糖尿病患者心脏舒张功能的超声心动图改变

本文应用多功能超声心动仪检测31例糖尿病(DM)患者及42名正常人,反映左、右心室舒张功能的20项指标。发现DM组EPSSb增高,EF斜率降低,左、右室的E峰流速积分及其与全舒张期流速积分比值降低,表明其左、右室均有舒张功能减退。经分析认为,DM组舒张功能减退重于收缩功能减退,右室更为明显,病变原因与糖尿病性心肌病(DCM)有关。     

超声心动图对高血压病患者右心室功能的研究

本文采用超声心动图测定了无心功能不全症状的高血压病患者右室结构和功能,并将其分为左室肥厚(LVH)组和非左室肥厚(NLVH)组.结果两组病人右室收缩功能和室腔大小均正常.NLVH组与正常组比较通过三尖瓣的E峰较低,A峰较高,E/A比值较小,快速充盈分数(RFF)、1/3充盈分数(1/3FF)和每搏量校正的最大充盈率(PFR)降低,下降时间延长;LVH组A峰、E/A比值、PFR进一步损害,右室壁厚度较正常组和NLVH组明显增加.表明高血压病患者早期右室舒张功能已受损害,但收缩功能正常,左室肥厚的同时存在右室肥厚.     

超声多普勒二尖瓣血流估计左心室舒张功能

本文用脉冲多普勒测量二尖瓣血流的快速充盈E峰,心房收缩A峰流速,A/E比值以及A峰流速积分占左室充盈量比值AI/FSV%来估测心肌梗塞患者左室充盈功能。与正常对照组36例结果相比,54例心肌梗塞患者,显示左室充盈功能受损,其A峰流速,A/E比值及A/FSV%显著增高,E峰降低但不够显著,以AI/FSV%指标比较敏感。     

高血压病患者的右室舒张功能

原发高血压对右室功能的影响尚不清楚,本文采用脉冲多普勒超声心动图研究了高血压患者的右室舒张功能。研究的50例轻度原发高血压患者均为男性,舒张压12.7～14.5KPa(95～109mmHg),除外各种心脏病,肺部疾病,胰岛素依赖性糖尿病等,检查前2周停用降压药,对照组10例无心脏病,血压正常,年龄与高血压组相仿。全部患者均进行了M型和二维超声心动图检查。多普勒取样标本置于三尖瓣环下方瓣叶之间,尽量使多普勒声束与血流方向一致(角度接近0)。流入速度曲线以100mm/S记录在录像带上。应用计算机分析5个心动周期流速曲线,计算早期迅速充盈(E)及晚期充盈速度(A)及其比率,1/2加速和1/2减速时间.     

急性前壁心肌梗死患者P波离散度与左心室舒张功能的相关性

目的 研究急性前壁心肌梗死患者心电图P波参数与超声心动图左心室舒张功能参数之间的相关性.方法 应用超声心动图对86例初次发生急性前壁心肌梗死的患者进行检查,测量左心室舒张早期充盈峰值流速、左心房收缩期充盈峰值流速和两者比值及其他常见超声心动图参数.所有入选患者记录12导联同步体表心电图并测算P波参数.结果 86例患者中有21例(24.4%)发生房颤.房颤患者P波最大宽度、P波离散度、左心室舒张早期充盈峰值流速和左心室舒张早期充盈峰值流速与左心房收缩期充盈峰值流速比值分别为(103±10)ms,(36±7)ms,(77±12)cm/s,1.71±0.66;均明显高于非房颤患者.所有患者P离散度和左心室舒张早期充盈峰值流速与左心房收缩期充盈峰值流速比值呈正相关(r=0.47,P<0.001).结论 P波离散度作为一个简便无创的心电指标不仅可以预测房颤的发生.而且可以评估急性前壁心肌梗死患者的左心室舒张功能,有助于舒张性心力衰竭的早期干预是一个很有临床应用价值的参考数值.     

肥胖对2型糖尿病患者左室舒张功能的影响

目的:通过超声心动图左室舒张功能各项指标的测定,探讨不同程度的肥胖对2型糖尿病患者左室舒张功能的影响。方法:对90例2型糖尿病患者测定身高、体重,计算体重指数(BMI)。根据体重指数的不同,分为三组:正常体重组、超重组、肥胖组。每组病人均测定左室舒张功能指标即左室舒张早期充盈峰值流速(Peak E)、晚期充盈峰值流速(Peak A)、A/E比值、等容舒张时间(IRT)、左房直径(LAD)、二尖瓣半压时间(MV1/2T)。比较各组心脏左室舒张功能情况。结果:BMI与Peak E呈负相关(r=-0.235,P<0.05);BMI与A/E比值呈正相关(r=0.195,P<0.05);BMI与IRT呈负相关(r=-0.163,P<0.05)。2型糖尿病早期亚临床心脏左室舒张功能异常的发生率分别36%;47%;58%。结论:2型糖尿病早期即存在左室舒张功能异常;肥胖加重心脏左室舒张功能异常。     

应用超声心动图评价2型糖尿病患者的左室功能

目的:利用超声心动图对2型糖尿病患者左室功能进行检测分析,旨在早期发现糖尿病患者的心功能改变。方法:入选糖尿病患者42例(糖尿病组),健康体检者30例(健康对照组);采用M型超声心动图测量左室射血分数(LVEF)、左室短轴缩短率(LVFS);利用脉冲多普勒超声心动图测量二尖瓣口及右上肺静脉血流参数,包括左室舒张早期E峰速度峰值(E)、舒张晚期A峰速度峰值(A)、计算E/A比值、心房收缩期肺静脉逆向流速峰值(ap)。结果:与健康对照组比较,糖尿病患者组舒张功能指标E/A[(1.12±0.14)比(0.95±0.56)]明显降低(P<0.05),ap[(23.54±2.91)cm/s比(31.73±9.97)cm/s]明显升高(P<0.001)。结论:糖尿病患者首先出现左室舒张功能下降,表现为E/A比值降低,肺静脉逆向流速峰值升高,对糖尿病患者应尽早进行心功能检查,以便早期发现心功能不全,早期治疗。     

老年原发性高血压患者心脏舒张功能的评价

目的观察老年原性发高血压(EH)患者血压水平及昼夜节律,探讨其与左心舒张功能的相关关系。方法选择因冠心病、糖尿病、缺血性脑血管病等在我院老年心血管内科住院的EH患者57例(EH组)。血压正常患者57例(NBP组)。对所有患者行24h动态血压监测、心脏超声及组织多普勒检查,测量二尖瓣舒张早期血流峰速(E)、二尖瓣环舒张早期运动峰值速度(E′),计算E/E′比值。结果 EH组糖尿病、冠心病的发病率明显高于NBP组(P0.05);行多重线性回归分析显示:年龄、24h平均收缩压(24hSBP)、脉压、24h收缩压负荷(24hSBPL)与E/E′比值呈显著正相关(P0.01),为E/E′比值的危险因素;24h平均舒张压(24hDBP),24h舒张压负荷(24h DBPL)为E/E′比值的保护性因素(P0.05,P0.01)。回归方程为E/E′比值=0.062+2.533×年龄+3.765×24hSBP-2.919×24hDBP+3.75×脉压+3.331×24hSBPL-1.933×24hDBPL。结论老年EH患者心脏舒张功能较显著下降,其收缩压升高、舒张压降低、脉压增加、SBPL增加,均是舒张功能降低的危险因素。     

超声心动图在老年女性继发肺动脉高压的类风湿关节炎患者右心室功能检测中的应用

目的探讨超声心动图在老年女性继发肺动脉高压(PAH)的类风湿关节炎(RA)患者右心室功能检测中的应用价值。方法回顾性分析RA老年女性患者超声心动图检查结果。其中,继发PAH 36例,无PAH 34例,测定两组患者的右室舒张末横径(RVDD)、右室游离壁舒张末厚度(RVDT)、三尖瓣环收缩期位移(TAPSE)、主肺动脉内径(MPA)、右室收缩末期面积(RVESA)和右室舒张末期面积(RVEDA),并计算右室面积变化率(RVFAC);测量三尖瓣舒张期血流峰值流速E/A比值;测量血流加速时间(AT)和肺动脉瓣收缩期血流最大频移(MFS),计算肺动脉僵硬度(PAS);通过三尖瓣反流峰值估测肺动脉收缩压(SPAP);采用组织多普勒成像技术(DTI)测量舒张早期、晚期峰值速度(Em、Am),并计算Em/Am,测量三尖瓣前叶瓣环处组织运动收缩期峰值速度(Sm)和右室肌射血时间(ET)、等容收缩(ICT)、舒张时间(IRT),计算右室Tei指数。结果 PAH组与无PAH组相比,RVDD和RVDT明显增大,TAPSE下降,RVFAC降低;MPA及PAS明显增大;三尖瓣舒张期血流峰值流速E/A比值下降;右室肌运动速度Em/Am、Sm降低,右室肌ET缩短,ICT+IRT延长,Tei指数增加(P<0.01)。结论患有RA的老年女性PAH患者,右心室功能显著下降,超声心动图对其具有良好的诊断价值。     

彩色超声心动图检测年轻吸烟者右心功能急性效应的相关分析

目的:研究吸烟对健康人右心结构及功能的即时影响。方法:入选标准的健康年轻男性吸烟者42人,于5分钟内吸完1支香烟,应用二维超声(2-DE)、脉冲多普勒(PDE)和多普勒组织成像技术(DTI)对吸烟前与吸烟后的右室结构及功能指标进行检测并对比分析。结果:吸烟后右房(RA)、右室(RV)较吸烟前增大(34.54±5.20mmvs36.38±5.38mm,P0.01;21.33±3.06mmvs23.56±2.19mm,P0.01),肺动脉收缩期峰值流速加速时间(PAAT)缩短(154.29±13.43msvs131.43±22.82ms,P0.01),肺动脉收缩期峰值流速(PAVp)增高(87.49±10.96cm/svs95.19±9.69cm/s,P0.01),均具有显著意义;右室舒张功能参数包括三尖瓣口早期充盈峰值速度(TVE)、舒张晚期峰值速度(TVA)、TVE/TVA值、E峰减速时间(TVEDT)、三尖瓣环的舒张早期运动速度(TVEm峰)、舒张晚期运动速度(TVAm峰)、TVEm/TVAm值在吸烟后发现有明显变化,均有显著意义。结论:吸烟可致健康年轻吸烟者右室结构及收缩、舒张充盈(松弛功能)明显的改变。     

Left Atrial Responses to Acute Right Ventricular Apical Pacing in Patients with Sick Sinus Syndrome

Chronic right ventricular apical (RVA) pacing can lead to an increased risk of heart failure and atrial fibrillation, but the acute effects of RVA pacing on left atrial (LA) function are not well known. Twenty‐four patients with sick sinus syndrome and intact intrinsic atrioventricular conduction were included. All patients received dual‐chamber pacemaker implants with the atrial lead in the right atrial appendage and the ventricular lead in the right ventricular (RV) apex. Transthoracic standard and strain echocardiography (measured by tissue Doppler imaging and speckle tracking image) were performed to identify functional changes in the left ventricle (LV) and LA before and after 1 hour of RVA pacing. The LA volume index did not change after pacing; however, the ratio of peak early diastolic mitral flow velocity (E) to peak early diastolic mitral annular velocity (Ea) was significantly increased and peak systolic LA strain (Sm), mean peak systolic LA strain rate (SmSR), peak early diastolic LA strain rate (EmSR), and peak late diastolic LA strain rate (AmSR) were significantly reduced after RV pacing. LV dyssynchrony, induced by RV pacing, had a significant correlation with E/Ea, Sm, and SmSR after pacing. E/Ea also had a negative correlation with Sm and SmSR after pacing. Multivariate regression analysis identified LV dyssynchrony and E/Ea as important factors that affect Sm, SmSR, EmSR, and AmSR after acute RVA pacing. Acute RVA pacing results in LA functional change and LV dyssynchrony and higher LV filling pressures reflected by E/Ea are important causes of LA dysfunction after acute RVA pacing.     

Diastolic ventricular interaction in normal and dilated heart during head-up tilting

BACKGROUND: The normal human heart behaves as a single functional unit during preload reduction; adaptations of the left ventricle to head-up tilting is mediated through ventricular interdependence and biventricular-lung interaction. HYPOTHESIS: We hypothesized that reduction of venous return in dilated cardiomyopathy is likely to have a great effect on ventricular chamber geometry and filling. The aim of this study was to evaluate the effects of gradual head-up tilting in normal subjects and in patients with dilated cardiomyopathy, addressing special attention to right (RV) and left ventricular (LV) dimensions, geometry, and filling, and to biventricular-lung interaction. METHODS: Twenty normal subjects and 23 patients with moderate heart failure due to dilated cardiomyopathy were studied with two-dimensional and Doppler echocardiography in supine position and after 20 degrees, 40 degrees, and 60 degrees tilting. Right ventricular and LV dimensions, LV geometry, and tricuspid, mitral, and pulmonary venous flow patterns were recorded at each step of the study. Geometric changes of the LV were evaluated by measurements of volumes and diameters in the apical four-chamber view (which identifies the interventricular septum and lateral wall) and apical two-chamber view (which identifies the inferior and anterior wall of the LV). RESULTS: In the two groups, tilting was associated with reduction of RV area and LV diameter and volumes; percent variations in LV diameter and volumes recorded in four-chamber view were lower at each step of tilting than with those derived from the two-chamber view in controls and in patients. In normal subjects, mitral and tricuspid peak early flow velocities were decreased at any tilting level; peak late velocities were unchanged; peak velocity of systolic forward flow of the pulmonary vein was reduced, diastolic forward flow was unchanged, and the difference in duration between reverse pulmonary flow and forward mitral A wave was reduced. Doppler findings were qualitatively similar in patients, but tilting induced a more marked redistribution of LV filling to late diastole because of a significant increase in atrial contribution. CONCLUSIONS: Preload reduction by tilting induces profound effects on left and right dimensions, geometry, and filling in normal and dilated heart; reduction or RV dimensions are associated with changes in LV ventricular geometry (minimal reduction in septal-lateral diameter, marked reduction in anterior-posterior diameter), redistribution of right and left diastolic filling to late diastole, and redistribution of pulmonary venous flow to early diastole. These mechanisms are probably due to a favorable interaction between heart and lungs, which increases compliance within the pericardial space and facilitates redistribution of flow from the lungs. Even a minimal amount of preload reduction causes more marked effects in LV filling patterns in dilated cardiomyopathy than in normal hearts, confirming that ventricular interaction and pericardial constraint are increased when heart volume enlarges.     

Right ventricular diastolic function in patients with hypertrophic cardiomyopathy--an invasive study.

To assess diastolic function of the right ventricle (RV) in patients with hypertrophic cardiomyopathy (HCM), biplane RV angiograms and RV pressures were analyzed in 19 HCM patients and in 13 normal subjects. RV and left ventricle (LV) pressures were measured using catheter-tip manometers. RV volumes were obtained from frame-by-frame tracings of angiograms. Ventricular relaxation was assessed by the time constant of isovolumic pressure decay (T). The peak filling rate (PFR) and the time to PFR (TPFR) were used as parameters of early diastolic filling, and the right atrial contribution to RV filling (%AF) was used as a parameter of late diastolic filling. The T for the RV was significantly prolonged in HCM patients. However, there was no significant correlation between the T for the RV and LV, nor did the T for the RV correlate with the RV ejection fraction or interventricular septal wall thickness. The TPFR, but not PFR, was significantly greater in HCM patients, and the %AF tended to be increased in HCM, but not significantly. The RV diastolic pressure-volume relations in the HCM patients shifted upward. In conclusion, impaired isovolumic relaxation and delayed diastolic filling and decreased diastolic distensibility are present in the RV of HCM patients.     

Left ventricular filling abnormalities in asymptomatic morbid obesity.

Indexes of left ventricular (LV) diastolic filling were measured by pulse Doppler echocardiography in 16 asymptomatic morbidity obese patients presenting for bariatric surgery and were compared with an age- and sex-matched lean control population. No patient had concomitant disorders known to affect diastolic function. All patients had normal systolic function. LV wall thickness and internal dimension were measured in order to calculate LV mass. Fifty percent of morbidly obese patients had LV diastolic filling abnormalities as assessed by the presence of greater than or equal to 2 abnormal variables of mitral inflow velocity. The ratio of peak early to peak late (atrial) filling velocity was significantly decreased in obese compared with control patients (1.16 +/- 0.26 vs 1.66 +/- 0.30, p less than 0.001). The peak velocity of early LV diastolic filling was significantly reduced in obese patients (75 +/- 15 vs 98 +/- 19 cm/s, p less than 0.001). The atrial contribution to stroke velocity as assessed by the time-velocity integral of late compared with total LV diastolic filling was significantly increased in obese patients (36 +/- 7 vs 27 +/- 4%, p less than 0.001). Obese patients had significantly increased LV mass (214 +/- 45 vs 138 +/- 37 g, p less than 0.001), even when corrected for body surface area (95 +/- 16 vs 76 +/- 16 g/m2, p less than 0.002). However, increased LV mass did not correlate with indexes of abnormal diastolic filling in obese patients. These data suggest that abnormalities of diastolic function occur frequently in asymptomatic morbidly obese patients and may represent a subclinical form of cardiomyopathy in the obese patient.     

Role of left atrial booster pump function in a worsening course of congestive heart failure.

We evaluated changes in left ventricular (LV) preload and the Doppler-derived transmitral late to early diastolic peak velocity ratio (A/E ratio) during the exercise in 27 patients with ischemic heart disease. After the exercise, A/E ratio decreased in 16 patients with a remarkable elevation in LV preload, and increased in 11 with a mild elevation. Further, Doppler transmitral flow in conjunction with pulmonary venous flow and hemodynamic parameters were analyzed in 11 dogs during a worsening course of heart failure induced by dextran infusion. The relationship of A/E ratio to LV end-diastolic pressure showed a quadratic curve concave to the pressure axis. A/E ratio, an index expressing left atrial (LA) contribution to LV filling, returned to that seen before volume loading under the condition of cardiac dysfunction. Pulmonary venous reflux fraction determined as the ratio of peak velocity of pulmonary venous reflux during LA systole to the sum of systolic and diastolic peak velocities of pulmonary venous antegrade flow, did not increase here. In this situation, blood could not be ejected from the left atrium into the left ventricle and even into the pulmonary veins during LA contraction. Finally, LV filling was not compensated by the left atrium, and LA booster pump function itself was deteriorated.     

The impact of hypertension and hypertension-related left ventricle hypertrophy on right ventricle function

AIM: The aim of our study is to determine the effect of hypertension and hypertension-related left ventricle hypertrophy on right ventricle (RV) morphology and function by using RV standard Doppler echocardiographic indices, myocardial Doppler imaging, and strain/strain rate imaging indices. METHODS: We studied 35 patients with arterial hypertension and 30 age- and sex-adjusted control subjects who had no other pathological conditions. Standard transthoracic Doppler echocardiographical measurements, pulsed-wave tissue Doppler from tricuspid anulus (Peak systolic-st, peak early diastolic-et, peak late diastolic velocity-at), reconstructed spectral pulsed-wave tissue Doppler velocities (peak systolic-S, peak early-E, peak late diastolic velocity-A), and strain/strain rate imaging of RV free wall mid region (peak systolic strain-in, peak systolic strain rate-SR) were obtained. RESULTS: Age, body surface area, blood pressure, and heart rate were comparable between two groups. Hypertensive subjects had significantly increased LV end-diastolic septal and posterior wall thickness, left atrial diameter, LV mass, LV mass index, and relative wall thickness during diastole. At the level of right ventricular lateral tricuspid annulus without systolic changes, the majority of diastolic measurements were altered in hypertensives (early diastolic velocity et; 13 +/- 2 vs. 18 +/- 4 m/sec, P < 0.0001, late diastolic velocity at; 20 +/- 4 vs. 14 +/- 3 m/sec, P < 0.0001, early to late diastolic velocity ratio; 0.69 +/- 0.14 vs. 1.32 +/- 0.38, P < 0.0001). The velocity data from two-dimensional color myocardial imaging at the level of RV free wall mid region again showed altered diastolic measurements in hypertensives (E; 8.01 +/- 2.6 vs. 10.4 +/- 3.14 m/sec, P < 0.001, A; 11.5 +/- 2.6 vs. 9.12 +/- 3.7 m/sec, P < 0.0001, E/A ratio; 0.75 +/- 0.41 vs. 1.87 +/- 0.48, P < 0.00). The peak systolic strain of RV free wall mid region was significantly lower in hypertensive individuals than controls (25.666 +/- 5.64 vs. 30.03 +/- 6.78%, P < 0.05). No significant differences were found in other parameters of RV function between hypertensive and control subjects. CONCLUSIONS: The present study demonstrates that besides the manifest morphologic LV adaptations, significant RV functional alterations can be determined by TDI and strain/strain rate imaging in patients arterial hypertension. Both tissue velocities by TDI and strain imaging may be new tools to define and quantitate subtle change in systolic and diastolic function of right ventricular function in arterial hypertension that cannot be determined in standard echocardiographic parameters.     

Effects of captopril on left ventricular systolic and diastolic function after acute myocardial infarction.

The left ventricle progressively dilates in some patients after acute myocardial infarction (AMI). Both systolic and diastolic left ventricular (LV) dysfunction can be of significance in the development of heart failure. Captopril has been shown to prevent dilatation, but the effect on LV diastolic function is unknown. In a placebo-controlled double-blind parallel study, 58 AMI patients with heart failure or low ejection fraction, or both, were consecutively randomized at day 7 to either placebo or captopril (25 mg twice daily). No differences were present between the groups at baseline. Fifty-three patients completed the 6-month study period. Both LV diastolic and systolic volume indexes increased significantly in the placebo group (17 and 14%, respectively); in the captopril group there was no change in LV diastolic volume index, but a 13% reduction in LV systolic volume index. Ejection fraction increased significantly in the captopril group. The peak flow velocities of the early and atrial filling phases were measured, and the ratio between the velocities was calculated. A significant reduction was observed during the study period in early peak flow velocity (65 to 52 cm/s) and in the ratio between early and atrial peak flow velocity (1.3 to 0.8) in the placebo group (p less than 0.05), but no significant changes occurred in the captopril group. No correlation was found between dilatation of the left ventricle and reduction in early peak flow velocity or the ratio between early and atrial peak flow velocity. In conclusion, captopril prevented LV dilatation, improved ejection fraction and prevented LV diastolic dysfunction in AMI patients with early signs of LV systolic dysfunction.     

Respiratory influence on right and left ventricular diastolic function in normal children

Doppler echocardiograms of the tricuspid and mitral valves were recorded with electrocardiogram and respirations in 20 normal children aged 1.5 to 11 years. Four variables of early diastolic left ventricular (LV) filling decreased with inspiration: the peak E velocity (mean decrease 8%, p less than 0.0001), the ratio of E/A areas (mean decrease 12%, p less than 0.001), the peak E/A velocity ratio (mean decrease 14%, p less than 0.005) and the 1/3 area fraction (mean decrease 12%, p less than 0.001). Variables of late active atrial emptying (peak A velocity and A/total area ratio) were unchanged with respiration. There was a significant increase in the right ventricular (RV) peak E (mean increase 26%, p less than 0.0001) and peak A velocities (mean increase 18%, p less than 0.0001) and mean heart rate (5% increase) with inspiration. The enhancement of RV filling was similar for early and late diastolic filling, since each of the variables generated from their ratios were not significantly changed with inspiration. Inspiration significantly enhances RV venous return, while the LV response to inspiration is a complex interplay among preload, afterload and ventricular interdependence. Assessment of pediatric RV and LV diastolic function should include standardization for phase of respiration.     

Right ventricular diastolic function in systemic hypertension

Right (RV) and left ventricular (LV) diastolic function was evaluated in 50 patients with mild, uncomplicated essential hypertension using pulsed-wave Doppler echocardiography. Patients with pulmonary, valvular or coronary artery disease were excluded and antihypertensive drugs were discontinued for the 2 weeks preceding the study. Ten normotensive patients without heart disease acted as control subjects. In the hypertensive patients, RV peak velocity of atrial filling was higher (42 +/- 10 vs 31 +/- 7 cm/s, p less than 0.01) and deceleration half-time was prolonged (96 +/- 20 vs 83 +/- 10 ms, difference not significant); ratio of early/atrial filling velocity (1.1 +/- 0.3 vs 1.7 +/- 0.4, p less than 0.001) and peak filling rate corrected to stroke volume (3.6 +/- 0.7 vs 5.3 +/- 0.9 SV/s, p less than 0.001) were lower. LV filling parameters showed similar changes. RV filling parameters did not correlate with age, LV mass or septal thickness but correlated weakly with LV radius/thickness ratio. There was good correlation between RV and the following corresponding LV filling parameters: peak filling rate, r = 0.68, p less than 0.001; ratio of early/atrial filling, r = 0.88, p less than 0.0001; and deceleration half-time, r = 0.62, p less than 0.001. Data indicate that RV diastolic function is abnormal in essential hypertension and these abnormalities are closely related to those of LV diastolic function.     

Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size.

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65 +/- 2 years) were studied by Doppler echocardiography. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velocity integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between pressure half-time and infarct size as measured by peak enzyme release (r = -0.64, p < 0.001). These data suggest that, depending on infarct size, patients exhibit a "restrictive" filling pattern early after the acute event. This is manifested by the greater proportion of filling occurring in early diastole, reflecting an overall increase in chamber stiffness. At 6 weeks, this pattern is less pronounced presumably due to the remodeling process.