Alternating contractility in pulsus alternans studied in the isolated canine heart

We examined pulsus alternans in seven isolated, perfused canine left ventricles ejecting into a simulated arterial impedance. Left ventricular pressure-volume loops were measured during pulsus alternans while filing-source pressure was lowered. In all cases two distinct linear end-systolic pressure-volume relationships (ESPVRs) were noted for the strong and weak beats. The slopes of the ESPVRs of the strong beats were significantly greater than those of the weak beats (mean difference 0.9 +/- 0.6 mm Hg/ml, p less than .01), while the intercepts were not significantly different (mean difference 0.06 +/- 0.5 ml). Diastolic pressure-volume relationships for the strong and weak beats were not significantly different, excluding incomplete relaxation as a cause of pulsus alternans. Although the weak beats had both a smaller preceding end-diastolic volume and a larger end-systolic volume, the presence of two distinct ESPVRS for the strong and weak beats shows there is alternating ventricular chamber contractility in pulsus alternans that is not solely due to the Starling mechanism. The magnitude of alternation in pump function parameters such as pressure and stroke volume during pulsus alternans reflects the complex interactions of alternating contractile state with alternations in preload and afterload.     

Alternating atrial electromechanical dissociation as contributing factor for pulsus alternans.

Ten patients with mechanical pulsus alternans were studied by echocardiography and mechanocardiography. All had been or were in congestive heart failure. An atrial mechanism for pulsus alternans could be identified in two patients: one with primary congestive cardiomyopathy and one after aortic valve replacement for calcific aortic stenosis. Each strong systole was preceded by an "a" wave, while each weak systole was not. This was documented on both the apexcardiogram and the M-mode echocardiogram. Since both patients were in normal sinus rhythm with regular PP intervals, it was concluded that alternating atrial electromechanical dissociation was either the underlying mechanism or contributed to the pulsus alternans. Thus, alternating atrial electromechanical dissociation exists and may cause pulsus alternans. Pulsus alternans is not necessarily the result of left ventricular myocardial dysfunction alone.     

Mechanical alternans in patients with chronic heart failure.

BACKGROUND: Clinical implications of mechanical alternans in patients with chronic heart failure have remained uncertain. In this study, prevalence, characteristics, and prognostic implications of mechanical alternans were investigated. METHODS AND RESULTS: Consecutive 51 patients with dilated cardiomyopathy underwent diagnostic cardiac catheterization using a micromanometer-tipped catheter. Under basal conditions, 7 of 35 patients with sinus rhythm showed mechanical alternans. Physiologic tachycardia (110 bpm) induced mechanical alternans in another 15 patients with sinus rhythm and in another 10 of 16 patients with atrial fibrillation. Low doses of dobutamine also induced mechanical alternans in another 8 patients, but a high dose of dobutamine eliminated mechanical alternans. Consequently, 40 patients (78%) showed mechanical alternans. Mechanical alternans was always accompanied by alternating changes of positive dP/dt, a parameter of contractility during isovolumetric contraction time, but negative dP/dt was occasionally constant. Concordant mechanical alternans between both ventricles was more prevalent than discordant alternans. The left ventricular end-diastolic volume indices and end-systolic volume indices of patients with mechanical alternans were larger than those of patients without. The left ventricular ejection fraction of patients with alternans was significantly lower than that of patients without. CONCLUSIONS: Mechanical alternans was highly prevalent in patients with chronic heart failure. The origin of mechanical alternans seems to exist before or at the isovolumetric contraction time.     

Significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship under acute hypoxia in the dog

Summary In 14 closed-chest dogs, the significance of right ventricular filling for left ventricular enddiastolic pressure-volume relationship was investigated under acute hypoxia by means of single plane cineventriculography and simultaneous intraventricular pressure recording.Both after 5 min asphyxia (respirator switched off) (n=5) and after 3 min hypoxia (ventilation with pure N₂) (n=9), there was a significant leftward shift (p<0.005) of the left ventricular enddiastolic pressure-volume curve as compared to the control curves under normoxia. To simulate the elevated filling of the right ventricle under acute hypoxia, rapid intraventricular infusion was applier under normoxic conditions to raise right ventricular enddiastolic pressure to the same values as that measured under hypoxia. The extent of the ensuing leftward shift of the left ventricular enddiastolic pressurevolume curve was on average 60% of the shift under hypoxia in both sets of experiments. Neither the slope of the relationship between volume stiffness and enddiastolic pressure, nor the relationship between tangent elastic modulus and left ventricular wall stress, was affected by hypoxia or asphyxia.Thus, the shift of the left ventricular enddiastolic pressure-volume curve in the early stage of hypoxia is predominantly due to the influence of increased right ventricular filling. Since the increased volume of the atria under acute hypoxia limits left ventricular distensibility additionally, the changes in left ventricular enddiastolic pressure-volume relationships, observed in the early stage of hypoxia are mainly, or even entircly, the result of interaction of the various heart compartments, and not a reflection of alterations in myocardial tissue elasticity.Preliminary results were presented at the symposium on Cardiac adaptation to hemodynamic overload, training and stress in Tübingen (1983)Supported by the Deutsche Forschungsgemeinschaft     

Types of left ventricular hypertrophy and their functional changes in essential hypertension

104 patients of hypertensive left ventricular hypertrophy (LVH) were studied by two-dimensional echocardiography. According to the changes of left ventricular wall thickness, wall mass, end-diastolic volume and ejection fraction, they were divided into three types (concentric, dilated, disproportionate): (1) Concentric LVH 83 cases (79.8%) with thickened ventricular wall and augmented mass. (2) Dilated LVH 13 cases (12.5%) with left ventricular cavity enlarged and both ventricular mass and volume increased, ejection fraction decreased. (3) Disproportionate LVH 8 cases (7.7%), similar to hypertrophic cardiomyopathy with excess increase in interventricular septal thickness. The thickness ratio between interventricular septal and left ventricular posterior wall was greater than or equal to 1.3.     

Determination of left ventricular volumes using 2-dimensional echocardiography in children

In the first part of the study we examined silicone rubber left ventricular casts of children and adolescents by cross-sectional echocardiography using the so-called two-chamber and four-chamber apical views. Left ventricular volumes calculated from the echocardiographic left ventricular silhouettes correlated very well (r = 0.99) with the titrated cast volumes. In the second part of the study we compared in 30 infants, children, and adolescents left ventricular volumes as calculated from the two-chamber and four-chamber apical echocardiographic views with those obtained from the frontal projection of the left ventricular cineangiogram. Volumes calculated from the apical four-chamber view showed an acceptable correlation with those determined by angiography (r = 0.96 for enddiastolic and r = 0.90 for endsystolic volume). Underestimation of left ventricular enddiastolic volume by echocardiography was corrected by a factor of 1.33; no correction factor was necessary for the endsystolic volume. The correlation between the endsystolic volumes obtained by echocardiographic two-chamber view and by cineangiography was poor. Finally, in 51 infants, children, and adolescents without heart disease we determined left ventricular volumes and derived variables by cross-sectional echocardiography, using the previously established correction factor for the calculation of enddiastolic volumes. Both enddiastolic and endsystolic volumes were found to correlate linearly to body surface area.     

Klinische Wertigkeit der intraven?sen Kontrastmittelechokardiographie zur Quantifizierung der linksventrikul?ren Volumina und Funktion bei Patienten mit reduzierter echokardiographischer Bildqualit?t

In the present study, we investigated whether the intravenous injection of air-filled albumin microspheres (Infoson) as a contrast medium improves the echocardiographic quantification of left ventricular enddiastolic and endsystolic volumes, stroke volume, ejection fraction, and regional wall motion in patients with suboptimal endocardial border definition on echocardiography. In 30 adult patients, apical two and four chamber views were performed. In comparison to biplane cineventriculography enddiastolic and endsystolic volumes, stroke volume, ejection fraction, and regional wall function were assessed for heart cycles with and without left ventricular contrast.In comparison to biplane cineventriculography echocardiography underestimates enddiastolic (167+/-64 ml, 111+/-43; p<0.0001) and endsystolic volumes (77+/-63 ml, 54+/-40 ml; p<0.0002), stroke volume (90+/-25 ml, 57+/-17 ml; p<0.0001), and ejection fraction (58+/-16%, 55+/-14%; p<0.03). By contrast echocardiography ejection fraction (58+/-16%) agreed with the angiocardiographically measured ejection fraction. Furthermore, after contrast injection correlations improved between cineventriculography and echocardiography for the assessment of left ventricular enddiastolic volumes (without contrast r = 0.90, SEE = 19 ml; with contrast r = 0.93, SEE = 19 ml), endsystolic volumes (without contrast r = 0.94, SEE = 14 ml; with contrast r = 0.95, SEE = 15 ml), stroke volume (without contrast r = 0.63, SEE = 14 ml; with contrast r = 0.67, SEE = 14 ml), ejection fraction (without contrast r = 0.84, SEE = 8%; with contrast r = 0.88, SEE = 7%), regional wall motion (p<0.01) and its reproducibility (p<0.02). In adult patients with suboptimal endocardial border delineation intravenous contrast echocardiography improves the assessment of left ventricular ejection fraction, regional wall motion, and its reproducibility without severe side effects.     

Left ventricular function in mitral valve stenosis]

In 12 patients with mitral stenosis left ventricular performance was assessed by pharmacologically (Methoxamine) induced increased afterload. At rest ventricular enddiastolic pressure (6.2 +/- 3.1 mm Hg), left ventricular enddiastolic volume (68 +/- 20 ml/m2), endsystolic volume (26 +/- 11 ml/m2) and left ventricular ejection fraction (0.63 +/- 0.06) were normal in each subject. Methoxamine induced a mean increment in peak systolic atrial pressure of 65 mm Hg. Left ventricular stroke volume, stroke work, stroke power, enddiastolic pressure and volume increased with Methoxamine in each patient. The mean left ventricular ejection fraction remained unchanged for the group and remained within the normal range for all patients. No difference was observed between the response of the mitral stenosis group and a control group of 10 normal subjects with the exception of the account of mitral regurgitation during the pressure load in 9 mitral stenosis patients. This study indicates the left ventricle in mitral stenosis is capable of a normal response to a pressure load. No evidence of impaired left ventricular function was detected in this group of patients.     

The importance of two-dimensional echocardiography in conjunction with trans-esophageal stimulation of the left atrium for the diagnosis of myocardial ischemia

In 27 patients with coronary heart disease (group 1) and in 15 persons of ontrol group (group 2) transoesophageal left atrial pacing was performed. 12-lead ECG and two-dimensional echocardiography were done before and on the peak of the pacing. Changes of ST-segment (ST) and R-wave amplitude of V5 in the ECG (RV5) were analyzed. Left ventricular wall motion in the 11 segments and left ventricular enddiastolic volume index (LVEDVI), left ventrivular endsystolic volume index (LVESVI), stroke volume index (SVI), cardiac index (CI) and ejection fraction were studied by echocardiography. Sensitivity, specifity and predictive value confirming and excluding of coronary heart disease of the analyzed parameters were determined. During the analysis of ST-segment these values were 0.81, 0.67, 0.81 and 0.67 respectively. Diagnostic values of the analysis of the left ventricular wall motion and the ejection fraction were not statistically different (p greater than 0.05) from the analysis of ST-segment. During the analysis of LVEDVI, LVESVI, CI sensitivity of the transoesophageal atrial pacing was decreased and specifity was increased (p less than 0.05). The greatest value in the diagnosis of myocardial ischaemia during the two-dimensional echocardiography combined with transoesophageal left atrial pacing has the finding of the segmental asynergy of systole, diminution of EF and augmentation of LVESVI.     

Mitral valve alternans

An echogram showing mitral valve alternans was recorded in a patient with advanced cardiomyopathy and pulsus alternans induced by premature ventricular depolarizations. Decreased left ventricular emptying by the weak beat was followed by blunting of the subsequent mitral valve E point, a finding compatible with a significant elevation of left ventricular pressure in early diastole. Both alternating systolic (contractile state) and diastolic (pressure and dimension) variables seemed to participate in the alternans phenomenon in this patient.     

The ischemic segment and left ventricular function during exercise angina

Improvement of the quality of transpulmonary left ventriculograms by exercise was demonstrated in 5 patients in a pre-study. In the main study transpulmonary left ventriculography was performed in 10 patients with coronary artery disease (CAD) at rest and during exercise, producing maximum angina pectoris (AP). Left ventricular pressure was recorded simultaneously. The extent of CAD, demonstrated in all patients by coronary angiography, was quantitated by a score. In the exercise ventriculograms, local wall motion was quantitated by 14 hemiaxes. During exercise AP, all patients developed wall motion abnormalities not present at rest. There was a significant linear correlation between coronary score and number of abmormally shortening hemiaxes (< 30% shortening) during exercise-AP (y = 0.16 × + 4.34; r = 0.933). The number of anormal hemiaxes correlated significantly (p < 0.05) with left ventricular enddiastolic pressure (LVEDP), dp/dt min, endsystolic volume index, enddiastolic volume index, ejection fraction, stroke work index, minute work, compliance SV/ Δ PD/ESV, and cardiac index. During exercise AP the extent of ischemic wall motion abnormalities is determined by localization and severity of coronary artery lesions. The extent of ischemic impairment of wall motion determines the severity of impairment of left ventricular pump function, filling pressure, and maximum speed of relaxation. Transpulmonary left ventriculography during exercise AP is a safe and relatively simple method to quantitate the extent of ischemic wall motion abnormalities. It could be useful in the selection of patients for coronary artery surgery and in the assessment of the results of this operation.     

Right and left ventricular volume parameters in cardiomyopathy (author's transl)

In 41 patients with different types of cardiomyopathy (19 congestive = COCM, 6 hypertrophic obstructive = HOCM, and 16 hypertrophic non-obstructive = HCM) ventricular enddiastolic volume (EDV), endsystolic volume (ESV), and ejection fraction (EF) were determined angiographically and values of both ventricles were compared. In the mean, volume parameters increased significantly and EF of both ventricles decreased as compared to control values of patients with coronary heart disease without myocardial infarction. In COCM volume parameters reached pathologic values as in the total patient group whereas in HOCM and in HCM values did not differ significantly from control. Left ventricular function was reduced more often and, in the mean, more severely than right ventricular function. This became evident e.g. from the incidence of enddiastolic volume increase and the course of the regression line. A similar finding can be derived from the reversal of the normal relation of volume parameters of both ventricles. Only in rare cases right ventricular function was more severely impaired than left ventricular function. These findings indicate a simultaneous impairment of both ventricles in cardiomyopathy. The more pronounced left ventricular function disturbance may be attributed to the higher left ventricular work load. Thus, left ventricular biopsies might be of greater diagnostic significance than right ventricular biopsies.     

Function of the right ventricle in patients with mitral valve diseases

To investigate right ventricular function in mitral valve disease, biplane cineventriculograms of the right and left ventricle were performed in 96 patients-35 with mitral stenosis, 26 with mitral regurgitation, 12 with combined mitral valve disease, 14 with mitral stenosis and tricuspid regurgitation, and nine with mitral regurgitation and tricuspid regurgitation, compared to 18 normals (N). Right ventricular enddiastolic volume index was moderately elevated in patients with mitral stenosis and concomitant tricuspid regurgitation (111.6 +/- 35.3 ml/m2, no significance compared to N: 95.9 +/- 21.8 ml/m2) and with mitral regurgitation and tricuspid regurgitation (107.9 +/- 45.1 ml/m2, no significance compared to N). A reduced right ventricular ejection fraction (RVEF less than or equal to 50%) was found in 40 of the 96 patients. Right ventricular ejection fraction was frequently reduced in patients with mitral regurgitation and tricuspid regurgitation (46.7% +/- 15.1%) and significantly reduced in patients with combined mitral valve disease (45.0 +/- 17.6%, compared to N: 58.0 +/- 7.1%, p less than 0.01). No significant correlations were found between right ventricular ejection fraction and left ventricular enddiastolic volume or left ventricular ejection fraction in patients with mitral valve disease. Moreover, right ventricular ejection fraction did not correlate with systolic pulmonary artery pressure, mean pulmonary artery pressure or mean pulmonary capillary wedge pressure. Local wall motion (mean systolic shortening) was determined for the anterior, anteroapical, and inferior segment in the RAO-projection and for the right ventricular free wall in the LAO-projection. 63% of the patients (n = 25) with reduced right ventricular function (RVEF less than of equal to 50%) showed local wall motion abnormalities, preferably in the anterior segment of the RAO- projection (48%) and the right ventricular free wall (30%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiocardiograms and hemodynamics in idiopathic cardiomyopathy, with reference to histology of biopsied ventricular myocardium.

Cardiac catheterization, angiocardiography and ventricular muscle biopsy were performed in forty patients with idiopathic cardiomyopathy and included 21 cases of hypertrophic cardiomyopathy and 19 cases of congestive cardiomyopathy. 1) Cardiac catheterization revealed normal cardiac index and stroke index in both types, although there was a slight tendency toward decrease in cases of CCM. HCM showed slightly elevated right ventricular end-diastolic pressure and left ventricular end-diastolic pressure with a high incidence of atrial kick. CCM showed an elevated mean pulmonary artery, mean pulmonary wedge and left ventricular end-diastolic pressure. 2) Angiocardiographic findings revealed that in HCM left ventricular end-diastolic volume as well as left ventricular end-systolic volume, ejection fraction, meanVcf and MNSER were within normal range, and left ventricular anterior wall thickness, left ventricular mass and shortening of short axis in systole were increased. In CCM left ventricular end-diastolic volume and end-systolic volume increased, and ejection fraction, meanVcf, MNSER were decreased. The left ventricular anterior wall thickness was normal, and the left ventricular mass was smaller compared to the volume. The shortening of long and short axes in systole was slight. Left ventricular asynergy and mitral regurgitation occurred frequently. Coronary cineangiograms revealed normal patterns in both types. 3) Histological findings revealed hypertrophy of myofibers, degenerative changes, i.e. scarcity of myofibrils, deformity of nucleus and vacuolization of myocardial fibers, and collagen proliferation in both types. 4) No definite relationship was seen between parameters of left ventricular function and the findings of biopsied left ventricular muscle except for increase in wall thickness which might be apparently due to hypertrophy of the myocardial fibers.     

Myocardial oxygen consumption in chronic heart disease: role of wall stress, hypertrophy and coronary reserve.

The relations between left ventricular mass, mass to volume ratio, systolic wall stress and myocardial oxygen consumption were analyzed in 187 patients with chronic heart disease. The degree of left ventricular hypertrophy is determined by mass, the mass to volume ratio, and pressure and, hence, systolic wall stress. For each condition an inverse relation exists between mass to volume ratio and peak systolic wall stress. In chronic heart disease at least two types of inappropriate left ventricular hypertrophy may occur: (1) low stress hypertrophy with an increased mass to volume ratio, normal left ventricular function and normal or reduced oxygen consumption (MVO₂), whereas (2) high stress hypertrophy has a normal or low mass to volume ratio, impaired left ventricular function and an increased MVO₂. The range of systolic wall stress was 100 to 450 × 10³, dynes/cm² and reflects the stress that could be altered by inotropic interventions and changes in systolic pressure. A similar reserve capacity is present for both the metabolic and the coronary reserves. Total left ventricular oxygen consumption is related to total left ventricular mass. This relation is influenced by the degree of viability of left ventricular mass, by the mass to volume ratio and by inotropic interventions. Left ventricular oxygen consumption per viable mass unit (MVO₂) is significantly correlated with the systolic force per unit cross-sectional area of the left ventricular wall, that is, to left ventricular systolic wall stress.It is concluded that peak systolic wall stress represents one of the major determinants of myocardial oxygen consumption and of ventricular performance. It closely relates to the appropriateness of left ventricular hypertrophy, which may be defined by the relation between systolic pressure, mass to volume ratio and peak systolic wall stress.     

Contractile and relaxation reserve of the left ventricle. III. Patients with cardiomyopathy (author's transl)

Seven of 22 patients with cardiomyopathy increased maximal rate of left ventricular pressure rise (max dP/dt) above 3200 mm Hg/s and dP/dt/P above 60/s. Relaxation reserve was normal with an increase of min dP/dt above 2400 mm Hg/s.--In 15 patients contractile and relaxation reserve was reduced. In congestive cardiomyopathy, contractility and relaxation reserve were equally reduced. Left ventricular enddiastolic pressure increased during exercise slightly or not (grade 1). Enddiastolic volume was elevated to 173 +/- 50 ml/1.73 m2 and endsystolic volume to 63 +/- 22 ml/1.73 m2; ejection fraction and mean circumferential fiber shortening were reduced (61 +/- 17%; 1.3 +/- 0.9 circ/s). In hypertrophic cardiomyopathy without obstruction, contractile and relaxation reserve and ejection phase parameters could be found to be normal. Enddiastolic pressure at rest was elevated. In severe cases, contractile and relaxation reserve were markedly reduced and enddiastolic pressure increased to a greater extent than in congestive cardiomyopathy. In addition, relaxation reserve was reduced, especially in patients with excessive hypertrophy of the myocardium. These had abnormal (grade 2) and pathological reaction to exercise: contractile and relaxation reserve were decreased and enddiastolic pressure (grade 3) increased. Left ventricular contractility was found to be almost normal in patients with hypertrophic obstructive cardiomyopathy. This was the case despite increases in enddiastolic pressure. Contractile reserve was reduced, however, in patients with excessive hypertrophy. Diastolic filling was impeded during exercise.--Measuring left ventricular function during exercise, different types of cardiomyopathy correlate with typical hemodynamic alterations.     

Quantitative study of left ventricular function by two-dimensional echocardiography

The results of two dimensional echocardiography and cineventriculography in the calculation of left ventricular volumes and ejection fractions were compared. The study was performed experimentally in dogs and also in 12 patients with ischaemic heart disease. 25 measurements were performed in the animal: 19 basal and 6 measurements one hour after occlusion of the LAD. Reconstruction by Simpson's method showed good correlations with angiography (p less than 0,001) for enddiastolic volume (r = 0,94), end systolic volume (r = 0,97) and ejection fraction (r = 0,89). A preliminary clinical study was performed in 12 patients. All had significant stenosis of at least one main coronary artery and 10 had segmental abnormalities of left ventricular wall motion. Left ventricular volumes were calculated from the simplified 5/6 AL formula which only requires one long axis view and one short axis view at the level of the papillary muscles. The comparison between echocardiography and angiography showed a better correlation for end systolic volume (r = 0,91) than for end diastolic volume (r = 0,73). Echo underestimated end diastolic volume by 14% and end systolic volume by 13%. The correlation obtained for ejection fraction was excellent (r = 0,97) with no underestimation of this parameter by echocardiography. In conclusion, left ventricular volumes and ejection fractions may be calculated by two dimensional echocardiography. The technique allows a sequential quantitative study from beat to beat and in real time of cardiac function. It is a simple non-invasive method of following the evolution of cardiac disease and of assessing the effects of therapy on left ventricular function.     

Coronary disease. II. Analysis of diastolic pressure-volume correlations and left ventricular elasticity in 110 patients]

Left ventricular pressure-volume relationships as well as diastolic compliance were determined in 110 patients with coronary heart disease during routine right and left heart catheterization, coronary angiography and ventriculography. 1. Enddiastolic and endystolic volume of the left ventricle were increased in severe coronary heart disease dependent on the degree of coronary stenosis; left ventricular ejection fraction was consecutively reduced. 2. Left ventricular enddiastolic pressure, diastolic pressure difference and diastolic rate of pressure rise were increased in corrleation with coronary artery stenosis. In contrast, last diastolic volume inflow into the left ventricle was nearly the same in all groups. Left ventricular stiffness, expressed as dP/dV, was significantly increased dependent on the severity degree of coronary artery disease. 3. Diastolic pressure-volume relationships revealed greater steepness in coronary artery disease, significantly dependent, on the corresponding severity degree. 4. Hemodynamic measures (stroke volume, cardiac index, ejection fraction) were decreased parallel to the increased left ventricular wall stiffness. The results demonstrated decreased left ventricular compliance in coronary heart disease. There was a striking correlation between the severity degree of coronary heart disease and the decrease of left ventricular compliance. Validity and limitations of the techniques of estimating left ventricular compliance from diastolic pressures and volumes as well as the effects of a decrease of left ventricular compliance on cardiac mechanics are discussed.     

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 remodeling after aortic valve replacement]

The aim of the study was the assessment of left ventricular (LV) systolic function and left ventricular mass following aortic valve replacement (AVR) due to aortic valve stenosis as well as the influence of regression of LV hypertrophy in patients with normal and impaired LV systolic function prior to surgery. 74 patients with severe aortic valve stenosis (29 female, 45 male, mean age 66 +/- 18 years) were divided into 2 groups according to LV ejection fraction (EF): Group 1 with EF > 50% (n = 40); Group 2 with EF < or = 50% (n = 34). Furthermore, patients were differentiated into a group A without (n = 53) and a group B with aortic regurgitation (< or = II degrees, n = 21). All patients were examined by transthoracic echocardiography before and 1 month after surgery. There was a significant decrease of LV enddiastolic and endsystolic volume indices following AVR in group 2 and group B. Patients with preoperatively lower EF (group 2) showed an increase in LV ejection fraction from 39 +/- 10% before AVR to 47 +/- 11% after AVR (p < 0.001), whereas patients with preoperative normal EF (group 1) showed a significant decrease in EF (from 62 +/- 8% to 57 +/- 10%, p < 0.05). Also patients with combined aortic valve disease before AVR had an increase of EF after surgery (from 45 +/- 14% to 56 +/- 14%, p < 0.03). There were significant decreases of interventricular septum thickness and LV posterior wall thickness in group 1 and group A, whereas a significant decrease of LV enddiastolic diameter index was noted only in group B. Improvement of the NYHA functional class could be demonstrated in group 2 from 2.8 +/- 0.7 before to 2.2 +/- 0.6 after AVR, as well as in group B from 2.9 +/- 0.7 before to 1.9 +/- 0.7 after surgery. In conclusion, patients with impaired LV function or combined aortic valve disease showed a significant improvement of left ventricular systolic function after AVR, while patients with normal LV function presented a slight decrease of EF. There was a significant regression of left ventricular muscle mass in all groups independent of the left ventricular functional status.