R-wave amplitude changes during exercise in adolescents with left ventricular pressure and volume overload

To determine the diagnostic value of exerciseinduced R-wave changes in adolescents with congenital heart disease, the responses of 50 adolescents without significant heart disease were compared with those of 72 patients with either a left ventricular (LV) pressure or volume overload lesion. Among the pressure overload group, 24 patients had valvular aortic stenosis (AS) and 27 had coarctation of the aorta. The volume overload group included 12 patients with mitral regurgitation (MR) and 9 with aortic regurgitation (AR). Severity of the cardiac lesion was assessed using cardiac catheterization in patients with AS, physical examination in patients with coarctation of the aorta and clinical or angiographiec criteria, or both, in patients with valvular regurgitation. The R wave was measured in 10 consecutive QRS complexes in leads II, aVF and V₅ at rest, maximal exercise and 1-minute recovery. At maximal exercise, control subjects had a mean decrease in amplitude (ΔR) of ?3.6 mm (p < 0.0001). Compared with the control group, the AS group had a similar decrease of ?3.5 mm, but the coarctation group had a ΔR of ?1.4 (p < 0.005) and the volume overload group a ΔR of ?1.1 mm (p < 0.003). Patients with AS and ischemic ST-segment changes during exercise (n = 12) had greater decreases in R-wave amplitude than did those with no ST changes (n = 12) (p < 0.04). In patients with AS and an LV end-diastolic pressure ? 12 mm Hg (n = 7), the decrease in ΔR was also greater than that in patients with LV end-diastolic pressure ≤ 12 mm Hg (n = 14) (p < 0.006). Among patients with volume overload, more severe valvular regurgitation was associated with a smaller ΔR (p < 0.03). In patients with AS an increased ΔR reflects ischemia or diminished LV compliance, or both, whereas in patients with volume overload a decrease in ΔR is an indicator of the severity of regurgitation.     

Abnormal left ventricular response to isometric exercise in pure, isolated aortic regurgitation: beneficial effects of nifedipine

To examine the effects of nifedipine on the left ventricular (LV) functional response to isometric exercise in patients with aortic regurgitation (AR), 20 patients with isolated, moderate to severe AR performed 3 minutes of handgrip exercise at 33% of their maximal voluntary contraction, before and after administration of 20 mg of sublingual nifedipine. Although handgrip exercise produced similar increases in heart rate and systolic blood pressure before and after nifedipine treatment, heart rate was higher and systolic blood pressure lower with handgrip exercise during nifedipine treatment. LV end-diastolic volume index was not different during the control period and nifedipine handgrip exercise, but the increase in end-systolic volume index was smaller and the ejection fraction was higher during nifedipine handgrip exercise. Nifedipine reduces afterload and ameliorates handgrip exercise-induced LV dysfunction in patients with AR.     

Effect of aortic valve stenosis (pressure overload) and regurgitation (volume overload) on left ventricular systolic and diastolic function.

In secondary hypertrophy from chronic pressure or volume overload, or both, systolic as well as diastolic abnormalities of left ventricular (LV) function have been described, but their relation has not been defined. In 58 patients with aortic valve disease (28 with aortic valve stenosis, and 30 with aortic regurgitation) and in 11 control subjects, LV biplane cineangiography was performed simultaneously with LV high-fidelity pressure measurements. LV ejection performance was assessed by ejection fraction, and diastolic function by the time constant of LV pressure decay, the early and late peak filling rates, and the constants of chamber (pressure-volume relation) and myocardial stiffness (stress-strain relation). In the entire cohort (n = 69), ejection fraction was inversely related to the time constant of LV relaxation (r = -0.58, p less than 0.001) and to the constant of myocardial stiffness (r = -0.62, p less than 0.001). Despite preserved systolic contractile function (as evaluated from the ejection fraction-mean systolic stress relation), abnormalities in LV diastolic function were present in 9 of 18 patients with pressure overload and 20 of 22 with volume overload. None of the 58 patients with aortic valve disease had a reduced early peak filling rate, whereas a reduction in late peak filling rate was observed in 3 with aortic stenosis, but in none with aortic regurgitation. This, it appears that abnormalities of relaxation and passive diastolic myocardial stiffness precede alterations in myocardial contractility. Assessment of peak filling rates is not helpful to detect diastolic dysfunction in patients with aortic valve disease.     

Prevalence and significance of reversible radionuclide ischemic perfusion defects in symptomatic aortic valve disease patients with or without concomitant coronary disease

To determine the prevalence and significance of exercise-induced localized perfusion defects in symptomatic patients with aortic valve disease, thallium-201 rest and exercise studies were performed in a consecutive series of 29 such patients prior to left heart catheterization with coronary arteriography. Eight patients had repeat studies after aortic valve replacement. Twelve of 17 patients with predominant aortic regurgitation (AR) had distinct LV apical defects during exercise despite normal coronary arteries, while 10 of 12 patients with aortic valve disease and associated coronary artery disease (CAD) had localized perfusion defects in LV areas other than the apex. In patients with AR, reversible apical perfusion defects can occur without CAD; these apical detects are probably a reflection of severe LV volume overload in AR. LV perfusion defects in areas other than the apex are specific for CAD in aortic valve disease, and concomitant CAD may not provoke regional LV perfusion deficits in aortic stenosis patients with severe LV hypertrophy.     

Systemic and left ventricular responses to exercise stress in asymptomatic patients with valvular aortic stenosis.

Patients with heart disease may have myocardial ischemia or left ventricular (LV) dysfunction without symptoms. The exercise responses of 14 asymptomatic patients with valvular aortic stenosis (AS) were studied using treadmill testing, thallium-201 scintigraphy and radionuclide angiography. Compared with age- and gender-matched control subjects, patients with AS demonstrated reduced exercise tolerance (10.7 +/- 2.5 vs 13.3 +/- 4.2 min; p = 0.06) and maximal oxygen consumption (26.7 +/- 6.3 vs 36.3 +/- 9.5 ml O2/min/kg; p = 0.004) associated with decreased peak systolic blood pressure response to exercise (177 +/- 18 vs 214 +/- 42 mm Hg; p less than 0.004). Ten of 14 patients developed ST-segment depression during exercise, only 3 of whom had reversible thallium defects. Patients with AS tended to have greater LV ejection fractions at rest (65 +/- 11 vs 58 +/- 7; p = 0.08) and significantly decreased early peak filling rates (4.8 +/- 1.3 vs 6.1 +/- 0.6 stroke volume/s; p = 0.003) compared with those of control subjects. During maximal supine exercise, patients with AS had less of an increase in ejection fraction (2 +/- 9 vs 15 +/- 7%; p less than 0.001) associated with a decrease in end-diastolic (-7 +/- 15 vs +5 +/- 16%; p = 0.06) and stroke (-6 +/- 17 vs +30 +/- 13%; p less than 0.001) volumes from baseline measurements.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanisms for an abnormal radionuclide left ventricular ejection fraction response to exercise in patients with chronic, severe aortic regurgitation.

To clarify the mechanisms for an abnormal radionuclide left ventricular (LV) ejection fraction response to exercise in patients with chronic, severe aortic regurgitation (AR), we studied seven control patients and 21 patients with AR. We used exercise radionuclide angiography and catheterization of the right and left sides of the heart to obtain a calculation of LV chamber elastance. The control and AR groups had similar heart rates, systolic blood pressure responses to exercise, and exercise durations. In both patient groups, LV end-diastolic volume did not change with exercise. In contrast to the decrease in LV end-systolic volume (p less than 0.05) and increase in LV ejection fraction (p less than 0.01) in the control group, LV end-systolic volume in the patients with AR increased, resulting in little change in their LV ejection fraction. By stepwise multiple regression analysis, the radionuclide LV ejection fraction at peak exercise in patients with AR was determined by the LV chamber elastance, LV end-systolic volume, and stroke volume at peak exercise (cumulative r = 0.79, p less than 0.02); the change in radionuclide LV ejection fraction from rest to peak exercise was determined by the corresponding change in systemic vascular resistance, regurgitant index, and LV end-diastolic and end-systolic volumes (cumulative r = 0.88, p less than 0.02). These data demonstrate that in patients with AR, the radionuclide LV ejection fraction at peak exercise is principally determined by the cumulative effects of chronic, severe AR on LV systolic chamber performance, and the change in radionuclide LV ejection fraction from rest to peak exercise is principally established by peripheral vascular responses.     

Left ventricular function at rest and by stress in patients with aortic valve diseases. Study using digital subtraction angiocardiography

Using digital subtraction angiocardiography left ventricular (LV) function and mean pulmonary artery pressure (PPA) at rest and during exercise were examined in 49 patients with aortic valve disease, 23 patients with aortic stenosis (AS), 12 patients with combined aortic valve lesions (kAV) and 14 patients with aortic regurgitation (AI). Muscular hypertrophy was present in all patients. LV-mass-to-volume ratio was significantly higher in patients with AS and kAV than in patients with AI. There was no significant difference in heart rate at rest or during exercise among the three groups. During exercise PPA increased significantly in all groups. The increase was significantly higher in patients with AS than in those with AI. End-diastolic and end-systolic volumes increased significantly in patients with AS and kAV on the average, showing no change in patients with AI. Ejection fraction decreased significantly in patients with AS and kAV and remained unchanged in patients with AI. Due to the increase in heart rate cardiac index increased significantly during exercise in all groups. In patients with pressure overloaded left ventricles (AS and kAV) the increase in filling pressure partly results in a decrease of compliance caused by hypertrophy. Thus in these ventricles LV function cannot be judged by LV filling pressures alone. In those patients in whom the indication for valve replacement was given without knowing the results of the exercise test, the changes of LV volumes and ejection fraction were abnormal during exercise on the average.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of Left Ventricular Contractility in Pressure and Volume Overload: A Strain Rate Study in the Clinical Model of Aortic Stenosis and Regurgitation

Objective: The aim of this study is to compare the impact of two different loading conditions on myocardial contractility in asymptomatic patients with normal EF by using stain rate imaging (SRI). Methods: A total of 27 patients with severe aortic regurgitation (mean age 50 ± 11 years) and 25 patients with severe aortic stenosis (mean age 53 ± 15 years) were prospectively recruited. Fifteen healthy subjects (mean age 50 ± 6 years) were enrolled as the control group. For the evaluation myocardial contractility, longitudinal LV function was chosen and, midventricular segment shortening was analyzed for the septum, LV lateral wall from apical four‐chamber view and for the anterior, inferior wall from apical two‐chamber view. Results: Longitudinal peak systolic strain rate values of each segment derived from analysis of a total of 804 segments were significantly decreased in the patients population (P < 0.001). Global longitudinal peak systolic strain rate was also significantly decreased in aortic stenosis and regurgitation compared to the control group (?1 ± 0.5, ?0.9 ± 0.3, and ?1.6 ± 0.3, P = 0.001). As far as the comparison between patients with aortic stenosis and aortic regurgitation, neither global strain rate nor strain rate for each wall was found to be different. Conclusion: We conclude that longitudinal LV function is reduced in both pressure and volume overload, and both of this overload patterns are equally harmful to the ventricle. (Echocardiography 2010;27:798‐802)     

Factors influencing left ventricular structure and stress-corrected systolic function in men and women with asymptomatic aortic valve stenosis (a SEAS Substudy)

To identify determinants of left ventricular (LV) structure and stress-corrected systolic function in men and women with asymptomatic aortic stenosis (AS), Doppler echocardiography was performed at baseline in 1,046 men and 674 women 28 to 86 years of age (mean 67 +/- 10) recruited in the Simvastatin Ezetimibe in Aortic Stenosis (SEAS) study evaluating placebo-controlled combined simvastatin and ezetimibe treatment in AS. LV hypertrophy was less prevalent in women despite older age, higher systolic blood pressure, and smaller aortic valve area/body surface area (all p values <0.05). In logistic regression analyses, LV hypertrophy was independently associated with male gender, severity of AS, hypertension, higher systolic blood pressure, and lower stress-corrected midwall shortening (scMWS) or stress-corrected fractional shortening (scFS; all p values <0.01). In men aortic regurgitation also was a predictor of LV hypertrophy (p <0.05). Women had greater scFS and scMWS when corrected for LV size or geometry (all p values <0.001). In multivariate analyses, female gender predicted 11% greater scFS and 4% greater scMWS independent of age, body mass index, heart rate, aortic valve area, LV mass, relative wall thickness, aortic regurgitation, hypertension, and end-systolic stress (R(2) = 0.23 and 0.59, respectively, p <0.001). In conclusion, the major determinants of LV hypertrophy in patients with asymptomatic AS are male gender, severity of AS, and concomitant hypertension. Women have higher stress-corrected indexes of systolic function independent of LV geometry or size, wall stress, older age, or more concomitant hypertension.     

Effects of upright and supine position on cardiac rest and exercise response in aortic regurgitation

The effects of upright and supine position on cardiac response to exercise were assessed by radionuclide ventriculography in 15 patients with moderate to severe aortic regurgitation (AR) and in 10 control subjects. In patients with AR, heart rate was higher during upright exercise, but systolic and diastolic blood pressure and left ventricular (LV) output were similar during both forms of exercise. LV stroke volume and end-diastolic volume were not altered during supine exercise. LV end-systolic volume increased and ejection fraction decreased during supine exercise, but both were unchanged during upright exercise. Of 15 patients, 5 in the upright and 12 in the supine position had an abnormal LV ejection fraction response to exercise (p less than 0.01). Right ventricular ejection fraction increased and regurgitant index decreased with both forms of exercise and was not significantly different between the 2 positions. Thus, posture is important in determining LV response to exercise in patients with moderate to severe AR.     

Comparison of effects of isometric and supine bicycle exercise on left ventricular performance in patients with aortic regurgitation and normal ejection fraction at rest

The effects of handgrip and supine bicycle exercise on hemodynamics and left ventricular (LV) performance were compared in 25 patients with moderate to severe aortic regurgitation (AR) and normal LV ejection fraction at rest (greater than or equal to 50%) and in 10 control subjects. In both groups, heart rate, systolic blood pressure, rate-pressure product, and LV output were higher during supine bicycle exercise. Compared with the controls, in patients with AR, stroke volume was unchanged during supine bicycle exercise. LV end-diastolic volume increased during handgrip exercise but was unchanged during supine bicycle exercise. LV end-systolic volume increased and ejection fraction decreased during both forms of exercise. Of 25 patients with AR, 15 (60%) during handgrip exercise and 19 (76%) during supine bicycle exercise had an abnormal ejection fraction response (p less than 0.05). In patients with moderate to severe AR and normal LV ejection fraction at rest, both handgrip and supine bicycle exercise induced LV dysfunction. An abnormal LV ejection fraction response occurred more often with supine bicycle exercise. Handgrip exercise may be a useful alternative method for detecting LV dysfunction in patients with AR in whom adequate bicycle exercise cannot be accomplished.     

Radionuclide evaluation of aortic regurgitation: assessment of ventricular function by Fourier phase analysis

Forty patients with chronic isolated aortic regurgitation werestudied by phase analysis of equilibrium radionuclide ventriculographyto see whether this technique could detect changes in left ventricular(LV) function before the onset of symptoms. This technique wascompared to the radionuclide ejection fraction and echocardiography.The severity of LV volume overload was assessed using the radionuclideregurgitant index.Patients with clinically severe aortic regurgitationhad severe volume overload (high regurgitant index), increasedechocardiographic left ventricular dimensions and significantlyincreased phase spread (loss synchrony of wall motion) comparedto mild and moderate groups. All but one had well maintainedglobal left ventricular function assessed by the ejection fraction.All seven patients with definite symptoms had a marked increasein phase spread and severe volume overload.     

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.     

Left ventricular function in chronic aortic regurgitation with reference to end-systolic pressure, volume and stress relations

Left ventricular muscle and pump performance were evaluated in 12 normal subjects and 21 patients with aortic regurgitation (10 with minimal symptoms and 11 with congestive heart failure). A computer-based quantitative analysis of biplane left ventriculograms was used. Both patient groups had significant aortic regurgitation documented by ventriculography. Contractile function measured by peak systolic stress/end-diastolic volume and end-systolic pressure/volume curves was poorer than that in normal subjects in patients with heart failure but not in asymptomatic patients. When normalized for muscle mass, stroke work was not depressed in either asymptomatic patients (mean +/- standard error of the mean 0.008 +/- 0.001 joules/g) or patients with heart failure (0.009 +/- 0.004) by comparison with the value in normal subjects (0.010 +/- 0.001). Angiographically determined cardiac index (CI) increased with increasing volume overload even though forward cardiac index measured by the Fick method remained essentially unchanged: normal subjects (total CI 3.7 +/- 0.4 liters/min per m2, Fick CI 2.4 +/- 0.1); asymptomatic patients (total CI 7.6 +/- 0.7, Fick CI 2.3 +/- 0.2); patients with heart failure (total CI 9.1 +/- 0.82, Fick CI 2.1 +/- 0.18). Left ventricular peak stress increased significantly in patients with heart failure (511 +/- 55 dynes/cm2 x 10(-3)) compared with values in normal subjects (360 +/- 33) and asymptomatic patients (428 +/- 50). The combination of decreased muscle function and increased demands on pump function causes a significant increase in end-diastolic pressure only in patients with heart failure (23 +/- 2 mm Hg), which results in pulmonary congestive symptoms.     

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.     

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.     

Reliable estimation of peak left ventricular systolic pressure by M-mode echographic-determined end-diastolic relative wall thickness: Identification of severe valvular aortic stenosis in adult patients

In compensated hearts, left ventricular systolic pressure (LVSP) can be estimated from the ratio of LV wall thickness to chamber radius (RWT). To determine the clinical value of such estimates, we examined echocardiographic RWT in an unscreened series of 81 individuals with aortic valve disease, hypertension, or normal hearts. Despite the presence, in many subjects, of symptoms of congestive heart failure, reduced ejection fraction, or coronary disease, end-diastolic RWT (RWT_D) correlated well with peak LVSP (r = 0.77); 45 of 55 patients with LVSP ≥ 140 mm Hg had RWT_D ≥ 0.45, while 26 of 26 with LVSP < 140 mm Hg had lower values (p < 0.005). RWT_D was ≥ 0.50 in 30 of 34 patients with LVSP ≥ 180 mm Hg and in 6 of 21 with LVSP 140 to 180 mm Hg. RWT_D correctly estimated LVSP range in 26 of 27 severe aortic stenosis (AS) patients and, combined with echocardiographic aortic valve calcification, correctly recognized the presence or absence of severe AS in 99% of the series. The RWT_D for any given LVSP was higher in patients on antihypertensive treatment and lower in patients with severe aortic regurgitation. In contrast to series based on patients with normal LV function, end-systolic RWT correlated poorly with LVSP.     

Comparison of left ventricular geometry and left atrial size and function in patients with aortic stenosis versus those with pure aortic regurgitation

Chronic aortic valve disease can result in distinct adaptive left ventricular (LV) geometric patterns, which has different effects on LV function and left atrial (LA) performance. In this study we assessed the effect of LV geometry on LA size and function, and we verified the relation between LA size and LV mass in patients with distinct LV overload subsets. We analyzed 183 patients with aortic valve disease who underwent a complete echocardiographic evaluation. Based on the type of valvular dysfunction, patients were classified into 2 groups: 141 patients with aortic stenosis (group AS) and 42 patients with pure aortic regurgitation (group AR). Each of these 2 groups were then divided into those with a concentric LV pattern and those with an eccentric pattern. Both LA size and LA ejection force were significantly greater in group AS than group AR, particularly in patients with a concentric LV pattern. The degree of LA enlargement depended on LV mass in the patients with a concentric LV pattern (group AS r = 0.61, p <0.00001; group AR r = 0.38, p = 0.04). In contrast, no relation was found between LA size and LV mass in the patients with an eccentric pattern, independently of the type of valve dysfunction. Our results indicate that the influence of LV geometry on LA size and function in patients with aortic valve disease is relevant. A concentric LV pattern is associated with greater LA size and higher ejection than an eccentric pattern, suggesting that chronic LV pressure overload more than volume overload has a greater effect on stimulating increases in LA performance. The degree of LA enlargement depends on LV mass in patients with a concentric LV pattern, whereas it was unpredictable in those with an eccentric LV pattern.     

Left ventricular volume and ejection fraction response to exercise in aortic regurgitation

To test the hypothesis that left ventricular (LV) performance in aortic regurgitation (AR) can be more completely characterized by measurement of LV volumes in addition to ejection fraction (EF), 27 asymptomatic patients (Group 1), and 22 symptomatic patients (Group 2), and 10 control subjects were studied at rest and during upright bicycle exercise using the first-pass technique and a multicrystal scintillation camera. LV end-diastolic volume was measured by the area-length method. In the control group end-diastolic volume increased 14%, end-systolic volume decreased 22%, and EF increased 22% with exercise. In contrast, in Group 1 patients with AR, end-diastolic volume was elevated at rest and during exercise. The 18% decrease in end-diastolic volume during exercise was significantly different from the control response (p less than 0.01). End-systolic volume was also elevated at rest and during exercise, but the 30% decrease during exercise was a response not significantly different from the control. Although mean EF increased 15% in these patients, EF at peak exercise was significantly lower than that in the controls. In Group 2 patients with AR, resting EF was reduced, the EF response to exercise was abnormal, and end-diastolic and end-systolic volume responses to exercise were significantly different from those in Group 1: end-diastolic volume did not change and end-systolic volume increased. In contrast to the fairly uniform volume responses among all Group 1 patients, there were 2 subgroups based on volume changes within Group 2: 7 of 22 had a decrease in end-diastolic volume and end-systolic volume during exercise and 8 of 22 showed an increase in end-diastolic and end-systolic volume during exercise. In conclusion, LV volumes at rest and exercise give more information about LV functional reserve in symptomatic patients with AR than do EF responses alone, and may be useful in separating symptomatic patients who show a normal end-systolic volume response to exercise from those in whom worsening failure develops during exercise.     

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.