The effect of exercise-induced myocardial ischemia on postischemic left ventricular diastolic filling.

To determine whether exercise-induced ischemia impairs left ventricular diastolic filling in the postischemic period in humans, 101 men (mean age 57 +/- 10 years) were studied before and 2 h after a symptom-limited thallium-201 tomographic treadmill with pulsed Doppler echocardiography of mitral valve inflow. In the postischemic period 2 h after exercise, diastolic filling was significantly impaired in the ischemia group (reversible thallium defect; n = 24) as reflected by a decrease in the peak early filling velocity (44.5 +/- 10.1 to 39.9 +/- 9.9 cm/s, p less than 0.01), peak early to atrial filling velocity ratio (0.91 +/- 0.27 to 0.76 +/- 0.25, p less than 0.001), and deceleration rate of early filling (281 +/- 104 to 245 +/- 86 cm/s2, p less than 0.01). Similar alterations in the postischemic period occurred in the myocardial infarction-ischemia group (partially reversible defect; n = 28) as seen by a decrease in the peak early filling velocity (47.6 +/- 11.6 to 41.8 +/- 12.0 cm/s, p less than 0.001), peak early to atrial filling velocity ratio (0.84 +/- 0.21 to 0.68 +/- 0.18, p less than 0.001), and early time-velocity integral (7.06 +/- 1.78 to 5.64 +/- 2.07 cm, p less than 0.001). In the control group (no defects; n = 33) and myocardial infarction group (fixed defect; n = 16), diastolic filling was unchanged in the postexercise period. Heart rate and blood pressure were unchanged post-exercise in all groups. Exercise-induced ischemia impairs diastolic filling in the postischemic period in humans.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of preload reduction on mitral flow velocity pattern in normal subjects

In the last few years, alterations in transmitral diastolic flow pattern have been used to assess changes in left ventricular diastolic properties. However, since diastolic flow primarily reflects the atrioventricular pressure gradient, loading conditions, as well as intrinsic left ventricular properties, should be able to affect this pattern. This study was selectively designed to decrease preload (a major determinant of the atrioventricular pressure gradient) in normal subjects to observe the effects on the Doppler transmitral flow pattern without pharmacologic interventions that may also affect left ventricular diastolic properties. In 12 normal subjects, preload was reduced by inflation of blood pressure cuffs placed at the level of the root of the 4 limbs. The peak velocity of early mitral flow (E wave) decreased from 62 +/- 8 to 51 +/- 7 cm/s (p less than 0.001), while no changes were found in the maximal velocity after atrial contraction; this caused a significant decrease in the ratio of these 2 velocities (the E to A ratio) from 1.5 +/- 0.3 to 1.1 +/- 0.1 (p less than 0.001). The time-velocity integral of early diastolic inflow decreased from 7.8 +/- 1.3 to 6.1 +/- 1.3 cm (p less than 0.001) with no significant changes of the time-velocity integral of inflow after atrial contraction. Therefore, preload reduction in normal subjects significantly reduces transmitral flow in early diastole with preserved late ventricular filling, producing a pattern that can mimic the changes previously described in left ventricular diastolic dysfunction.     

The effect of premature ventricular contraction on left ventricular relaxation, chamber stiffness, and filling in humans

To investigate the influence of single spontaneous premature ventricular ectopic beats on left ventricular contraction, relaxation, chamber stiffness, and filling, we examined 21 patients with simultaneous micromanometer left ventricular pressure tracings and echocardiograms. Instantaneous left ventricular diameter and mitral valve inflow velocity were obtained by using of M-mode and pulsed Doppler echocardiography, respectively. The isovolumic relaxation time constants (TL and TD) were calculated by mean of a zero (TL) and variable (TD) asymptote pressure. The chamber stiffness constants were derived from the diastolic pressure-diameter (kd) and pressure-volume (kv) relationships. The extrasystolic beat was associated with marked impairments of relaxation, systolic function, and diastolic filling as seen by an increased TL (53 to 71 msec; p less than 0.001), TD (59 to 89 msec; p less than 0.005), time from maximum negative dp/dt to the lowest diastolic pressure (147 to 170 msec; p less than 0.05), and decreased number of elasped TDs (3.1 to 2.4; p less than 0.05), end-systolic pressure-diameter ratio (2.4 to 1.7; p less than 0.001), maximum positive dp/dt (1904 to 1326 mm Hg/sec; p less than 0.001), shortening fraction (31% to 21%; p less than 0.001), and peak early filling velocity (59 to 49 cm/sec; p less than 0.001). Chamber stiffness constants were unchanged. Relaxation and chamber stiffness were unchanged during the postextrasystolic beat as reflected by TL, TD, maximum negative dp/dt, and kd and kv.(ABSTRACT TRUNCATED AT 250 WORDS)     

Dynamic determinants of left ventricular early diastolic filling in old myocardial infarction.

The determinants of left ventricular early diastolic filling were assessed in 15 patients with old myocardial infarction. The left atrial pressure (LAP) and left ventricular pressure (LVP) were simultaneously measured by a Millar's multisensor micromanometer with the pusled Doppler mitral inflow velocity at baseline and during angiotensin infusion (20 ng/kg/min). Cardiac output was measured by a thermodilution method. LV peak systolic pressure and end-diastolic pressure were significantly (p less than 0.001) increased during angiotensin infusion from 137 +/- 19 to 170 +/- 21 mmHg and from 13.3 +/- 5.9 to 20.4 +/- 6.2 mmHg, respectively. Cardiac index was significantly decreased during angiotensin infusion. Heart rate, diastolic time, and peak positive dP/dt were unchanged. Although the LA-LV peak pressure gradient[(LAP-LVP) max] was unchanged (from 2.8 +/- 1.0 to 3.0 +/- 1.4 mmHg), the pressure gradient interval (the interval between the first and second points of transmitral pressure crossover) was significantly (p less than 0.001) decreased from 154 +/- 38 to 117 +/- 26 msec during angiotensin infusion. Peak early diastolic mitral inflow velocity (peak E) and the time-velocity integral of E wave (Ei) were significantly decreased during angiotensin infusion from 51 +/- 10 to 45 +/- 11 cm/sec (p less than 0.002) and from 7.47 +/- 1.96 to 5.70 +/- 1.66 cm (p less than 0.001), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic function: comparison of pulsed Doppler echocardiographic and hemodynamic indexes in subjects with and without coronary artery disease

To evaluate the influence of left ventricular chamber stiffness and relaxation on Doppler echocardiographic indexes of diastolic function, 35 patients (mean age 60 +/- 12 years) were examined; 24 had coronary artery disease and 11 (Group I) had no cardiovascular disease. Micromanometer left ventricular pressure was recorded simultaneously with Doppler echocardiograms of mitral valve inflow and M-mode echocardiograms of left ventricular diameter. The chamber stiffness constant (k) was derived from the pressure-diameter relation. Relaxation was assessed by the isovolumic relaxation time constant (tau) derived from the exponential left ventricular pressure decay. The patients with coronary artery disease were classified into two groups on the basis of complete (Group II; n = 10) and incomplete (Group III; n = 14) relaxation. In Group I (no coronary disease), significant correlations were demonstrated between the chamber stiffness constant and the peak early filling velocity (r = 0.73; p less than 0.02), peak early to atrial filling velocity ratio (r = 0.82; p less than 0.005), atrial time-velocity integral (r = -0.73; p less than 0.02), early to atrial time-velocity integral ratio (r = 0.70; p less than 0.05), percent atrial contribution to filling (r = -0.64; p less than 0.05) and one-half filling fraction (r = 0.73; p less than 0.02). In Group II (coronary disease with complete relaxation), the chamber stiffness constant correlated with peak early filling velocity (r = 0.68; p less than 0.05), early filling time-velocity integral (r = 0.65; p less than 0.05) and early to atrial time-velocity integral ratio (r = 0.74; p less than 0.02). No correlations between k and Doppler indexes were found in Group III (coronary disease with incomplete relaxation). However, Group III demonstrated significant correlations between tau and the peak early filling velocity (r = -0.71; p less than 0.005), percent atrial contribution to filling (r = 0.56; p less than 0.05) and mean acceleration rate of early filling (r = -0.79; p less than 0.002). Thus, in subjects with normal relaxation, increasing chamber stiffness was associated with an enhanced peak early filling velocity and volume and decreased filling during atrial systole. This finding differs strikingly from the proposed influence of chamber stiffness on diastolic filling postulated by several researchers.(ABSTRACT TRUNCATED AT 400 WORDS)     

Left ventricular diastolic reserve during acute pressure loading in hypertrophic cardiomyopathy and dilated cardiomyopathy

To evaluate left ventricular diastolic reserve during acute pressure loading, changes in mitral flow velocity patterns before and after the elevation of blood pressure were analyzed by pulsed Doppler echocardiography in 11 cases of hypertrophic cardiomyopathy (HCM), nine cases of dilated cardiomyopathy (DCM), and 11 control subjects. Systolic blood pressure was elevated 25% above basal values by methoxamine infusion (0.01 mg/kg/min). Before and after methoxamine, left ventricular dimension and mitral flow velocity pattern were obtained by M-mode and pulsed Doppler echocardiography, respectively. The peak velocity in the rapid filling and atrial contraction phases and time-velocity integrals were measured from the flow pattern. After methoxamine, left ventricular diastolic dimension was significantly increased in all groups, from 43.8 +/- 4.7 mm to 47.4 +/- 4.9 mm in the control subjects, from 43.7 +/- 6.3 mm to 47.2 +/- 6.0 mm in HCM, and from 57.9 +/- 6.4 mm to 60.6 +/- 5.9 mm in DCM. Left ventricular systolic dimension was significantly increased from 48.6 +/- 8.4 mm to 52.8 +/- 8.3 mm in DCM, but not in the control subjects or HCM. The peak velocity in the rapid filling phase was significantly increased from 60 +/- 16 cm/sec to 69 +/- 14 cm/sec in the control subjects and tended to be increased from 44 +/- 13 cm/sec to 52 +/- 12 cm/sec in HCM. The extent of this increase tended to be less in HCM. However, the peak velocity in the rapid filling phase tended to decrease in DCM. There were no consistent trends of changes in the peak velocity in the atrial contraction phase in any groups. The mitral velocity integral increased from 502 Hz-sec to 621 Hz-sec in the controls and from 525 Hz-sec to 613 Hz-sec in HCM, but it did not increase in DCM. These findings suggest that there is impaired diastolic reserve during acute pressure loading in HCM and DCM and that the diastolic disturbance might be reflected in the early diastolic phase, rather than in the late diastolic phase.     

Influence of postural change on transmitral flow velocity profile assessed by pulsed Doppler echocardiography in normal individuals and in patients with myocardial infarction

The influence of postural change from lying to sitting on transmitral flow velocity profile was investigated by pulsed Doppler echocardiography in eight normal individuals and in eight patients with myocardial infarction. The postural change decreased early and atrial filling velocities in the normal individuals (61 +/- 10 to 49 +/- 7 cm/sec and 66 +/- 8 to 55 +/- 7 cm/sec, p less than 0.01, respectively), and also decreased early filling but increased atrial filling velocity in the eight patients (62 +/- 13 to 43 +/- 12 cm/sec and 56 +/- 11 to 65 +/- 14 cm/sec, p less than 0.01 and p less than 0.05, respectively). These changes were associated with a reduction in pulmonary artery wedge pressure in the normal subjects and in the patients (5 +/- 2 to 2 +/- 2 mm Hg and 12 +/- 4 to 8 +/- 3 mm Hg, p less than 0.01, respectively). These observations indicate that a preload reduction alters the left ventricular diastolic filling profile. The differences in Doppler alterations between the groups may be attributed to the fundamental differences in intrinsic left ventricular diastolic properties of normal subjects and patients with myocardial infarction.     

Immediate and short-term effects of aortic balloon valvuloplasty on left ventricular diastolic function and filling in humans

The effect of aortic balloon valvuloplasty on left ventricular diastolic function and filling was investigated in 44 adult patients with severe aortic stenosis. Two-dimensional and Doppler echocardiography was performed in all patients before and 24 h after valvuloplasty. In 19 patients (short-term group) repeat studies were performed at 3 (n = 2) and 6 (n = 17) months. Left ventricular relaxation, chamber stiffness and filling were assessed in 16 patients (immediate post-valvuloplasty group) before and immediately after valvuloplasty by simultaneous micromanometer left ventricular pressure tracings and echocardiograms. Immediately after valvuloplasty, relaxation was slightly impaired in the immediate post-valvuloplasty group, as reflected by the isovolumic relaxation time constant (56 +/- 26 to 68 +/- 39 ms; p less than 0.01) and maximal negative dP/dt (2,063 +/- 640 to 1,767 +/- 495 mm Hg/s; p less than 0.001). The chamber stiffness constants and diastolic filling dynamics were unchanged immediately after valvuloplasty. Twenty-four hours after valvuloplasty, patients without mitral regurgitation (n = 24) showed increases in the peak early filling velocity (72 +/- 31 to 83 +/- 28 cm/s; p less than 0.05) and peak early to atrial filling velocity ratio (0.8 +/- 0.6 to 1.0 +/- 0.7; p less than 0.05). However, in patients with mitral regurgitation (n = 20), the diastolic filling dynamics were not significantly changed. In the short-term group at the 3 to 6 month follow-up period, patients without mitral regurgitation (n = 12) showed striking increases compared with pre-valvuloplasty values in the peak early filling velocity (66 +/- 21 to 93 +/- 31 cm/s; p less than 0.02), peak early to atrial filling velocity ratio (0.6 +/- 0.2 to 0.9 +/- 0.4; p less than 0.02) and early time-velocity integral (9 +/- 4 to 16 +/- 6 cm; p less than 0.002). In patients with mitral regurgitation (n = 7) decreases occurred in the peak early filling velocity (123 +/- 32 to 106 +/- 28 cm/s; p less than 0.05) and peak early to atrial filling velocity ratio (1.5 +/- 0.7 to 1.1 +/- 0.6; p less than 0.05). Functional class in hospital improved after valvuloplasty (3.1 +/- 1.0 to 2.6 +/- 0.9; p less than 0.001) and correlated modestly with the percent decrease in Doppler-derived peak gradient (rs = 0.41, p less than 0.02) and mean gradient (rs = 0.36, p less than 0.05), but did not correlate with changes in aortic valve area, left ventricular ejection fraction or diastolic filling variables.(ABSTRACT TRUNCATED AT 400 WORDS)     

Determination of parameters of left ventricular diastolic filling with pulsed Doppler echocardiography: comparison with cineangiography

To determine the relationship between Doppler-derived flow velocity through the mitral anulus and angiographic parameters of left ventricular filling, 30 patients were studied by two-dimensional echocardiography combined with pulsed Doppler echocardiography followed within 1 hr by left ventricular angiography. The average heart rate for each test was 69 beats/min. Doppler-derived parameters included: early peak diastolic velocity (E) and peak atrial velocity, peak filling rate computed as E X cross-sectional area of the mitral anulus derived from the annular diameter, normalized peak filling rate computed as peak filling rate divided by the left ventricular end-diastolic volume determined by two-dimensional echocardiography, and half filling fraction derived from the time-velocity integral of the Doppler-determined velocity curve. Frame-by-frame left ventricular volumes were obtained throughout diastole from single-plane cineangiograms. A volume-time curve with its derivative was generated by computer processing from which peak filling rate, normalized peak filling rate, and half filling fraction were measured. Morphologically, the Doppler-derived velocity profile resembled the derivative of the angiographic volume curve. In patients with reduced angiographic peak filling rates, early peak diastolic velocity was often decreased less than 45 cm/sec with a relative increase in peak atrial velocity resulting in an early peak diastolic velocity to peak atrial velocity ratio less than 1.0. There were no significant differences in mean values for peak filling rate, normalized peak filling rate, and half filling fraction by Doppler echocardiography vs angiography (296 vs 283 ml/sec, 1.9 vs 2.0 sec-1 and 0.55 vs 0.55, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic function in PTCA: a Doppler echocardiographic study

The measurement of left ventricular inflow by Doppler echocardiography provides a continuous, non-invasive assessment of parameters of diastolic function. We studied changes in left ventricular diastolic function during percutaneous transluminal coronary angioplasty (PTCA) of the left anterior descending coronary artery (LAD). In ten patients, the diastolic flow velocity profile across the mitral valve was measured by Doppler echocardiography, before and 60 s after inflation and 60 s after deflation of the balloon. The peak velocity of early diastolic filling (VE) significantly decreased during angioplasty, from 68 +/- 12 to 56 +/- 10 cm/s (p less than 0.001), while the peak velocity of late diastolic filling caused by atrial contraction (VA) showed no change. This resulted in a significant decline in the diastolic velocity ratio (VE/VA) from 1.11 +/- 0.47 to 0.92 +/- 0.35 (p less than 0.01). The total area under the diastolic flow velocity profile representing the total filling volume fell from 14.3 +/- 4.1 to 10.9 +/- 3.6 cm (p less than 0.001). The early diastolic filling fraction decreased from 68 +/- 5% to 64 +/- 7%, in favor of the filling fraction due to atrial contraction, which increased from 32 +/- 5%, to 36 +/- 7% (p less than 0.01). 60 s after deflation of the balloon, the parameters of diastolic filling returned to baseline values. We conclude from our results that diastolic dysfunction caused by angioplasty of the LAD results in a decrease in early diastolic left ventricular filling, which is completely reversible after 60 s.     

Restrictive diastolic abnormalities identified by Doppler echocardiography in patients with thalassemia major

The consequences of transfusional iron overload on left ventricular diastolic filling have never been investigated systematically in patients with thalassemia major. In the present study, the pattern of left ventricular filling was assessed by Doppler echocardiography in 32 patients with thalassemia major (age, 17 +/- 5 years) who had not experienced symptoms of heart failure and had normal left ventricular systolic function. Data were compared with those obtained in 32 age-matched and sex-matched normal subjects. An abnormal Doppler pattern of left ventricular filling with increased flow velocity at mitral valve opening followed by an abrupt and premature decrease of flow velocity in early diastole was identified in the patients with thalassemia. Peak flow velocity in early diastole was increased in patients compared with controls (90 +/- 10 vs. 81 +/- 15 cm/sec; p less than 0.01), and rate of deceleration of flow velocity after the early diastolic peak and the ratio between the early and late (atrial) peaks of flow velocity were also increased (1,050 +/- 325 vs. 762 +/- 193 cm/sec2 and 2.7 +/- 0.7 vs. 2.2 +/- 0.5, respectively; p less than 0.001), whereas flow velocity deceleration time was reduced (97 +/- 22 vs. 119 +/- 19 msec; p less than 0.001). This Doppler pattern of diastolic filling is usually described as "restrictive" and reflects a decrease in left ventricular chamber compliance. A restrictive pattern of left ventricular filling was also identified in the subgroup of 16 study patients who had undergone optimal iron chelation therapy with deferoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of Doppler-derived left ventricular diastolic filling variables in dilated cardiomyopathy.

To determine the prognostic significance of pulsed wave Doppler-derived left ventricular diastolic filling velocity profiles and the relationship between Doppler variables and clinical functional status, the follow-up outcomes of 62 consecutive patients with dilated cardiomyopathy and symptoms of left ventricular dysfunction were analyzed. All patients had echocardiographic left ventricular end-diastolic dimension > or = 6.0 cm, fractional shortening < 25%, increased E pointseptal separation, and diffuse hypokinesia or akinesia. During a mean follow-up period of 30.5 +/- 13.9 months, 27 patients experienced cardiac events: 23 died of either progressive pump failure or an episode of sudden death and four required cardiac transplantation because of refractory heart failure. Peak early filling velocity (78 +/- 23 cm/sec vs 65 +/- 25 cm/sec; p < 0.03) was higher and late atrial filing velocity (34 +/- 13 cm/sec vs 55 +/- 19 cm/sec; p < 0.001) was lower in patients with cardiac events than in cardiac event-free survivors. The ratio of early to late transmitral filling velocities was higher (2.6 +/- 1.2 vs 1.5 +/- 1.3; p < 0.001), and the deceleration time of early diastole was shorter (133 +/- 48 msec vs 175 +/- 71 msec; p < 0.001) in patients with cardiac events. The cardiac event rate was significantly higher in patients with an early to late filling velocity ratio greater than 2 (77% vs 19%; p < 0.001) or a deceleration time less than 150 msec (58% vs 23%; p < 0.05) than in those without. Stepwise multivariate regression analysis revealed that the pattern of transmitral early to late filling velocity ratio was the only significant independent Doppler echocardiographic predictor of outcome for these patients. Repeat Doppler echocardiographic examinations, which were performed in 31 survivors after intensive treatment (mean, 38.6 +/- 6.5 months), showed that early filling velocity was decreased (55 +/- 20 cm/sec vs 75 +/- 25 cm/sec; p < 0.02), late atrial filling velocity was increased (74 +/- 27 cm/sec vs 57 +/- 21 cm/sec; p < 0.01), early to late filling velocity ratio was reduced (0.8 +/- 0.3 vs 1.7 +/- 1.3; p < 0.001), and deceleration time was prolonged (227 +/- 60 msec vs 167 +/- 82 msec; p < 0.01) in 18 patients with clinical functional improvement, whereas these measurements were unaltered in the remaining 13 patients whose functional status was unchanged or had deteriorated.(ABSTRACT TRUNCATED AT 400 WORDS)     

Diastolic abnormalities in young asymptomatic diabetic patients assessed by pulsed Doppler echocardiography

Indexes of left ventricular diastolic filling were measured by pulsed Doppler echocardiography in 21 insulin-dependent diabetic patients and 21 control subjects without clinical evidence of heart disease. No patient had chest pain or electrocardiographic changes during exercise testing. The mean age of patients was 32 years. All patients had a normal ejection fraction. Six (29%) of the 21 diabetic patients had evidence of diastolic dysfunction as assessed by the presence of at least two abnormal variables of mitral inflow velocity. The ratio of peak early to peak late (atrial) filling velocity was significantly decreased in diabetic compared with control subjects (1.24 +/- 0.21 versus 1.66 +/- 0.30, p. less than 0.001). Atrial filling velocity was significantly increased in diabetic patients (74.3 +/- 16.7 versus 60.3 +/- 12.2 cm/s, p less than 0.004), whereas early filling velocity was reduced by a nearly significant degree (88.8 +/- 12.6 versus 98.5 +/- 18.8 cm/s, p less than 0.057). The atrial contribution to stroke volume as assessed by area under the late diastolic filling envelope compared to total diastolic area was also significantly increased in diabetic compared with control subjects (35 versus 27%, p less than 0.001). Left ventricular diastolic filling abnormalities in diabetic patients did not correlate with duration of diabetes, retinopathy, nephropathy or peripheral neuropathy. These data suggest that approximately one-third of such patients have subclinical myocardial dysfunction unrelated to accelerated atherosclerosis. Doppler echocardiography may offer a reliable noninvasive means to assess diastolic function and to follow up diabetic patients serially for any deterioration in cardiac status before the appearance of clinical symptoms.     

Influence of short atrioventricular delay on late diastolic transmitral flow and stroke volume.

Atrial transport function and the corresponding transmitral flow and stroke volume depend on the timing of atrial contraction. To study the influence of short atrioventricular delay (AVD) on these hemodynamic parameters, transmitral flow velocity (by pulsed wave Doppler) and aortic flow (by electromagnetic technique) were studied and compared (paired t test) during normal and short AVD at fixed rate DDD pacing (80 bpm) in AV-blocked, open-chest canine preparations (n:16). The short AVD resulted in a shorter acceleration (difference 4.1 +/- 4.9 msec, mean +/- SD, p less than 0.05), a lower peak velocity (difference: 7.1 +/- 3.2 cm/sec, p less than 0.001), a shorter (difference: 26.9 +/- 16.2 msec, p less than 0.001) and more rapid deceleration (difference: 220.7 +/- 291.7 cm/sec2, p less than 0.005) of the late diastolic transmitral flow elicited by atrial systole. Stroke volume decreased (7.8 +/- 5.2%, p less than 0.001) during short AVD as a consequence of a reduced left ventricular filling due to the interruption of the active atrial transport by the onset of the ventricular contraction.     

Age-related alterations of Doppler left ventricular filling indexes in normal subjects are independent of left ventricular mass, heart rate, contractility and loading conditions

The purpose of this study was to determine whether age-related alterations in Doppler diastolic filling indexes occur independent of cardiovascular disease and confounding physiologic variables. Ten old (62 to 73 years) and 10 young (21 to 32 years) healthy male volunteers were rigorously screened for cardiovascular disease and underwent comprehensive Doppler echocardiography, radionuclide ventriculography and invasive measurements of right heart and left atrial pressures. There were no differences between the two groups in the physiologic variables of left ventricular mass, volumes, ejection fraction, end-systolic wall stress, left atrial size, heart rate and right atrial, pulmonary artery, pulmonary capillary wedge and systemic arterial pressures. However, there were marked differences in Doppler left ventricular filling indexes. Compared with the young group, the old group had reduced peak early diastolic flow velocity (56 +/- 13 vs. 82 +/- 12 cm/s, p = 0.0002) and increased atrial diastolic flow velocity (59 +/- 14 vs. 43 +/- 10 cm/s, p = 0.009) and had a peak atrial/early flow velocity (A/E) ratio twice that of the young group (1.09 +/- 0.29 vs. 0.54 +/- 0.15, p less than 0.0001). Similar results were obtained for the time-velocity integrals of the peaks. Subjects in the old group also had a markedly reduced peak filling rate (274 +/- 62 vs. 448 +/- 152 ml/s, p = 0.004). In univariate and multivariate regression analyses, peak early and atrial flow velocities were not related to any of the physiologic variables measured once age was accounted for, although peak filling rate, a volumetric measure flow, was related to body surface area as well as age.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler echocardiographic evaluation of left ventricular diastolic function in patients with systemic lupus erythematosus

Subclinical myocardial involvement frequently occurs in patients with systemic lupus erythematosus (SLE). In this study, left ventricular diastolic function was assessed in 58 patients (54 female and 4 male; mean age 32 +/- 11 years) and in 40 sex-matched and age-matched healthy control subjects (37 female and 3 male; mean age 33 +/- 9 years) by means of pulsed Doppler echocardiography. All subjects had no clinical evidence of overt myocardial disease or abnormal left ventricular systolic function. Compared with the control group, patients with SLE had significantly prolonged isovolumic relaxation time (62 +/- 12 vs 80 +/- 14 msec; p less than 0.01), reduced peak early diastolic flow velocity (peak E) (82 +/- 18 vs 76 +/- 16 cm/sec; p less than 0.05), increased peak late diastolic flow velocity (peak A) (45 +/- 7 vs 53 +/- 8 cm/sec; p less than 0.01), reduced E/A ratio (1.81 +/- 0.32 vs 1.46 +/- 0.29; p less than 0.001), and lower deceleration rate of early diastolic flow velocity (EF slope) (489 +/- 151 vs 361 +/- 185 cm/sec2; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

The transmitral pressure-flow velocity relation. Effect of abrupt preload reduction

Although recent animal and clinical studies suggest that Doppler-derived indexes may be useful for the characterization of ventricular diastolic behavior, the hemodynamic basis for the preload dependency of these indexes has not previously been fully elucidated. Accordingly, effects of reduction of left atrial load on the pressure-flow velocity relation were characterized in 10 anesthetized, closed-chest dogs during transient inferior vena caval occlusion by means of simultaneously recorded left atrial and left ventricular micromanometric pressure measurement and transesophageal Doppler echocardiograms. Within four or five beats after inferior vena caval balloon occlusion, left atrial loading was reduced as evidenced by a decrease in the slope of the left atrial v wave from 21 +/- 4 to 13 +/- 4 mm Hg/sec (p less than 0.001) and by a decrease in the first crossover point of left atrial and left ventricular pressures from 5.6 +/- 1.1 to 2.9 +/- 1.5 mm Hg (p less than 0.001). This decrease in left atrial loading resulted in reductions during early diastole of minimum left ventricular pressure (from 1.0 +/- 0.8 to -0.4 +/- 1.2 mm Hg, p less than 0.001), the maximum early forward (i.e., left atrial pressure greater than left ventricular pressure) transmitral pressure gradient (from 2.8 +/- 0.8 to 2.4 +/- 0.5 mm Hg, p less than 0.01); the slope of the rapid filling pressure wave (from 44 +/- 11 to 38 +/- 10 mm Hg/sec, p less than 0.025); and the area of the reversed (i.e., left ventricular pressure greater than left atrial pressure) transmitral pressure gradient (from 79 +/- 42 to 53 +/- 33 mm Hg.msec, p less than 0.05). During late diastole, both the heights and slopes of the left atrial and left ventricular a waves fell, resulting in a decrease in the maximum late transmitral pressure gradient (from 1.2 +/- 0.7 to 0.9 +/- 0.5 mm Hg, p less than 0.05). Vena caval occlusion also altered Doppler transmitral velocity profiles during both the early and late phases of diastole. Peak velocity of the E wave decreased (from 50 +/- 11 to 41 +/- 7 cm/sec, p less than 0.01) as did acceleration (from 880 +/- 222 to 757 +/- 258 cm/sec2, p less than 0.025) and deceleration (from 597 +/- 260 to 429 +/- 197 cm/sec2, p less than 0.025). Peak velocity of the A wave also fell (from 29 +/- 9 to 22 +/- 5 cm/sec, p less than 0.005). Abrupt inferior vena caval occlusion did not significantly change heart rate or mean aortic pressure.(ABSTRACT TRUNCATED AT 400 WORDS)     

Pattern of left ventricular diastolic filling associated with right ventricular enlargement

Right ventricular (RV) dilatation associated with pressure overload may alter left ventricular (LV) geometry resulting in abnormal diastolic function as demonstrated by a smaller LV diastolic volume for a given LV diastolic pressure. To determine whether abnormalities in LV geometry due to RV dilatation result in abnormalities in the LV diastolic filling pattern, we obtained pulsed Doppler transmitral recordings from 23 patients with RV dilatation with RV systolic pressure estimated to be less than 40 mm Hg (group 1), 18 patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg (group 2) and 33 normal patients. RV systolic pressures were estimated from continuous wave Doppler peak tricuspid regurgitation velocities using the modified Bernoulli equation. Diastolic filling parameters in group 1 patients were similar to normals. In group 2 patient, increased peak atrial filling velocity (76 +/- 14 vs 57 +/- 12 cm/s, p less than 0.001), decreased peak rapid filling velocity/peak atrial filling velocity (1.1 +/- 0.4 vs 1.5 +/- 0.4, p less than 0.01), increased atrial filling fraction (41 +/- 14 vs 30 +/- 10%, p less than 0.01) and prolongation of the atrial filling period (171 +/- 47 vs 152 +/- 39 ms, p less than 0.05) were noted compared with the normal group. RV end-diastolic size and LV end-systolic shape were significantly correlated with the atrial filling fraction in group 2 patients. In patients with RV dilatation and RV systolic pressures greater than or equal to 40 mm Hg, there is increased reliance on atrial systolic contribution to the LV filling volume.     

Pulmonary venous flow dynamics before and after balloon mitral valvuloplasty as determined by transesophageal Doppler echocardiography.

The pattern of left atrial filling was studied in 14 patients with severe mitral stenosis in sinus rhythm before and immediately after successful balloon mitral valvuloplasty by transesophageal pulsed Doppler echocardiography of the left superior pulmonary vein. Mean mitral valve orifice area increased from 0.8 +/- 0.1 to 2.2 +/- 0.3 cm2 (p less than 0.0001), and left atrial mean pressure decreased from 30 +/- 5 to 12 +/- 4 mm Hg (p less than 0.0001) after the procedure. After balloon mitral valvuloplasty, significant increases in peak systolic pulmonary velocity (35 +/- 16 to 44 +/- 10 cm/s; p less than 0.01), systolic flow velocity time integral (3.3 +/- 1.5 to 5.9 +/- 2.0 cm; p less than 0.001) and the ratio of systolic/diastolic pulmonary venous flow velocity time integrals (0.8 +/- 0.4 to 1.4 +/- 0.5; p less than 0.001) were observed. An acute increase in mitral valve orifice area caused no significant changes in peak diastolic forward flow velocity (40 +/- 7 to 41 +/- 9 cm/s; p = not significant [NS]), diastolic forward flow velocity time integral (4.3 +/- 1.7 to 4.6 +/- 1.8 cm; p = NS) and atrial flow reversal velocity (30 +/- 3 to 35 +/- 3 cm/s; p = NS) compared with at baseline. The results suggest that in patients with severe mitral stenosis and sinus rhythm, left atrial filling is biphasic with a diastolic preponderance, and successful mitral valvuloplasty is associated with an immediate increase in pulmonary venous systolic forward flow.     

Abnormalities of diastolic filling of the left ventricle associated with aging are less pronounced in exercise-trained individuals.

To determine whether exercise training has an effect on left ventricular diastolic dysfunction associated with the normal aging process, we studied a group of 20 normal healthy adult distance runners (mean miles currently run per week was 45 for an average of 15 years) and 20 normal healthy sedentary individuals (who currently walk less than 1 mile per day and are not involved in a regular exercise program) matched for age and systolic and diastolic blood pressure with the runners. Doppler echocardiographic indices of left ventricular diastolic filling were significantly different between the two groups. The exercise group when compared with the sedentary group had significantly decreased late diastolic peak filling velocity (0.51 +/- 0.11 m/sec versus 0.66 +/- 0.20 m/sec; p = 0.003), late diastolic velocity-time integral (5.2 +/- 1.5 cm versus 6.6 +/- 2.2 cm; p = 0.02), increased early-to-late peak filling velocity ratio (1.29 +/- 0.38 versus 0.96 +/- 0.24; p = 0.001), and early-to-late velocity-time integral ratio (2.08 +/- 0.51 versus 1.42 +/- 0.47; p less than 0.001). We conclude that the left ventricular diastolic dysfunction associated with "normal" aging is less pronounced in those persons who are exercise-trained.