Doppler characteristics of late-diastolic flow in the left ventricular outflow tract

This study characterizes the relationship between late-diastolic Doppler detected forward flow in the left ventricular outflow tract and diastolic transmitral flow. Pulsed-wave Doppler interrogation of the left ventricular outflow tract, in a prospective consecutive series (n = 137), revealed the presence of end-diastolic forward flow in 83% of the patients studied. Further quantification of both flow signals was performed in 67 patients. Pulsed-wave mapping demonstrated that peak velocity of the end-diastolic left ventricular outflow tract signal (J wave) was maximal, 2.6 +/- 0.7 cm from the aortic valve anulus, and occurred 48 +/- 34 milliseconds after the peak transmitral atrial velocity flow signal. Peak J velocity ranged from 25 to 118 cm per second and correlated with peak A velocity (r = 0.69, p less than 0.001). Peak J velocity was inversely related to left ventricular end-diastolic dimension (r = -0.53, p less than 0.0001) and left ventricular end-diastolic volume (r = -0.43, p less than 0.004). There was no relationship between J wave velocity and early diastolic filling. We concluded that a late-diastolic forward flow signal is commonly observed in the left ventricular outflow tract. It is a manifestation of transmitral atrial systolic flow in the left ventricular outflow tract and is determined predominantly by peak transmitral atrial velocity and left ventricular size.     

Noninvasive indexes of left atrial diastolic function in hypertrophic cardiomyopathy.

OBJECTIVES: Our goal was to noninvasively assess left atrial diastolic function and its relation to the impaired left ventricular filling in patients with hypertrophic cardiomyopathy. METHODS AND RESULTS: We studied 34 patients with hypertrophic cardiomyopathy, 26 patients with secondary forms of left ventricular hypertrophy (aortic stenosis, fixed subaortic stenosis, hypertension), and 21 control subjects. Left atrial diastolic function was assessed by measuring acceleration time (SAT), deceleration time (SDT), and the EF (mean deceleration rate) slope of the pulmonary venous flow systolic wave (SW). Left ventricular diastolic function assessed by transmitral Doppler included peak early left ventricular and peak atrial filling velocities, the ratio of early-to-late peak velocities, isovolumic relaxation time, deceleration time, and EF slope. In patients with hypertrophic cardiomyopathy, acceleration time was significantly reduced (P<.05), deceleration time was significantly prolonged (P<.0001), and EF slope was significantly reduced (P<.01). These indexes were similar among the other two groups. No statistically significant difference existed between the subgroups of hypertrophic cardiomyopathy in the above indexes. Patients with hypertrophic cardiomyopathy and secondary forms of left ventricular hypertrophy had evidence of left ventricular diastolic dysfunction. In patients with hypertrophic cardiomyopathy, no correlation existed between left atrial and left ventricular diastolic function indexes (r = -0.26 to 0.33). CONCLUSIONS: Echocardiographic indexes of left atrial relaxation and filling are abnormal in patients with hypertrophic cardiomyopathy but not in secondary forms of left ventricular hypertrophy. These indexes are abnormal in all forms of hypertrophic cardiomyopathy irrespective of left ventricular outflow tract obstruction and distribution of hypertrophy; they are not solely attributable to left ventricular diastolic dysfunction. The above may imply that hypertrophic cardiomyopathy is a cardiac myopathic disease that involves the heart muscle as a whole, irrespective of distribution of hypertrophy and obstruction.     

Detection of early abnormalities of left ventricular function by hemodynamic, echo-tissue Doppler imaging, and mitral Doppler flow techniques in patients with coronary artery disease and normal ejection fraction.

We have investigated the possibility of detecting early abnormalities of left ventricular function at the initial phase of ischemic cardiomyopathy. Sixteen normotensive patients with coronary artery disease and normal left ventricular ejection fraction and 6 control patients were studied by invasive hemodynamic techniques in combination with transmitral Doppler flow or with echo-tissue Doppler imaging. The extent of the percentage of left ventricular longitudinal shortening and the systolic peak velocity at echo-tissue Doppler were significantly higher in the control patients than in patients with ischemic cardiomyopathy (P <.01). Left ventricular end-diastolic pressure was higher (P <.05), whereas mean values of isovolumic contraction and relaxation indexes (dP/dt/P: P <.05; +dP/dt: P <.05; -dP/dt: P <.01) were lower in patients with ischemic cardiomyopathy. Tau was significantly longer in ischemic patients (42.7 +/- 8.8 versus 34.5 +/- 3.7 ms, P <.05). In the control patients, the aortic valve closure to peak E interval by transmitral Doppler flow was significantly longer than that measured by echo-tissue Doppler (P <.001), whereas in patients with ischemic cardiomyopathy, this interval difference was still present and significantly shorter (P <.05). In patients with coronary artery disease and normal ejection fraction, minor and early abnormalities of left ventricular function related to isovolumic contraction and relaxation as well as to longitudinal shortening could be detected. In addition, a suction-like effect, detected during early filling evaluation with echo-tissue Doppler, is significantly decreased but not abolished during the early stages of coronary artery disease.     

国产氨氯地平对高血压病患者左室舒张功能的影响

目的评价国产氨氯地平的降压疗效及对高血压患者左室舒张功能的影响.方法观察29例轻-中度高血压患者服用国产氨氯地平4周后的降压效果,并采用多普勒超声心动图(UCG)测定4周前后左室舒张功能的变化.结果国产氨氯地平治疗4周,SBP、DBP及脉压均有显著降低(P＜0.01～0.05).E峰峰值流速和EDV增加,IVRT缩短,从而使A峰峰值流速、A/E及心房充盈分数降低,E波持续时间及EDFP/DFP减少(P＜0.01～0.05),左室舒张功能得到改善.左室舒张功能与SBP、DBP和脉压呈负相关.结论国产氨氯地平能安全有效地降低血压,并能够改善左室舒张功能.     

Left ventricular diastolic dysfunction in patients with hypertension and preserved systolic function

OBJECTIVE: To assess prospectively diastolic function in hypertensive patients with preserved left ventricular function, particularly focusing on the limitation of the transmitral flow velocity curve alone to detect diastolic dysfunction. PATIENTS AND METHODS: Comprehensive Doppler analysis was performed in 51 hypertensive patients with preserved left ventricular systolic function. RESULTS: The ratio of the peak early diastolic filling wave velocity to the peak velocity of filling wave at atrial contraction was less than the age-adjusted mean value minus 2 SD in 16 patients, and the other 35 patients had a "normal" transmitral Doppler signal. However, the combined transmitral and pulmonary venous Doppler analysis revealed that 12 of these 35 patients had a "pseudonormal" pattern. The prevalence of diastolic dysfunction was estimated at 31% with use of transmitral Doppler alone but increased to 55% when comprehensive Doppler analysis was used (P < .05). CONCLUSION: The presence of diastolic dysfunction has been frequently overlooked in hypertensive patients with transmitral Doppler analysis alone, and an assessment of diastolic function with a comprehensive Doppler analysis is needed in patients at risk for diastolic dysfunction.     

Left ventricular diastolic dysfunction in end-stage dilated cardiomyopathy: simultaneous Doppler echocardiography and hemodynamic evaluation

Left ventricular diastolic dysfunction is an integral component of end-stage dilated cardiomyopathy. To better characterize this disorder we studied 15 patients undergoing catheterization during cardiac transplant screening evaluation. Pulsed-wave Doppler echocardiographic recordings of mitral inflow were obtained with simultaneous high-fidelity left ventricular and phase-corrected pulmonary capillary wedge pressures. Doppler-derived isovolumic relaxation times were within normal limits, despite a prolonged coefficient of relaxation (tau), and correlated with pulmonary capillary wedge--left ventricular crossover pressure. Peak velocity of early diastolic filling was similar to that reported in normal subjects and did not correlate with crossover pressure or tau. Early diastolic acceleration and deceleration times were shortened compared with reported normal values. Acceleration time correlated with mean negative dP/dt from mitral valve opening to left ventricular minimum pressure and with crossover pressure, and deceleration time correlated with mean dP/dt from left ventricular minimum pressure to the peak of the rapid filling wave. Late diastolic filling at atrial contraction was absent in 12 patients, all of whom had a significant early diastolic rapid filling wave and an elevated end-diastolic pressure. Despite an increase in pulmonary capillary wedge pressure during atrial contraction, the failing ventricles were unable to generate detectable forward transmitral flow. Poor cardiac pump function was shown by low left ventricular stroke volume, which correlated with the diastolic flow velocity integral. Thus, in end-stage cardiomyopathy, the transmitral flow velocity pattern is characterized by normal peak early filling velocity, low normal isovolumic relaxation time, shortened acceleration and deceleration times of early diastolic flow, decreased early flow velocity integral, and absent or decreased filling during atrial contraction. This pattern reflects interaction between elevated transmitral driving pressure and the compromised relaxation and compliance of a left ventricle functioning on an elevated pressure-volume curve.     

Mitral regurgitation and left ventricular diastolic dysfunction similarly affect mitral and pulmonary vein flow Doppler parameters: the advantage of end-diastolic markers.

Enhanced early mitral flow and reduced systolic pulmonary vein flow may be caused both by increased left ventricular pressure as the result of diastolic dysfunction and by increased transmitral flow as the result of mitral regurgitation. Nevertheless, Doppler parameters are widely used to predict left ventricular filling pressure. We aimed to analyze the interference of mitral regurgitation with Doppler parameters usually used to estimate left ventricular filling pressure and to identify markers independent of mitral regurgitation, which could reliably estimate increased left ventricular filling pressure. Eighty-four patients (age, 62 +/- 9 years; 82% men) had a complete echocardiographic Doppler examination. Transmitral E- and A-wave velocity, E deceleration time and A duration, pulmonary vein systolic and diastolic velocities, and reversal flow duration and maximal and minimal left atrial volumes were measured. The difference between the duration of pulmonary vein and mitral A waves was calculated (A'-A). Mitral regurgitant volume was quantitatively assessed by echocardiography. Left ventricular end-diastolic pressure was measured invasively. Patients had a wide range of left ventricular ejection fraction (14% to 70%), mitral regurgitant volume (0 to 94 mL), and left ventricular end-diastolic pressure (3 to 37 mm Hg). E velocity, E/A, pulmonary vein systolic and diastolic, and systo-diastolic ratios were significantly and independently correlated with both left ventricular end-diastolic pressure and mitral regurgitant volume. A'-A showed a strong correlation with left ventricular end-diastolic pressure (r = 0.70; P <.0001), but the relation with mitral regurgitant volume was not significant (r = 0.19; P =.08). Mitral regurgitation affects the majority of Doppler parameters widely used to predict filling pressure but does not influence Ad'-Ad, which proved to be the strongest predictor of left ventricular end-diastolic pressure.     

The spectrum of left ventricular filling in severe aortic stenosis

To assess left ventricular diastolic filling in valvular aortic stenosis, pulsed Doppler echocardiography was used prospectively in 35 patients with severe aortic stenosis (valve area < 1 cm²) and in 38 age-matched normal subjects. Twenty-seven patients had a normal left ventricular systolic function at rest (ejection fraction > 0.50) and a normal or only slightly increased mean pulmonary capillary wedge pressure (mean 11±4 mm Hg). Eight patients had a poor left ventricular systolic function (ejection fraction: 0.28±0.10) and an elevated mean pulmonary capillary wedge pressure (mean: 36±9 mm Hg). The Doppler derived filling parameters were correlated with hemodynamic data, left ventricular wall thickness derived from M-mode echocardiograms, heart rate and atrio-ventricular (A-V) conduction delay using stepwise multiple correlation. The data of this study suggest that left ventricular filling is significantly impaired in patients with severe aortic stenosis and left ventricular hypertrophy with an increase in late diastolic (A-wave) velocity, an increase in the A/E ratio, a decrease in the first one-half filling fraction and a prolongation of early diastolic deceleration time. These changes in filling hemodynamics are associated with alterations in mean pulmonary capillary wedge pressure, left ventricular wall thickness, heart rate and A-V conduction delay. When heart failure develops as a result of impaired left ventricular systolic function, an increase in left atrial filling pressure is associated with a shift of left ventricular filling towards early diastole with a ‘normalisation’ of the transmitral flow velocity curve. In extreme cases, a progression towards a ‘restrictive’ filling pattern is found with a marked shortening of the left ventricular early diastolic deceleration time. In the presence of high filling pressures, increased left atrial driving pressure (derived from the mean pulmonary capillary wedge pressure) is associated with changes in the left ventricular filling pattern irrespective of the presence and the degree of myocardial hypertrophy.     

Non-invasive cardiac assessment in beta-thalassaemia major

Iron deposition in the heart occurs in beta-thalassaemia major and contributes to cardiac dysfunction. Eighteen patients with beta-thalassaemia major were assessed clinically and had non-invasive investigations. They were young (15.5 +/- 3.6 years). Two patients had clinical heart failure. Doppler echocardiography demonstrated higher transmitral peak flow velocity in early and late diastole compared with controls (e: p<0.05, a: p<0.01). Transtricuspid peak late diastolic flow velocity was higher in patients (p<0.005). Isovolumic relaxation time was shortened (p<0.001). Pulmonary venous flow velocity was higher in diastole than systole (S: 0.51 +/- 0.11 m/s, D: 0.62 +/- 0.08 m/s). Reversal of pulmonary venous flow during atrial systole was seen in eight patients. These diastolic filling abnormalities did not significantly change with blood transfusion. Left ventricular ejection fraction was normal in patients. Two patients had cardiomegaly on chest X-ray. In beta-thalassaemia with iron overload, there is a restrictive pattern of diastolic dysfunction. This is not altered by recent blood transfusion. Left ventricular function remains relatively intact.     

Heart remodeling in case of isolated systolic arterial hypertension

Examination of 32 patients with isolated systolic arterial hypertension (office blood pressure 171.9 = -3.3/79.7 +/- 0.2 mm Hg) and 54 ones with systolic/diastolic hypertension) 179.8 +/- 3.9/114.8 +/- 1.9 mm Hg) showed that the former are characterized by isolated hypertrophy of interventricular septum, the latter by symmetric hypertrophy of the septum and free left ventricular wall. Septal hypertrophy affects the initial phase of diastolic filling of the left ventricle as appears from longer time of isovolume relaxation and low peak rate of early transmitral blood flow; it does not influence diastolic function of the right ventricle. Hypertrophy of the free left ventricular wall disturbs the final stage of early diastolic filling of both right and left ventricles manifest as increased duration of their slowed early filling.     

脉冲多普勒与组织多普勒技术对原发性高血压伴左室肥厚患者的右心室舒张功能的评价

目的:探讨组织多普勒与脉冲多普勒2种方法对原发性高血压伴左室肥厚患者右心室舒张功能的评价。材料与方法:对48例原发性高血压患者经超声检测左室肥厚患者和50例健康体检者先采用脉冲多普勒超声心动图测量右室舒张期三尖瓣口充盈早期血流峰值速度(E)和心房收缩峰值(A),并计算E/A值;再应用组织多普勒测量三尖瓣环舒张早期运动速度(e)、舒张晚期运动速度(a)及计算e/a值,并与健康组进行比较。结果:原发性高血压伴左室肥厚组脉冲多普勒与组织多普勒E、A比值均小于1(E/A1),而健康组E、A比值均大于1(E/A1);高血压伴左室肥厚组e、e/a值均较健康组显著减低(P0.01)。结论:原发性高血压患者伴左室肥厚可引起右室舒张功能减低,组织多普勒与脉冲多普勒显像均适合应用于评价原发性高血压伴左室肥厚对右室舒张功能的影响。组织多普勒与脉冲多普勒2种方法所测e、e/a值在原发性高血压伴左室肥厚患者的右心室舒张功能评价中均具有临床应用价值。     

Tei指数评价原发性高血压病患者左室舒张功能

目的探讨Tei指数评价原发性高血压病左室不同构型的舒张功能的临床价值。方法原发性高血压病患者115例,以Ganau分类法分为4组:正常构型组36例,向心性重构组36例,向心性肥厚组31例,离心性肥厚组12例;另选择体检健康者35例为对照组。应用M型超声测量左室的舒张末期内径(LVEDD)、后壁厚度(LVPWT)、室间隔厚度(IVST);改良Simpson法测量左室射血分数(LVEF);脉冲多普勒测量二尖瓣舒张早期血流峰值流速(E)、舒张晚期血流峰值流速(A)、E峰减速时间(EDT),计算E/A;测量肺静脉血流频谱收缩期肺静脉血流峰值(PVS)、舒张早期血流峰值(PVD),计算PVS/PVD,组织多普勒测量左室Tei指数。结果高血压病组左室舒张功能均减低。正常构型组、向心性重构组、向心性肥厚组E/A1,EDT延长;离心性肥厚组E/A1,其EDT较正常构型组、向心性重构组、向心性肥厚组缩短,收缩功能减低,LVEF与对照组比较差异有统计学意义(P0.05);对照组、高血压病各组Tei指数依次增加,组间差异均有统计学意义(均P0.05);左室Tei指数与LVEF、A峰呈负相关,与IVST、LVPWT、LVEDD、RWT、LVMI、E峰、E/A呈正相关;Tei指数ROC曲线下面积为0.986,以Tei指数为0.425鉴别有无左室舒张功能不全的敏感性为97%,特异性为83%。结论 Tei指数与原发性高血压病患者左室不同构型具有良好的相关性,原发性高血压病早期Tei指数即发生改变,随舒张功能不全的加重而增高;Tei指数可作为评价鉴别二尖瓣血流"假性正常化"的参考指标之一。     

高血压不同左室构型左室舒张功能的超声心动图研究

目的联合应用二维、M-型超声心动图与脉冲多普勒技术评价高血压左心室不同构型的舒张功能。方法采用M-型和二维超声技术测量高血压患者左室几何构型，测量各组左房功能指标及二尖瓣、肺静脉血流频谱。结果与对照组相比，高血压各组左室舒张功能均有不同程度损害，向心性肥厚及离心性肥厚组受损最严重。高血压早期即可出现舒张功能异常，表现为正常构型组舒张功能的异常改变。左房灌注分数(LAT)是比二尖瓣及肺静脉血流频谱更加可靠地反映早期左室舒张功能异常的指标。结论左室舒张功能异常特别是左房灌注分数(LAT)的异常，可以早期体现左室重构超声心动图变化。     

Decreased and abnormal left ventricular filling in acute heart failure: role of pericardial constraint and its mechanism.

Pericardial constraining force is minimal in normal hearts; however, it is considered to be prominent in moderate to severe heart failure. Thus, effects of the pericardium on pulsed Doppler transmitral flow velocity pattern were examined in 17 dogs with acute left ventricular dysfunction. Left ventricular dysfunction with left ventricular end-diastolic pressure > or = 15 mm Hg was produced by injection of microspheres into the left coronary artery. Transmitral flow velocity pattern, left atrial and left ventricular diameters, and high-fidelity left atrial and left ventricular pressures were recorded before and after pericardiectomy. In five of the 17 dogs, mitral regurgitation with giant "v" wave of left atrial pressure occurred with reductions of left ventricular systolic pressure and peak rate of the left ventricular pressure fall (dP/dt) after pericardiectomy. In the other 12 dogs, peak early and late diastolic filling velocities increased with a decrease in left ventricular minimal pressure and increases in left arterial and left ventricular diameters and left atrial and left ventricular compliance after pericardiectomy. In these 12 dogs, left atrial to left ventricular crossover pressure, left ventricular end-diastolic pressure, and references for left ventricular relaxation did not change after pericardiectomy. Thus the release from pericardial constraining force in severe heart failure may increase chamber compliance of the left ventricle and left atrium and, in turn, increase peak early and late diastolic filling velocities through an increment in forward transmitral pressure gradient. Increased pericardial constraining force is a possible cause limiting left ventricular filling and hence cardiac output in heart failure.     

超声心动图评价高血压病患者左心功能

目的运用超声心动图技术综合评价高血压病患者左室收缩功能和舒张功能。方法高血压病组56例和对照组36例,M-型和二维(2D)超声心动图检测:左房内径(LAd),舒张期室间隔厚度(IVST)和左室后壁厚度(PWT),左室舒张末期内径(LVDd),二尖瓣EF斜率,室间隔及左室后壁运动幅度,左室射血分数(EF),左室短轴缩短率(FS),每搏量(SV);脉冲多普勒(PW)检测二尖瓣口舒张早期充盈峰速度(VE),舒张晚期充盈峰速度(VA),E/A比值,等容舒张时间(IVRT)。结果高血压病患者左室壁与室间隔收缩期运动幅度普遍增强,与对照组比较P<0.01;左室收缩功能各项参数(EF、FS、SV)高于对照组(P<0.05),高血压病组左室舒张功能各参数异常,表现为VE减低,VA升高,E/A<1,IVRT延长,MV-EF斜率减慢,与对照组比较P<0.001;左房扩大(P<0.001)。结论超声心动图技术可反映高血压病患者左心结构和功能变化,为临床诊治提供客观依据。     

Compensatory responses of left atrial conduit flow to atrial fibrillation with acute myocardial infarction in a canine model.

The aim of this study was to examine the interaction of acute atrial fibrillation (Af) and acute myocardial infarction (AMI) on left atrial (LA) and left ventricular (LV) filling in atrioventricular (A-V) sequential paced, open chest, anesthetized dogs. Left atrial conduit function was determined from pulmonary venous flow (PVF) and detailed analysis of early diastolic flow with the use of micromanometers and transmitral Doppler echocardiography. We studied 8 dogs with regular ventricular rates to avoid the confounding effect of ventricular arrhythmia in Af. In the control stage, Af increased the diastolic PVF volume to the left atrium compared with that during regular A-V pacing (from 0.58 +/- 0.11 mL/beat to 0.70 +/- 0.13 mL/beat, P <.05), as a compensatory response to the impaired systolic PVF volume (from 0.56 +/- 0.12 mL/beat to 0.41 +/- 0.11 mL/beat, P <.05). As a result, cardiac output was maintained. However, in the AMI stage, Af decreased cardiac output (from 0.95 +/- 0.32 L/min to 0.80 +/- 0.23 L/min, P <.05 versus AMI with A-V pacing), and decreased diastolic PVF volume (from 0.46 +/- 0.13 mL/beat to 0.33 +/- 0.14 mL/beat, P <.05 versus AMI with A-V pacing). These changes were associated with a prolonged LV isovolumic pressure decay rate. Our study demonstrates that Af does not affect cardiac output in the setting of normal LV function at a controlled ventricular rate because enhanced LA conduit flow compensates for impaired LA reservoir function. In contrast, in the setting of AMI, the compensatory response to Af is attenuated because of abnormal LV relaxation, resulting in a decrease in cardiac output.     

Echocardiographic Doppler assessments of left ventricular filling and ejection during upright exercise in endurance athletes

Doppler echocardiography was used to describe left ventricular filling and ejection during upright bicycle exercise in 24 healthy male endurance athletes. The transmitral pressure gradient was estimated and isovolumetric relaxation, filling and ejection time and transmitral and aortic flow velocities were measured at rest and during exercise. From rest to peak exercise (at a heart rate of 160 bpm), the mean left ventricular filling time was shortened by 73%, the ejection time by 31%, while the isovolumetric relaxation time was shortened by 62%. At peak exercise, the maximum aortic flow velocity almost doubled and the maximum transmitral flow velocity more than doubled, with a tenfold increase in the mean transmitral pressure gradient. The increase was significant (P<0.001) at each level of exercise. The left ventricular filling rate measured as volume per time was 185 +/- 62 ml s(-1) at rest and it increased to 986 +/- 192 ml s(-1) at peak exercise. This study demonstrates large changes in diastolic filling indices during upright exercise and it shows that the heart is able to increase its filling rate five times from rest to peak exercise.     

Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy

BACKGROUND: Left atrial systolic dysfunction, unexplained by altered loading conditions, has been reported in idiopathic dilated cardiomyopathy suggesting left atrial involvement in the myopathic process. MATERIALS AND METHODS: Seventeen patients with idiopathic dilated cardiomyopathy, 16 with ischemic dilated cardiomyopathy and 18 normal controls were studied with transthoracic echocardiography and cardiac catheterization. Transmitral diastolic flow was evaluated with pulsed Doppler. Left atrial volume (cm3/m2) at mitral valve opening (maximal, Vmax.), onset of atrial systole (P wave of the electrocardiogram, Vp), and mitral valve closure (minimal, Vmin. ) was determined with two-dimensional echocardiography using the biplane area-length method. The left atrial active emptying fraction (ACTEF = [Vp-Vmin.] x 100/Vp) served as an index of systolic function. RESULTS: The peak early diastolic transmitral flow velocity (cm/sec) was similar in the three groups (idiopathic: 60 +/- 16, ischemic: 58 +/- 20, control: 56 +/- 22; P = NS), whereas the late diastolic transmitral flow velocity was lower but not significantly different in idiopathic compared to ischemic cardiomyopathy, and in both was lower than control (26 +/- 12 vs. 34 +/- 13 vs. 44 +/- 14, respectively; P < 0.05). Vmax. and Vp were similar in idiopathic and ischemic cardiomyopathy and greater than control (44.6 +/- 13.6 vs. 48.2 +/- 18.3 vs. 26.9 +/- 6.2; P < 0.05, and 34.6 +/- 13.4 vs. 30.8 +/- 10.9 vs. 16.7 +/- 3.7, respectively; P < 0.05). ACTEF was lower in idiopathic than in ischemic cardiomyopathy and in the latter it was similar to control (18 +/- 10% vs. 32 +/- 10% vs. 36 +/- 10%, respectively; P < 0.05). Moreover, ACTEF was inversely related to left atrial tension at end-of atrial systole both in idiopathic and in ischemic cardiomyopathy (r2 = 0.52, P = 0.001 and r2 = 0.57, P = 0.0007, respectively). However, at any given level of left atrial tension at end of atrial systole, ACTEF was lower in idiopathic than ischemic cardiomyopathy. CONCLUSION: Left atrial systolic function is depressed in idiopathic and preserved in ischemic dilated cardiomyopathy despite similar left atrial loading conditions. This finding suggests left atrial myopathy in the former, and may be related to the differences in the response to medical treatment and clinical outcome observed between the two conditions.     

The diastolic dysfunction of the left ventricle in patients with systemic lupus erythematosus and system scleroderma

The subjects of the study were 22 patients with systemic lupus erythematosus (SLE) and 18 patients with system scleroderma (SS). The mean age of the subjects was 36.3 +/- 2.4 years, the onset of the disease had taken place 5 to 10 years ago. The control group consisted of 20 practically healthy individuals with no complaints, clinical signs or instrumental data suggesting cardiovascular pathology. In order to evaluate the character of left ventricular (LV) diastolic filling, all the patients underwent transthoracal Doppler analysis with measurement of transmitral flow in four-chamber heart position using apical approach with the control volume at the level of the ends of mitral valvular cusps (computed sonography system ACUSON 128 XP/10). The study found no significant difference between SLE and SS patients in such parameters as LV myocardial mass and LV mass index. All the patients with rheumatic diseases, with or without arterial hypertension (AH), had diastolic dysfunction, which was manifested by increase of atrial systolic contribution into LV filling, prolongation of blood flow slowdown time in the stage of its early filling, and prolongation of LV isometric relaxation time; heart diastolic disorder was accompanied by significant increase of end diastolic pressure in LV cavity. It should be noted that the most prominent changes were found in rheumatic patients with AH, which must be caused by the hypertrophy and remodeling of the myocardium. Myocardial hypertrophy was associated with substantial changes in the ventricular septum, which consisted in its hypokinesia, associated with impairment of myocardial contractility (ejection fraction of 48.3 +/- 3.5%).     

Improvement in left ventricular diastolic filling by septal myectomy in hypertrophic cardiomyopathy

Abnormalities in left ventricular diastolic function or filling are considered to be responsible for some of the symptoms in patients with hypertrophic cardiomyopathy. To clarify whether the abnormalities in left ventricular diastolic filling are improved by septal myectomy, 13 patients with hypertrophic cardiomyopathy and intracavitary pressure gradient were studied preoperatively and postoperatively by use of pulsed Doppler echocardiography. Peak early diastolic filling velocity (E), the ratio of peak early diastolic filling to peak atrial filling velocities (E/A ratio), and deceleration time were measured from the transmitral flow velocity pattern before and after septal myectomy. Although E and E/A ratio did not change after septal myectomy, deceleration time significantly shortened from 314 +/- 72 to 271 +/- 53 milliseconds (n = 10; p less than 0.05). Further, if seven patients with significant changes in heart rate (greater than 30%) or in the Doppler-determined severity of mitral regurgitation (more than one degree) were excluded (because these parameters may effect E and E/A ratio), there were also significant changes in E (81 +/- 21 versus 98 +/- 25 cm/sec, p less than 0.05) and in E/A ratio (0.84 +/- 0.17 versus 1.14 +/- 0.33, p less than 0.05). Because left ventricular systolic function has been demonstrated to remain constant or to decrease by most measures after septal myectomy, relief of some symptoms may be largely the result of the improvement in diastolic filling suggested by these criteria.