uniform but vary in relation to h/r, irrespective of changes in L V mass; (2) early L Vfilling, expressed as E and DHT, is clearly impaired in patients with increased h/r, whereas it is only mildly affected in those with normal h/r; (3) atrial contribution to LV overall filling, expressed as A and A/E is increased in both hypertensive subgroups.
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