End-systolic Stress Research Articles

The imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension

The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively. Myocardial supply-demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN). Fractional shortening (%) and end-systolic stress (10(3) x dyn x cm(-2)) were determined using echocardiography, and coronary reserve was calculated using transesophageal Doppler echocardiography. Coronary reserve/stress (cm2 x dyn(-1)) was utilized as a measure of supply-demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening > or = 30), HTN2 (19 patients, 20 < or = fractional shortening < 30), and HTN3 (21 patients, fractional shortening < 20) were constituted. Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end-systolic stress (NL = 72 +/- 16, HTN1 = 72 +/- 23, HTN2 = 143 +/- 32, HTN3 = 186 +/- 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 +/- 0.6, HTN1 = 3.4 +/- 1.0, HTN2 = 3.1 +/- 1.0, HTN3 = 2.6 +/- 1.1), but coronary reserve/stress was reduced in both HTN2 and HTN3 (NL = 50 +/- 12, HTN1 = 53 +/- 21, HTN2 = 22 +/- 7, HTN3 = 15 +/- 7). Stepwise regression analysis identified diastolic internal dimension, end-systolic stress, and coronary reserve/stress as independently associated with fractional shortening. The imbalance between supply-demand explains the severity of hypertensive cardiac dysfunction and adds information to cardiac enlargement and elevated wall stress.

Relationship between left ventricular geometry and left atrial size and function in patients with systemic hypertension.

Arterial hypertension determines distinct adaptive left ventricular geometric responses, which may differently affect left ventricular function and left atrial performance. In this study, the effect of left ventricular geometry on left atrial size and function, and the relationship between left atrial size and left ventricular mass were assessed in 336 patients with systemic arterial hypertension who had undergone Doppler echocardiography. Patients were classified into concentric (110 patients with concentric left ventricular geometry defined as relative wall thickness > or = 0.44) and eccentric groups (226 patients with relative wall thickness < 0.44). Comparison to the latter, the former had greater left atrial size, left atrial ejection force, left ventricular mass and lower left ventricular midwall fractional shortening. Left ventricular concentric, rather than eccentric, geometry emerged by multivariate analysis as a factor independently associated with the highest degree of left atrial ejection force. Left atrial size was positively related to left ventricular mass in the whole population (r = 0.65, SEE = 6 ml, P < 0.00001). This relationship was maintained in the subgroups with concentric (r = 0.65, SEE = 6 ml, P < 0.00001) or eccentric geometry (r = 0.59, SEE = 6 ml, P < 0.00001). Our results indicate that the relationship of left ventricular geometry to both left atrial size and ejection force in hypertensive patients is relevant. Concentric left ventricular geometry is associated with greater left atrial size and ejection force than eccentric geometry, suggesting that increased left ventricular stiffness has a greater effect in stimulating left atrial performance than left ventricular end-systolic stress. The degree of left atrial enlargement similarly depends on left ventricular mass in patients with concentric and eccentric geometry.

Midwall mechanics in physiologic and hypertensive concentric hypertrophy

Objective We sought to analyze and compare midwall fractional shortening (mFS), and its relations with circumferential end-systolic stress (cESS) and relative wall thickness (RWT), among subjects with physiologic concentric left ventricular (LV) hypertrophy, patients with hypertension and concentric LV hypertrophy, and control subjects. Methods A total of 51 normotensive athletes and 56 young patients with hypertension and echocardiographic evidence of concentric LV hypertrophy were enrolled. In addition, 49 age- and sex-matched control subjects were recruited. LV cavity size and wall thicknesses, LV mass, RWT, cESS, and mFS were determined by echocardiography. Results The 3 groups were similar in age, sex, height, weight, body surface area, LV diameters, and conventional indices of systolic function. LV thicknesses, RWT, LV mass, and LV mass index were similarly increased in the athletes and in the hypertensive group when compared with the control subjects. A similar depression in mFS was observed in both the athletes (22.4 ± 2.6%) and hypertensive group (22.5 ± 3.6%) in comparison with the control group (24.5 ± 2.5%, P = .0003). The depression in mFS was still significant after taking into account the effect of cESS, but was no more evident after indexation of mFS by RWT or LV mass. At regression analysis, the relation between mFS and cESS showed a steeper negative slope in the patients with hypertension than in the other 2 groups. Conclusions MFS is similarly depressed in physiologic and hypertensive concentric LV hypertrophy. The depression is abolished by adjustment for RWT or LV mass, suggesting that geometric factors are the major determinants of midwall performance in both types of concentric LV hypertrophy. However, an impaired response to different values of cESS seems to exist only in hypertensive concentric LV hypertrophy, because increasing levels of cESS may be associated with more evident mFS depression in patients with hypertension than in the athletes and control subjects.

LEFT VENTRICULAR MECHANICS IN PATIENTS WITH SYSTOLIC HEART FAILURE

The end systolic stress–strain relationship (mean end‐systolic fiber stress (MESFS) and the logarithm ln(h0/h) [h0 = wall thickness extrapolated to a “cero” ventricular volume; h = end‐systolic wall thickness]), evaluates the mechanics of the left ventricle (LV) independently of its mass and geometry. Objectives: To compare the LV mechanics in patients without and with compensated systolic heart failure (HF) using the MESFS–ln(h0/h) relationship. Methods: We perform echo Doppler studies in 37 patients with compensated HF (11 women) 65±15 years old (18–85) and 162 patients without HF (102 women) 50±16 years old (18–83). MESFS and ln(h0/h) were calculated and compared between the groups, and the resulting curve was plotted. Results. (o) without HF; with HF. Conclusion: Patients with compensated HF have higher‐end systolic MESFS and ln(h0/h). Consequently, they show a rightward shift in the end‐systolic MESFS‐ ln(h0/h) curve.

Left ventricular structure and systolic function in African Americans: the Atherosclerosis Risk in Communities (ARIC) study.

To estimate prevalence of left ventricular (LV) hypertrophy and its relation to systolic function in a population-based sample of African Americans. A baseline 2D guided M-mode echocardiogram was conducted as part of a longitudinal cohort study to assess prevalence and cross-sectional relationships between echocardiographic and clinical parameters. Data were collected as part of the Atherosclerosis Risk in Communities study. Analysis is limited to 1543 African Americans, aged 51-70 years, without clinically apparent cardiovascular or echocardiographically determined valvular disease. LV hypertrophy prevalence was defined as LV mass/ height2.7 > or = 51 g/m2.7. LV systolic chamber function was assessed at the midwall using the ratio of observed midwall fractional shortening (MWS%) to the value predicted from circumferential end-systolic stress. The prevalence of LV hypertrophy was 33% in men, 38% in women. The prevalence of concentric hypertrophy (LV hypertrophy with relative wall thickness > or = 0.45) was greater than that of eccentric hypertrophy (men: 24% vs 9%; women: 27% vs 11% women). Observed/predicted (O/P) MWS% was strongly and inversely related to LV mass/ height2.7 (P<.001) and LV hypertrophy (P<.001). The O/P MWS% was inversely related to LV mass/height2.7 quartile: O/P MWS% was 106% and 99% in the first and 97% and 89% in the fourth quartile of LV mass/height2.7 for men and women, respectively. Adjusting for age, adiposity, diabetes, blood pressure, antihypertensive medication use, and smoking did not remove association between O/P MWS% and LV mass/height2.7. LV hypertrophy was highly prevalent in this population-based middle-aged sample of African Americans and was associated with poorer LV systolic chamber function.

Myosplint decreases wall stress without depressing function in the failing heart: a finite element model study

Background The Myocor Myosplint is a transcavitary tensioning device designed to change left ventricular (LV) shape and reduce wall stress. Regional wall stress cannot be measured in the intact heart and LV function after surgical remodeling is often confounded by inotropic agents and mitral repair. We used a realistic mathematical (finite element) model of the dilated human LV to test the hypothesis that Myosplint decreased regional ventricular fiber stress and improved LV function. Methods A finite element model was used to simulate the effects of Myosplint on the LV stroke volume/end-diastolic pressure (Starling) relationship and regional distributions of stress in the local muscle fiber direction (fiber stress) for a wide range of diastolic and end-systolic material properties. The nonlinear stress-strain relationship for the diastolic myocardium was anisotropic with respect to the local muscle fiber direction. An elastance model for active fiber stress was incorporated in an axisymmetric geometric model of the globally dilated LV wall. Results Both diastolic compliance and end-systolic elastance shifted to the left on the pressure-volume diagram. LV end-diastolic volume and end-systolic volumes were reduced by 7.6% and 8.6%, respectively. Mean end-diastolic and end-systolic fiber stress was decreased by 24% and 16%, respectively. Although the effect of Myosplint on the Starling relationship was not significant, there were trends toward an improvement in this relationship at low diastolic stiffness, C, high peak intracellular calcium concentration, Ca 0 , and high arterial elastance, E A . Of note, the effect of C was twice that of Ca 0 and E A . Diastolic function would, therefore, be expected to be the prime determinant of success with Myosplint. Conclusions Myosplint reduces fiber stress without a decrement in the Starling relationship. Myosplint should be much more effective than partial ventriculectomy as a surgical therapy for patients with dilated cardiomyopathy and end-stage congestive heart failure.

Severe aortic insufficiency and normal systolic function: determining regional left ventricular wall stress by finite-element analysis

Background Because severe aortic insufficiency in the setting of preserved left ventricular function is often associated with a long asymptomatic period and unpredictable course on medical therapy, sensitive indices of left ventricular systolic performance are necessary for the optimal direction of therapeutic intervention. Because myocardial wall stress is closely related to both pathologic cardiac remodeling and ultimately to left ventricular decompensation, an accurate description of regional wall stress distribution may improve our ability to clinically manage these patients appropriately. The objectives of this study were (1) to define sensitive, noninvasive indices of left ventricular systolic performance to assist the clinician in the serial evaluation and early detection of increased left ventricular wall stress and, therefore, inadequate left ventricular remodeling and subsequent myocardial decompensation of patients with aortic insufficiency, and (2) to quantify differences in instantaneous global and regional end-systolic wall stress between normal subjects and patients. Methods Magnetic resonance imaging was performed on 23 normal volunteers and 19 patients with aortic insufficiency and normal systolic function (ejection fraction, 57% ± 6%). Finite-element analysis was used to estimate global and regional end-systolic stress. Results End-systolic stress was significantly higher in the patient group globally (154,700 ± 31,711 versus 96,781 ± 23,185 dyne/cm 2; p < 0.001) and regionally ( p < 0.001 in all segments) despite normal systolic function and similar end-systolic pressures. Conclusions End-systolic stress as determined by magnetic resonance imaging and finite-element analysis may have considerable potential as a noninvasive, clinically applicable index of regional left ventricular function that may help in the serial evaluation, optimal management, and early identification of left ventricular decompensation in patients with aortic insufficiency.

The late consequences of anthracycline treatment on left ventricular function after treatment for childhood cancer.

The purpose of this study was to determine the incidence of changes in left ventricular function in patients in long-term remission after treatment with anthracyclines for a childhood malignancy. The authors examined 155 patients in disease remission who underwent treatment protocols utilising anthracyclines in childhood. The group comprised 90 males and 65 females aged 15+/-4.9 years (range 5-29 years, median 15 years). The age at the time of diagnosis and start of treatment was 8.6+/-4.9 years (range 1-18 years, median 8 years). The time of follow-up was 7.3+/-4 years (range 1-21 years, median 6.3 years). The patients were given a cumulative dose of doxorubicin or daunorubicin of 250+/-131 mg/m2 (range 50-1200 mg/m2, median 240 mg/m2). The values of ejection fraction below 55% and fractional shortening below 30% assessed by means of echocardiography were considered as pathological. The control group consisted of 41 volunteers. Pathological values of fractional shortening were found in 12 patients (8%). Only one patient (0.64%) showed the development of heart failure due to cardiomyopathy. The group of the patients after chemotherapy revealed significantly worse values of left ventricular endsystolic wall stress, mean velocity of circumferential fibre shortening, Tei index, and isovolumic relaxation period in comparison with the control group. We found a correlation between the given cumulative dose of anthracyclines and indicators of systolic function of the left ventricle, but not a relation to the time indicators (age at diagnosis, time of follow-up). in the mean period of 6 years after chemotherapy, subclinical cardiotoxicity was found in 11 patients (7%) and cardiomyopathy with heart failure in one patient. Further indicators of subclinical damage are elevation of afterload (end-systolic stress), impaired relaxation and increased value of the Doppler index of global left ventricular function. Further monitoring and evaluation of the relevant subclinical abnormalities over a longer period of time are needed.

Associations of aortic and mitral regurgitation with body composition and myocardial energy expenditure in adults with hypertension: the Hypertension Genetic Epidemiology Network study

Background It has been reported that aortic regurgitation, mitral valve regurgitation, or both are associated with lower body mass index, an index of body adiposity. However, the relations of valvular regurgitation to body composition and myocardial bioenergetic expenditure have not been previously investigated in a population-based sample. Methods We selected 1496 patients with hypertension who did not have diabetes mellitus to participate in the Hypertension Genetic Epidemiology Network (HyperGEN) study. We excluded participants with severe aortic or mitral stenosis or with known coronary heart disease. Bioimpedance was used to assess body composition. Echocardiography was used to assess left ventricular (LV) structure and function and to calculate myocardial workload (expressed as energy expenditure) from end-systolic stress, ejection time, and stroke volume. The study sample was divided into groups without mitral or aortic regurgitation (control subjects, n = 1175), with mild valvular regurgitation (1+, n = 246), and with at least moderate (≥2+) mitral or aortic regurgitation (n = 75). Results The mean patient age was higher with more severe valvular insufficiency. Sex distribution and blood pressure were similar among the 3 groups. Body mass index and fat mass were significantly lower with more severe valvular regurgitation, whereas fat-free mass was only slightly lower in the group with ≥2+ regurgitation compared with control subjects. Skinfold thicknesses (brachial and subscapular) were lower with more severe valvular regurgitation, whereas self-reported physical activity per week was similar among the 3 groups. LV mass and circumferential end-systolic stress were higher with more severe valvular regurgitation. Noninvasively estimated myocardial energy expenditure was slightly higher in participants with 1+ valvular regurgitation and was significantly higher with ≥2+ regurgitation. Ejection fraction was mildly lower with ≥2+ aortic insufficiency, mitral insufficiency, or both. Midwall shortening and stress-corrected midwall shortening did not differ among groups. Conclusions In a population-based sample of adults with hypertension and without diabetes mellitus, known coronary heart disease, or significant valvular stenosis, mitral and aortic regurgitation were associated with higher LV mass and total myocardial biomechanical workload but with lower body fat mass and slightly lower body fat-free mass, which suggests that global myocardial bioenergetic expenditure is elevated by concomitant valvular regurgitation beyond the effect of pressure overload caused by hypertension.

Prognostic significance of the left ventricular contractility index in patients with essential hypertension

The aim of the study was to assess the relationship between the left ventricular (LV) contractility index, cardiac function and extracardiac organ damage in essential hypertension (EH). We have studied 142 patients (pts) with EH, age 43–52 years, free of signs of heart failure, normal values of the LV ejection fraction and fractional shortening. From M-mode Echo midwall fractional shortening (mFS)(de Simone method), end-systolic stress ESS (Reichek method) were calculated. LV contractility index was assessed as mFS in relation to ESS(mFS/ESS). Early filling velocity (E), late filling velocity (A), E/A ratio, isovolumic relaxation time (IVRT) and deceleration time (DT) were determined by Doppler-Echo. Albuminuria was measured as albumin to creatinine ratio (ACR). Retinal vascular changes were evaluated by direct ophthalmoscopy (Keith-Wagener classification). The prevalence of LV hypertrophy and depressed LV contractility were 68.0 and 43.0%, respectively. The pts with depressed LV contractility index showed high prevalence of LV hypertrophy (86.7% vs 32.3%, p<0.001), especially eccentric hypertrophy (58.0% vs 14.2%, p<0.001). Pts with depressed mFS/ESS had longer IVRT and DT with significant difference in peak E-, A-wave and E/A ratio (IVRT-157.5±9.40 vs 120.0±10.0 ms; 292.5 ±23.4 vs 214.0±6.1 ms; E-60.5±2.43 vs 70.2±1.28 cm/s; A-71.2±2.70 vs 52.0±1.64 cm/s; E/A-0.96 ±0.04 vs 1.20 ±0.08, p<0.01 for all). IVRT and DT showed a strong relation to mFS/ESS (r=−0.67 and r=−0.69, respectively, p<0.01 for both). Moreover hypertensives with depressed mFS/ESS showed early signs of extracardiac damage namely increased ACR (3.2±0.6 vs 1.2 ±0.08, p<0.01) and serum creatinine (3.6±1.2 vs 1.0±0.06 mg%, p<0.05), a higher prevalence of retinopathy (fundoscopy grade II or beyond) compared with subjects with preserved contractility (89.0% vs 40.0%, p<0.001). Furthermore, mFS/ESS was strongly associated with ACR and serum creatinine level in an univariate analysis (r=−0.59 and r=−0.62, respectively, p<0.01 for both) and these associations were still present after stepwise multivariate analysis. Pts with depressed contractility show a higher prevalence of LV hypertrophy, diastolic dysfunction and early signs of extracardiac vascular damage. The evaluation of LV contractility index might improve the prognostic stratification of hypertensive pts and it might be suitable to recognize subset of pts at higher risk.

Late anthracycline cardiotoxicity after childhood cancer: a prospective longitudinal study.

The objective of the current study was to examine the risk factors for progression in severity of anthracycline-induced cardiac dysfunction, thereby providing information that is useful in refining cancer treatment regimes and guiding follow-up. Serial echocardiograms were performed on 101 acute lymphoblastic leukemia survivors and 83 Wilms tumor survivors after a mean interval of 6.2 years and 6.7 years since last anthracycline dose, respectively, at first study, and after 10.3 years and 11.1 years, respectively, at second study. The paired data were contrasted with data from 100 normal subjects, and potential correlations with follow-up interval, cumulative dose, cancer diagnosis, gender, age at diagnosis, and growth were explored using univariate and multiple regression techniques. The most important predictor of worsening cardiac performance was total anthracycline dose. As a group, patients receiving < 240 mg/m(2) showed no deterioration of left ventricular end systolic stress at > 10 years from the end of treatment. Survivors who have received low-dose anthracycline require cardiac surveillance infrequently. In good prognosis tumors, cumulative anthracycline dose should be maintained at < 250 mg/m(2).

Pulse pressure/stroke index and left ventricular geometry and function

To evaluate the relationship between arterial stiffness estimated by the pulse pressure/stroke index ratio (PP/SVi) and prognostically relevant abnormalities of left ventricular geometry and function. Baseline data from the echocardiographic substudy of the Losartan Intervention For Endpoint (LIFE) Reduction in Hypertension Study were used. Patients involved in the present study had stage II-III hypertension and electrocardiographic left ventricular hypertrophy; those with a history of coronary heart disease or segmental wall motion abnormalities were excluded. Plasma glucose, total and high-density lipoprotein (HDL) cholesterol and creatinine concentrations and urinary albumin/creatinine were assessed by standard methods. The study sample (n = 667) was subdivided into tertiles of PP/SVi. With greater PP/SVi, age, proportion of women and prevalence of type 2 diabetes, systolic and mean blood pressures were greater, whereas body mass index, body height and diastolic blood pressure were lower. Total and HDL cholesterol, creatinine and albuminuria did not differ among the three groups. After adjustment for age, sex and body size, greater PP/SVi was related to concentric left ventricular geometry, but showed a weak negative relationship to left ventricular mass and aortic root diameter; the prevalence of aortic fibrocalcification and left atrial diameter did not differ among tertiles of PP/SVi. PP/SVi was related to greater left ventricular end-systolic stress; stress-corrected left ventricular chamber function was greater with greater PP/SVi, whereas myocardial contractility did not differ significantly among the three groups. Greater PP/SVi was related to greater mitral E-wave/A-wave ratio and shorter isovolumic relaxation time independently of age, sex, left ventricular geometry, systolic function and other confounders. Increased estimated arterial stiffness is associated with concentric left ventricular geometry and with diastolic left ventricular abnormalities suggestive of increased diastolic left ventricular stiffness.

Left ventricular remodeling, mechanics, and tissue characterization in congenital aortic stenosis

Background: As the response of the myocardium to pressure overload is age-dependent, this study was designed to examine left ventricular (LV) remodeling, mechanics, and tissue characterization in children with moderate congenital aortic stenosis. Methods: We studied by echocardiography Doppler 22 patients (mean age 12.4 ± 5.6 years) with peak and mean transvalvular gradient of 63 ± 6 and 32 ± 4 mm Hg, respectively. In addition, 30 age- and body surface area-matched participants with structurally normal hearts were used as a control group. Sex- and age-specific cut-off levels for LV mass/height2.7 and relative wall thickness were defined to assess LV geometry. As a load-independent index of myocardial contractility, the relation between the rate-corrected velocity of circumferential fiber shortening both at endocardium and midwall, and meridional end-systolic stress was assessed. In addition, LV diastolic function was also evaluated by the mitral flow indexes. Finally, ultrasonic tissue characterization of the LV myocardium was performed by calculating the magnitude of cyclic variation, which reflects the intramural contractile function, and the averaged myocardial intensity of integrated backscatter, which is directly related to the myocardium collagen content. Results: The endocardial velocity of circumferential fiber shortening endocardium and meridional end-systolic stress relationship was within the normal range (mean ± 2SD) in 18 of 22 patients (81.8%), and midwall velocity of circumferential fiber shortening at endocardium and meridional end-systolic stress was normal in all 22 patients. No mitral flow index of LV diastolic function was significantly different between aortic stenosis group and normal participants. In our study population, 16 of 22 patients (72.7%) showed normal LV geometry, 3 (13.6%) had a pattern of concentric remodeling, and 3 (13.6%) concentric hypertrophy. LV hypertrophy was not marked (left ventricular mass index [LVMI] < 51 g/m2.7) in any patient. Finally, compared with control participants our study population showed, both at interventricular septum and posterior wall, comparable values of cyclic variation integrated backscatter, but significantly higher values of averaged myocardial integrated backscatter intensity (P <.01). Conclusions: In children with moderate congenital aortic stenosis, the total amount of myocardial collagen was increased despite normal LV myocardial contractility and diastolic function. Furthermore, LV remodeling was abnormal in only about a quarter of our patients and none had more than mild hypertrophy. Although the majority of these patients do not have markers now recognized to predict higher risk of cardiovascular events, the long-term significance of myocardial fibrosis and its response to treatment remain to be investigated. (J Am Soc Echocardiogr 2003;16:214-20.)

Release of Preformed Ang II from Myocytes Mediates Angiotensinogen and ET-1 Gene Overexpression In Vivo via AT1 Receptor

P. A. Modesti, S. Zecchi-Orlandini, S. Vanni, G. P olidori, I. Bertolozzi, A. M. Perna, L. Formigli, I. Cecioni, M. Coppo, M. Boddi and G. G. Neri Serneri. Release of Preformed Ang II from Myocytes Mediates Angiotensinogen and ET-1 Gene Overexpression in vivo via AT1 Receptor. Journal of Molecular and Cellular Cardiology (2002) 34, 1491–1500. The role of angiotensin II in pressure overload is still debated because notwithstanding its effects on myocyte contractility angiotensin II is not an obligatory factor for the development of hypertrophy. To define the role of angiotensin II in acute pressure overload we studied the effects of AT1 blockade (valsartan 80mg per day) on myocardial contractility, cardiac growth factor gene expression, and myocardial hypertrophy in aortic banded (60mmHg) pigs. Acute pressure overload caused an abrupt reduction of myocardial contractility, measured by the end-systolic stiffness constant, and a sharp increase in end-systolic stress which rapidly normalized (within 12h) in the placebo group. In AT1-blocked animals end-systolic stiffness constant remained significantly depressed up to 24h and end-systolic stress was still elevated up to 48h (both P<0.05 vs placebo). In both groups confocal microscopy revealed that granular staining of angiotensin II in cardiomyocyte cytoplasm disappeared after 30min of pressure overload. AT1 blockade abolished following cardiac overexpression of angiotensinogen and endothelin-1 genes as shown in RT-PCR studies and the consequent angiotensin II and endothelin-1 release in the coronary circulation. Conversely, insulin-like growth factor-I and ACE mRNA overexpression, as well as the onset of left ventricular mass increase, were not significantly affected by AT1 blockade. In conclusion: (1) mechanical stress releases preformed angiotensin II from myocyte in vivo; (2) the AT1 blockade abolishes cardiac angiotensin II and endothelin-1 production with delayed recovery of myocardial contractility; whereas (3) the overexpression of insulin-like growth factor-I gene and the development of myocardial hypertrophy are not angiotensin II-mediated effects.

Left ventricular mass and hemodynamic overload in normotensive hemodialysis patients

It remains uncertain whether the hemodynamic parameters are important determinants of left ventricular mass (LVM) in normotensive chronic hemodialysis (NTHD) patients, as has been found in their hypertensive counterparts. Forty NTHD patients (mean age, 53.7 +/- 14.4 years; male/female, 18/22) without the requirement of antihypertensive drugs for at least six months were studied. Controls were 41 hypertensive hemodialysis patients (HTHD) and 46 normotensive subjects with normal renal function (NTNR). The influence of anthropometrics, cardiovascular structure and function, and volume status on LVM (by two-dimensional echocardiography) was analyzed by steps of multiple linear regression. As compared with the NTNR and NTHD group, the HTHD group had obvious pressure and volume/flow overload, and greater LV wall thickness, chamber size and mass. In contrast, NTHD subjects had similar blood pressure, large artery function, LV chamber size and stroke volume as the NTNR subjects. However, the NTHD patients still had greater wall thickness and LVM, along with greater cardiac output, lower total peripheral resistance and lower end-systolic meridional stress to volume ratio (ESSV) than the NTNR group. LVM in the NTHD group was significantly positively related to averaged systolic blood pressure (SBPavg), body surface area, extracellular fluid (ECF), carotid intima-media thickness (IMT), aortic pulse wave velocity (PWV), and negatively related to ESSV and Kt/V. The independent significant noncardiac structural determinants of LVM in NTHD subjects were ESSV, SBPavg, PWV and SV (model r2 = 0.617, P < 0.001). The NTHD patients, without significant pressure and volume overload, still had increased LVM that was partially explained by the persistent flow overload and subclinical LV dysfunction.

Structural and functional changes in left ventricle during normotensive and preeclamptic pregnancy.

Increased cardiac output in pregnancy is associated with cardiac remodeling and possible reduction in contractility, which may worsen in preeclampsia. Left ventricular (LV) geometry and function were compared between nonpregnant controls (n = 12) and normotensive (n = 44) and preeclamptic (n = 15) pregnant women using echocardiography. Load-independent comparisons of LV systolic function compared end-systolic stress (ESS) and rate-corrected velocity of circumferential fiber shortening (V(CFC)). Mean arterial pressures were 101 +/- 14 mmHg in preeclampsia, 76 +/- 6 mmHg in normotensive pregnancy, and 78 +/- 6 mmHg in controls (P < 0.005 vs. preeclampsia). LV mass increased during normotensive pregnancy (66 +/- 13 to 76 +/- 16 g/m(2); P < 0.05; controls, 65 +/- 10 g/m(2); P < 0.05) and was greater in preeclampsia (90 +/- 18 g/m(2); P < 0.05). In normotensive pregnancy, ESS decreased (59 +/- 9 to 52 +/- 11 g/cm(2); P < 0.05; controls, 66 +/- 14 g/cm(2); P < 0.005). ESS was greater in preeclampsia (60 +/- 14 g/cm(2); P < 0.05). In controls, there was an inverse relationship between ESS and V(CFC) (r = -0.78). The ESS-V(CFC) relationships in normotensive and preeclamptic pregnancy were unchanged from controls. We conclude that LV hypertrophy in normotensive and preeclamptic pregnancy matches changes in cardiac work, and LV contractility is preserved.

Association between left ventricular structure and cardiac performance during effort in two morphological forms of athlete’s heart

Aim: The aim of the study was to evaluate in 263 competitive athletes possible correlations between changes induced by different sport activities in left ventricular (LV) structure and cardiac response during maximal physical effort. Methods: A total of 160 top-level endurance athletes (ATE; swimmers, runners; 28±4 years; 98 male) and 103 strength-trained athletes (ATS; weight-lifters, body-builders; 27±5 years; male), selected on the basis of training protocol (dynamic vs. static exercise), underwent standard Doppler echocardiography, heart rate variability analysis and maximal exercise stress test by bicycle ergometry. M- and B-mode echocardiographic LV measurements were determined at rest, while the following functional indexes were assessed during effort: maximal heart rate (HR), maximal systolic blood pressure (SBP) and maximal workload (Watts reached by bicycle test). Results: The two groups were comparable for age and sex, but ATS at rest showed higher HR, SBP, and body surface area (BSA). By echo analysis, LV mass index and ejection fraction did not significantly differ between the two groups. However, ATS showed increased sum of wall thickness (septum+posterior wall), relative wall thickness and LV end-systolic stress, while LV stroke volume and LV end-diastolic diameter ( P<0.01) were greater in ATE. HR variability analysis underlined in ATE increased indexes of vagal tone ( P<0.01). During maximal physical effort, ATE showed a better functional capacity, with greater maximal workload ( P<0.001) reached with lower maximal HR and SBP. After adjusting for HR, age, sex, BSA and SBP, distinct multiple linear regression models evidenced in ATE independent associations of maximal effort workload with LV end-diastolic diameter ( P<0.001), HR ( P<0.001) at rest and LV end-systolic stress ( P<0.01) were found in ATE. On the other hand, independent direct correlation of SBP max during effort with sum of wall thickness ( P<0.001), BSA ( P<0.05) and LV end-systolic stress ( P<0.001) was evidenced in ATS. Conclusions: LV structural changes in competitive athletes represent adaptation to hemodynamic overload induced by training and are consistent with different kinds of sport activity. Work capacity during exercise is positively influenced by preload increase in ATE, while increased afterload due to isometric training in ATS determines higher systemic resistance during physical effort.

Echocardiographic comparison of left ventricular structure and function in hypertensive patients with primary aldosteronism and essential hypertension

Background In experimental renovascular hypertension, aldosterone has been implicated in myocardial remodeling and fibrosis, but it is uncertain whether excess aldosterone effects left ventricular structure and function in hypertensive patients. Methods Hypertensive patients from the Cardiovascular Center of the New York Presbyterian Hospital-Weill Cornell Medical Center in New York and the Russian Cardiovascular Research Institute, Moscow, Russia, were studied. The sample included 35 patients with primary aldosteronism and 35 controls with essential hypertension matched for age, gender, and blood pressure (BP). Left ventricular (LV) mass, endocardial and midwall fractional shortening, and circumferential end-systolic stress were calculated. The observed/predicted midwall shortening ratio was used as an index of LV performance corrected for afterload. Results: Primary aldosteronism and essential hypertension patients had comparable LV dimensions, wall thickness, mass, mass/body surface area, and mass/height 2.7. Endocardial and midwall fractional shortening, and afterload-corrected midwall shortening were similar in primary aldosteronism and essential hypertension groups from both clinics. Moreover, logistic regression analysis using BP, body mass index, height, gender, and center as covariates failed to identify statistical differences in LV geometry or systolic function between primary aldosteronism and essential hypertension patients. Conclusions Patients with primary aldosteronism, a state characterized by chronic aldosterone excess, had similar LV geometry and systolic function compared to essential hypertension patients matched for age, gender, and BP. This argues against important independent associations between aldosterone and these aspects of LV response to human hypertension.

Coronary flow velocity reserve in hypertensive patients with left ventricular systolic dysfunction

Hypertensive microvascular disease is speculated to be a limiting factor for the ability of left ventricular (LV) hypertrophy to maintain LV systolic function in systemic hypertension. The role of coronary reserve, which may be affected by microvascular disease, remains uncertain in the pathophysiology of hypertensive heart disease. A progressive impairment of coronary flow velocity reserve (CFVR) according to the presence and severity of LV systolic dysfunction is anticipated to occur in hypertension. According to the absence or presence of LV dysfunction (LV fractional shortening - FS% < 30), two groups of hypertensive patients were investigated: HP1 (n = 9, FS% = 36+/-6) and HP2 (n = 13, FS% = 18+/-6). Eight normal subjects (NL) served as controls (LVFS% = 35+/-3). Doppler blood flow velocity was obtained from the left anterior descending coronary artery using transesophageal echocardiography before, and during 6-min continuous adenosine infusion (140 microg x kg(-1) x min(-1) intravenous). The CFVR was calculated as the ratio of maximal to baseline peak diastolic flow velocities. The comparison among NL, HP1, and HP2 groups showed statistically different (p < 0.05) mass index (101+/-18, 172+/-46, and 257+/-54 g x m(-2)), end-systolic wall stress (76.9+/-14.4, 78.4+/-23.9, and 174.5+/-43.0 10(3) x dyn x cm(-2)), and CFVR (3.5+/-0.6, 3.2+/-0.4, and 2.6+/-0.8), respectively. The CFVR correlated significantly and directly with LVFS% (r = 0.40) and correlated inversely with both mass index (r = -0.54) and end-systolic stress (r = -0.40). These results indicate that CFVR impairment is weakly related to LV dysfunction in hypertension.

Wall tension or stress in ischemic heart disease

Wall stress or wall tension is a conception derived from physics (Laplace's law) and represents the systolic force or work per surface unit. It is the systolic force made by myocardial tissues. Stress increase indicates enlargement of the left ventricle or increase of intracavitary pressure. This investigation included 170 subjects; control group consisted of 50 patients (pts) with normal coronary angiographic finding without valvular anomalies and the examination group included 120 pts with coronary disease. Transthoracic echocardiography was performed in the left lateral position using computerized Hewlett Packard SONOS 1000 apparatus. Invasive hemodynamic procedure was performed using GENERAL ELETRICS CGR 300. Meridional and equatorial systolic and diastolic stress were calculated according to Grossman formula. The meridional end-diastolic equatorial stress was 18.55 +/- 12.12 dyn/cm2 x 10(3) in the control group, while in coronary patients it was 28.15 +/- 13.42 dyn/cm2 x 10(3). In healthy persons the meridional end-systolic stress established by echocardiography was 190.37 +/- 23.15 dyn/cm2 x 10(3), while in coronary patients 203.82 +/- 17.88 dyn/cm2 x 10(3). End-diastolic equatorial stress was 34.32 +/- 17.18 dyn/cm2 x 10(3) in the control group and 46.13 +/- 17.82 dyn/cm2 x 10(3) in coronary patients. Systolic equatorial stress in the control group was 357.42 +/- 32.15 dyn/cm2 x 10(3) and in coronary patients 385.34 +/- 35.72 dyn/cm2 x 10(3). The same parameters determined by invasive hemodynamic procedure were slightly higher, but without statistical significance in relation to the values determined by echocardiography (P > 0.05). Values of equatorial and particularly meridional stress were higher in coronary patients in relations to healthy persons, but without significant difference. The correlation coefficients of all investigated parameters established by noninvasive 2D echocardiography and invasive hemodynamic procedure were in one domain of medium high and high values. Meridional stress increases in coronary patients, equatorial in hypertensive patients or valvular anomalies with severe myocardial hypertrophy. In regard to high correlation between these two techniques, echocardiography may be considered a highly reliable method in evaluation of wall tension.