Regression of left ventricular hypertrophy after aortic valve replacement for aortic stenosis with different valve substitutes

OBJECTIVE: Stentless biologic aortic valves are less obstructive than stented biologic or mechanical valves. Their superior hemodynamic performances are expected to reflect in better regression of left ventricular hypertrophy. We compared the regression of left ventricular hypertrophy in 3 groups of patients undergoing aortic valve replacement for severe aortic stenosis. Group I (10 patients) received stentless biologic aortic valves, group II (10 patients) received stented biologic aortic valves, and group III (10 patients) received bileaflet mechanical aortic valves. METHODS: Echocardiographic evaluations were performed before the operation and after 1 year, and the results were compared with those of a control group. Left ventricular diameters and function, left ventricular wall thickness, and left ventricular mass were assessed by echocardiography. RESULTS: Group I patients had a significantly lower maximum and mean transprosthetic gradient than the other valve groups (P = .001). One year after operation there was a significant reduction in left ventricular mass for all patient groups (P < .01), but mass did not reach normal values (P = .05). Although the rate of regression in the interventricular septum and posterior wall thickness differed slightly among groups, their values at follow-up were comparable and still higher than control values (P = .002). The ratio between interventricular septum and posterior wall and the ratio between wall thickness and chamber radius did not change significantly at follow-up. CONCLUSIONS: Because the number of patients was relatively small, we could not use left ventricular mass regression after I year to distinguish among patients undergoing aortic valve replacement for aortic stenosis by means of valve prostheses with different hemodynamic performances.     

Clinical significance of magnetic resonance and echocardiographic correlations in the evaluation of hypertrophic cardiomyopathy

Relatively few clinical studies have investigated the role of MRI in the patients with hypertrophic cardiomyopathy. To assess MR capabilities in defining the presence, distribution and severity of left ventricular hypertrophy, the prevalence and clinical correlations of right ventricular hypertrophy and the prevalence and clinical implications of structural myocardial abnormalities, MRI and echocardiography were performed on 37 unselected patients with hypertrophic cardiomyopathy. The two methods were in agreement in 100% of cases in diagnosing the disease and classifying left ventricular hypertrophy as asymmetric, concentric or apical, and in 92% of cases in assessing the topographic distribution of hypertrophy of ventricular segments. A statistically significant linear correlation was found between echocardiographic and MR measurements of interventricular septum (r = 0.69, p < 0.0001, SEE = 4) and left posterior wall of the left ventricle (r = 0.67, p < 0.0001, SEE = 2.4). Right ventricular hypertrophy (right anterior wall diastolic thickness > 5 mm) was demonstrated by MRI in 23 of 33 patients (70%). In this group, left posterior wall thickness and left atrial diameter were higher (15 +/- 4 vs 11 +/- 2, p < 0.01 and 45 +/- 9 vs 38 +/- 5 mm, p < 0.05, respectively). On T2-weighted sequences, areas of reduced signal intensity, probably due to myocardial fibrosis, were detected in 16 cases (43%). This group was characterized by higher max. septal thickness (25 +/- 7 vs 21 +/- 6 mm, p < 0.05) and max. left posterior wall thickness (15 +/- 9 vs 7 +/- 8 mm, p < 0.05). All the three cases with dilated and hypokinetic left ventricle showed this kind of tissue abnormality. In conclusion, MRI provided clear, accurate and exhaustive data on the presence and distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. Right ventricular hypertrophy and structural abnormalities of ventricular myocardium can also be detected and quantified. Right ventricular involvement is associated with more severe hypertrophy of left ventricular posterior wall. Structural myocardial abnormalities, probably due to fibrosis, are related to the extent of left ventricular hypertrophy.     

Effect of the treatment with amlodipine on left ventricular hypertrophy in hypertensive patients

BACKGROUND: Left ventricular hypertrophy (LVH) is one of the physiopathological effects of hypertension and one of the main risk factors for sudden death, myocardial infarction and congestive heart failure. Drugs to treat hypertension must not only reduce blood pressure, but also modify the facts which lead to ventricular hypertrophy. This study has been designed to assess the effect of amlodipine, a calcium-antagonist, on LVH in hypertensive patients. METHODS: 20 hypertensive patients (mild to moderate, both sexes, mean age 45.0 yr) were included in a single-blind study. After an initial, four weeks placebo period, active treatment was given (amlodipine 5 mg a day). Dose titration was made after 4-8 weeks to 10 mg a day if necessary and continued until the end of the study. Systolic (SBP) and diastolic blood pressure (DBP), as well as pulse rate (PR) and adverse events were recorded at every visit. Blood and urine analysis, catecholamine, plasmatic renin activity and Mode M echocardiography were made at the beginning and the end of the study. RESULTS: Only one patient was excluded. SBP and DBP showed a significantly fall (p < 0.001). In 80% of patients DBP fell under 90 mm Hg. Every echocardiographic parameter, but left ventricular diastolic dimension, showed significantly reductions at the end of the study: septum thickness (p = 0.001), posterior wall thickness (p = 0.001), left ventricular systolic dimension (p = 0.014), wall relative thickness (p = 0.015), shortening fraction (p = 0.009), left ventricular mass (p = 0.001) and corrected left ventricular mass (p = 0.001). Blood parameters did not modify. CONCLUSIONS: Amlodipine has a beneficial effect on LVH and also is an effective and safe drug to treat mild to moderate hypertension.     

M-mode echocardiographic diagnosis of dilated cardiomyopathy in giant breed dogs

M-mode echocardiograms were recorded from 62 giant breed dogs without historical, clinical, electrocardiographic and roentgenologic signs of heart disease, from six dogs with asymptomatic dilated cardiomyopathy (DCM, NYHA class I), and 13 dogs with symptomatic DCM (NYHA class III-IV). There was a general trend that several echocardiographic parameters were significantly in control Great Danes as compared to Newfoundlands and Irish Wolfhounds. There were substantial differences in left ventricular size both in systole and diastole and in systolic indices of the left ventricle between the control group, the asymptomatic dogs and symptomatic dogs with DCM (P = 0.0001). There was also a significant decreased in the interventricular septum thickness (P = 0.0001) and left ventricular free wall thickness in systole (P = 0.002) and diastole (P = 0.005) between the three groups. Furthermore, the left atrial/aortic ratio was significantly different between the three groups (P = 0.0001). It was concluded that this study established echocardiographic reference values in giant breed dogs which may be useful in the study of heart diseases in giant breed dogs.     

Left ventricular geometry as an independent predictor for extracardiac target organ damage in essential hypertension

Left ventricular hypertrophy (LVH) is an independent cardiovascular risk factor. It has not been established, however, whether left ventricular geometry is an independent predictor of extracardiac target organ damage in essential hypertension. Study groups were classified according to relative wall thickness: 27 patients with concentric LVH and 50 patients with eccentric LVH. Age and left ventricular mass indexes of two groups were matched. As indexes of extracardiac target organ damage, retinal funduscopic grade, and serum creatinine level were measured. The severity of hypertensive retinopathy and the renal involvement were more severe in patients with concentric LVH than in patients with eccentric LVH. Extracardiac target organ damage was consistently higher in patients with concentric LVH than in those with eccentric LVH. Systemic hemodynamics paralleled ventricular geometric patterns, with higher peripheral resistance and lower aortic compliance in patients with concentric LVH, whereas end-diastolic volumes and stroke volumes were higher in patients with eccentric LVH than in patients with concentric LVH. In addition, total peripheral resistance was related to retinal fundoscopic grade (r = 0.41, P < .01), and serum creatinine level (r = 0.28, P < .05). Even in the presence of an identical degree of LVH, echocardiographically determined left ventricular geometry may provide a further independent stratification of extracardiac target organ damage in essential hypertension.     

Preoperative localization procedures for initial surgery in primary hyperparathyroidism

BACKGROUND: Left ventricular hypertrophy (LVH) has been identified as a main target organ change resulting from hypertension, also being a long-term predictor of myocardial infarction, stroke and cardiovascular death. However, very few longitudinal studies exist following the development of LVH in the hypertensive process. METHODS: The present longitudinal study investigated a population based group of borderline hypertensive men (BHT, n = 66, diastolic blood pressure (BP) 85-94 mm Hg). M-mode echocardiography was performed at baseline and after 3 years, and anthropometrical data recorded. RESULTS: There was no increase in LVH indices over the 3-year period, while there was a statistically significant increase in aortic root dimension (P < 0.001), left atrial diameter in diastole (LADD, P < 0.001), left ventricular diameter in diastole (LVDD, P < 0.001) and peak systolic wall stress (PSWS, P < 0.01) and a significant decrease in left ventricular ejection time (LVET, P < 0.01). Baseline BP levels correlated to PSWS (P < 0.05) but not to LVH indices, whereas body mass index (BMI) correlated significantly to wall thickness (P < 0.05) and LV mass (P < 0.05). CONCLUSIONS: LVH indices did not increase over a 3-year period. However, there was a significant increase in aortic root dimension, LADD, LVDD and PSWS, and a significantly shortened LVET, suggesting that these changes precede any increase in LVH. Finally, BMI showed stronger correlation to LVH indices than did BP levels.     

Death receptor 5, a new member of the TNFR family, and DR4 induce FADD-dependent apoptosis and activate the NF-kappaB pathway

The relationships between angiotensin-converting enzyme (ACE) gene insertion (I) / deletion (D) polymorphism and left ventricular hypertrophy induced by hypertension or idiopathic hypertrophic cardiomyopathy have been studied. However, little is known about the association between this polymorphism and left ventricular hypertrophy induced by volume overload. The relationship between left ventricular hypertrophy and the ACE gene I/D polymorphism was examined in 80 maintenance hemodialysis patients (mean age: 60.1+/-1.4 years). Multivariate regression analysis showed that the left ventricular mass index calculated by M-mode echocardiography was associated with serum creatinine (p = 0.040), male gender (p = 0.027), antihypertensive drug treatment (p = 0.026), weight gain between hemodialysis (p = 0.018) and mean blood pressure after hemodialysis (p=0.010), but not with ACE I/D genotype (p = 0.69). These findings suggest that although hemodialysis patients seem to be under volume overload, ACE genotype may not be involved in their left ventricular hypertrophy. Hypertension and other factors related to renal failure are involved in the left ventricular hypertrophy in chronic hemodialysis patients.     

Left ventricular hypertrophy and ambulatory blood pressure monitoring in chronic renal failure

BACKGROUND: Left ventricular hypertrophy (LVH) is both common and an important predictor of risk of death in end-stage renal failure (ESRF). In mild to moderate chronic renal failure (CRF), the timing of onset of LVH and the factors involved in its initial development have not been fully elucidated. The present study was undertaken to examine the prevalence and potential determinants of echocardiographically determined LVH in this connection, and to compare 24-h ambulatory blood pressure (BP) recordings with BP measured at a previous clinic visit. METHODS: From a cohort of 120 non-diabetic patients who had been attending a nephrology clinic, 118 agreed to participate in the study. Of these we selected for analysis 85 stable patients (37 male). Patients with known cardiovascular disease, those with a history of poor compliance with antihypertensive medication, and those in whom such medication had been changed in the previous 3 months were excluded. Clinic BP, 24-h ambulatory BP, echocardiography, body mass index (BMI), serum creatinine (SCr), creatinine clearance (CrCl), haemoglobin (Hb), fasting cholesterol (CHOL), triglyceride TRIGL), plasma glucose, calcium (Ca), phosphate (PO4), alkaline phosphatase (ALK PHOS), parathyroid hormone (PTH) concentrations, and 24-h urinary protein were assessed in all patients. Seventy-seven per cent were on antihypertensive medication. RESULTS: LVH was detected in 16% of patients with CrCL > 30 ml/min, and 38% of patients with CrCl < 30 ml/min. By stepwise regression analysis, ambulatory systolic BP (P < 0.0001), male gender (P < 0.0001), BMI (P < 0.0002), and Hb concentration (P < 0.002) were the only independent determinants of left ventricular (LV) mass. Nocturnal systolic BP (P < 0.02) was the main determinant of LVH in the group of patients with advanced CRF. The correlation between left ventricular mass index (LVMI) and mean 24-h ambulatory systolic BP (r = 0.52, 95% confidence interval 0.50-0.54) was statistically significantly stronger than with outpatient systolic BP (r = 0.25, 95% confidence interval 0.23-0.27). The same was true for the correlation between LVMI and mean 24-h ambulatory diastolic BP (r = 0.42, 95% confidence interval 0.40-0.44), and outpatient diastolic BP (r = 0.22, 95% confidence interval 0.20-0.24). CONCLUSIONS: Twenty-four hour ambulatory BP recording and echocardiography are required for accurate diagnosis of inadequate BP control and early LVH in patients with chronic renal impairment, independent determinants of which are hypertension, male sex, BMI, and anaemia.     

Evaluation of electrocardiographic left ventricular hypertrophy with both QRS voltage and ST-T change using echocardiography

The purpose of the present study is to determine whether electrocardiographic QRS voltage criteria with ST-T change is useful in the diagnosis of left ventricular hypertrophy (LVH) using echocardiography. One hundred men including 59 with hypertension (HT), 9 with hypertrophic cardiomyopathy (HCM), and 32 without any cardiovascular disease were enrolled in this study. All of them had the electrocardiographic evidence of LVH by Sokolow-Lyon voltage criteria (RV5 or RV6 > 2.6 mV, SV1+RV5 or SV1+RV6 > or = 3.5 mV). They were classified into three groups based on ST-T pattern as follows: Normal ST-T (group N): normal ST-T in twelve leads; Early strain ST-T (group ES): ST depression, flat T (T/R < 1/10), diphasic T or T wave inversion < 0.1 mV in V5 or V6; and Strain ST-T (group S): inverted T wave in V5 and V6. Echocardiographic LVH was determined when either interventricular septal thickness (IVST) or left ventricular posterior wall thickness (LVPWT) > or = 12 mm was present. According to this echocardiographic evidence, 31.7%(20/63) of group N, 75.0% (12/16) of group ES, and 100% (21/21) of group S were diagnosed. There were significant correlations between QRS voltage indices (RV5, RV6, SV1+RV5 and SV1+RV6) and IVST, (IVST+LVPWT)/2, and LV mass in group S(r = 0.650 to 0.858, p < 0.05) but not in group N. Values for IVST and LV mass were significantly greater in group S than in group ES or N. The electrocardiographic diagnosis of LVH with both QRS voltage and ST-T change thus appeared to be more useful than that with QRS voltage criteria alone.     

Left ventricular hypertrophy, blood pressure and ACE genotype in untreated hypertension

It has been suggested that the deletion polymorphism of the angiotensin-converting enzyme (ACE) genotype may be important in the development of left ventricular hypertrophy (LVH). In order to test this hypothesis we investigated the interaction between blood pressure (BP), LVH and ACE genotype in 86 previously untreated hypertensive patients. Each underwent two-dimensional and Doppler echocardiography and ACE genotyping. There were no significant differences in BP, the parameters of left ventricular structure (including left ventricular mass index) or diastolic function between the three genotype groups. Additionally, there were no significant differences in the relationship between systolic BP and left ventricular mass index among the three genotype groups (II genotype, r = 0.46, P = 0.02; ID genotype, r = 0.42, P = 0.01; DD genotype, r = 0.34, P = 0.10; F = 0.38). In contrast to some previous studies, we have found in this group of previously untreated hypertensive subjects no evidence to suggest that the deletion polymorphism of the ACE genotype is important in the development of LVH.     

Cardiac effects of short course dexamethasone in preterm infants

AIM: To examine the incidence and natural history of left ventricular hypertrophy (LVH) associated with the shorter 2-3 week course of dexamethasone, now more usual, for chronic lung disease. METHOD: Thirty one infants, gestational age 23-34 (median 26) weeks, birthweight 500-2054 (median 815)g, received dexamethasone, starting at 0.4-0.6 mg/kg/day, at a median of 11 days of age (range 2-34), weaning over a period of 2-3 weeks. Eighteen preterm neonates were studied as controls over a similar time period. Serial echocardiographic measurements of end diastolic interventricular septum (IVSd) and left ventricular posterior wall (LVPWd) thicknesses were taken before, and up to 48 days after, starting dexamethasone. Maximum Doppler blood flow velocities from the left ventricular outflow tract (LVOT) were measured. RESULTS: Left ventricular hypertrophy (LVH) occurred in 29 babies (94%). Median hypertrophy of the IVSd in those receiving dexamethasone was 67% and LVPWd 56% of baseline measurements, significantly greater than control infants (p < 0.001). LVH appeared by a median of three days, peaking by a median of 10 days. All resolved by a median of 27 days. LVOT obstruction was not seen. There was no significant correlation with birthweight, gestation, blood pressure, or glucose tolerance. CONCLUSIONS: LVH developed in almost all preterm neonates receiving a 2-3 week course of dexamethasone, but was of little clinical importance and always resolved. Echocardiography is probably not required routinely in infants receiving such short course dexamethasone for chronic lung disease.     

Left ventricular geometric patterns and QT dispersion in untreated essential hypertension

The spectrum of left ventricular adaptation to hypertension, different types of hypertrophy patterns, and QT dispersion in different types of hypertrophy was investigated in 107 patients with untreated essential hypertension and 30 age- and gender-matched normal adults studied by 12-derivation electrocardiogram (ECG), two-dimensional, and M-mode echocardiography. Left ventricular mass (LVM), body mass index, total peripheral resistance (TPR), relative wall thickness (RWT), and QT dispersion were found to be statistically significantly higher in the hypertension group (P < .001 for all). Among hypertensive patients, 41.1% had both normal LVM and RWT, here called normal left ventricle in hypertension; 10.3% had concentric hypertrophy with increased LVM and RWT; 14.95% had eccentric hypertrophy with increased LVM and normal RWT; and 32.7% had concentric remodeling with normal LVM and increased RWT. Echocardiographically derived cardiac index was higher in the concentric hypertrophy and eccentric hypertrophy patterns (P = .002 and P < .0001, respectively), whereas TPR was higher in the concentric hypertrophy and concentric remodeling patterns (P = .017 and .02, respectively). QT dispersion values were found to be increased in the hypertensive group (P = .001), whereas similar values were calculated for different types of hypertrophy patterns. We conclude that the more common types of ventricular adaptation to essential hypertension are eccentric hypertrophy and concentric remodeling. Concentric hypertrophy is found to be associated with both volume and pressure overload, whereas eccentric hypertrophy is associated with volume overload only and concentric remodeling is associated with pressure overload. But different left ventricular geometric patterns seem to have similar effects on QT dispersion.     

Role of p53 in the regulation of irradiation-induced apoptosis in neuroblastoma cells

Myocardial texture analysis of two-dimensional echocardiographic gray level distribution is abnormal in hypertensive patients with severe increase of left ventricular mass. The aim of this study was to investigate the behavior of this parameter in hypertensive patients with absent-to-moderate left ventricular hypertrophy, more representative of the overall hypertensive population. We compared male essential hypertensive patients, with absent or mild-to-moderate left ventricular hypertrophy, with normotensive sedentary healthy subjects as controls. The groups (n = 18 each) were age- (+/- 2 years) and sex-matched. All subjects performed ambulatory blood pressure measurements for the evaluation of 24 h mean systolic and diastolic blood pressure. Quantitative analysis of echocardiographic digitized imaging was performed through a calibrated 256 gray level digitization system to calculate midseptum and midposterior end-diastolic and end-systolic first and second order textural analysis. In particular were observed the mean gray level cyclic variations to deriving the cyclic variation index (CVI). The hypertensives showed a significantly lower CVI compared with controls both for septum (P < .001) and for posterior wall (P < .0001). No significant relationships were found between CVI and relative diastolic thickness both of septum and posterior wall. Conversely, a significant inverse relationship was found between systolic arterial pressure values and CVI both of septum and posterior wall. Abnormalities of two dimensional echocardiographic gray level distribution are present also in hypertensive patients with absent or with mild-to-moderate levels of left ventricular hypertrophy, but seem unrelated to the degree of echocardiographic hypertrophy as such. Changes in collagen network distribution or microcirculatory alterations, secondary to pressure-volume overload per se or to other complex humoral factors, could explain these abnormalities. Further work is needed to establish the clinical, therapeutic, and prognostic implications of these findings.     

Increased myocardial ultrasonic reflectivity is associated with extreme hypertensive left ventricular hypertrophy: a tissue characterization study in humans

We assessed myocardial reflectivity pattern in a large spectrum of left ventricular mass values, covering the extremes from absent to severe myocardial hypertensive hypertrophy. Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to the morphometrically evaluated collagen content in humans. We enrolled 88 essential hypertensives. With an echo prototype implemented in our Institute, integrated values of the radiofrequency signal of myocardial walls were obtained and normalized for those of the pericardium (Integrated Backscatter Index, IBI, %). Left ventricular mass index (LVMI) was measured by Devereux formula. There was a weak correlation between septal IBI and LVMI (r = 0.35; P < .001). On the basis of LVMI values, three groups of hypertensives were identified, with absent (Group I, n = 23; LVMI < 125 g/m2), mild to moderate (Group II, n = 44; LVMI from 125 to 174 g/m2), or severe (Group III, n = 21; LVMI > 175 g/m2) left ventricular hypertrophy. The Integrated Backscatter Index in the septum was lower in patients of Group I (IBI = 23.3% +/- 3.6%) and II (IBI = 26.5 +/- 7.6; P = NS v Group I), in comparison with patients of Group III (IBI = 31.1 +/- 5.9; P < .02 v II; P < .0001 v I). An increased myocardial wall reflectivity is detectable only in the presence of extreme forms of hypertensive left ventricular hypertrophy.     

Direct evidence of impaired cardiac sympathetic innervation in essential hypertensive patients with left ventricular hypertrophy

Increased sympathetic nervous activity has been proposed as one of the causes of left ventricular hypertrophy (LVH) associated with hypertension. However, the precise relationship is not fully understood. METHODS: To elucidate the relationship between myocardial sympathetic nervous activity and LVH in patients with essential hypertension EHT), we performed 123I-metaiodobenzylguanidine (MIBG) myocardial scintigraphy in 49 patients with EHT and 17 normotensive control subjects. Sympathetic innervation of the left ventricle was evaluated using SPECT, and the whole heart uptake of the tracer was quantitatively assessed as the heart-to-mediastinum uptake ratio on both the early (15-min) and delayed (5-hr) images. Myocardial washout rate (MWR) of the tracer from 15 min to 5 hr after the isotope administration was also calculated. The left ventricular mass index (LVMI) was determined echocardiographically. RESULTS: In 49 hypertensive patients, there was a negative correlation between LVMI and heart-to-mediastinum uptake ratio on both the early and delayed images (r=-0.55, p < 0.0001; r=-0.63, p < 0.0001, respectively). In addition, there was a positive correlation between the LVMI and MWR of 123I-MIBG in these hypertensive patients (r=0.59, p < 0.0001). As for the regional uptake of the tracer, there was no significant difference between control subjects and hypertensive patients without cardiac hypertrophy, but a significant decrease of the uptake in the inferior and lateral regions was observed in hypertensive patients with cardiac hypertrophy. CONCLUSION: Patients with EHT had decreased accumulation and increased MWR of 123I-MIBG in proportion to the degree of LVH. Hypertensive patients with cardiac hypertrophy had impaired sympathetic innervation in the inferior and lateral regions of the left ventricle.     

Increased myocardial echo density in left ventricular pressure and volume overload in human aortic valvular disease: an ultrasonic tissue characterization study

Quantitatively assessed ultrasonic backscatter is an index of ultrasonic tissue characterization directly related to morphometrically evaluated collagen in human beings. Our objective was to assess myocardial reflectivity pattern of patients with severe left ventricular hypertrophy caused by either aortic stenosis (AS) or aortic regurgitation (AR). Ten patients with AS, 10 patients with AR, and 10 closely age- and gender-matched healthy controls were studied by two-dimensional Doppler echocardiography. By using an echocardiographic prototype, we performed a radiofrequency analysis to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall (integrated backscatter index: IBI, expressed in percentage). All patients with stenosis or aortic insufficiency showed a normal regional and global resting systolic function (fractional shortening: AS = 36.0 +/- 6.6 versus AR = 40.3 +/- 6.2 versus control = 40.2 +/- 8.7; p = not significant [NS]) Left ventricular mass index (Devereux's formula) was markedly increased in patients with stenosis or aortic insufficiency (AS = 199.3 +/- 18 versus AR = 208.8 +/- 60 versus control = 97.3 +/- 11 g/m2; p < 0.0001). Myocardial echo density was increased in patients with stenosis or aortic insufficiency in comparison with controls, both in the septum (IBI%: AR = 40.7 +/- 7.9 versus AS = 33.4 +/- 4.2 versus control = 23.0 +/- 6.2; p < 0.0001) and in the posterior wall (IBI%: AR = 27.1 +/- 4.3 versus AS = 23.0 +/- 2.6 versus control = 15.0 +/- 4.2; p < 0.0001). No significant correlations were found between septal and posterior wall IBI and their thickness. Abnormally increased myocardial echo density--possibly related to disproportionate collagen deposition--can be detected in patients with pressure or volume overload caused by aortic valve disease and without overt systolic dysfunction.     

Temporal pattern of IGF-I expression during mouse preimplantation embryogenesis

PURPOSE: To evaluate the role of casual and exercise blood pressure as well as the importance of clinical factors on the presence and degree of left ventricular hypertrophy in hypertension. METHODS: Fifteen normotensives (control group) and 30 hypertensives, 14 of them with and 16 without left ventricular hypertrophy (groups with LVH and without LVH, respectively) were studied. LVH diagnosis was established when mass index was higher than 2 standard-deviations of the mean values calculated for each sex in control group. Resting, casual determined, and bicycle exercise systolic and diastolic blood pressures along with age, body surface area, sex and race distribution were compared between groups. In addiction, their relation with mass index as independent variables were also tested. RESULTS: Hypertensives in group with LVH had higher diastolic septal, posterior wall, and relative wall thicknesses. No significant statistical difference was observed neither in sex and race distribution, nor in age and body surface area between groups. Otherwise, there were significant differences in both resting and exercise blood pressure. In the entire population studied, left ventricular mass index significantly correlated with age (r=0,33, p=0,03) as well as with both casual (systolic - r=0,72, p=0,0001; diastolic - r=0,69, p=0,0001) and exercise (systolic - r=0,62, p=0,0001; diastolic - r=0,66, p=0,0001) blood pressures. However, linear regression analysis demonstrated that only resting systolic (p=0,0001) and exercise diastolic (p=0,0303) blood pressures were significant and independent determinants of mass index. CONCLUSION: Resting and exercising blood pressures are the main determinants of left ventricular hypertrophy in hypertension.     

Various ways of calculating echocardiographic left ventricular mass and their relative prognostic values

OBJECTIVE: To compare the calculations of left ventricular mass according to thick-wall [American Society of Echocardiography (ASE) and Penn convention] and thin-wall (Wikstrand formula) models. METHODS: We have reexamined the data from the cross-sectional study on the general population sample of Vobarno and from a prospective longitudinal study of hypertensive patients assessing the prognostic significance of changes in left ventricular mass during a follow-up period of 10 years on average (Brescia population). RESULTS: For the Vobarno and Brescia populations, we found a close relationship between values of left ventricular mass calculated by using a thin-wall ellipsoidal model (Wikstrand formula) and those calculated using a thick-wall model with Penn convention or ASE left ventricle measurements (r = 0.99, for both the Vobarno and Brescia populations). Highest values of Penn left ventricle mass were slightly underestimated by use of the thin-wall formula. The numbers of nonfatal cardiovascular events and the relative risks, evaluated by Cox proportional hazard models for 151 patients seen at follow-up did not differ for patients with persistence of left ventricular hypertrophy (LVH), those with regression of LVH, and those with normal left ventricle mass, both at baseline and at follow-up, when these different ways of measuring left ventricle mass and partition values for LVH were used. CONCLUSIONS: The calculation of left ventricle mass according to the ASE recommendations or to the Penn convention, both of which are based on the assumption that the left ventricle can be represented by a prolate ellipsoid with both the internal and external long axes twice the short axis, produces results similar to those obtained using an alternate formula for the calculation of left ventricle mass, considering wall thickness constant around the ellipsoidal cavity. The cardiovascular risk stratification, in relation both to baseline left ventricular mass and to its change during long-term antihypertensive treatment, does not differ significantly among the results of these three different calculations.     

Diminished contractile reserve in patients with left ventricular hypertrophy and increased end-systolic stress during Dobutamine stress echocardiography

Left ventricular hypertrophy (LVH) is associated with decreased contractile response to inotropic stimulation in animal models, but this has not been documented in humans. To determine whether LVH is associated with decreased myocardial contractile reserve, we measured left ventricular mass, heart rate-corrected velocity of circumferential fiber shortening (Vcfc), end-systolic stress, and LV ejection fraction (LVEF) in patients with LVH and increased end-systolic stress (n = 6) and in patients without LVH (n = 7) who had a normal response to dobutamine stress echocardiography (increased LVEF and no wall motion abnormalities). The afterload-dependent indexes of left ventricular systolic performance were normal at baseline and showed significant increases at peak dobutamine dose (LVH group: Vcfc 0.91 +/- 0.11 to 1.76 +/- 0.59, p = 0.006; LVEF 49 +/- 5 to 65 +/- 6, p = 0.001; group without LVH: Vcfc 1.16 +/- 0.24 to 1.99 +/- 0.36, p = 0.001; LVEF 61 +/- 6 to 68 +/- 6, p = 0.05). The Vcfc/ end-systolic stress relation, a load-independent index of myocardial contractility, rose in a dose-dependent fashion in both groups, but the increment was significantly less for patients with LVH (p < 0.02), suggesting a blunted myocardial contractile reserve to inotropic stimulation. The change in heart rate-corrected velocity of circumferential fiber shortening per unit of change in end-systolic stress in each patient at each dobutamine dose showed a linear and inverse relationship. The increment in heart rate-corrected velocity of circumferential fiber shortening for a given reduction in end-systolic stress was larger in patients without LVH than in patients with LVH (p = 0.01). These results suggest that in patients with LVH and increased end-systolic stress, ventricular performance is maintained at the expense of limited myocardial contractile reserve, and that inotropic stimulation unmasks this abnormality, despite a normal response in LVEF and velocity of circumferential fiber shortening. This approach may identify patients with LVH at risk of developing systolic dysfunction and heart failure.     

Influence of the angiotensin II antagonist valsartan on left ventricular hypertrophy in patients with essential hypertension

BACKGROUND: Left ventricular hypertrophy (LVH) represents an independent risk factor in patients with essential hypertension. Because reversal of LVH may be associated with an improvement of prognosis, the influence of new antihypertensive compounds, such as angiotensin II AT1 receptor antagonists, on LVH should be determined. METHODS AND RESULTS: In a randomized, double-blind trial, 69 predominantly previously untreated hypertensive patients with echocardiographically proven LVH, ie, left ventricular mass index (LVMI) >134 g/m2 in men and >110 g/m2 in women and/or end-diastolic septal thickness >12 mm, received either the angiotensin II antagonist valsartan or atenolol for 8 months. Echocardiographic data of 58 patients were available. After 8 months of valsartan treatment (n=29), LVMI decreased from 127+/-23 to 106+/-25 g/m2 (ratio [R]=0.83; 95% CI, 0.79 to 0.87; P<0.0001 versus baseline). Under atenolol (n=29), LVMI decreased to a smaller extent, from 127+/-25 to 117+/-27 g/m2 (R=0.92; 95% CI, 0.86 to 0.98; P=0.0082 versus baseline). The mean reduction of LVMI came to 21 g/m2 under valsartan and only to 10 g/m2 under atenolol (R=0.91; 90% CI, 0.85 to 0.97 versus atenolol). Baseline mean blood pressure values were determined to be 163+/-12/101+/-6 mm Hg before treatment with valsartan and 160+/-14/103+/-6 mm Hg before atenolol treatment. After 8 months of treatment, mean blood pressure decreased to 146+/-13/90+/-7 mm Hg with valsartan and to 147+/-18/90+/-7 mm Hg with atenolol. Nine patients in the valsartan group and 8 patients in the atenolol group required additional medication with hydrochlorothiazide. CONCLUSIONS: Antihypertensive treatment with the angiotensin II antagonist valsartan for 8 months produced a significant regression of LVH in predominantly previously untreated patients with essential hypertension. The drug may be safely administered in this subset of hypertensive patients; however, the long-term benefit in terms of risk reduction has still to be evaluated in further trials.