Left ventricular radius to wall thickness ratio

Left ventricular relative wall thickness, expressed as the ratio of enddiastolic radius to wall thickness (R/Th ratio), has a constant relation with left ventricular systolic pressure in children and adults with a normal heart, subjects with physiologic forms of cardiac hypertrophy (athletes) and patients with compensated chronic left ventricular volume overload (chronic aortic regurgitation). Greatly increased values for the radius/ thickness ratio, suggesting inadequate hypertrophy, indicate a poor prognosis in patients with chronic aortic regurgitation and in those with congestive cardiomyopathy; decreased values for this ratio are found in patients with hypertrophic cardiomyopathy (inappropriate hypertrophy) and in patients with compensated aortic stenosis (appropriate hypertrophy). In patients with compensated aortic stenosis, echocardiographic measurement of the left ventricular end-diastolic radius/wall thickness ratio has been used to estimate left ventricular systolic pressure. Measurement of left ventricular relative wall thickness appears to provide diagnostic and prognostic data in patients with a broad variety of cardiac disorders.     

Left ventricular relaxation and filling pattern in different forms of left ventricular hypertrophy: An echocardiographic study

To study left ventricular relaxation and filling in different forms of left ventricular hypertrophy, echocardiograms of the left ventricle in 24 patients with hypertrophic obstructive cardiomyopathy and in 24 patients with chronic left ventricular pressure overload (due to aortic stenosis in 6 and to severe arterial hypertension in 18) were analyzed by computer and compared with those of 28 normal subjects. The relaxation time index (minimal left ventricular dimension to mitral valve opening) was 13 ± 15 ms in normal subjects. This index was prolonged in patients with cardiomyopathy (93 ± 37 ms) and overload (66 ± 31 ms). During the interval from minimal left ventricular dimension to mitral valve opening both groups with left ventricular hypertrophy showed a marked increase in left ventricular dimension of 4.0 ± 2.2 mm and 3.0 ±1.8 mm, respectively, which was significantly greater (p < 0.001) than in normal subjects (0.6 ± 0.5 mm). This was probably a result of an abnormal change in left ventricular shape during isovolumic relaxation.The rapid filling phase and the increase in dimension during this period were significantly reduced in hypertrophic obstructive cardiomyopathy and chronic pressure overload. In contrast to findings in the patients with cardiomyopathy, in those with pressure overload the reduced increase in left ventricular dimension during the rapid diastolic filling period was compensated for by a greater dimensional increase due to atrial contraction, resulting in a normal end-diastolic dimension. These data indicate that significant prolongation of isovolumic relaxation is seen in different forms of left ventricular hypertrophy and is often associated with an abnormal diastolic filling pattern.     

Supernormal ejection performance is isolated to the ipsilateral congenitally pressure-overloaded ventricle

Congenital left ventricular pressure overload is associated with "excessive" hypertrophy that leads to subnormal afterload (wall stress), permitting enhanced ventricular ejection performance. Whether congenital right ventricular pressure overload is associated with a similar phenomenon is uncertain. It is also unknown whether supranormal ejection performance affects only the overloaded ventricle or is a general process affecting both ventricles. Conflicting data exist about whether the hypertrophic process associated with pressure overload is induced primarily by local loading conditions or by neuroendocrine influences. If the former postulate is true, the hypertrophic response should be confined to the overloaded ventricle; if the latter is true, one might predict that both ventricles would be affected by a less specific response to circulating catecholamines. To help resolve these issues, both right and left ventricular performance was examined in seven patients with isolated congenital pulmonary stenosis (average pulmonary pressure gradient 78 +/- 13 mm Hg), six patients with isolated congenital aortic stenosis (average gradient 80 +/- 10 mm Hg) and six normal subjects. Right ventricular ejection fraction was increased in patients with pulmonary stenosis (61 +/- 2%) compared with the value in normal subjects (53 +/- 2%, p less than 0.01) and in patients with aortic stenosis (50 +/- 3%, p = 0.007). Left ventricular ejection fraction was increased in patients with congenital aortic stenosis (84 +/- 4%) compared with the value in normal subjects (70 +/- 4%, p less than 0.01) and in patients with congenital pulmonary stenosis (65 +/- 2%, p less than 0.002).(ABSTRACT TRUNCATED AT 250 WORDS)     

Echocardiographic measurement of right ventricular wall thickness in hypertrophic cardiomyopathy: relation to clinical and prognostic features

Hypertrophic cardiomyopathy is characterized by unexplained left ventricular hypertrophy. It is uncertain, however, to what extent the right ventricle is also thickened. Right ventricular hypertrophy is found at autopsy in patients who die suddenly but, until recently, systematic evaluation of right ventricular morphology has not been feasible. In this two-dimensional echocardiographic study, a total of 4 to 10 (median 7) right ventricular wall thickness measurements were made from six right ventricular views in 73 patients with hypertrophic cardiomyopathy. Forty-one normal subjects were also studied for comparison. Thirty-two (44%) of the 73 patients had right ventricular hypertrophy with at least two of the wall thickness measurements exceeding 2 standard deviations (SD) from the mean value in the normal subjects. Right ventricular hypertrophy was mild (less than or equal to 8 mm) in 24 patients, moderate (9 to 12 mm) in 7 and severe (greater than 12 mm) in 1. The coefficient of variation of right ventricular wall thickness measurements was similar in normal subjects and patients with and without right ventricular hypertrophy (17 +/- 7, 11 +/- 8 and 10 +/- 8, respectively). The hypertrophy was concentric, with a coefficient of variation of 25% in all but one patient. There was a strong correlation of maximal right and mean left ventricular wall thickness (r = 0.643, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Left ventricular diastolic function in elite athletes with physiologic cardiac hypertrophy

Left ventricular hypertrophy due to aortic stenosis, hypertension and other forms of heart disease is associated with abnormalities of diastolic function. It is uncertain whether these changes are an inherent consequence of the hypertrophic process or represent additional pathologic factors. To investigate this issue, echocardiographic indexes of left ventricular early diastolic function in highly trained athletes were compared with those in age-matched normal control subjects. Athletes were equally classified into two groups: 11 swimmers who had a pattern of myocardial hypertrophy with normal wall thickness to dimension ratio and 11 power lifters whose wall thickness to dimension ratio was increased. The peak rates of left ventricular dimension increase and wall thinning in swimmers and power lifters were greater than in control subjects despite significantly higher left ventricular wall thickness and left ventricular mass index in the athletes. This increase in diastolic function indexes was associated with greater ventricular size and systolic performance. Normalization of the peak rate of dimension increase for end-diastolic dimension and adjustment of the peak rate of wall thinning for the fractional systolic thickening resolved any differences between groups. Thus, after the effects of ventricular size and systolic function were taken into consideration, diastolic function was normal in these subjects with considerable physiologic hypertrophy. This is in contrast to the findings in patients with hypertrophy associated with left ventricular pressure or volume overload, and suggests that abnormalities of diastolic function seen in pathologic hypertrophy are due to factors other than cardiac hypertrophy itself.     

Alterations in left ventricular geometry, wall stress, and ejection performance after correction of congenital aortic stenosis

Children with congenital aortic stenosis have "excessive" left ventricular hypertrophy with reduced resting systolic wall stress that allows for supernormal ejection performance. If aortic stenosis is uncorrected, this pattern persists until adulthood. The effect of removing the aortic pressure gradient on left ventricular hypertrophy and wall stress in children with congenital aortic stenosis is unknown. To test the hypothesis that removal of the stimulus for hypertrophy by aortic valve replacement or repair would normalize left ventricular mass and wall stress, we measured left ventricular ejection performance, wall stress, and contractile function in seven patients at cardiac catheterization before and 36 +/- 7 months after surgical correction of congenital aortic stenosis. After aortic valve replacement or repair, the aortic valve gradient fell from 87 +/- 12 to 7 +/- 4 mm Hg, and peak left ventricular pressure fell from 187 +/- 14 to 128 +/- 8 mm Hg. Left ventricular ejection fraction decreased postoperatively from 86 +/- 4% to 74 +/- 4% (p less than 0.001), whereas velocity of circumferential fiber shortening decreased from 2.15 +/- 0.15 to 1.6 +/- 0.11 (p less than 0.002). Left ventricular mass remained unchanged preoperatively (121 +/- 14 g/m2) and postoperatively (121 +/- 16 g/m2), but wall thickness (h) decreased in relation to ventricular radius (r) (h/r = 0.55 +/- 0.05 preoperatively, 0.36 +/- 0.02 postoperatively; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Computerized echocardiographic analysis to detect abnormal systolic and diastolic left venticular function in children with aortic stenosis.

Experience with computer analysis of M mode echocardiograms for the evaluation of left ventricular function in patients with left ventricular pressure overload is reported. In order to study systolic and diastolic left ventricular function, endocardial surfaces of the septum and posterior wall were digitized and analyzed by minicomputer. The subjects included 52 normal children and 30 children with catheterization-proved aortic stenosis with (13) and without (17) coarctation. Compared with the normal children, the patients with aortic stenosis had a statistically smaller and thicker walled left ventricle and increased fractional shortening of the left ventricular minor axis. Continuous tracings of minor axis dimension and the first derivative of these tracings were plotted. The tracings allowed measurement of the maximal velocity of shortening and lengthening. Maximal velocity of shortening (normal = 96.8 ± 3 mm/sec [mean ± standard error of the mean]) was depressed to 80.8 ± 4.7 mm/sec) in the group with pressure overload. Maximal velocity of lengthening (normal = 116.4 ± 3 mm/sec) was also depressed (88.4 ± 5.2 mm/sec) in this group. Although the velocity measurements allowed separation of the normal from the abnormal group, they did not correlate closely with either left ventricular wall thickness or left ventricular systolic pressure and therefore they cannot be used to assess the severity of the left ventricular pressure overload or the need for surgical correction. Nonetheless, the study provides a method for analyzing left ventricular diastolic and systolic dynamic function from a ventricular M mode echo alone and suggests abnormal systolic and diastolic left ventricular performance in some children with aortic stenosis and left ventricular hypertrophy.     

Effects of labetalol on left ventricular mass and function in hypertension--an assessment by serial echocardiography

We determined echocardiographic (M-mode) indices of left ventricular mass and function serially at 1-month intervals in 10 patients with uncomplicated mild or moderate essential hypertension, before and after adequate control of blood pressure with labetalol, a combined alpha- and beta-receptor blocking agent. Seven patients had pretreatment echocardiographic evidence of left ventricular hypertrophy with disproportionate septal thickness in 4. Systolic blood pressure in the untreated state correlated well (r = 0.96) with left ventricular mass but poorly (r = 0.30) with diastolic pressure. Following a satisfactory blood pressure reduction, achieved in all patients, left ventricular mass decreased from 240.5 +/- 71.1 g to 159.5 +/- 40.7 g (P less than 0.01), interventricular septal thickness from 1.33 +/- 0.3 cm to 0.92 +/- 0.25 cm (P less than 0.01) and posterior wall thickness from 1.03 +/- 0.23 cm to 0.93 +/- 0.23 cm (P less than 0.05). While the maximum changes in left ventricular mass were noted by the end of first month (P less than 0.01) with insignificant changes thereafter, the correlation of fall in blood pressure with change in left ventricular mass was significant only after 2 months of treatment (P less than 0.05). Indices of left ventricular function (end-diastolic volume, ejection fraction, fractional diameter shortening, left atrial dimension and posterior aortic wall motion) were normal before treatment and remained unchanged during 3 months of treatment. In this short-term study, labetalol reduced left ventricular hypertrophy (expressed as left ventricular mass and wall thickness) without altering left ventricular function indices in patients with uncomplicated essential hypertension. This has important implications in the treatment of hypertensive patients.     

Left ventricular structural characteristics in unilateral renovascular hypertension and primary aldosteronism

To assess the importance of the renin-angiotensin system and plasma volume as determinants of hypertensive left ventricular hypertrophy and its anatomy, patients with unilateral renovascular hypertension and primary aldosteronism were studied by echocardiography. Blood pressure, age and sex were matched as closely as possible. The 19 patients with unilateral renovascular hypertension and the 19 patients with primary aldosteronism were similar in age, sex and blood pressure (168 +/- 19/97 +/- 11 and 163 +/- 17/99 +/- 10 mm Hg, respectively), but plasma volume was increased in the patients with primary aldosteronism. Interventricular septal thickness, left ventricular posterior wall thickness, left ventricular mass index and relative wall thickness did not differ between the 2 groups of patients. There was a significant correlation between the level of systolic blood pressure and either left ventricular mass index (r = 0.34, p less than 0.05) or relative wall thickness (r = 0.58, p less than 0.001) in both groups of patients. Left ventricular end-diastolic dimension index was increased in the patients with primary aldosteronism compared with those with unilateral renovascular hypertension (3.2 +/- 0.4 vs 2.9 +/- 0.3 cm/m2, p less than 0.02). When confined to the patients with systolic pressure greater than or equal to 150 mm Hg, relative wall thickness was significantly increased in the patients with unilateral renovascular hypertension. Patients with primary aldosteronism and unilateral renovascular hypertension of similar blood pressure levels, age and sex have almost identical degrees of left ventricular hypertrophy and anatomy. In contrast, the patients with primary oldosteronism had increased left ventricular dimension index.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early diastolic left ventricular function in children and adults with aortic stenosis

Pressure overload hypertrophy of the left ventricle is associated with abnormal left ventricular early diastolic filling. The roles of the extent of cardiac hypertrophy, depressed left ventricular systolic function and aging in the pathogenesis of left ventricular diastolic dysfunction have not, however, been fully defined. To determine the relative importance of these factors in the pathogenesis of diastolic dysfunction in pressure overload hypertrophy, 16 children and 25 adults with aortic stenosis were compared with 48 normal children and adults, using rates of left ventricular early diastolic filling and wall thinning derived from M-mode echocardiography. Left ventricular early diastolic filling and wall thinning rates were significantly depressed in both children and adults with aortic stenosis as compared with values in normal subjects. Filling and thinning rates correlated negatively with age, left ventricular peak systolic pressure and wall thickness in all subjects. Furthermore, the effect of age on diastolic function appeared to be mediated by age-related increases in systolic pressure and wall thickness. In adults with aortic stenosis, early diastolic filling and wall thinning rates were depressed to a similar extent in subjects with normal and abnormal systolic function; thus, diastolic dysfunction does not appear to be a manifestation of abnormal systolic loading and ejection performance. These results suggest that extent of hypertrophy itself plays a dominant role in the mechanism of impaired left ventricular early diastolic filling in pressure overload due to aortic stenosis.     

Echocardiographic left ventricular dimensions in pressure and volume overload. Their use in assessing aortic stenosis.

Left ventricular 'relative wall thickness', determined from the ratio between echocardiographic measurements of end-systolic wall thickness and cavity transverse dimension, was related to peak systolic intraventricular pressure in 15 normal subjects, in 15 patients with left ventricular volume or pressure overload without aortic stenosis, and in 23 patients with aortic stenosis. All these patients had a mean rate of circumferential fibre shortening greater than 1.0 circumference per second and were regarded as having good ventricular function. Relative wall thickness was found to be normal in cases of volume overload and to be increased in pressure overload, being proportional to the systolic intraventricular pressure. Values for the ratio of systolic intraventricular pressure to relative wall thickness in the normal subjects and patients without aortic stenosis were similar (mean 30 +/- 2.5). Based on this relation, estimates of peak systolic intraventricular pressure were made in the cases of aortic stenosis using the formula: systolic intraventricular pressure (kPa) equals 30 x wall thicknes divided by transverse dimension. Peak systolic aortic value gradients derived by subtracting brachial artery systolic pressure, measured by sphygmomanometer, from the echocardiographic estimates of intraventricular pressure compared favourably with the gradients measured at left heart catheterization (r equals 0.87, P less than 0.001). Aortic value orifice areas, derived from echocardiographic estimates of stroke volume, ejection time, and value gradient, ranged from 0.21 to 3.16 cm2 and appeared to correlate with the severity of aortic stenosis. All patients with aortic stenosis, with or without coexistent mild aortic regurgitation, who were recommended for aortic valve surgery, had estimated valve orifice areas of less than 0.8 cm2. A further 10 patients with pressure or volume overload had mean rates of circumferential fibre shortening of less than 1.0 circumference per second and were regarded as having poor ventricular function. In these cases values for relative wall thickness were lower than in those with good ventricular function and were not proportional to systolic intraventricular pressure. In patients with good left ventricular function systolic intraventricular pressure is proportional to, and can be estimated from, echocardiographic measurement of relative wall thickness.     

Left ventricular geometry and function in patients with aortic stenosis: gender differences.

BACKGROUND: Gender differences in cardiac size have been described in normal and pathological conditions in human and animals. Sex determination of a pattern of hypertrophy as a response to pressure overload has not been extensively evaluated and is still poorly understood in humans. METHODS AND RESULTS: To investigate the influence of gender in the left ventricle remodelling and preservation of the left ventricle function 195 adults (140 men and 55 women) with isolated aortic stenosis were evaluated. The mean age was 52 +/- 11 years for men and 53 +/- 13 years for women. All the patients had similar degree of aortic stenosis finally treated with valve replacement, similar clinical status and no signs of coronary artery disease in coronary angiograms. On echocardiography the left ventricle of women had a smaller the end systolic (30.5 +/- 7.8 vs. 39.4 +/- 11.2, P<0.001) and the end diastolic (49.4 +/- 9 vs. 57.3 +/- 11, P<0.001) chamber size. The female left ventricle generated a higher relative wall thickness (0.65 +/- 0.21 vs. 0.52 +/- 0.12, P<0.01), a greater fractional shortening (35.3 +/- 8.5 vs. 32.0 +/- 9.0, P<0.01) and a higher ejection fraction (64.4 +/- 12.7 vs. 57.5 +/- 14.6, P<0.001). The left ventricle posterior wall thickness and the septal thickness indexes were similar in both groups. There were also significant differences between the two groups in the left ventricle mass index. CONCLUSIONS: Gender has an important influence on the left ventricle adaptation pattern to pressure overload due to aortic stenosis. Women developed a greater degree of left ventricle hypertrophy documented as changes in left ventricle geometry (increased relative wall thickness, left ventricular mass) and left ventricle function (fractional shortening and ejection fraction).     

Echocardiographic left ventricular dimensions in pressure and volume overload. Their use in assessing aortic stenosis.

Left ventricular 'relative wall thickness', determined from the ratio between echocardiographic measurements of end-systolic wall thickness and cavity transverse dimension, was related to peak systolic intraventricular pressure in 15 normal subjects, in 15 patients with left ventricular volume or pressure overload without aortic stenosis, and in 23 patients with aortic stenosis. All these patients had a mean rate of circumferential fibre shortening greater than 1.0 circumference per second and were regarded as having good ventricular function. Relative wall thickness was found to be normal in cases of volume overload and to be increased in pressure overload, being proportional to the systolic intraventricular pressure. Values for the ratio of systolic intraventricular pressure to relative wall thickness in the normal subjects and patients without aortic stenosis were similar (mean 30 +/- 2.5). Based on this relation, estimates of peak systolic intraventricular pressure were made in the cases of aortic stenosis using the formula: systolic intraventricular pressure (kPa) equals 30 x wall thicknes divided by transverse dimension. Peak systolic aortic value gradients derived by subtracting brachial artery systolic pressure, measured by sphygmomanometer, from the echocardiographic estimates of intraventricular pressure compared favourably with the gradients measured at left heart catheterization (r equals 0.87, P less than 0.001). Aortic value orifice areas, derived from echocardiographic estimates of stroke volume, ejection time, and value gradient, ranged from 0.21 to 3.16 cm2 and appeared to correlate with the severity of aortic stenosis. All patients with aortic stenosis, with or without coexistent mild aortic regurgitation, who were recommended for aortic valve surgery, had estimated valve orifice areas of less than 0.8 cm2. A further 10 patients with pressure or volume overload had mean rates of circumferential fibre shortening of less than 1.0 circumference per second and were regarded as having poor ventricular function. In these cases values for relative wall thickness were lower than in those with good ventricular function and were not proportional to systolic intraventricular pressure. In patients with good left ventricular function systolic intraventricular pressure is proportional to, and can be estimated from, echocardiographic measurement of relative wall thickness.     

Diastolic left ventricular pressure-volume and stress-strain relations in patients with valvular aortic stenosis and left ventricular hypertrophy.

Left ventricular (LV) chamber and myocardial stiffness were determined in 17 patients, four subjects with normal LV function and 13 subjects with valvular aortic stenosis and concentric myocardial hypertrophy, using simultaneous catheter micromanometry and LV cineangiography. Pressure (P), volume (V), and wall thickness (h) were measured. Variability in both chamber and myocardial stiffness parameters was found with five of the aortic stenosis patients (Group 1, left ventricular end-diastolic pressure = 15 +/- 2 (SEM) mm Hg) exhibiting normal values for end-diastolic dP/dV and dP/dV/V, for chamber stiffness constants (a,a') derived from P-V and normalized P-V relations, respectively, for end-diastolic myocardial elastic stiffness (ES or EE, where S = spherical model and E = ellipsoidal model) at the midwall of the minor axis circumference, and for the myocardial stiffness constants (KS or KE) of the circumferential stress-strain relation. Eight other patients with aortic stenosis (Group II, left ventricular end-diastolic pressure = 20 +/- 3 (SEM) mm Hg) exhibited significant increases in end-diastolic dP/dV,dP/dV/V,ES and EE and a tendency for increase in the chamber stiffness constants (a,a') and myocardial stiffness constants (KS, KE). These observations suggest that concentric increase in muscle mass (increase in wall thickness/minor axis radius ratio and wall volume/chamber volume ratio) is an important determinant of elevated mid- and late diastolic pressures in patients with valvular aortic stenosis, while concurrently mitigating increases in both systolic and diastolic wall stress. In some patients with aortic stenosis, however, diastolic filling pressures are elevated more severely, not only as a result of concentric hypertrophy, but also in response to augmented muscle stiffness. Reversibility of increased ventricular diastolic stiffness and elevated filling pressures was documented as concentric hypertrophy regressed post-aortic valve replacement in one patient, suggesting that fibrosis is not invariably the cause of enhanced myocardial stiffness in this secondary and compensatory form of hypertrophy.     

Relationship between instantaneous trans-mitral blood flow velocity and instantaneous left ventricular volume in normal and hypertrophied hearts.

We examined the relationship between trans-mitral blood flow velocity and left ventricular volume in normal and hypertrophied hearts using cross-sectional Doppler echocardiography. We studied 10 normal subjects and 19 patients with left ventricular hypertrophy, 9 with aortic stenosis and 10 with dilated cardiomyopathy. Trans-mitral Doppler flow velocity signals and cross-sectional echocardiograms of the left ventricular short and long axes were digitized in each patient to obtain instantaneous mitral flow velocity, instantaneous left ventricular volume, left ventricular mass, and left ventricular mass/volume ratio at end-diastole. Peak velocities during rapid filling (E wave) were similar in all three groups. Peak velocities during atrial systole (A wave) were significantly increased in aortic stenosis, (124 +/- 28 cm/sec); but were not different from normal in dilated cardiomyopathy (43 +/- 20 cm/sec versus 32 +/- 9 cm/sec). The peak A/E velocity ratio was elevated in aortic stenosis 1.47 +/- 0.30, but in dilated cardiomyopathy it was similar to normal hearts (0.47 +/- 0.23 versus 0.54 +/- 0.15). The percentages of left ventricular filling achieved at the time of the peak E wave, the end of rapid filling, and at the time of the peak A wave were similar in all three patient groups. There was no correlation between blood flow velocities at peak E wave, peak A wave or the A/E velocity ratio and left ventricular volume or mass. There was a significant correlation between peak A velocities and left ventricular muscle/cavity areas (r = 0.81; P less than 0.001). There was a similarly close correlation between the peak A/E velocity ratios and left ventricular muscle/cavity areas (r = 0.80; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiocyte cytoskeleton in patients with left ventricular pressure overload hypertrophy

OBJECTIVES: We sought to determine whether the cardiocyte microtubule network densification characteristic of animal models of severe pressure overload cardiac hypertrophy occurs in human patients. BACKGROUND: In animal models of clinical entities causative of severe right and left ventricular (LV) pressure overload hypertrophy, increased density of the cellular microtubule network, through viscous loading of active myofilaments, causes contractile dysfunction that is normalized by microtubule depolymerization. These linked contractile and cytoskeletal abnormalities, based on augmented tubulin synthesis and microtubule stability, progress during the transition to heart failure. METHODS: Thirteen patients with symptomatic aortic stenosis (AS) (aortic valve area = 0.6 +/- 0.1 cm2) and two control patients without AS were studied. No patient had aortic insufficiency, significant coronary artery disease or abnormal segmental LV wall motion. Left ventricular function was assessed by echocardiography and cardiac catheterization before aortic valve replacement. Left ventricular biopsies obtained at surgery before cardioplegia were separated into free and polymerized tubulin fractions before analysis. Midwall LV fractional shortening versus mean LV wall stress in the AS patients was compared with that in 84 normal patients. RESULTS: Four AS patients had normal LV function and microtubule protein concentration; six had decreased LV function and increased microtubule protein concentration, and three had borderline LV function and microtubule protein concentration, such that there was an inverse relationship of midwall LV fractional shortening to microtubule protein. CONCLUSIONS: In patients, as in animal models of severe LV pressure overload hypertrophy, myocardial dysfunction is associated with increased microtubules, suggesting that this may be one mechanism contributing to the development of congestive heart failure in patients with AS.     

Relation of hemodynamic load to left ventricular hypertrophy and performance in hypertension

Left ventricular hypertrophy and dysfunction in patients with hypertension are often poorly related to the level of blood pressure. To evaluate the reasons for this, 100 untreated patients (44 +/- 14 years) with essential hypertension were studied using cuff blood pressure and quantitative echocardiography to measure left ventricular mass index and end-diastolic relative wall thickness as 2 indexes of left ventricular hypertrophy. Left ventricular hypertrophy, as measured by either left ventricular mass index or end-diastolic relative wall thickness, correlated weakly with all indexes of blood pressure including systolic, diastolic, and mean blood pressure (r = 0.16 to 0.32). In contrast, end-diastolic relative wall thickness, an index which assesses the severity of concentric hypertrophy, showed a closer direct relation with total peripheral resistance (r = 0.52 p less than 0.001) and a significant inverse relation with cardiac index (r = -0.47, p less than 0.001). Left ventricular performance as assessed by fractional systolic shortening of left ventricular internal dimensions was not significantly related to left ventricular mass index, blood pressure, or peak systolic wall stress, but declined significantly with increasing mean systolic wall stress (r = -0.42, p less than 0.001) and even more with increasing end-systolic wall stress (r = -0.71, p less than 0.001). It is concluded that in patients with hypertension (1) left ventricular hypertrophy is correlated only modestly with measurements of resting blood pressure; and (2) the classic pattern of concentric left ventricular hypertrophy, as measured by relative wall thickness, is more closely related to the "typical" hypertensive abnormality of elevated peripheral resistance, suggesting that these anatomic and hemodynamic changes may be pathophysiologically interdependent. Furthermore, left ventricular performance declines when the pressure overload in hypertension is not offset by compensating hypertrophy, allowing wall stresses to increase.     

Echocardiographic detection of right ventricular hypertrophy

M-mode echocardiographic right ventricular wall thickness (RVW) and diastolic right ventricular internal diameter (RVID), when above the accepted normal range (RVW less than or equal to 5 mm, RVID less than or equal to 26 mm), are frequently used clinically to predict the presence of right ventricular hypertrophy. RVID was compared to anatomic right ventricular mass (RVM) in 27 patients and to RVW in 13 patients to determine their accuracy for predicting right ventricular hypertrophy (RVM greater than 65 gm). When increased, both measurements were specific for right ventricular hypertrophy. The specificity for RVW above 5 mm was 100% and for RVID greater than 26 mm was 79%. Neither was a sensitive indicator of hypertrophy. Only 36% of those with anatomic right ventricular hypertrophy had an echocardiographically dilated ventricle, and 67% had a thickened free wall. Neither measurement proved to be an accurate predictor of RVM, with a correlation for RVW of 0.56 and for diastolic RVID of 0.19.     

Usefulness of measuring right ventricular anterior wall thickness in patients with right ventricular overload using M-mode echocardiography

Right ventricular anterior wall thickness measured by M-mode echocardiography and right ventricular systolic pressure obtained by right heart catheterization were correlated in 62 patients with chronic right ventricular overload including congenital heart disease and primary pulmonary hypertension. The patients were divided into two groups; one, with right ventricular systolic pressures of 39 mmHg or less; the other, 40 mmHg or more. The following results were obtained. 1. The correlation coefficient for right ventricular anterior wall thickness and right ventricular systolic pressure was r = 0.90 (p less than 0.001), and the regression equation was y = 13.2x-1.3. 2. Right ventricular end-diastolic dimension increased significantly in both groups, but no statistically significant differences were detected between the two. Right ventricular anterior wall thickness increased significantly in the group with higher right ventricular pressures (7.1 +/- 0.5 mm vs 3.1 +/- 0.5 mm). 3. When right ventricular anterior wall thickness was more than 4.0 mm, pulmonary hypertension was detected, with a sensitivity of 97.5% and a specificity of 90.9%. In conclusion, measurements of right ventricular anterior wall thickness by M-mode echocardiography via the anterior chest wall proved to be potentially useful in predicting right ventricular systolic pressures in patients with chronic right ventricular overloads.     

Patterns of left ventricular hypertrophy and geometric remodeling in essential hypertension.

The spectrum of left ventricular geometric adaptation to hypertension was investigated in 165 patients with untreated essential hypertension and 125 age- and gender-matched normal adults studied by two-dimensional and M-mode echocardiography. Among hypertensive patients, left ventricular mass index and relative wall thickness were normal in 52%, whereas 13% had increased relative wall thickness with normal ventricular mass ("concentric remodeling"), 27% had increased mass with normal relative wall thickness (eccentric hypertrophy) and only 8% had "typical" hypertensive concentric hypertrophy (increase in both variables). Systemic hemodynamics paralleled ventricular geometry, with the highest peripheral resistance in the groups with concentric remodeling and hypertrophy, whereas cardiac index was super-normal in those with eccentric hypertrophy and low normal in patients with concentric remodeling. The left ventricular short-axis/long-axis ratio was positively related to stroke volume (r = 0.45, p less than 0.001), with cavity shape most elliptic in patients with concentric remodeling and most spheric in those with eccentric hypertrophy. Normality of left ventricular mass in concentric remodeling appeared to reflect offsetting by volume "underload" of the effects of pressure overload, whereas eccentric hypertrophy was associated with concomitant pressure and volume overload. Thus, arterial hypertension is associated with a spectrum of cardiac geometric adaptation matched to systemic hemodynamics and ventricular load. Concentric left ventricular remodeling and eccentric hypertrophy are more common than the typical pattern of concentric hypertrophy in untreated hypertensive patients.