Alteration of the longitudinal function of the left ventricle in hypertensives with systolic function of normal appearance]

Left ventricular (LV) transverse function is often used by the echocardiography to evaluate the systolic function in arterial hypertension (HTN). It would be interesting to know whether the LV long axis systolic dysfunction may precede the abnormalities of the transverse function in hypertension (HTN). For that purpose we evaluated by echo 36 patients (24 males, 12 females) with LV concentric hypertrophic (Lvmi > 134 g/m2 for men and > 110 g/m2 for women). All subjects were free of coronary heart disease and heart failure. According to the dimensions of the LV wall chickness (WTh) the HTN were subdivided in two groups: Group 1: Wth (12-14 mm) and Group 2: WTh (> 14 mm). The patients were compared to 30 healthy persons (control group) matched for age and LV systolic function (Fractional Shortening). METHODS: LV long axis shortening was measured at the septal and lateral sides of the mitral annulus using M-mode from the apical four chamber view. RESULTS: Compared to control group, septal long axis shortening fell significantly (p < 0.05) in proportion to the degree of the wall thickness: control group: 21 +/- 2 mm. Group 1: 16 +/- 1 mm and Group 2: 14 +/- 1 mm. Lateral shortening was reduced only in the Group 2 (15 +/- 2 vs 20 +/- 2 mm) (p < 0.05). LV wall thickness correlated significantly (p < 0.05) to septal and lateral shortening respectively (r = -0.51) and (r = -0.48). CONCLUSIONS: 1. Significant impairment of LV long axis function occurs in arterial hypertension with concentric hypertrophy even with normal transverse systolic function. 2. This alteration seems to be related to the dimensions of the LV wall thickness. 3. The prognostic implication of this disorder should be investigated further.     

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.     

Effect of angiotensin type I-receptor blockade on left ventricular remodeling in pressure overload hypertrophy.

BACKGROUND: The renin-angiotensin system is involved in cardiac remodeling. In contrast to the well-recognized salutary effects of angiotensin-converting enzyme inhibition, the value of angiotensin II type I (AT(1))-receptor blockade on left ventricular (LV) hypertrophy and dysfunction is controversial. METHODS AND RESULTS: Descending thoracic aorta-banded and sham-operated guinea pigs were given either losartan (30 mg x kg(-1) x day(-1) intraperitoneally) or vehicle for 8 weeks (n = 7 in each group). LV end-diastolic and end-systolic dimensions and wall thicknesses were measured echocardiographically, and LV fractional shortening, relative wall thickness, and LV mass normalized by body weight were calculated. Isolated heart function (Langendorff perfusion) was studied 8 weeks after surgery, and LV performance was assessed by maximum LV pressure and +/-dP/dt normalized by LV mass. Eight weeks after banding guinea pigs developed concentric LV hypertrophy and had decreased maximum LV pressure and +/-dP/dt normalized by LV mass; LV end-diastolic dimension and LV fractional shortening were unchanged. In band-operated guinea pigs treatment with losartan had no significant effects on any of these measurements. CONCLUSIONS: In guinea pigs with descending aortic banding, treatment with losartan for 8 weeks neither attenuates progression of pressure overload hypertrophy nor significantly improves impaired mass-normalized pressure-derived indices of LV contraction and 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.     

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     

Systolic and diastolic dysfunction during atrial pacing in conscious dogs with left ventricular hypertrophy

To determine the extent to which the hypertrophied left ventricle responds to the chronotropic stress induced by graded atrial pacing rates, we studied conscious, chronically instrumented dogs with severe compensated pressure overload left ventricular (LV) hypertrophy induced by aortic banding in puppies 8-10 weeks of age. At 1-2 years, dogs with severe LV hypertrophy (LV free wall/body wt ratio 6.8 +/- 0.6 g/kg) and sham-operated littermates (LV free wall/body wt ratio 4.0 +/- 0.3 g/kg) were instrumented with ultrasonic dimension crystals to measure LV short axis internal diameter and wall thickness, miniature LV pressure transducers, and aortic and LV catheters. During atrial pacing (240 beats/min) in eight control dogs, LV pressure did not change from 119 +/- 2 mm Hg, and mean velocity of circumferential fiber shortening (VCF) did not change from 1.25 +/- 0.09/sec. In seven dogs with LV hypertrophy, atrial pacing (240 beats/min) decreased systolic LV function; that is, LV systolic pressure decreased (p less than 0.01) by 65 +/- 12 from 254 +/- 14 mm Hg, and VCF decreased (p less than 0.01) by 0.19 +/- 0.03 from 0.97 +/- 0.15/sec. Diastolic dysfunction was also observed in the dogs with LV hypertrophy. In the control dogs during atrial pacing (240 beats/min), LV end-diastolic pressure decreased (p less than 0.01) by 8 +/- 1 from 9 +/- 1 mm Hg, end-diastolic stress decreased (p less than 0.01) by 18 +/- 2 from 22 +/- 2 g/cm2, and the radial myocardial stiffness constant did not change from 5.6 +/- 1.0.(ABSTRACT TRUNCATED AT 250 WORDS)     

Marked regional left ventricular heterogeneity in hypertensive left ventricular hypertrophy patients: a losartan intervention for endpoint reduction in hypertension (LIFE) cardiovascular magnetic resonance and echocardiographic substudy

Concentric hypertensive left ventricular (LV) hypertrophy is presumed to be a symmetrical process. Using MRI-derived intramyocardial strain, we sought to determine whether segmental deformation was also symmetrical, as suggested by echocardiography. High echocardiographic LV relative wall thickness in hypertensive LV hypertrophy allows preserved endocardial excursion despite depressed LV midwall shortening (MWS). Depressed MWS is an adverse prognostic indicator, but whether this is related to global or regional myocardial depression is unknown. We prospectively compared MWS derived from linear echocardiographic dimensions with MR strain(in) in septal and posterior locations in 27 subjects with ECG LV hypertrophy in the Losartan Intervention for Endpoint Reduction in Hypertension Study. Although MRI-derived mass was higher in patients than in normal control subjects (124.0+/-38.6 versus 60.5+/-13.2g/m(2); P<0.001), fractional shortening (30+/-5% versus 33+/-3%) and end-systolic stress (175+/-22 versus 146+/-28 g/cm(2)) did not differ between groups. However, mean MR(in) was decreased in patients versus normal control subjects (13.9+/-6.8% versus 22.4+/-3.5%), as was echo MWS (13.4+/-2.8% versus 18.2+/-1.4%; both P<0.001). For patients versus normal control subjects, posterior wall(in) was not different (17.8+/-7.1% versus 21.6+/-4.0%), whereas septal(in) was markedly depressed (10.1+/-6.6% versus 23.2+/-3.4%; P<0.001). Although global MWS by echocardiography or MRI is depressed in hypertensive LV hypertrophy, MRI tissue tagging demonstrates substantial regional intramyocardial strain(in) heterogeneity, with most severely depressed strain patterns in the septum. Although posterior wall 2D principal strain was inversely related to radius of curvature, septal strain was not, suggesting that factors other than afterload are responsible for pronounced myocardial strain heterogeneity in concentric hypertrophy.     

Left ventricular hypertrophy in hypertension: functional aspects

The purpose of this study was to detect the anatomical and functional response of the left ventricle in essential, uncomplicated hypertension. Fifty outpatients, whose hypertension (DBP greater than 95 mmHg on three separate visits) had been documented from few weeks to a maximum of 5 years, showing neither electrocardiographic abnormalities nor other signs referable to target organ damage, underwent an M-mode, computerised echocardiographic study. Twenty-seven patients has never been treated, and 23 patients were withdrawn from previous treatments for at least one month. Echocardiographic data of the left ventricle were compared with those of 38 normals, matched by sex, age and body surface area. Hypertensives showed a significant increase in both LV mass index (p less than 0.001) and relative wall thickness (p less than 0.001), a pattern of concentric hypertrophy, which prevented an inappropriate rise in wall tension. Twenty-four patients, whose LV mass was above the mean normal value plus two standard deviations, were considered to have left ventricular hypertrophy. The remaining 26 patients were classified as non hypertrophic, for their mass resulted lower than the mean value of controls plus 2 SD: left ventricular mass was 152 +/- 32 g/m2 and 97 +/- 19 g/m2, respectively (p less than 0.001). Systolic performance was enhanced in both subgroups of hypertensives, since their values of fractional shortening and those of mean-Vcf were both above the line which represents the normal relationship with end-systolic stress. Diastolic relaxation, evaluated by means of time to peak filling rate, was impaired only in the hypertensive subjects with increased LV mass (p less than 0.001 vs. normotensive), being retained in the non-hypertrophic patients. In the whole hypertensive group, LV mass index poorly correlated with casual systolic blood pressure (r = 0.31; p less than 0.05), while time to peak filling rate showed a good correlation with LV mass index (r = 0.76; p less than 0.001). We conclude that: 1) in essential hypertension without electrocardiographic abnormalities or target organ damage, echocardiographic left ventricular hypertrophy is a rather frequent finding; 2) the pattern of concentric hypertrophy, by reducing the increase in wall tension due to pressure load, contributes to the retained, or enhanced, systolic performance seen in our series; 3) on the other hand, left ventricular filling seems to be impaired in relation to the degree of myocardial hypertrophy.     

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.     

Association of left bundle branch block with left ventricular structure and function in hypertensive patients with left ventricular hypertrophy: the LIFE study

Electrocardiographic (ECG) left bundle branch block (LBBB) is associated with left ventricular hypertrophy (LVH), but its relation to left ventricular (LV) geometry and function in hypertensive patients with ECG LVH is unknown. Echocardiograms were performed in 933 patients (548 women, mean age 66+/-7 years) with essential hypertension and LVH by baseline ECG in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. LBBB, defined by Minnesota code 7.1, was present in 47 patients and absent in 886 patients. Patients with and without LBBB were similar in age, gender, body mass index, blood pressure, prevalence of diabetes, and history of myocardial infarction. Despite similarly elevated mean LV mass (126+/-25 vs 124+/-26 g/m(2)) and relative wall thickness (0.41+/-0.07 vs 0.41+/-0.07, P=NS), patients with LBBB had lower LV fractional shortening (30+/-6 vs 34+/-6%), ejection fraction (56+/-10 vs 61+/-8%), midwall shortening (14+/-2 vs 16+/-2%), stress-corrected midwall shortening (90+/-13 vs 97+/-13%) (all P<0.001), and lower LV stroke index (38+/-7 vs 42+/-9 ml/m(2)) (P<0.05). Patients with LBBB also had reduced LV inferior wall and lower mitral E/A ratio (0.75+/-0.18 vs 0.87+/-0.38) (all P<0.05). The above univariate results were confirmed by multivariate analyses adjusted for gender, age, blood pressures, height, weight, body mass index, heart rate, and LV mass index. Among hypertensive patients at high risk because of ECG LVH, the presence of LBBB identifies individuals with worse global and regional LV systolic function and impaired LV relaxation without more severe LVH by echocardiography.     

Racial differences in left ventricular structure in healthy young adults.

Racial differences in cardiac structure and function were evaluated in 62 black and 71 white healthy young adults. Left ventricular (LV) mass index, relative wall thickness, fractional shortening, resting cardiac index and resting systemic vascular resistance index were estimated using M-mode echocardiography. Pulsed Doppler interrogation of transmitral flow was used to characterize LV filling. Average daytime blood pressure (BP) was determined by ambulatory monitoring during a typical work or school day. Ambulatory daytime BP averaged 127 +/- 12/80 +/- 7 mm Hg in black subjects, and 127 +/- 9/80 +/- 6 mm Hg in white subjects (p = not significant). The 2 groups were also similar in resting BP, age and gender composition. Relative wall thickness was significantly greater in black than in white subjects (0.37 +/- 0.06 vs 0.34 +/- 0.05; p less than 0.01). This difference was found in both men and women. Black subjects also had a higher resting systemic vascular resistance index (2,110 +/- 570 vs 1,920 +/- 500 dynes.s.cm-5.m2; p less than 0.05) and lower resting cardiac index (3.14 +/- 0.84 vs 3.46 +/- 0.85 L/min/m2; p less than 0.05). There were no significant differences between black and white subjects in LV mass index, fractional shortening and normalized peak filling velocity. These results suggest that racial differences in LV structure and systemic hemodynamics exist even in patients without sustained hypertension. In our study population, the greater relative wall thickness in black subjects was not accompanied by significant differences in LV systolic function or diastolic filling.     

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.     

Left ventricular diastolic function in physiologic and pathologic hypertrophy

BACKGROUND: Patients with hypertensive heart disease and left ventricular hypertrophy demonstrate an impaired left ventricular diastolic filling pattern. The aim of this study was to find out whether physiologic left ventricular hypertrophy induced by endurance training causes disturbances in left ventricular systolic and diastolic filling. METHODS: We examined 49 athletes with left ventricular (LV) hypertrophy due to endurance training, 49 patients with LV hypertrophy due to arterial hypertension, and 26 untrained healthy control subjects by conventional echocardiography. Parameters of LV diastolic filling using pulse wave and color flow Doppler were also assessed. RESULTS: All three study groups showed normal fractional shortening and mid-wall fractional shortening. Conventional echocardiography revealed a higher LV muscle mass index in the two study groups compared with the controls (athletes, 99 +/- 10 g; hypertensive patients, 95 +/- 11 g: controls: 52 +/- 7 g; P < .01 for athletes and hypertensive patients). In patients with arterial hypertension, a diastolic dysfunction consisting of a delayed relaxation pattern with a decrease in maximal early velocity of diastolic filling (0.44 +/- 0.1 m/sec) and a compensatory increase of the maximal late velocity of diastolic filling (0.53 +/- 0.1 m/sec) was demonstrated. In athletes with physiologic LV hypertrophy, a normal LV diastolic filling pattern was documented. CONCLUSIONS: Doppler echocardiographic parameters of LV diastolic function can be of diagnostic importance for discrimination between pathologic and physiologic LV hypertrophy.     

Heart failure in pressure overload hypertrophy. The relative roles of ventricular remodeling and myocardial dysfunction

OBJECTIVES: We sought to explore the relative contributions of ventricular remodeling and myocardial dysfunction to heart failure in pressure overload hypertrophy (POH). BACKGROUND: The mechanism that underlies heart failure in POH is adverse left ventricular (LV) chamber remodeling or decreased myocardial function, or a combination of these. METHODS: Twenty weeks after suprarenal aortic banding in rats, animals with POH were classified as those with heart failure (POH-HF) or those with no heart failure (POH-NHF). The LV chamber and myocardial systolic and diastolic functions were determined from in vivo and ex vivo experiments. RESULTS: The LV mass was similar in both POH groups. Chamber remodeling in the POH-HF group was characterized by marked LV enlargement with a normal relative wall thickness (eccentric remodeling), whereas remodeling in the POH-NHF group was characterized by a normal chamber size and increased relative wall thickness (concentric remodeling). The LV systolic function, as determined in vivo from the end-systolic pressure-diameter relationship and ex vivo from the pressure-volume relationship, was lower in the POH-HF group than in the POH-NHF and sham-operated control groups. In contrast, myocardial function was similar in both POH groups, as determined in vivo from the stress-midwall fractional shortening relationship and myocardial systolic stiffness, and ex vivo from the slope of the LV systolic stress-strain relationship. The diastolic chamber stiffness constant was lower in the POH-HF group than in the POH-NHF group, but the myocardial stiffness constant was similar in the two POH groups. CONCLUSIONS: The two POH groups differed primarily in their remodeling process, which led to a chronically compensated state in one group and to heart failure in the other. Hence, heart failure in POH is more closely related to deleterious LV remodeling than to depressed myocardial function.     

Effect of increased wall thickness on indices of left ventricular pump function in children.

OBJECTIVE--To investigate whether augmented chamber performance in children with a concentric hypertrophied left ventricle is due to increased myocardial shortening or a geometric effect of the thickened ventricular wall. DESIGN--Chamber performance in terms of fractional area change and myocardial shortening--that is, circumferential midwall shortening--were measured by cross sectional echocardiography in young people with normal left ventricles and those with concentric hypertrophy of the left ventricle. PATIENTS--52 healthy infants, children, and young people (age range 3 1/2 weeks to 26 years; body weight 1.8-89 kg (mean 23.6 kg)) and 29 infants, children, and adolescents with ventricular hypertrophy (mean body weight 31.4 kg, age range 4 weeks to 18.7 years). MAIN OUTCOME MEASURES--Chamber areas, fractional area change, midwall circumferential shortening normalised to body weight. RESULTS--In the controls normalised reference values were: end diastolic cavity area, 1.47 (0.25) cm2/kg0.65; fractional area change, 0.56 (0.03); end diastolic myocardial area, 1.62 (0.25) cm2/kg0.55; midwall circumferential shortening, 0.21 (0.03). By comparison, the patients had normal chamber areas (end diastolic myocardial area, 1.57 (0.42) cm2/kg0.65), increased fractional area change, 0.68 (0.05) (P < 0.001), and normal midwall circumferential shortening, 0.21 (0.03). There was a significant relation between the degree of hypertrophy (in terms of end diastolic myocardial area) and pump function while midwall shortening remained constant: 0.08 x end diastolic myocardial area + 0.44 (r = 0.74, P < 0.001). CONCLUSIONS--The relation between myocardial shortening, wall thickness, and fractional area change emphasises that the augmentation of pump function variables in left ventricular hypertrophy in young people is an effect of the thickened wall and not necessarily due to increased myocardial shortening. This relation offers the possibility of assessing the adequacy of chamber performance with respect to the degree of hypertrophy.     

Left ventricular mass regression in the LIFE study: effect of previous antihypertensive treatment

BACKGROUND: Whether to include only those patients who have not had prior hypertension treatment in clinical trials of left ventricular (LV) mass reduction is controversial. Accordingly, our aim was to study the relationship between prior treatment and both baseline and 1-year echocardiographic LV mass in subjects enrolled in the Losartan Intervention For Endpoint reduction (LIFE) study. METHODS: We studied clinical and baseline echocardiographic data on 960 patients with electrocardiographically confirmed left ventricular hypertrophy enrolled in the electrocardiographic substudy of the LIFE study, 847 of whom had LV mass remeasured after 1 year of blinded treatment. The majority (75%) of these patients had prior medical treatment for hypertension. RESULTS: In multivariable regression analysis, controlling for age, sex, blood pressure (BP), body mass index, and indices of pump and myocardial function, prior antihypertensive treatment was not associated with either greater LV mass or relative wall thickness on the baseline study. Moreover, there was no significant difference between the 637 subjects who were previously treated and the 210 who were not treated with regard to the mean reduction in systolic or diastolic pressures (-25 +/- 17 v -24 +/- -16 and -13 +/- 9 mm Hg v -12 +/- 9 mm Hg), LV mass (-27 +/- 38 v -29 +/- 34 g), or LV mass/body surface area (-14 +/- 20 v -15 +/- 18 g/m(2)), all P >.05. CONCLUSIONS: Prior treatment is not associated with either greater LV mass or greater relative wall thickness when age, body mass index, sex, systolic BP, heart rate, or indices of LV volume load and systolic function are taken into account. In addition, prior treatment is not associated with lesser degrees of LV mass reduction. For design of future clinical trials, restriction of inclusion criteria to only previously untreated patients does not appear to be necessary when the selection criterion is electrocardiographically determined left ventricular hypertrophy.     

Left ventricular structure and function in primary hyperparathyroidism before and after parathyroidectomy

OBJECTIVE: Our aim was to study the effect of primary hyperparathyroidism (PHPT) and parathyroidectomy (PTX) on left ventricular (LV) wall thicknesses and systolic and diastolic function. METHODS: Fifteen patients with untreated PHPT were evaluated by applying Doppler and digitized M-mode echocardiography before and 2-3 months after PTX. Fifteen age- and sex-matched healthy controls were also examined echocardiographically. RESULTS: Prior to PTX, interventricular septal thickness (IVST), LV mass (LVM), aortic root dimension and left atrium dimension were greater and LV fractional shortening was slightly decreased in patients as compared to controls. Significantly increased LV peak late diastolic velocity (A(max)) and isovolumic relaxation time, and a slightly decreased ratio of peak early to peak late diastolic velocities (E/A(max)) in the patients indicated impairment of LV diastolic function in hyperparathyroidism. PTX reduced serum total Ca from 2. 79 +/- 0.13 to 2.39 +/- 0.09 mmol/l (p < 0.001) and tended to reduce IVST [10.6 +/- 2.1 vs. 10.4 +/- 2.0 mm; not significant (n.s.)], LV posterior wall thickness (9.6 +/- 2.0 vs. 9.2 +/- 1.0 mm, n.s.) and LVM (250 +/- 102 vs. 213 +/- 42 g; n.s.). Before PTX, there was a significant correlation between serum total Ca and LVM (r = 0.63, p < 0.05), and the PTX-induced change in serum total calcium correlated with the change in LVM (r = 0.59, p < 0.05). PTX induced no significant changes in LV systolic or diastolic function during the follow-up of 2-3 months. CONCLUSIONS: The present findings indicate that PHPT induces LV hypertrophy, slight impairment of LV systolic function and significant impairment of LV diastolic function, which are not substantially improved after TX and 2-3 months of normocalcemia.     

Influence of left ventricular hypertrophy and function on the occurrence of ventricular tachycardia in hypertrophic cardiomyopathy.

Sixty-nine patients with hypertrophic cardiomyopathy were studied by 2-dimensional and Doppler echocardiography and 72-hour Holter monitoring to examine the relation between the degree of left ventricular (LV) hypertrophy and dysfunction and the occurrence of ventricular tachycardia (VT). Episodes of nonsustained VT were detected in 20 patients (29%). Maximal wall thickness was not different between patients with (22 +/- 5 mm) and without (21 +/- 5 mm) VT. Total hypertrophy score, calculated as the sum of 10 segmental wall thicknesses, was also similar in both groups (157 +/- 22 and 153 +/- 32 mm, respectively; p = not significant). Furthermore, no significant differences were found between the 2 groups in LV end-diastolic dimension (41 +/- 7 vs 40 +/- 6 mm), fractional shortening (33 +/- 7 vs 34 +/- 10%) and left atrial size (40 +/- 10 vs 41 +/- 11 mm). An LV outflow tract gradient was detected in 25% of patients with and 35% without VT (p = not significant). One or more Doppler indexes of diastolic function were abnormal in 70% of patients, but no difference in any of these indexes was found between those with and without VT. In summary, the occurrence of VT in hypertrophic cardiomyopathy is not related to the degree of LV hypertrophy, outflow tract gradient or dysfunction. This finding suggests a dissociation between the arrhythmogenic substrate and echocardiographic features of the disease.     

Relative wall thickness is an independent predictor of left ventricular systolic and diastolic dysfunctions in essential hypertension.

The objective of this study was to elucidate the relationship between left ventricular geometry and left ventricular (LV) function in patients with untreated essential hypertension. We evaluated LV systolic and diastolic functions by M-mode echocardiography in 24 normotensive control subjects (NC) and 129 patients with essential hypertension. Patients were divided into four groups according to the relative wall thickness and LV mass index: a normal left ventricle (n=57), a concentric remodeling (n=7), a concentric hypertrophy (n=31), and an eccentric hypertrophy (n=34) group. LV systolic function as measured by midwall fractional shortening (FS) was significantly decreased in both the concentric remodeling and concentric hypertrophy groups; no differences were observed for endocardial FS. LV diastolic function as measured by isovolumic relaxation time (IRT) was also decreased in both the concentric remodeling and concentric hypertrophy groups. In multivariate analysis, relative wall thickness (p<0.0001), end-systolic wall stress (p<0.0001), and systolic blood pressure (p=0.002) were independently associated (r2=0.72) with midwall FS in a model including age, LV mass index, body mass index, diastolic blood pressure and IRT. In addition, relative wall thickness (p=0.0008) and age (p<0.0001) were independently associated (r2=0.31) with IRT in a model including LV mass index, end-systolic wall stress, body mass index, systolic and diastolic blood pressures and midwall FS. We conclude that LV geometry as evaluated by relative wall thickness may provide a further independent stratification of LV systolic and diastolic functions in essential hypertension.     

Treatment with a growth hormone secretagogue in a model of developing heart failure: effects on ventricular and myocyte function

BACKGROUND: Exogenous administration of growth hormone (GH) and subsequently increased production of insulin-like growth factor-1 can influence left ventricular (LV) myocardial growth and geometry in the setting of congestive heart failure (CHF). This study determined the effects of an orally active GH secretagogue (GHS) treatment that causes a release of endogenous GH on LV function and myocyte contractility in a model of developing CHF. METHODS AND RESULTS: Pigs were randomly assigned to the following treatment groups: (1) chronic rapid pacing at 240 bpm for 3 weeks (n=11); (2) chronic rapid pacing and GHS (CP-424,391 at 10 mg x kg(-1) x d(-1), n=9); and (3) sham controls (n=8). In the untreated pacing CHF group, LV fractional shortening was reduced (21+/-2% versus 47+/-2%) and peak wall stress increased (364+/-21 versus 141+/-5 g/cm(2)) from normal control values (P:<0.05). In the GHS group, LV fractional shortening was higher (29+/-2%) and LV peak wall stress lower (187+/-126 g/cm(2)) than untreated CHF values (P:<0.05). With GHS treatment, the ratio of LV mass to body weight increased by 44% from untreated values. Steady-state myocyte velocity of shortening was reduced with pacing CHF compared with controls (38+/-1 versus 78+/-1 microm/s, P:<0.05) and was increased from pacing CHF values with GHS treatment (55+/-7 microm/s, P:<0.05). CONCLUSIONS: The improved LV pump function that occurred with GHS treatment in this model of CHF was most likely a result of favorable effects on LV myocardial remodeling and contractile processes. On the basis of these results, further studies are warranted to determine the potential role of GH secretagogues in the treatment of CHF.