Echocardiographic criteria of normal left atrial size in adults

Although the measurement of left atrial diameter (LAD) is a standard part of anyechocardiographic examination, the normal range for adults has never been well established or correlated with body surface area (BSA) and sex. We studied 100 males and 100 females whose ages ranged from 15 to 70 years, with no evidence of mitral value disease or other form of heart disease which might cause left atrial enlargement. All measurements were obtained between the external surface of posterior aortic root (AR) and the internal surface of the left atrial wall and were recorded at ventricular end diastole (ED) as well as end systole (ES). The LAD at ED ranged from 9.5 to 29.5 mm with a mean of 19 mm ± 5.0 S.D.; the diameter at ES ranged from 18.3 mm to 38.7 mm with a mean of 28.5 mm ± 5.1 S.D. The mean LAD at ED was 20.7 mm ± 4.8 S.D. in males compared to the mean diameter of 18.3 ± 4.9 S.D. in females which represents a significant difference (p<0.001). The LAD did not correlate with BSA. The left atrial dimension by ultrasound in these 200 normal patients was compared with the same measurement in 50 catheterized patients with mitral valve disease and proven left atrial enlargement. When absolute values of the left atrial dimension both at end systole and end diastole were determined by ultrasound, there was a clear separation between normal and abnormal (p<0.0001).     

Pulmonary vein blood flow velocity waveform--with special reference to pulmonary "systolic runoff" in patients with atrial septal defect

In order to evaluate the magnitude of pulmonary "systolic runoff", we studied the pulmonary vein blood flow velocity waveform by positioning a catheter-tip velocity-pressure transducer into the extraparenchymal pulmonary vein just distal to the left atrium. We recorded blood flow velocity and pressure simultaneously, and subsequently identified the zero blood flow velocity with blood flow velocity level of the pulmonary artery in diastole. Patients with atrial septal defect were used as subjects because of the technical ease although the altered hemodynamics were present. Two kinds of flow velocity waveforms were consistently demonstrated. One was a waveform of two peaks with the first peak in late systole and the second peak in early diastole (n = 9). The other was a waveform of one peak with a summit near the end of systole (n = 5). On the assumption that the blood flow velocity waveform obtained with this method is roughly equivalent to the flow volume waveform, we initiated the second study. The area encompassed between the actual flow velocity waveform and the line of zero flow velocity was divided into two compartments, i.e., ventricular systole (S) and diastole (D). The ratios of the area in systole to the sum of the areas in systole and diastole, i.e., (S)/[S) + (D], which are analogous to the pulmonary "systolic runoff", were 0.45 +/- 0.07 (mean +/- SD, n = 13). This suggests that about 40% of the right ventricular stroke volume flows into the pulmonary veins, the left atrium and a portion of the right atrium through the atrial septal defect during ventricular systole.     

Non-compaction cardiomyopathy is associated with mitral annulus enlargement and functional impairment: a real-time three-dimensional echocardiographic study

BACKGROUND AND AIM OF THE STUDY: Non-compaction cardiomyopathy (NCCM) is a disorder characterized by loosened, spongy myocardium associated with a high incidence of heart failure and systemic embolization. The mitral annulus (MA) is an important component of the mitral valve apparatus, and plays a role in left ventricular and left atrial function. The study aim was to use real-time three-dimensional echocardiography (RT3DE) in the assessment of MA size and function in patients with NCCM. METHODS: The study comprised the following patient populations: 20 patients with an established diagnosis of NCCM; 20 with an established diagnosis of dilated cardiomyopathy (DCM); and 16 control subjects. RT3DE was used to measure MA annulus diameter, MA fractional area change (MAFAC(3D)) and MA fractional shortening (MAFS(3D)). RESULTS: The left ventricular ejection fraction (LVEF) in NCCM patients (38.0 +/- 18.3%) was higher than in DCM patients (18.0 +/- 4.1%), but lower than in controls (56.9 +/- 9.2%) (p <0.05). The prevalence and severity of mitral regurgitation were comparable in the NCCM and DCM groups, but higher than in controls (p <0.05). The MA area was significantly larger, while MAFAC(3D) and MAFS(3D) were significantly impaired in NCCM patients compared to controls. Both, in systole and diastole, the MA diameter and area were larger in DCM than NCCM patients, but no difference was observed in MAFAC(3D) and MAFS(3D). The number of non-compacted segments did not correlate with MA diameter and area, MAFAC(3D) and MAFS(3D). MAFAC(3D) was significantly correlated with LVEF in NCCM (r = 0.43, p <0.05) and in DCM (r = 0.47, p <0.05). CONCLUSION: Mitral annulus enlargement and functional impairment were both present in NCCM patients, with a higher incidence and severity of mitral regurgitation.     

Influence of recipient atrial contraction on left ventricular filling dynamics of the transplanted heart assessed by Doppler echocardiography

Recipient atrial remnants retain electrical and mechanical activity after orthotopic cardiac transplantation. This study investigated the influence of recipient atrial contraction timing on Doppler ultrasound mitral flow velocity curves, isovolumic relaxation time, peak early mitral flow velocity (M1), mitral valve pressure half-time and peak mitral flow velocity due to atrial systole (M2). Clearly identifiable recipient atrial electrical activity (P waves) was present in 7 of 10 patients studied early postoperatively 2 to 6 months (mean 2.5) (early group) and in 20 of 24 patients seen 1 to 11 years (mean 3) after transplantation (late group). Median age and gender distribution were similar in both groups. For analysis of its influence on isovolumic relaxation time, pressure half-time and M1, recipient atrial contraction was classified by its position in the cardiac cycle as early systole, late systole or diastole. For analysis of M2, it was classified as early diastole, late diastole or systole. Compared with its occurrence in diastole, recipient atrial contraction in late systole was associated with a shorter isovolumic relaxation time, shorter pressure half-time and higher M1. In early systole it was associated with a longer pressure half-time and lower M1 than in diastole; isovolumic relaxation time was unchanged. Recipient atrial contraction in early diastole resulted in a lower M2 than in systole, whereas simultaneous contraction of recipient and donor atria in late diastole resulted in an increase in M2. These results indicate that the timing of recipient atrial contraction and relaxation significantly influences left ventricular filling dynamics.     

Relation of filling pattern to diastolic function in severe left ventricular disease.

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

Mitral regurgitation after cardiac transplantation

The contribution of the left atrium to mitral valve competence was assessed using the model of altered atrial size and geometry created by atrial anastomosis during cardiac transplantation. Sixteen patients underwent Doppler and 2-dimensional echocardiography after orthotopic transplantation. Mitral regurgitation was present in 14 of 16 patients. Left atrial geometry was uniformly abnormal, in a "snowman" configuration. Compared with 16 normal control subjects, the transplanted left atria were dilated (23 +/- 6 vs 13 +/- 3 cm2 during ventricular systole, p less than 0.001). Mitral valve anular diameter indexes, anular systolic reduction and ventricular function were normal in both groups. Ventricular volumes were small in the transplanted heart relative to donor body size (15 +/- 5 vs 20 +/- 8 cm3/m2 in systole, p less than 0.05). The ratio between ventricular length and anular diameter was smaller in the transplant patients (0.87 +/- 0.1 vs 1.0 +/- 0.2, p less than 0.05). In the presence of abnormal left atria, mitral regurgitation may occur without other structural abnormalities of the mitral apparatus. This study suggests that the left atrium plays an important role in mitral valve competence for primary cardiac disease associated with left atrial enlargement, even in the absence of intrinsic mitral valve disease or left ventricular dysfunction.     

Relation of filling pattern to diastolic function in severe left ventricular disease

M mode and Doppler echocardiograms, apex cardiograms, and phonocardiograms were recorded in 50 patients with severe ventricular disease of varying aetiology to examine how left ventricular filling is disturbed by cavity dilatation. The size of the left ventricular cavity was increased in all with a mean (SD) transverse diameter of 7.2 (0.8) cm at end diastole and 6.3 (0.8) cm at end systole. All were in sinus rhythm and 35 had functional mitral regurgitation. In nine patients, in whom filling period was less than 170 ms, transmitral flow showed only a single peak, representing summation. In the remainder there was a strikingly bimodal distribution of filling pattern. In 12 the ventricle filled dominantly with atrial systole (A fillers). Isovolumic relaxation was long (75 (35) ms) and wall motion incoordinate; mitral regurgitation was present in only one. In most (29) the left ventricle filled predominantly during early diastole (E fillers). Mitral regurgitation, which was present in 26, was much more common than in the A fillers, while the isovolumic relaxation time (10 (24) ms) was much shorter and the normal phase relations between flow velocity and wall motion were lost. In 24 E fillers no atrial flow was detected. In four there was no evidence of any mechanical activity, suggesting "atrial failure". In 20, either the apex cardiogram or the mitral echogram showed an A wave, implying that atrial contraction had occurred but had failed to cause transmitral flow, showing that ventricular filling was fundamentally disturbed in late diastole. A series of discrete abnormalities of filling, beyond those shown by Doppler alone, could thus be detected in this apparently homogeneous patient group by a combination of non-invasive methods. The presence and nature of these abnormalities may shed light on underlying physiological disturbances.     

Kinking of the atrioventricular plane during the cardiac cycle

Systolic descent of the atrioventricular plane toward the relatively stationary left ventricular apex is well described. As the atrioventricular plane includes two separate valvular units, systolic atrioventricular plane displacement should not be homogenous. In 6 sheep, sonomicrometric crystals were implanted at the base of the right coronary sinus, anterolateral and posteromedial fibrous trigones, posterior mitral annulus, left ventricular apex, and the tips of the anterior and posterior mitral leaflets. The aortomitral angle was calculated and related to simultaneous left ventricular and aortic pressures and mitral valve movement. The aortomitral angle was largest at end diastole (150.73 degrees +/- 15.48 degrees ). During isovolumic contraction, it narrowed rapidly to 144.90 degrees +/- 16.64 degrees , followed by a slower narrowing during ejection until it reached its smallest angle at end systole (139.66 degrees +/- 16.78 degrees ). During isovolumic relaxation, the aortomitral angle increased to 143.66 degrees +/- 16.02 degrees at the beginning of diastole. During the first third of diastole, it narrowed again to 141 degrees +/- 16.24 degrees before re-expanding to maximum at end diastole. During systole, the atrioventricular plane descended non-homogeneously toward the apex, with kinking at the hinge between the aortic and mitral annulus plane. This deformation of the atrioventricular plane has relevance in valve surgery.     

The posterior left atrial echocardiogram of mitral regurgitation

The motion of the posterior wall of the normal left atrium has not been studied systematically. The superoposterior portion of the left atrium is adynamic throughout the cardiac cycle, whereas the inferoposterior portion is displaced posteriorly with left atrial filling during ventricular systole. In the present study, the left atrial diameter (LAD), the left atrial systolic motion (LASM) and the left atrial systolic velocity (LASV), were determined in the following groups of patients: 34 normals; eight patients with either coronary artery disease or aortic stenosis; six patients with aortic insufficiency; and three patients with ventricular septal defect. The results obtained were compared to 15 patients with angiographically documented mitral regurgitation. In the last group, the LAD (4.2 +/- .19 cm) and LASV (12.3 +/- 1.23 cm) and LASM (1.2 +/- 0.4 cm) were significantly greater reflecting the early accentuated filling of the left atrium induced by mitral regurgitation. As well, the product of these three parameters was greater in the mitral regurgitation group (63.2 +/- 7.34 cm3/sec) than in the other groups and patients with mild to moderate regurgitation had a significantly lower value than those with moderate to severe regurgitation (45.7 +/- 4.1 vs 78.5 +/- 10.9, P less than 0.02). The left atrial echocardiogram, therefore, is an aid in the diagnosis of mitral regurgitation and provides a rough index of the severity of the lesion.     

Obstruction of inferior vena caval orifice by giant left atrium in patients with mitral stenosis. A Doppler echocardiographic study from the right parasternal approach.

BACKGROUND. To examine whether an extremely enlarged left atrium (giant left atrium) obstructs the venous return from the inferior vena cava (IVC), the velocity of IVC flow was measured at its junction with the right atrium (IVC orifice) in patients with mitral stenosis by use of color and pulsed-wave Doppler echocardiography from a right parasternal longitudinal plane. METHODS AND RESULTS. The maximum dimension of the IVC orifice by two-dimensional echocardiography and the maximum IVC orifice flow velocity by pulsed-wave Doppler echocardiography were measured in 74 patients with mitral stenosis and atrial fibrillation (mean age, 59 years). The control population consisted of 16 subjects with atrial fibrillation alone (mean age, 61 years). Flow velocities in the superior vena cava and hepatic vein were also obtained by pulsed-wave Doppler echocardiography from the supraclavicular and subcostal views, respectively. Fifty-one mitral stenosis patients without severe tricuspid regurgitation were divided into two groups according to the left atrial dimension (LAD), which was measured by the standard left parasternal long-axis view (group A: n = 33, LAD less than 65 mm; group B: n = 18, LAD greater than or equal to 65 mm). Peak inspiratory and expiratory velocities of IVC orifice flow in diastole averaged over three consecutive inspirations in group B (mean +/- SD, 93.4 +/- 32.0 and 47.6 +/- 19.8 cm/sec) were significantly greater (p less than 0.01) than in the control subjects (67.9 +/- 12.8 and 34.5 +/- 7.0 cm/sec) and in group A (70.2 +/- 18.4 and 38.1 +/- 11.5 cm/sec, respectively). However, there were no significant differences in superior vena caval and hepatic vein flow velocities among the three groups. The maximum IVC orifice dimension in group B (11.4 +/- 4.4 mm) was significantly smaller than in the control subjects (20.1 +/- 2.1 mm) and in group A (18.6 +/- 5.4 mm) because of displacement of the atrial septum into the right atrium. There were significant negative correlations between the IVC orifice dimension and the peak IVC orifice flow velocity (r = -0.62, SEE = 0.33 cm/sec, n = 67, y = e(-0.01x + 3.6), p less than 0.01) as well as the left atrial dimension (r = -0.71, SEE = 0.32 mm, n = 67, y = e(-0.02x + 3.8), p less than 0.01) in these 51 patients and control subjects. In the remaining 23 patients with severe tricuspid regurgitation, the peak inspiratory IVC orifice velocity (n = 9, 88.6 +/- 30.0 cm/sec) was significantly greater (p less than 0.05) and the IVC orifice dimension (23.8 +/- 9.7 mm) significantly smaller (p less than 0.05) in patients with a giant left atrium than in those without (n = 14, 69.9 +/- 15.3 cm/sec and 30.5 +/- 9.6 mm, respectively); in the latter, the IVC orifice dimension was significantly (p less than 0.05) greater than in the controls. CONCLUSIONS. A giant left atrium in patients with mitral stenosis obstructs venous return at the IVC orifice by marked displacement of the atrial septum toward the right atrium.     

Percutaneous transarterial balloon mitral valvuloplasty: 30 months experience

Between February, 1985, and August, 1987, 76 patients with mitral stenosis underwent percutaneous transarterial mitral balloon valvuloplasty (MVP). There were 58 females and 18 males aged from 15 to 69 years (mean 39 +/- 11). In 31 patients the mitral valve was pliable (40%) and in 45 patients (60%) the valve was nonpliable. Calcified mitral stenosis was found in 24 patients (31%). Transseptal catheterization was used to place one or two 0.035" (350 cm long) exchange wires into the ascending aorta in order to be snared, retrieved and exteriorized, each one through a femoral artery. Over these wires, the balloon dilation catheters were advanced through the femoral artery, retrogradely, across the mitral valve, for mitral dilation. Single (25 mm in diameter, trefoil 3 x 12 mm, bifoil 2 x 19 mm) and double (18 and 15 mm, 18 and 18 mm, 18 and 20 mm) balloons were used in 24 and 52 patients respectively. Transarterial mitral valvuloplasty produced immediate improvement of mitral valve area (MVA = 1.1 +/- 0.3 to 2.4 +/- 0.4 cm2, p less than 0.001), mitral valve gradient (19 +/- 4 to 8 +/- 6 mmHg, p less than 0.001), echocardiographic left atrial diameter (LAD = 58 +/- 6 to 54 +/- 5 mm, p greater than 0.05) and echo-MVA (0.9 +/- 0.4 to 2.1 +/- 0.7, p less than 0.001). In three patients no MVA enlargement was achieved. A significant mitral regurgitation was produced in two patients. A stroke occurred in three patients (3.9%), one of these patients subsequently died (1.3%), one recovered and one remained hemiplegic. No atrial septal defect was found after valvuloplasty.(ABSTRACT TRUNCATED AT 250 WORDS)     

Assessment of the tilting properties of the human mitral valve during three main phases of the heart cycle: an echocardiographic study

RATIONALE AND OBJECTIVES: In experimental models of the left heart, the mitral valve (MV) is commonly implanted perpendicular to a central axis of the apex/MV. To adapt this to a more correct anatomical model, as well as for further studies of the left ventricle, we created a database of implantation angles of the MV and annulus during three main phases of the heart cycle, based on standard cardiac ultrasound measurements. MATERIALS AND METHODS: Twenty-eight patients were studied with the standard cardiac ultrasound equipment. From the apical echo window, an anteroposterior (AP) plane and a perpendicular commisure-commisure (CC) plane were generated during three critical moments in the heart cycle: systole (S); diastole early filling (E); and diastole late filling (A). In both planes, the angles between the annular plane and each mitral leaflet, as well as the angle between a theoretical longitudinal axis through the apex and center of the MV orifice and the mitral annulus plane, were measured with a custom-made application of Matlab R14. RESULTS: We observed an inclination of the angle mitral annulus/central left ventricle axis, with its lowest point in the direction of the aortic valve (AP plane) of 85 degrees+/-7 degrees in systole (S), 88 degrees+/-8 degrees in early diastole (E), and 88 degrees+/-7 degrees in late diastole (A). In the CC plane, we observed an almost horizontal implantation of 91 degrees+/-5 degrees in systole (S), 91 degrees+/-8 degrees in early diastole (E), and 91 degrees+/-7 degrees in late diastole (A).     

Quantitative analysis of regional systolic function with left ventricular aneurysm

Left ventricular aneurysm (LVA) remains a poorly understood entity, often resulting in congestive failure that is not consistently improved by standard resection with linear closure. Although other surgical approaches have been proposed, current methods to assess their effect on left ventricular function are not adequate. The purpose of the present study was to quantitatively define regional systolic function in patients with LVA and to assess acute changes in regional function after standard repair. Seven patients underwent resection of an anteroapical LVA. Intraoperative two-dimensional echocardiography was performed off cardiopulmonary bypass immediately before and after resection. In all patients, short-axis views at the papillary muscle (apex) level showed anteroseptal paradox and distorted geometry, whereas at the mitral valve (base), symmetric wall motion and geometry were preserved. Videotaped echo images were divided into octants by a floating axis fitted to internal landmarks. Myocardial area and midwall perimeter were obtained for each octant, and wall thickness was calculated at end diastole (ED), isovolumetric systole (IS), and end systole (ES). Wall thickening (delta t) for each segment was calculated as the percent increase in thickness from ED and averaged for all seven patients. At the apex level before resection, isovolumetric thinning occurred in the aneurysm as well as bordering segments, with delta t ranging from -17 +/- 5% (+/- SEM) in the anteroseptal segment to 12 +/- 6% posterolaterally (p less than 0.05). The isovolumetric bulge was followed by late-systolic thickening, however, with delta t ranging from 13 +/- 7% to 27 +/- 8% (NS).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of atrial fibrillation on the dynamics of mitral annular area

BACKGROUND AND AIMS OF THE STUDY: The mitral annulus shows dynamic changes in shape and size during the cardiac cycle. A smaller size in end-diastole is attributed to the sphincteric action of atrial systole, and this may be important for functional integrity of the mitral valve. However, the effect of atrial fibrillation (AF) on dynamic changes in mitral annular size in humans is not known. METHODS: Mitral annular diameters in apical four- and two-chamber views were measured using echocardiography in 25 patients in atrial fibrillation, and in 37 subjects in normal sinus rhythm at mid-diastole, end-diastole and end-systole. Mitral annular area was computed assuming elliptical geometry. RESULTS: Patients in sinus rhythm showed a significant increase in mitral annular area of 25.9 +/- 12.8% with ventricular systole compared to its area in end-diastole (p < 0.0001), and a 10.5 +/- 8.4% reduction with atrial systole compared to mid-diastole (p < 0.001). Patients in AF had larger mitral annuli which showed non-significant changes in size between these three phases of the cardiac cycle. Percent reduction in mitral annular area in the latter half of diastole correlated significantly with left atrial (LA) diameter (r = -0.54, p < 0.0001), LA volume (r = -0.50, p < 0.0001), left ventricular (LV) fractional shortening (r = 0.37, p = 0.0036), mitral annular area in mid-diastole (r = -0.41, p = 0.0011) and mitral annular area in end-diastole (r = -0.64, p < 0.0001). That is, atrial sphincteric action on the mitral annulus was less in the presence of larger left atrium or the mitral annulus. Stepwise multiple regression analysis showed rhythm and mitral annular size to be independent predictors of dynamic changes in mitral annular area. CONCLUSION: It is concluded that AF blunts or eliminates the phasic changes in mitral annular size during the cardiac cycle with loss of its presystolic sphincteric action; this may have implications in the genesis and surgical correction of mitral regurgitation.     

Mitral anulus motion. Relation to pulmonary venous and transmitral flows in normal subjects and in patients with dilated cardiomyopathy

The dynamics between mitral anulus motion, and, thus, motion of the base of the heart, and filling of the left atrium and ventricle were studied by Doppler echocardiography in 12 normal subjects and 28 patients with dilated cardiomyopathy. The normal motion of the mitral anulus is associated with two phases of inflow from the pulmonary veins. The first phase (J) of pulmonary venous inflow occurs during ventricular systole, concomitant with the descent of the mitral anulus toward the ventricular apex, the extent of which is 12.8 +/- 1.4 mm. The end of the descent of the anulus occurs at the cessation of aortic ejection. About 100 msec later, a rapid recoil of the mitral anulus toward the atrium coincides with the onset of transmitral filling. This rapid recoil contributes to the displacement of blood from the atria into the ventricles in early diastole. The second phase (K) of pulmonary venous flow begins in early diastole, with its peak occurring about 50 msec after the peak of transmitral flow. During atrial contraction, the mitral anulus moves slightly (2.4 +/- 0.7 mm) toward the atrium and then returns toward its initial position within 120 msec. This motion coincides with the A wave of transmitral flow. In patients with dilated cardiomyopathy, pulmonary venous flow and mitral anulus motion are markedly altered in comparison with normal subjects. In all patients, motion of the mitral anulus is either reduced or absent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of left ventricular filling profile on the effect of atrioventricular synchronous pacing.

We correlated the percentage of atrial contribution to left ventricular filling (percent AC) assessed by Doppler echocardiography with the hemodynamic benefit from atrioventricular synchronous pacing assessed by direct hemodynamic measurements. Subjects comprised 40 patients who underwent electrophysiologic catheterization because of unexplained syncope or bradycardia (< 40 beats/min). Femoral arterial and pulmonary capillary wedge pressure were recorded by catheterization, and cardiac output was measured by thermodilution during temporary atrioventricular synchronous (DDD, 70 beats/min with 150 ms of atrioventricular delay) and ventricular (VVI, 70 beats/min) pacing. Mitral inflow velocity by pulsed-wave Doppler echocardiography was recorded during DDD pacing and percent AC was obtained by calculating the ratio of mitral inflow velocity area during atrial systole to total mitral inflow velocity area during early diastole and atrial systole. The mean arterial pressure and the cardiac output increased significantly (99 +/- 16 mm Hg vs 90 +/- 15 mm Hg, p < 0.001; 4.6 +/- 1.0 L/min vs 3.9 +/- 0.9 L/min, p < 0.001), and the mean pulmonary capillary wedge pressure decreased (7 +/- 4 mm Hg vs 10 +/- 4 mm Hg, p < 0.001) during DDD compared with VVI pacing. A significant positive correlation was observed between the percent AC and the increase in cardiac output (r = 0.58, n = 40, p < 0.01) or the increase in mean arterial pressure (r = 0.62, n = 38, p < 0.01) during DDD pacing. The percent AC did not significantly correlate with the decrease in pulmonary capillary wedge pressure. In conclusion, patients with larger percent AC may receive major benefit from atrioventricular synchronous pacing.     

Pulsed Doppler evaluation of left ventricular filling in subjects with pathologic and physiologic third heart sound

Haemodynamic studies suggest that the rapid deceleration of left ventricular inflow at the end of early diastole may play an important role in the genesis of the third heart sound (S3). To confirm this hypothesis noninvasively, pulsed Doppler of transmitral flow was used. Mitral flow velocity wave was recorded in 20 post-infarction patients with audible S3 (Group 1), in 20 young healthy individuals with physiologic S3 (Group II), in 20 postinfarction patients without S3 (Group III) and in 20 normal adults (Group IV). Peak flow velocity in early diastole (Ev), peak flow velocity during atrial systole (Av), the Ev/Av ratio, the deceleration of early diastolic flow (EF slope), the ratio of the time velocity integral of early diastole to the total time velocity integral (TVle/TVlt) and the isovolumic relaxation time (IVRT) were measured from Doppler recordings. The time relation between S3, the mitral valve motion on M-mode tracing, and the mitral flow velocity wave were analysed comparing the intervals from the second sound to Ev (A2-Ev), to the E point of mitral valve motion (A2-Em) and to the S3 (A2-S3). In groups I and II Ev/Av ratio was higher (respectively 4.4 +/- 2.2 and 2.8 +/- 1.1) than in group III (0.8 +/- 0.4) and IV (1.3 +/- 0.3). Similar results were found for the TVle/TVlt ratio. In both groups with S3, EF slope was significantly steeper (respectively 9 +/- 1.8 and 7.5 +/- 1.1 m s) than in normal adults (4.4 +/- 1.1 m s) and patients without S3 (3.6 +/- 1.1 m s).(ABSTRACT TRUNCATED AT 250 WORDS)     

超声心动图评价成人房间隔缺损封堵术后心脏结构和功能的变化

目的探讨超声心动图评价成人房间隔缺损(atrial septal defects,ASD)介入封堵术后心脏形态和功能变化。方法经超声心动图和心电图检查确诊为ASD并成功施行ASD封堵术的患者74例,年龄(35.63±12.74)岁,ASD直径为(16.29±5.11)mm。于封堵器堵闭术后24h、1个月、3个月、6个月和12个月进行经胸超声心动图追踪测量主动脉内径、左心室舒张末内径、左心室收缩末内径和右心室前后径,肺动脉内径和肺动脉瓣血流速度,右心房和右心室的上下径、主动脉瓣口血流速度、二尖瓣口血流速度、三尖瓣口血流速度和左心室射血分数,同时测量封堵器的直径和长度,并进行统计学分析。结果术后24h与术前相比,右心房内径、右心室内径、肺动脉内径、三尖瓣口血流速度和肺动脉瓣口血流速度均显著减少(P0.01);左心房内径、左心室内径、主动脉内径、二尖瓣口血流速度和主动脉瓣口血流速度均显著增加(P0.05);左心室射血分数无明显变化。房室大小和血流速度在术后24h内变化明显,在术后1个月后的随访中逐渐趋于稳定。结论封堵器介入封堵ASD,既纠正了解剖畸形,又改善了左心和右心系统的几何结构。     

PtfV1与左心舒张期血流动力学参数的多元偏相关分析

研究38例单纯二尖瓣狭窄患者二尖瓣球囊扩张前后左室舒张期血流动力学参数的变化,发现 Ptfv_1分别与左房内径(LAD)高度负偏相关,与平均左房压(MLAP)及二尖瓣口面积(MVA)正偏相关(-0.9167.0.6551和0.8433,P 均<0.01)。标准偏回归系数显示诸参数对 Ptfv_1的相对贡献率分别为LAD45%,MLAP24%和 MVA31%。风湿性心脏病 Ptfv_1异常的机制是左房收缩超负荷或左房内径增大。     

Atrial contribution to ventricular filling in mitral stenosis

BACKGROUND. The importance of the contribution of atrial systole to ventricular filling in mitral stenosis is controversial. The cause of reduced cardiac output following the onset of atrial fibrillation may be due to an increased heart rate, a loss of booster pump function, or both. METHODS AND RESULTS. We studied the atrial contribution to filling under a variety of conditions by combining noninvasive studies of patients with computer modeling. Thirty patients in sinus rhythm with mild-to-severe stenosis were studied with two-dimensional and Doppler echocardiography for measurement of mitral flow velocity and mitral valve area (MVA). The mean +/- SD atrial contribution to left ventricular filling volume was 18 +/- 10% and varied inversely with mitral resistance. Patients with mild mitral stenosis (MVA, 1.8 +/- 0.7 cm2) and severe mitral stenosis (MVA, 0.9 +/- 0.2 cm2) had atrial contributions of 29 +/- 4% and 9 +/- 5%, respectively. The pathophysiological mechanisms responsible for these trends were further investigated by the computer model. In modeled severe mitral stenosis, increasing heart rate from 75 to 150 beats/min caused an increase of 5.2 mm Hg in mean left atrial pressure, whereas loss of atrial contraction at a heart rate of 150 beats/min caused only a 1.3 mm Hg increase. CONCLUSIONS. The atrial booster pump contributes less to ventricular filling in mitral stenosis than in the normal heart, and the loss of atrial pump function is less important than the effect of increasing heart rate as the cause of decompensation during atrial fibrillation.