糖尿病对冠状动脉狭窄左室舒张末压的影响

目的:探讨糖尿病对冠状动脉狭窄患者左室舒张末压的影响。方法:选择行冠状动脉造影及左室造影的冠脉狭窄的患者662例,将之分为冠状动脉狭窄并发糖尿病组（CHD+DM组）110例,及单纯冠状动脉狭窄组（CHD组）552例,所有患者都进行左室造影,测定左室射血分数（LVEF）及左室舒张末压（LVEDP）。结果:两组患者LVEF间无明显差异,但CHD+DM组患者的LVEDP显著高于CHD组。结论:糖尿病可以加重冠状动脉狭窄对左室舒张功能的损害,引起LVEDP增高。     

The Effects of Simvastatin on Left Ventricular Hypertrophy and Left Ventricular Function in Patients with Essential Hypertension

This study is to evaluate the effects of Simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension. Untreated or noncompliance with drug treatment patients with simple essential hypertension were treated with a therapy on the basis of using Telmisartan to decrease blood pressure (BP). There were 237 patients who had essential hypertension combined with left ventricular hypertrophy as diagnosed by echocardiography, taken after their BPs were decreased to meet the values of the standard normal. Among them, there were only 41 out of the original 237 patients, 17.3%, who had simple essential hypertension combined with left ventricular hypertrophy without any other co-existing disease. They were the patients selected for this study. All patients were randomly, indiscriminately divided into two groups: one was the control group (Group T), treated with the Telmisartan-based monotherapy; the other was the target group (Group TS), treated with the Telmisartan-based plus simvastatin therapy. The changes of left ventricular hypertrophy and left ventricular function were rediagnosed by echocardiography after 1 year. The results we obtained from this study were as follows: (i) The average BPs at the beginning of the study, of simple essential hypertension combined with left ventricular hypertrophy, were high levels (systolic blood pressure (SBP) 189.21 ± 19.91 mm Hg, diastolic blood pressure 101.40 ± 16.92 mm Hg). (ii) The Telmisartan-based plus simvastatin therapy was significantly effective in lowering the SBP (128.26 ± 9.33 mm Hg vs. 139.22 ± 16.34 mm Hg). (iii) After the 1-year treatment, the parameters of left ventricular hypertrophy in both groups were improved. Compared to group T, there were no differences in the characteristics of the subjects, including interventricular septum, left ventricular mass, left ventricular mass index, ejection fraction, left atrium inner diameter at baseline. The patients’ interventricular septum (Group TS 10.30 ± 1.80 mm vs. Group T 10.99 ± 1.68 mm, P < .05), LVM (Group TS 177.43 ± 65.40 g vs. Group T 181.28 ± 65.09 g, P < .05), and LVMI (Group TS 100.97 ± 37.33 g/m² vs. Group T 106.54 ± 27.95 g/m², P < .05), all dropped more prominently (P < .05) in group TS; the ejection fraction rose more remarkably in group TS (Group TS: 57.50 ± 16.41% to 65.43 ± 11.60%, P < .01 while showing no change in Group T); the left ventricular hypertrophy reversed more significantly and the left ventricular systolic function improved more. (iv) The left atrium inner diameter of Group TS decreased (P < .01), the ratio of E/A, which indicates the left ventricular diastolic function, continued to drop further, showing no change to the trend of left ventricular diastolic function declination. Patients who have hypertension with left ventricular hypertrophy usually suffer other accompanying diseases at the same time. Telmisartan-based plus Simvastatin treatment can significantly reduce SBP, reverse left ventricular hypertrophy, improve the left ventricular systolic function, but it has no effect on reversing the left ventricular diastolic function. This experiment indicated that Simvastatin can reverse left ventricular hypertrophy and improve left systolic function.     

Echocardiographic evaluation of left ventricular end diastolic pressure in patients with diastolic heart failure: A comparative study with real-time catheterization

To evaluate the left ventricular end diastolic pressure (LVEDP) in patients with diastolic heart failure by echocardiography and explore the clinical value of echocardiography.From July 2017 to January 2018, 120 patients were prospectively selected from the affiliated hospital of Jiangsu university diagnosed as diastolic heart failure (York Heart Association class ≥II, LVEF ≥50%). The patients were divided into group with LVEDP ≤15 mm hg (1 mm hg = 0.133 kpa) (43 cases) and the group with LVEDP >15 mm hg (77 cases) according to the real-time measurement of LVEDP. Receiver operator characteristic curves of each parameter of echocardiography in diagnosis of LVEDP were compared between the 2 groups.Common ultrasonic parameters such as left ventricular inflow tract blood flow propagation velocity, mitral valve diastole e peak velocity/mitral valve diastole a peak velocity, e peak deceleration time, a peak duration, and early diastole interventricular septum bicuspid annulus velocity e’ (e''sep) were used to evaluate LVEDP elevation with low accuracy (AUC is only between 0.5 and 0.7). Other ultrasonic parameters such as left atrial volume index (LAVI), tricuspid regurgitation maximum flow rate (TRmax), early diastole left ventricular sidewall bicuspid annulus velocity e’ (e’lat), average e’, E/e''sep, E/e’lat, average E/e’ were used to evaluate LVEDP elevation with a certain improvement in accuracy (AUC between 0.7 and 0.9). Propagation velocity, mitral valve diastole e peak velocity/mitral valve diastole a peak velocity, e peak deceleration time, a peak duration, e''sep, average e’, E/e''sep have very low correlation with LVEDP (r = −0.283 to 0.281); LAVI, TRmax, e’lat, E/e’lat, average E/e’ and LVEDP are not highly correlated (r = 0.330–0.478). Through real-time left ventricular manometry, multiple regression analysis showed that TRmax, average e’, e’lat, LAVI were independently correlated with the actual measured LVEDP.Echocardiography can recognize the increase of LVEDP in patients with heart failure preserved by LVEF, and estimate the value of LVEDP roughly, which can reflect LVEDP to a certain extent, with high feasibility and accuracy.     

Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives

Summary Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p<0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p=ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s^-5, p<0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p<0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p<0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm², p<0.0001) and mass/volume ratio (2.14 to 2.01 p=0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r=–0.558 before and r=–0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.     

Effects of morphine on left ventricular dimensions and function in patients with previous myocardial infarction

To assess the effects of morphine sulfate on left ventricular function and dimensions we administered 15 mg of this agent to 11 stable patients with previous transmural myocardial infarction. All studies were carried out in the supine position. Before morphine administration an echocardiogram was obtained, and this procedure was repeated at 15, 30, 60, 120, and 240 min after morphine. Heart rate decreased from a control value of 69 +/- 4 to 62 +/- 5 beats/min 2 h after morphine (p less than 0.01, analysis of variance); this slower heart rate persisted for 4 h after morphine. Serial measurements of blood pressure, echocardiographic ejection fraction, percent of fractional shortening, and mean normalized velocity of circumferential fiber shortening also showed no significant alterations after morphine. We conclude that in stable patients with chronic ischemic heart disease studied in the supine position, 1) morphine exerts no effect on left ventricular dimensions, an observation which does not support the concept that this agent acts in humans by producing a 'pharmacologic phlebotomy'; and 2) morphine does not alter left ventricular function at rest. Whether different results will be found in patients with increased sympathetic activity, such as occurs in the setting of an acute myocardial infarction or during an episode of acute pulmonary edema, remains to be investigated.     

Diastolic left ventricular function after renal transplantation in patients with normal and hypertrophied myocardium

While diastolic left ventricular (LV) dysfunction is frequent and associated with cardiovascular complications in end-stage renal disease treated with dialysis, controversial information exists on diastolic LV function after renal transplantation. Therefore, Doppler echocardiographic parameters of LV diastolic filling were analyzed in 17 transplanted patients with normal LV mass (< 150 g/m2; mean: 128 +/- 17 g/m2) and 24 transplanted patients with LV hypertrophy (> 150 g/m2; mean: 197 +/- 36 g/m2) and compared with 28 normal controls without and 11 controls with LV hypertrophy. Mean age (normal vs. increased LV mass: 46 +/- 13 vs. 48 +/- 11 years; p = NS) and transplantation duration (60 +/- 35 vs. 50 +/- 37 months; p = NS) were comparable between renal patients, while systolic blood pressure (136 +/- 12 vs. 149 +/- 14 mmHg; p < 0.02) and serum creatinine (1.55 +/- 0.45 vs. 1.98 +/- 0.76 mg/dl; p < 0.05) were higher in patients with than without LV hypertrophy. In transplanted patients with LV hypertrophy, peak early/atrial filling velocity ratios were decreased (1.17 +/- 0.34 vs. 0.94 +/- 0.34; p < 0.05), mean atrial filling fractions were increased (37 +/- 7% vs. 42 +/- 7%; p < 0.05), and isovolumic relaxation periods were prolonged (86 +/- 23 vs. 106 +/- 26 ms; p < 0.02) compared with transplanted patients with normal LV mass. The frequency of pathologic peak early/atrial filling velocity ratios (12 vs. 42%; p < 0.05), atrial filling fractions (12 vs. 25%; p = NS) and isovolumic relaxation periods (6 vs. 29%; p = NS) was higher in transplanted patients with than without LV hypertrophy. Individual ratios of peak early/atrial filling velocity were inversely correlated with age in transplanted patients with normal LV mass (p < 0.002), and atrial filling fractions were correlated with LV mass index in transplanted patients with LV hypertrophy (p < 0.01). Diastolic LV function was comparable in both groups of transplanted patients with their corresponding non-renal controls. It is concluded that, in transplanted patients, diastolic LV filling is comparable to nonrenal controls; it is age-dependent in patients with normal LV mass and mass-dependent in those with LV hypertrophy.     

Left ventricular diastolic filling in patients with left ventricular dysfunction

The pattern of abnormal left ventricular diastolic filling and its specificity in coronary disease patients with severe left ventricular dysfunction has received little attention. We evaluated the left ventricular diastolic filling curve derived from gated blood pool scans in 21 normals, 61 coronary disease patients with ejection fractions less than or equal to 30%, and 51 congestive cardiomyopathy patients with ejection fraction less than or equal to 30%. The peak filling rate (PFR), peak ejection rate (PER), PFR/PER and the % stroke volume filled at 1/3 of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined for each group. The PFR and PER were reduced in both coronary disease and congestive cardiomyopathy groups. The PFR/PER was increased in the coronary disease group (1.19 +/- 0.28) and congestive cardiomyopathy group (1.21 +/- 0.32) as compared to normals (0.93 +/- 0.20, P less than 0.001). A greater %SV-1/3 DT and %SV-RFP were noted in both coronary disease and congestive cardiomyopathy groups. Coronary disease and congestive cardiomyopathy patients with a mean pulmonary capillary pressure (PCP) greater than or equal to 18 mm Hg had a greater PFR/PER, %SV-1/3 DT, and %SV-RFP than patients with a PCP less than 18 mm Hg. An abnormal and nonspecific pattern of left ventricular diastolic filling is present in both coronary disease and congestive cardiomyopathy patients and is characterized by an increased PFR/PER, a greater %SV-1/3 DT, and a greater %SV-RFP. This pattern may be related to elevated PCPs.     

Regression of left ventricular hypertrophy and systolic function in hypertensive patients during long-term treatment with ketanserin

Summary It is now generally accepted that antihypertensive therapy can induce regression of left ventricular hypertrophy (LVH) in hypertensive subjects. However, the influence of LVH reversal on both the systolic and diastolic functions, and particularly the ability of the heart to meet sudden overloads caused by exercise and/or recurrence of hypertension, remain unanswered questions. The long-term effects of ketanserin, a selective serotonin S₂-receptor antagonist with additional alpha₁-adrenergic blocking properties, on LVH and systolic function were studied in 13 untreated subjects (age range 35–55 years) with mild-to-moderate essential hypertension, echocardiographic evidence of LVH, and normal ejection fraction. Blood pressure values and echocardiographic measurements of dimensions, wall thicknesses, and indices of LV mass were determined before and after 3, 6, and 12 months treatment; ejection fractions at rest and during exercise were evaluated by equilibrium multigated radionucleide angiocardiography at baseline and after 12 months of therapy. Mean arterial pressure was significantly reduced from the first month of treatment (p<0.001) and remained well controlled up to the end of the trial. Both posterior and septum wall thicknesses decreased after 3 months of therapy and remained stable throughout the whole study period. LV mass index decreased from a mean ± SD of 187.7±47.6 g/m² to a mean of 157.81±31.63 g/m² (p<0.01) at the third month, reaching greater decreases after 6 months (156.05±31.00 g/m²) and after 12 months (153.21±28.80 g/m²) of treatment. A significant correlation was found between LV mass and posterior wall thickness at the different observation times in the study. Finally, the regression of LVH at the end of therapy was not associated with impairment of systolic function, as assessed by measurements of ejection fraction at rest and during exercise.     

Aging and left ventricular mass and function in people with end-stage renal disease

OBJECTIVES: To identify the main age‐related factors responsible for cardiomyopathy in people with end‐stage renal disease (ESRD). DESIGN: Cross‐sectional. SETTING: Dialysis unit. PARTICIPANTS: Two hundred fifty‐four individuals undergoing chronic dialysis. MEASUREMENTS: Left ventricular (LV) systolic function (assessed according to midwall fractional shortening (mwFS)) and LV mass index (LVMI). RESULTS: At echocardiography, 196 (77%) participants displayed LV hypertrophy (LVH) and 123 (48%) had LV systolic dysfunction. On univariate analysis, age was related directly to LVMI (correlation coefficient (r)=0.33, P<.001) and inversely to mwFS (r=?0.23, P<.001) and a 10‐year increase in age was associated with 4.2‐g/m^2.7 greater LVMI and 0.5% lower mwFS. Albumin, pulse pressure, cardiovascular comorbidities, and C‐reactive protein were age‐related risk factors for LVMI and mwFS, whereas hemoglobin was an age‐dependent risk factor only for LVMI and heart rate and diabetes mellitus only for mwFS. After adjusting for age‐related risk factors, the predictive value of age for cardiomyopathy was substantially less (–67%) and the age‐dependent variability in LVMI and mwFS was much attenuated (?61%), and neither was significant. CONCLUSION: This study suggests that in people with ESRD, the relationship between age and cardiomyopathy is largely dependent on age‐related risk factors and that interventions focused on modifiable risk factors linked to age (e.g., malnutrition and inflammation) could attenuate the detrimental effect of aging on cardiovascular risk in the dialysis population.     

超声观察高血压左室重构的临床意义

应用心脏超声按Ganau法对82例高血压患者的左室重构进行观察。结果显示:正常构形36例（占44％）;向心性重构6例（7％）;向心性肥厚11例（14％）和偏心性肥厚29例（35％）。     

Left ventricular muscle mass and diastolic function in patients with essential hypertension under long-term clonidine monotherapy

To determine whether alterations of left ventricular (LV) structure are associated with improved LV function under chronic clonidine monotherapy (300-450 g/day) of essential hypertension, 11 male patients (age range 47-61 years) were followed for 5.4 +/- 0.9 months using echocardiography and Doppler echocardiography. Blood pressure decreased from a mean of 168/105 to 150/96 mmHg (p less than 0.01), heart rate remained unchanged (73 +/- 10 vs. 71 +/- 10 beats/min). LV muscle mass decreased from 350 +/- 73 to 297 +/- 56 g (p less than 0.02), LV volume/muscle mass ratio increased from 0.58 +/- 0.13 to 0.69 +/- 0.12 ml/g (p less than 0.005). Ejection time increased from 276 +/- 17 to 296 +/- 17 ms (p less than 0.01), whereas no significant change was found for pre-ejection period, ejection fraction, cardiac index and LV dimensions. Doppler analysis revealed improved isovolumic relaxation time (116 +/- 17 vs. 84 +/- 28 ms; p less than 0.05), but no change in isovolumic contraction duration, maximal inflow velocities, time-velocity integrals and their duration, rate of acceleration and deceleration of early and atrial filling, and of their ratios. It is concluded that no reliable improvement in diastolic or systolic LV function is observed in chronic clonidine monotherapy of essential hypertension despite a normalization of blood pressure and a regression of LV hypertrophy.     

Cross-sectional multiplane transesophageal echocardiographic measurements: comparison with standard transthoracic values obtained in the same setting

BACKGROUND: Several algorithms developed for cost-effective use of transesophageal echocardiography (TEE) propose elimination of "screening" transthoracic echocardiographic (TTE) studies. Cross-sectional measurements obtained by TTE (left atrial diameter [LAD], left ventricular internal dimensions in diastole and systole [LVIDd, LVIDs], septal and posterior wall thickness in diastole [VSTd, PWTd], LV end-diastolic and end-systolic volumes [LVEDV and LVESV], and LV ejection fraction [LVEF]) have not been standardized for TEE. METHODS: Forty-six patients (age 27 to 85 years, 60 +/- 13 years, 25 [54%] women) underwent TEE and TTE studies. TTE was performed while the TEE probe was in place and the patient was still sedated. Standard TTE measurements were compared with corresponding TEE values obtained from mid-esophageal and transgastric views. RESULTS: Standard TTE measurements compared favorably with those obtained by TEE at the mid-esophageal three-chamber view for LAD (3.9 +/- 0.6 cm vs 4.0 +/- 0.7 cm, P = NS) and at the transgastric long-axis view for LVIDd (4.6 +/- 0.8 cm vs 4.7 +/- 0.8 cm, P = NS), LVIDs (3.1 +/- 0.9 cm vs 3.1 +/- 0.9 cm, P = NS), and VSTd (0.95 +/- 0.18 cm vs 0.98 +/- 0.19 cm, P = NS). Biplane TTE and TEE measurements of LVEDV (106 +/- 35 ml vs 112 +/- 38 ml, P = NS), LVESV (37 +/- 23 ml vs 37 +/- 25 ml, P = NS), and LVEF (67 +/- 14% vs 69 +/- 14%, P = NS) also correlated closely. The negative predictive values of TEE measurements for excluding abnormal LAD, LVIDd, VSTd, PWTd, and LVEF as defined by TTE were 83%, 94%, 95%, 97%, and 97%, respectively. CONCLUSION: Cross-sectional TEE measurements as obtained in this study are equivalent to standard TTE dimensions and provide reliable information that may facilitate interpretation of TEE studies in the absence of TTE information.     

Relationship between left ventricular geometry and left ventricular systolic and diastolic functions in patients with chronic severe aortic regurgitation

Background: Chronic aortic regurgitation (AR) is a form of volume overload inducing left ventricle (LV) dilatation. Myocardial fibrosis, apoptosis, progressive LV dilatation, and eventually LV dysfunction are seen with the progression of disease. The aim of the study was to assess the relation between LV geometry and LV systolic and diastolic functions in patients with chronic severe AR. Methods: The study population consisted of 88 patients with chronic severe AR and 42 healthy controls. The LV ejection fraction (LVEF) was calculated. Subjects were divided as Group I (controls, n = 42), Group II (LVEF > 50%, n = 47), and Group III (LVEF < 50%, n = 41). Transmitral early and late diastolic velocities and deceleration time were measured. The annular systolic (Sa) and diastolic (Ea and Aa) velocities were recorded. Diastolic function was classified as normal, impaired relaxation (IR), pseudonormalization (PN), and restrictive pattern (RP). Results: The LVEF was similar in Group I and II, while significantly lower in Group III. Sa velocity was progressively decreasing, but LV long- and short-axis diameters were increasing from Group I to Group III. Forty-six, 31 and 11 patients had IR, PN, and RP, respectively. LV long-axis systolic and diastolic diameters were significantly increasing, while LVEF and Sa velocity were significantly decreasing from patients with IR to patients with RP. The LV long-axis diastolic diameter is independently associated with LV systolic and diastolic functions. Conclusions: The LV long-axis diastolic diameter is closely related with LV systolic and diastolic functions in patients with chronic severe AR.     

左室舒张性心功能障碍超声左心形态、功能及运动耐量的改变50例分析

对核素心血池扫描证实的５０例左室舒张性心功能障碍（ＬＶＤＤ）病例、２６例左室收缩性心功能障碍（ＬＶＳＨＦ）病例进行Ｍ型、二维、多普勒超声心动图及活动平板运动试验检测，并以２０例正常人为对照组（ＣＧ）。结果表明：（１）左心形态学改变：与ＬＶＳＨＦ组比较，ＬＶＤＤ组左房内径（ＬＡＤ）、左室内径（ＬＶＤ）无明显增加，室间隔厚度（ＩＶＳＴ）、左室后壁厚度（ＰＷＴ）增加。与ＣＧ组比较，ＬＶＤＤ组ＬＡＤ、ＩＶＳＴ、ＰＷＴ增加，但ＬＶＤ差异无显著性。（２）ＬＶＤＤ组收缩功能指标：左室射血分数（ＬＶＥＦ）、心脏指数（ＣＩ）与ＣＧ组比较差异无显著性，ＬＶＳＨＦ组与ＣＧ组比较，ＬＶＳＨＦ组ＬＶＥＦ、ＣＩ减低。与ＣＧ组比较，ＬＶＤＤ组左室舒张功能指标：二尖瓣舒张早期流速峰值（ＥＰＦＶ）、二尖瓣舒张早、晚期流速峰值比（Ｅ／Ａ）、舒张早期减速度（ＤＣ）比ＣＧ组减低，二尖瓣舒张晚期流速峰值（ＡＰＦＶ）、等容舒张时间（ＩＲＴ）较ＣＧ组增高。ＬＶＤＤ组各左室舒张功能指标与ＬＶＳＨＦ组差异无显著性。（３）ＬＶＤＤ组运动时间、运动当量显著低于ＣＧ组，但高于ＬＶＳＨＦ组。     

The Relationship Between Aortic Stiffness and Left Ventricular Dyssynchrony in Hypertensive Patients with Preserved Left Ventricular Systolic Function

Left ventricular (LV) dyssynchrony is often seen in patients with hypertension, even without heart failure. Arterial stiffness is well accepted as an important factor of increasing blood pressure and influencing ventricular function. The purpose of this study was to determine the relationship between aortic stiffness and LV dyssynchrony in hypertensive patients with preserved LV systolic function. Eighty hypertensive patients with preserved LV systolic function (LV ejection fraction > 50%) and 30 controls were studied. The LV systolic and diastolic dyssynchrony indices were determined as the standard deviation of the time interval from onset of the QRS complex to peak myocardial systolic velocity (Ts-SD) and to early diastolic velocity (Te-SD) and the maximal differences in Ts (Ts-Max) and Te (Te-Max) in 12 LV segments. Aortic stiffness index was calculated from aortic diameters in the systolic and diastolic phases, as measured by echocardiography and blood pressure. No relationship was observed between LV systolic and diastolic dyssynchrony indices (r = 0.057, P = .61). In simple regression, aortic stiffness parameter was related to left ventricular mass index (LVMI), E/A ratio, and LV diastolic dyssynchrony index. But using multiple linear regression, Te-Max remained as a single variable related to aortic strain and aortic stiffness index (r = ?0.271, P = .008 and r = 0.269, P = .008). LVMI was related to aortic distensibility using multiple linear regression (r = ?0.239, P = .02). Aortic stiffness index was related to LV diastolic dyssynchrony index and LVMI. These findings suggest that LV diastolic dyssynchronous changes may be caused by increased LV mass and arterial stiffness.     

Patients with ankylosing spondylitis have evidence of left ventricular asynchrony

Objectives: Ankylosing spondylitis (AS) is a chronic inflammatory disease that often leads to cardiovascular complications including aortic regurgitation and conduction disturbances. Left ventricular (LV) systolic asynchrony is defined as loss of the simultaneous peak contraction of corresponding cardiac segments. The aim of this study was to evaluate LV systolic asynchrony noninvasively in patients with AS by using tissue synchrony imaging (TSI). Methods: Asynchrony was evaluated in 77 AS patients (61 male, mean age 36.4 ± 10 years) and 40 controls (35 male, mean age 39.1 ± 8.2 years). All study population underwent a comprehensive echocardiographic evaluation including TSI. The time to regional peak systolic velocity (Ts) during the ejection phase in LV was measured from TSI images by the six‐basal and six‐midsegmental model, and four TSI parameters of systolic asynchrony were computed. Results: The baseline demographic and echocardiographic characteristics were similar between the patients enrolled and controls. All TSI parameters of LV asynchrony were prolonged in patients with AS compared to controls: the standard deviation (SD) of the 12 LV segments Ts (39.6 ± 19.6 vs. 24.7 ± 11.6, P < 0.001); the maximal difference in Ts between any 2 of the 12 LV segments (122.1 ± 52.9 vs. 82.2 ± 38.6, P < 0.001); the SD of the six basal LV segments (33.5 ± 20.2 vs. 23 ± 13.3, P = 0.008); and the maximal difference in Ts between any two of the six basal LV segments (84.6 ± 48.1 vs. 60.4 ± 34.6, P = 0.008). The asynchrony parameters were significantly correlated with index of myocardial performance (Tei index) and peak systolic mitral annular velocity. Conclusion: TSI showed presence of LV systolic asynchrony in patients with AS which may account for the cardiovascular complications of AS. (Echocardiography 2012;29:661‐667)     

Left ventricular mechanical efficiency in hypertensive patients with and without increased myocardial mass and with normal pump function

Left ventricular hypertrophy (LVH) is a physiologic process of adaptation of the heart to mechanical load increase. Despite depression of left ventricular contractile performance, mechanical efficiency and ventriculoarterial coupling are preserved in hypertensive patients with LVH. To assess the differences between patients with and without LVH, left ventricular contractile performance and the ventriculoarterial coupling were compared in two groups of hypertensive patients with similar body surface area and arterial pressures, and normal pump function: 30 patients with LVH (group 1) and 23 without LVH (group 2). Left ventricular angiography coupled with simultaneous recording of pressures with a micromanometer were used to determine end-systolic stress-to-volume ratio (ESSVR), end-systolic elastance (Ees), effective arterial elastance (Ea), external work (EW), and pressure–volume area (PVA). Myocardial contractile performance, assessed by Ees normalized by myocardial mass and by ESSVR, was lower in group 1 than in group 2 (1.23 ± 0.28 v 1.89 ± 0.48 mm Hg/mL/100 g, and 3.85 ± 0.99 v 5.13 ± 0.56 g/cm²/mL, respectively, both P < .001). Ventriculoarterial coupling evaluated through Ea/Ees ratio, and mechanical efficiency evaluated through EW/PVA ratio, were similar in the two groups (0.53 ± 0.08 v 0.51 ± 0.05, and 0.78 ± 0.03 v 0.80 ± 0.02, respectively, NS). In conclusion, this study shows that ventriculoarterial coupling and mechanical efficiency are comparable in hypertensive patients with and without LVH. These results suggest that in hypertensive patients, the matching between left ventricular performance and arterial load and the energy transfer are preserved either through left ventricular hypertrophy with moderate depression of myocardial contractile performance or through enhancement of myocardial contractile performance in patients with normal left ventricular mass.