Instantaneous assessment of left ventricular midwall mechanics with tissue Doppler tracking technique

BACKGROUND: Left ventricular (LV) systolic function is better characterized by midwall mechanics in patients with LV hypertrophy than by endocardial LV function, and the midwall mechanics is an independent predictor of prognosis. However, a complex calculation is currently required to assess it, and it is not routinely assessable in clinical practice. Tissue Doppler imaging enables tracking of a point within the LV wall though a cardiac cycle; we tested our hypothesis that the tissue Doppler tracking technique provides an instantaneous and reliable evaluation of midwall mechanics. METHODS: LV M-mode echocardiogram was recorded in 18 subjects with conventional echocardiography and with tissue Doppler imaging. The midwall shortening was calculated from the data obtained with conventional echocardiography for the comparison with that measured with the tissue Doppler tracking technique. The tissue Doppler-determined midwall shortening correlated well with conventionally calculated value (r=.84, P<.0001), and their difference was small irrespective of absolute value of the midwall shortening. CONCLUSIONS: The midwall mechanics can be instantaneously and accurately evaluated with the tissue Doppler tracking technique.     

Analysis of left ventricular systolic function using midwall mechanics in patients >60 years of age with hypertensive heart disease and heart failure

Normal ejection fraction (EFs) is often equated with normal systolic function. However, midwall mechanics reveal systolic dysfunction in hypertensive heart disease accompanied by hypertrophic remodeling. Midwall mechanics are unstudied in patients with acute diastolic heart failure (HF). This study analyzed left ventricular (LV) midwall stress-shortening relations in 61 patients aged >60 years with hypertensive heart disease, HF, and normal EF. Sixty-one hypertensive patients (mean age 78 +/- 10 years) who presented with HF, each with an EF >50%, underwent echocardiography. Midwall mechanics were compared with those of 79 controls (mean age 75 +/- 8 years) without structural heart disease. Relative wall thickness (0.63 +/- 0.11 vs 0.46 +/- 0.10 mm) and LV mass (237 +/- 67 vs 177 +/- 57 g) were significantly greater in patients with HF compared with controls. Mean EFs were similar in patients with HF and controls (64 +/- 9% vs 67 +/- 9%). Although mean endocardial fractional shortening (35 +/- 7% vs 37 +/- 7%) was not significantly different, midwall shortening in patients with HF was significantly less compared with controls (16 +/- 2% vs 19 +/- 3%, p <0.05). Eighteen of the 61 patients with HF (30%) had midwall shortening that was <95% confidence intervals of the normal midwall stress-shortening relations. By this criterion, these patients had systolic dysfunction despite normal EF; they had smaller LV chambers (in dimension and volume), greater relative wall thickness, and smaller stroke volumes. In conclusion, almost 1/3 of patients hospitalized with diastolic HF had systolic dysfunction, characterized by abnormal midwall stress-shortening relations.     

Association of inappropriate left ventricular mass with systolic and diastolic dysfunction: the HyperGEN study

BACKGROUND: Left ventricular mass (LVM) exceeding values appropriate for individual workload is associated with concentric LV geometry and systolic dysfunction at both the midwall and chamber levels, even independently of clearcut LV hypertrophy, and is a marker of adverse prognosis. No information is available on whether inappropriate LVM is associated with alterations of LV diastolic properties in unselected population-based studies. METHODS: We examined 1513 hypertensive participants from the HyperGEN population who were without prevalent cardiovascular disease. The LVM prediction from stroke work (systolic blood pressure x Doppler stroke volume), sex, and height (in meters2.7) was derived in 210 nonobese, normal individuals. Observed/predicted LVM >133% defined inappropriate LVM. RESULTS: Participants with inappropriate LVM (229 subjects [15%]) exhibited higher LV dimensions and relative wall thickness, lower ejection fraction, midwall shortening and cardiac output, and prolonged isovolumic relaxation time (IVRT; P < or = .001). Other diastolic abnormalities were not associated with inappropriate LVM. After accounting for demographic and hemodynamic confounders, IVRT was directly related to excess LVM, whereas deceleration time of E velocity was negatively related to excess LVM. Nonechocardiographic correlates of prolonged relaxation included aging, African American ethnicity, male gender, and diabetes. CONCLUSIONS: The LVM exceeding the compensatory needs for workload is associated with delayed LV relaxation as well as mild midwall and chamber systolic dysfunction, independently of demographic, clinical, and hemodynamic confounders. Inappropriately high LVM also correlates with features of increased myocardial stiffness, coexisting with evidence of prolonged LV relaxation.     

Ventricular and myocardial function following treatment of hypertension

This study assesses and evaluates left ventricular (LV) contractile function after treatment of hypertension, with an emphasis on LV midwall mechanics. Although prior studies have assessed cardiac function after hypertension treatment, none has performed an analysis of LV midwall mechanics. The Veterans Affairs Study of monotherapy in hypertension was a study large enough to permit analysis of midwall mechanics across a wide spectrum of mass changes accompanying hypertension treatment. LV chamber function was assessed by computing fractional shortening at the endocardial surface; LV midwall shortening was used to define myocardial function. Both shortening indexes were related to end-systolic circumferential stress in the entire population by partitioning values of mass and relative wall thickness changes. Two hundred sixty-eight patients were studied at baseline and again after a 1- or 2-year period. In the entire group, there was no significant change in circumferential shortening either at the endocardium (38 +/- 8% at baseline vs 37 +/- 7% at follow up, p = 0.29) or in shortening at the midwall (20 +/- 3% vs 20 +/- 3%, p = 0.53). However, 83 patients had a reduction in relative wall thickness and an increase in midwall shortening. The change in midwall shortening was significantly related to changes in relative wall thickness (r = -0.53, p = 0.0001). Thus, reductions in LV mass associated with antihypertensive therapy are generally not accompanied by a decrement in LV chamber or myocardial function. Improvement in midwall shortening is more closely related to normalization of LV geometry than to reduction in LV mass.     

Left ventricular systolic and diastolic function after anthracycline chemotherapy in childhood

BACKGROUND: In childhood, late cardiotoxicity is characterized by inappropriately thin wall and consequent increased end-systolic wall stress, but the associations of impaired left ventricular geometry and function occurring under these circumstances need further investigation. HYPOTHESIS: The purpose of this study was to assess anthracycline late effects on the relationships occurring between increased end-systolic stress (ESS) and changes in both M-mode systolic measurements (i.e., endocardial and midwall fractional shortening) and Doppler diastolic indices in the pediatric age. METHODS: The population consisted of 101 children treated with anthracyclines for at least 12 months and 91 healthy children. Using M-mode echocardiography, end-systolic wall stress was calculated as index of afterload, and endocardial and midwall fractional shortening as systolic indices. Doppler transmitral measurements were made as diastolic indices. RESULTS: Patients treated with anthracyclines showed significantly lower relative wall thickness and left ventricular mass index, greater end-systolic wall stress, reduced endocardial and midwall fractional shortening and peak E/A ratio, prolonged deceleration, and isovolumic relaxation times. Direct relationships were found between end-systolic wall stress and both endocardial and midwall shortening. The use of midwall shortening in the relation showed a greater, but not significant increase (from 3 to 6%) in the proportion of patients with depressed systolic function than did endocardial shortening. In the anthracycline group, end-systolic wall stress was also inversely related to relative wall thickness and directly to isovolumic relaxation time. CONCLUSIONS: In childhood, reduced myocardial thickness and increased afterload explain much of systolic and diastolic dysfunction of late anthracycline toxicity. Midwall fractional shortening does not seem to add useful information for identifying subsets of children more prone to the development of heart failure.     

Improvement in midwall myocardial shortening with regression of left ventricular hypertrophy

Despite normal indices of left ventricular (LV) chamber function, patients with LV hypertrophy (LVH) due to hypertension are thought to have depressed midwall systolic shortening compared with normotensives. The aims of the present study were (1) to confirm this observation and (2) to assess the effects of antihypertensive therapy that cause regression of LVH on LV systolic function assessed at both the midwall and endocardium. Thirty-eight previously untreated hypertensive subjects with LVH underwent echocardiography and were compared with 38 normotensive control subjects. Comparisons between the group with LVH and the control group revealed no significant differences in cardiac output (4. 32+/-0.23 versus 4.55+/-0.21 L/min), ejection fraction (62.5+/-2% versus 66.4+/-1.07%), or endocardial fractional shortening (34.5+/-1.45% versus 37.0+/-0.82%), but shortening assessed at the midwall was significantly less in the group with LVH (17.9+/-1.11% versus 21.6+/-0.63%, P<0.01). Subsequently, 32 patients with uncontrolled hypertension (24 previously untreated and 8 on existing antihypertensive therapy) underwent treatment with ramipril, with the addition of felodipine and bendrofluazide if required, to reduce blood pressure to <140/90 mm Hg. These 32 patients underwent echocardiography at baseline, after blood pressure control, and after an additional 6 months of tight blood pressure control. Good blood pressure control was achieved after 6 months compared with baseline (143/86+/-2.8/1.4 versus 174/103+/-4.1/1.9 mm Hg; P<0.01) with significant regression of LV mass index (124+/-3.4 versus 145+/-3.8 g/m(2), P<0.01). LV fractional shortening assessed at the midwall improved with regression of LVH (21.9+/-0.84 and 18.7+/-1. 19%, P<0.05), with posttreatment midwall shortening being similar to that of the normal control subjects evaluated in the first study. Hypertensive patients with LVH have depressed midwall systolic shortening despite normal indices of LV chamber function. Regression of LVH after good blood pressure control improved midwall shortening to normal levels.     

Effect of electrocardiographic left ventricular hypertrophy on left ventricular systolic function in systemic hypertension (The LIFE Study). Losartan Intervention For Endpoint

Left ventricular (LV) ejection fraction is normal in most patients with uncomplicated hypertension, but the prevalence and correlates of decreased LV systolic chamber and myocardial function, as assessed by midwall mechanics, in hypertensive patients identified as being at high risk by the presence of LV hypertrophy on the electrocardiogram has not been established. Therefore echocardiograms were obtained in 913 patients with stage I to III hypertension and LV hypertrophy determined by electrocardiographic (Cornell voltage duration or Sokolow-Lyon voltage) criteria after 14 days' placebo treatment. The 913 patients' mean age was 66 years, and 42% were women. Fourteen percent had subnormal LV endocardial shortening, 24% had subnormal midwall shortening, and 13% had reduced stress-corrected midwall shortening. Nineteen percent had normal LV geometry, 11% had concentric remodeling, 47% had eccentric hypertrophy, and 23% had concentric hypertrophy. LV systolic performance evaluated by LV endocardial shortening and midwall shortening was impaired in 10% of patients with normal geometry, 20% with concentric remodeling, 27% with eccentric hypertrophy, and 42% with concentric hypertrophy. Relative wall thickness, an important independent correlate of LV chamber function, was related directly to endocardial shortening and negatively to midwall shortening and stress-corrected midwall shortening. LV mass was the strongest independent correlate of impaired endocardial shortening, midwall shortening, or both. In hypertensive patients with electrocardiographic LV hypertrophy, indexes of systolic performance are subnormal in 10% to 42% with different LV geometric patterns. Depressed endocardial shortening is most common in patients with eccentric LV hypertrophy, whereas impaired midwall shortening is most prevalent in patients with concentric remodeling or hypertrophy. Thus, in hypertensive patients with electrocardiographic LV hypertrophy, impaired LV performance occurs most often, and is associated with greater LV mass and relative wall thickness and may contribute to the high rate of cardiovascular events.     

Left ventricular midwall mechanics in subjects with aortic stenosis and normal systolic chamber function

BACKGROUND AND AIM OF THE STUDY: Endocardial indices of left ventricular (LV) systolic function overestimate myocardial performance in hypertrophic left ventricles. Midwall fractional shortening (mFS) is a more reliable index of systolic performance. Aortic stenosis (AS) is a common cause of LV hypertrophy (LVH), but midwall mechanics in this condition have not been analyzed. Also, a tendency towards hyperdynamic LV chamber function has been reported in women with AS in comparison with men, but whether there exist gender-related discrepancies in midwall performance is not known. METHODS: The study group included 147 patients with AS and normal chamber systolic function. LV diameters and thicknesses, LV mass, relative wall thickness (RWT), endocardial fractional shortening, stroke volume, ejection fraction (EF), mFS and stress-corrected mFS were determined. RESULTS: Patients with AS showed depressed mFS (16.2 +/- 2.5% versus 18.8 +/- 2.4%, p <0.0001) and stress-corrected mFS (84.3 +/- 13.8% versus 100.0 +/- 12.6%, p <0.0001) when compared to controls. The subset with moderate AS had lower mFS (15.9 +/- 2.0%) than those with mild AS (16.9 +/- 2.4%), and further depression was present in subjects with severe AS (13.8 +/- 2.2%, p <0.0001). A similar trend was observed for stress-corrected mFS (mild AS, 88.5 +/- 13.3%; moderate AS, 82.0 +/- 11.5%; severe AS, 71.2 +/- 12.0%, p <0.0001). Multivariate analysis identified RWT as the best predictor of mFS and stress-corrected mFS. Logistic regression showed that depressed stress-corrected mFS was independently associated with the presence of symptoms. Endocardial fractional shortening and EF were increased in women compared to men, but there were no gender-related differences in mFS (16.2 +/- 2.5% versus 16.1 +/- 2.4%, p = 0.84) and stress-corrected mFS (84.0 +/- 14.1% versus 84.5 +/- 13.5%, p 0.82). CONCLUSION: Aortic stenosis is associated with depression in LV midwall mechanics. Systolic midwall performance reduces as the severity of valve disease increases, and this relationship is mediated by parallel changes in LV geometry.     

Gender differences in systolic left ventricular function in hypertensive patients with electrocardiographic left ventricular hypertrophy (the LIFE study)

Echocardiography was performed in 944 untreated hypertensive patients (391 women and 553 men, mean age 66 years) who had electrocardiographic left ventricular (LV) hypertrophy at baseline in the Losartan Intervention For End point reduction in hypertension (LIFE) study to evaluate gender-associated differences in systolic LV function. Women had significantly lower diastolic blood pressure (175/97 vs 173/99 mm Hg) and body surface area and a higher body mass index (all p < 0.01). Women also had higher LV ejection fraction (EF), endocardial and midwall fractional shortening (63% vs 60%, 35% and 33%, and 16% vs 15%, respectively, all p < 0.01), higher stress-corrected midwall fractional shortening (98% vs 96%, p < 0.05), and lower circumferential end-systolic wall stress (178 vs 187 kdynes/cm(2), p < 0.01). There was no difference in age or LV mass indexed for height(2.7), but relative wall thickness was higher in women (0.42 vs 0.41, p < 0.05). In multiple regression analyses: (1) EF and endocardial fractional shortening were 2% to 3% higher in women than men, independent of the effects of LV stress, body mass index, and height (multiple r = 0.77 and 0.75, respectively, gender p < 0.02 in both models); (2) midwall fractional shortening was 0.5% higher in women, independent of the effects of age, body mass index, circumferential end-systolic stress, and absence of diabetes (multiple r = 0.36, p = 0.014 for gender); and (3) stress-corrected LV midwall fractional shortening was 2% higher (p = 0.004) in women, independent of the effects of age, height, heart rate, body mass index, and diabetes (multiple r = 0.33). Thus, female gender is an independent predictor of higher systolic LV function in hypertensive patients with electrocardiographic LV hypertrophy.     

Subclinical left ventricular dysfunction in systemic hypertension and the role of 24-hour blood pressure

The relation between blood pressure (BP) and left ventricular (LV) systolic function in systemic hypertension is controversial. We assessed the relation of LV midwall fractional shortening (FS) to 24-hour BP in 1,702 never-treated hypertensive subjects (age 48 +/- 12 years), who underwent 24-hour BP monitoring and echocardiography. Stress-corrected endocardial and midwall FS (the latter calculated taking into account the epicardial migration of midwall during systole) were predicted in hypertensives on the basis of the values observed in 130 healthy normotensives (age 43 +/- 13 years, office BP 126/78 mm Hg). Subjects below the fifth percentile of observed-to-predicted FS had depressed LV function. The use of midwall FS resulted in an increase from 3.5% to 17.5% in the proportion of patients with depressed chamber function. Compared with the group with normal function, subjects with low midwall LV function had similar office systolic BP (155 +/- 21 vs 154 +/- 17 mm Hg), but increased 24-hour systolic BP (140 +/- 17 vs 133 +/- 12 mm Hg, p <0.001). Midwall FS had a closer negative relation to 24-hour systolic BP than to office systolic BP (r = -0.27 vs -0.08, p <0.001), whereas this difference was not apparent for diastolic BP (r = -0.23 vs -0.20). Compared with endocardial FS, midwall FS had a stronger inverse association to LV mass (r = -0.45 vs -0.16, p <0.001). Thus, an increased 24-hour BP load may chronically lead to depressed myocardial function in systemic hypertension in the absence of clinically overt heart disease.     

Apical left ventricular asynergy in chronic aortic regurgitation

Apical left ventricular (LV) wall motion abnormalities have been described in chronic volume overload. To evaluate if these abnormalities are due to an actual hypokinesia we analyzed the percent shortening of apical LV radiants (PS%) by an angiographic computerized method and the endocardial systolic movement (ESM) and thickening (%Th) of the same region using M-mode echocardiographic technique in 11 patients affected by pure aortic regurgitation (AR). In these patients mean apical radii shortening was reduced with respect to normal values. Both %Th and ESM were significantly reduced in AR when compared to normal subjects (24.5 +/- 31.7% vs. 63.8 +/- 35.8%, p less than 0.01 and 4 +/- 7 vs. 10 +/- 3 mm, p less than 0.01, respectively). In addition, %Th and ESM directly correlated with PS% (r = 0.79, p less than 0.01 and r = 0.77, p less than 0.01, respectively). PS% correlated positively with systolic eccentricity and inversely with end-systolic volume index (r = 0.64, p less than 0.05 and r = 0.57, p less than 0.05, respectively). Finally, in AR %Th was related to a normalized peak rate of systolic wall thickening (r = 0.85, p less than 0.01) and to a normalized peak rate of diastolic wall thinning (r = 0.68, p less than 0.05). These results showed that in AR a reduced apical radii percent shortening was associated with a reduced normalized peak rate of systolic wall thickening and of diastolic wall thinning, thus indicating an actual hypokinesis and an impaired contractility. Moreover, the observed abnormalities correlated with an altered LV dynamic geometry linked to chronic volume overload.     

Left ventricular mass and systolic dysfunction in essential hypertension

A relation between left ventricular (LV) hypertrophy and depressed midwall systolic function has been described in hypertensive subjects. However, a strong confounding factor in this relation is concentric geometry, which is both a powerful determinant of depressed midwall systolic function and a correlate of LV mass in hypertension. To evaluate the independent contribution of LV mass to depressed systolic function, 1827 patients with never-treated essential hypertension (age 48 +/- 12 years, men 58%) underwent M-mode echocardiography under two-dimensional guidance. Relative wall thickness was the strongest determinant of low midwall fractional shortening (r = -0.63, P < 0.0001). The significant inverse relation observed between LV mass and midwall fractional shortening (r = -0.43, P < 0.0001) persisted after taking into account the effect of relative wall thickness (partial r = -0.27, P < 0.0001). Within each sex-specific quintile of relative wall thickness, prevalence of subnormal afterload-corrected midwall systolic function was greater in subjects with, than in subjects without, LV hypertrophy (P < 0.05 for the first, third, fourth and fifth quintile). In a multiple linear regression analysis, both LV mass (P < 0.0001) and relative wall thickness (P < 0.0001) were independent predictors of a reduced midwall fractional shortening. In conclusion, the inverse association between LV mass and midwall systolic function is partly independent from the effect of relative wall thickness. LV hypertrophy is a determinant of subclinical LV dysfunction independently of the concomitant changes in chamber geometry.     

Midwall myocardial shortening in athletic left ventricular hypertrophy

BACKGROUND: Patients with pathological left ventricular hypertrophy have depressed midwall systolic shortening in spite of normal indices of left ventricular chamber function and a reduced midwall function has been observed to be an independent predictor of cardiovascular risk. Whether midwall shortening is depressed in physiological hypertrophy is unknown. METHODS: Forty-two subjects, 27 athletes and 15 age- and sex-matched normal control subjects (group 1) were studied. The athletes were divided into those with eccentric hypertrophy (group 2) and those with concentric hypertrophy (group 3). Systolic left ventricular function was assessed at the midwall and endocardium using two-dimensional echocardiography in all subjects. RESULTS: Left ventricular mass index was significantly greater in both athletic groups than in controls (group 1, 101+/-5.8 g/m(2), group 2, 141+/-11.1*, group 3, 155+/-5.8*; *P<0.01 compared with group 1). Left ventricular systolic function assessed at the endocardium was similar among all three groups (ejection fraction: group 1, 66.2+/-2.38, group 2, 66.8+/-1.44, group 3, 63.7+/-1.66%; endocardial fractional shortening: group 1, 37.1+/-1.71, group 2, 37.6+/-1.13, group 3, 35.1+/-1.25%). However, fractional shortening at the midwall was reduced in the concentric hypertrophy athletes compared with the other two groups (midwall fractional shortening: group 1, 21.9+/-1.1, group 2, 21.9+/-0.86, group 3, 18.4+/-0.96*%; P<0.05 compared with groups 1 and 2). CONCLUSION: Subjects with physiological concentric hypertrophy have depressed midwall fractional shortening. This suggests that the observed discrepancy between midwall and endocardial shortening in patients with left ventricular hypertrophy is likely to be a function of the geometry and not necessarily a reflection of pathology within the myocardium.     

M-mode echocardiography overestimates left ventricular mass in patients with normal left ventricular shape: a comparative study using three-dimensional echocardiography.

AIMS: We sought to evaluate whether left ventricular (LV) mass (M) determined by M-mode echocardiography is overestimated compared with LVM calculated by three-dimensional (3D) echocardiography (E) in patients with normal LV shape. METHODS AND RESULTS: A total of 112 studies in 56 patients (60+/-13 years) with hypertension (n=25) or aortic stenosis (n=31) and 30 control subjects (57+/-14 years) evaluated for cardiac sources of embolism were analyzed. LVM by M-mode and 3DE was highly correlated (r=0.85; p<0.001). However, there were broad limits of agreement (-58 to 110 g) demonstrating large variability between the methods. M-mode overestimated 3DE LVM by a mean of 15+/-24% (p<0.001) with overestimation in controls and the different patient groups. Variability was unrelated to increasing quartiles of LVM values. Using technique-specific partition values for normal LVM, the agreement between M-mode and 3DE for the detection of LV hypertrophy was 83% (Kappa=0.59; p<0.001). CONCLUSION: Although M-mode and 3DE correlate well for the calculation of LVM, there is a systematic difference between the two techniques leading to overestimation of LVM by the 1D technique. Thus, previously published cutoff values for normal LVM derived from M-mode may not apply for 3DE. However, the use of technique-specific partition values allows stratification of patients for the presence of LV hypertrophy with reasonable agreement.     

Left ventricular chamber and wall mechanics in the presence of concentric geometry.

BACKGROUND: To test the hypothesis that in the presence of left ventricular concentric geometry the definition of 'normal' ejection fraction should be reconsidered, and normality should rather be considered to have a higher than usual lower limit METHODS: M-mode echocardiographic endocardial shortening (eS) was studied in 148 hypertensive patients with left ventricular concentric geometry (relative wall thickness > or = 0.42), 78 with normal (54 +/- 10 years, 27 women) and 70 with depressed midwall shortening (mS) (53 +/- 10 years, 26 women), based on normal distribution of stress-corrected mS, and compared to a reference adult population of 297 age-matched normal subjects (54 +/- 8 years, 121 women) with eS > or = 28%. RESULTS: Patients with low mS exhibited higher heart rates and body mass indices than control individuals (both P < 0.01); blood pressure, left ventricular mass, relative wall thickness and peripheral resistance were higher than in patients with normal mS, whereas cardiac index was reduced (all P< 0.01). Adjustment for body mass index and race attenuated but did not eliminate the differences between the two groups of patients (0.05 < P < 0.0001). In contrast, eS was higher than normal in patients with normal midwall shortening, whereas was 'normal' in patients with low left ventricular midwall function. More than 80% of patients in the lowest quartile of apparently normal eS exhibited clear-cut low left ventricular midwall function. CONCLUSIONS: 'Normal' left ventricular chamber function in the presence of concentric geometry is associated with depressed midwall performance, more severe left ventricular hypertrophy, lower cardiac output and higher peripheral resistance. 'Normal' eS is the hallmark of normal myocardial function when left ventricular geometry is normal, but should be considered as a marker of systolic dysfunction when associated with concentric left ventricular geometry. Normal limits for eS should be therefore reset to upper values.     

Changes in midwall systolic performance and cardiac hypertrophy reduction in hypertensive patients

OBJECTIVE: To investigate changes in left ventricular (LV) performance, as evaluated by measurement of midwall LV fractional shortening (FS), after reduction of cardiac hypertrophy. DESIGN AND METHODS: Echocardiographic evaluation of LV anatomy and function was performed by M-mode echocardiography at baseline, after long-term antihypertensive therapy, and after treatment withdrawal in 68 asymptomatic hypertensive patients (50 males, 18 females, age range 22-62 years). Patients were divided according to the presence of LV hypertrophy (LVH) at baseline (LV mass index, LVMI, > or = 51 g/m(2.7)). RESULTS: At baseline patients with concentric (relative wall thickness > 0.44) LV hypertrophy (n = 38) or remodelling (n = 7) had reduced midwall shortening with respect to patients with normal LV geometry (n = 4) or eccentric LVH (n = 19); no differences were observed for endocardial FS. After long-term treatment (average 15 months), in 11 patients LV mass remained within normal limits, in 45 patients LVH reduction was obtained, while in 12 patients LV mass remained persistently elevated. Midwall FS was significantly increased in patients with reduction of LVH both during treatment and after withdrawal of treatment, while it remained significantly lower in patients with persistently elevated LV mass. Changes in midwall fractional shortening were independently associated with modifications in relative wall thickness (P < 0.00001), with changes in end-diastolic dimensions (P < 0.0001) and those of LVMI (P< 0.02) as shown by multivariate analysis. CONCLUSION: LV midwall systolic performance significantly improved after reduction of LVH, even in the presence of high blood pressure values. Modifications in relative wall thickness are more independently associated with changes, in LV diastolic dimensions and mass, to midwall improvement     

Relations of longitudinal left ventricular systolic function to left ventricular mass, load, and Doppler stroke volume.

AIMS: To evaluate whether the peak systolic velocities of the displacement of the lateral mitral anulus (Sa) and of the mid-portion of the interventricular septal wall (Sm) correlate with measures of left ventricular load, left ventricular mass, and Doppler stroke volume in normotensive and hypertensive subjects without clinically overt cardiovascular disease. METHODS AND RESULTS: Tissue Doppler imaging was used to evaluate Sa and Sm in apical 4-chamber view; standard echocardiographic procedures were used to assess left ventricular structure and traditional parameters of systolic function (ejection fraction, stress-corrected midwall shortening, meridional and circumferential end-systolic stress); pulsed Doppler was employed to evaluate stroke volume. In 87 subjects meeting inclusion criteria, Sa and Sm were not significantly correlated either with left ventricular end-diastolic volume and end-systolic stress, or with stroke volume; in contrast, endocardial and midwall fractional shortening were lower with higher afterload, as expected. Fractional shortening at endocardium and midwall, and Sm were lower with higher left ventricular mass. Mean Sa and Sm values were lower in subjects with low vs. those with normal stress-corrected midwall shortening, but low Sa was not associated with lower stress-corrected midwall shortening in our study sample. CONCLUSIONS: While Sa and Sm might be indices of longitudinal left ventricular systolic mechanics, they should not be considered as measures of left ventricular contractility alternative to well-established parameters of systolic function, such as stress-corrected midwall shortening, in subjects at rest without overt heart disease.     

Left ventricular structural and functional characteristics in Cushing's syndrome

OBJECTIVES: This study was designed to evaluate left ventricular (LV) anatomy and function in patients with Cushing's syndrome. BACKGROUND: A high prevalence of LV hypertrophy and concentric remodeling has been reported in Cushing's syndrome, although no data have been reported on LV systolic and diastolic function. METHODS: Forty-two consecutive patients with Cushing's syndrome and 42 control subjects, matched for age, gender, and blood pressure, were studied. Left ventricular mass index (LVMI) and relative wall thickness (RWT) were measured by echocardiography, endocardial and midwall fractional shortening (FS) were assessed, and diastolic filling was measured by Doppler transmitral flow. RESULTS: The RWT was significantly greater in Cushing patients than in controls. Left ventricular hypertrophy and concentric remodeling were observed in 10 and 26 patients with Cushing's syndrome, respectively. In Cushing patients, midwall FS was significantly reduced compared with controls (16.2 +/- 3% vs. 21 +/- 4.5%, p = 0.01). The ratio of transmitral E and A flow velocities was reduced and E deceleration time was prolonged in Cushing patients compared with controls (p = 0.03 and p < 0.001, respectively). CONCLUSIONS: In patients with Cushing's syndrome, cardiac structural changes are associated with reduced midwall systolic performance and with diastolic dysfunction that may contribute to the high risk of cardiovascular events observed in these patients.     

Effect of regression of left ventricular hypertrophy from systemic hypertension on systolic function assessed by midwall shortening (HOT echocardiographic study)

Depressed midwall shortening has been shown to be an independent predictor of cardiovascular morbid events in hypertensive patients with left ventricular (LV) hypertrophy despite normal endocardial fractional shortening. The effects of LV mass changes in hypertensive patients on midwall shortening are unclear. To determine the impact of LV hypertrophy regression on LV systolic function assessed at the endocardium and the midwall level, 508 patients (58% men, 57% Caucasians, mean age 60 +/- 7 years) participating in the Hypertension Optimal Treatment study were prospectively studied by serial echocardiography at baseline, year 1, year 2, and at the end of the study. The Hypertension Optimal Treatment study was designed to challenge the existence of the J-curve phenomenon in hypertension. This study enrolled men and women between 50 and 80 years of age with mild to moderate hypertension. Patients were treated with a regimen based on felodipine with the addition of other antihypertensive drug classes as needed to reduce the diastolic blood pressure to a predefined target of < or =80, < or =85, or < or =90 mm Hg. From baseline to year 1, year 2, and end of the study, body mass index was unchanged (30.4, 30.1, 30.2, and 30.5 kg/m(2)); however, diastolic blood pressure was significantly reduced (99, 83, 80, and 80 mm Hg, p <0.0001), as was systolic blood pressure (161, 139, 137, and 134 mm Hg, p <0.0001) and LV mass index (117, 119, 107, and 106 g/m(2), p <0.0001). Over the same period of observation the endocardial fractional shortening did not change significantly (40%, 42%, 43%, and 44%); however, shortening at the midwall level showed improvement (20%, 21%, 22%, and 30%, p <0.001). In conclusion, midwall shortening is a more sensitive index of systolic function in subjects with pressure-overload hypertrophy, and it identifies high-risk patients who may benefit from a more aggressive antihypertensive program. The disparity between midwall and endocardial shortening suggests reduced myofibril function in patients with hypertension-induced hypertrophy.     

Left ventricular midwall mechanics in systemic arterial hypertension. Myocardial function is depressed in pressure-overload hypertrophy

BACKGROUND. Left ventricular (LV) midwall geometry has been described conventionally as the sum of the chamber radius and half of the wall thickness; this convention is based on the assumption of uniform transmural thickening during systole. However, theoretical considerations and experimental data indicate that the inner half (inner shell) of the LV wall thickens more than the outer half (outer shell). Thus, an end-diastolic circumferential midwall fiber exhibits a relative migration toward the epicardium during systole. As a result, the conventional method provides an overestimate of the extent of the midwall fiber shortening. METHODS AND RESULTS. We developed an ellipsoidal model with a concentric two-shell geometry (nonuniform thickening) to assess midwall fiber length transients throughout the cardiac cycle. This modified midwall method was used in the analysis of LV cineangiograms from 15 patients with systemic arterial hypertension and 14 normal subjects. Study groups were classified according to LV mass index (LVMI): 14 normal subjects (group I), eight hypertensive patients with a normal LVMI (group II), and seven hypertensive patients with an increased LVMI (group III). There were no significant differences in LV end-diastolic pressure or volume among the three groups; the ejection fraction was slightly greater in group II (70 +/- 5%) than in groups I (65 +/- 8%) and III (66 +/- 4%), but this trend did not achieve statistical significance. Values for endocardial and conventional midwall fractional shortening (FS) were also similar in the three groups. By contrast, FS by the concentric two-shell geometry (modified midwall method) in group III (16 +/- 2%) was significantly less than that seen in groups I and II (21 +/- 4% and 21 +/- 5%, respectively; both p less than 0.05). This difference achieves greater importance when it is recognized that mean systolic circumferential stress was lower in group III (151 +/- 22 g/cm2) than in groups I and II (244 +/- 37 g/cm2 and 213 +/- 38 g/cm2, respectively; both p less than 0.01). The midwall stress-shortening coordinates in six of the seven group III patients were outside the 95% confidence limits for the normal (group I) subjects. Thus, despite a normal ejection fraction, systolic function is subnormal in hypertensive patients with LV hypertrophy. CONCLUSIONS. Chamber dynamics provide an overestimate of myocardial function, especially when LV wall thickness is increased. This is due to a relatively greater contribution of inner shell thickening in pressure-overload hypertrophy.