Frequency spectra of the first heart sound and of the aortic component of the second heart sound in patients with degenerated porcine bioprosthetic valves

To determine the usefulness of the frequency of heart sounds in the assessment of porcine bioprosthetic valve degeneration, frequency spectra of phonocardiograms of the first heart sound and the aortic component of the second sound were analyzed in 31 patients with degenerated porcine bioprosthetic valves. Comparisons were made with 35 control patients whose valves were inserted 1 month or less. Among 23 patients with degenerated porcine bioprosthetic valves in the mitral position, the dominant frequency of the first heart sound was 95 ± 11 Hz, which exceeded the first sound in 18 controls (51 ± 3 Hz) (p < 0.01). The degenerated mitral porcine bioprosthetic valves of 14 patients showed calcification or fibrosis and the first heart sound in these patients was 115 ± 16 Hz, which exceeded that of control subjects (p < 0.001). The degenerated mitral porcine bioprosthetic valves of 9 patients showed torn leaflets only, and the first heart sound in these patients was 64 ± 9 Hz, which did not differ from that of control subjects. In the aortic position, 8 valves were degenerated and the aortic component of the second sound was 109 ± 12 Hz, which was higher than that in 17 control subjects (63 ± 4 Hz) (p < 0.001). Only 2 of these degenerated valves showed tears unaccompanied by calcific deposits or fibrosis, and the frequencies were comparable to that of control subjects. These observations indicate that the frequency of heart sounds in patients with degenerated porcine bioprosthetic valves becomes abnormally elevated when degeneration is accompanied by calcification or fibrosis, which causes the cusps to stiffen.     

Genesis of pericardial knock in constrictive pericarditis

A pericardial knock is a common finding in constrictive pericarditis. However, its origin has been uncertain. One hypothesis suggests that it is due to sudden deceleration of ventricular filling. To validate this hypothesis, left ventriculograms, phonocardiograms and external pulse recordings were obtained in seven patients with hemodynamic and pathologic findings of constrictive pericarditis and in seven normal subjects. Left ventriculographic silhouettes were digitized and left ventricular volumes were calculated by computer at 16 ms intervals. Curves of left ventricular volume versus diastolic filling time were constructed for each patient. Pericardial knock was recognized as an early high frequency sound recorded between 90 to 120 ms after the aortic closing sound and occurring at the trough of the Y descent of the jugular venous pressure tracing. The timing of the pericardial knock in five patients with constrictive pericarditis corresponded to a sudden and premature plateau of the diastolic left ventricular volume curve representing 85 ± 4 percent (mean ± standard deviation) of ventricular filling. The diastolic plateau was missing in two patients with constrictive pericarditis who had no pericardial knock. In these cases, the rate of ventricular filling was faster than normal in the first 20 percent of diastole.Thus, this study related pericardial knock to an abrupt plateau in the diastolic left ventricular volume curve, supporting the view that sudden cessation of ventricular filling generates the pericardial knock of constrictive pericarditis. Two mechanisms are proposed by which the filling plateau may produce the knock, and it is postulated that both ventricles may participate in the knock phenomenon.     

Investigation of symptom free patients after myocardial infarction

The dicrotic pulse is an abnormal carotid pulse found in conjunction with certain conditions characterised by low cardiac output. It is distinguished by two palpable pulsations, the second of which is diastolic and immediately follows the second heart sound. In the course of open chest canine studies of the second heart sound, micromanometers and an electromagnetic flow meter were used to study proximal aortic haemodynamic function in both strong and weak beats. It was found that the incisural notch of the aortic pressure signal is not strongly dependent on the extent of left ventricular ejection, and is of essentially normal amplitude even in beats having greatly reduced aortic flow. In contrast, the magnitude of the systolic upstroke of the aortic pressure pulse is strongly determined by the magnitude of left ventricular ejection and is considerably reduced in weak beats. With low cardiac output the relative size of the incisural notch becomes exaggerated in comparison with the overall pulsation, thus creating the characteristic M shaped waveform of the dicrotic pulse.     

Investigation of symptom free patients after myocardial infarction.

The dicrotic pulse is an abnormal carotid pulse found in conjunction with certain conditions characterised by low cardiac output. It is distinguished by two palpable pulsations, the second of which is diastolic and immediately follows the second heart sound. In the course of open chest canine studies of the second heart sound, micromanometers and an electromagnetic flow meter were used to study proximal aortic haemodynamic function in both strong and weak beats. It was found that the incisural notch of the aortic pressure signal is not strongly dependent on the extent of left ventricular ejection, and is of essentially normal amplitude even in beats having greatly reduced aortic flow. In contrast, the magnitude of the systolic upstroke of the aortic pressure pulse is strongly determined by the magnitude of left ventricular ejection and is considerably reduced in weak beats. With low cardiac output the relative size of the incisural notch becomes exaggerated in comparison with the overall pulsation, thus creating the characteristic M shaped waveform of the dicrotic pulse.     

Hemodynamic correlates of late diastolic posterior motion of the aortic root

Motion of the posterior aortic root on echocardiography is related to left atrial volume change. Early diastolic posterior motion of the aortic root reflects both LA emptying and filling and has been measured as the atrial emptying index. To study late diastolic motion of the aortic root, we measured the slope of posterior motion of the aortic root after left atrial systole (following the P wave of the ECG) in 25 subjects without heart disease (Group 1), in 15 patients with left ventricular hypertrophy due to pressure overload (Group 2), and in 10 patients (Group 3) with mitral stenosis. The aortic root slope measured (mean ± SEM) 58.0 ± 1.9 mm./sec. in Group 1, 50.6 ± 4.5 mm./sec. in Group 2 (NS vs 1) and 28.8 ± 4.5 mm./sec. in Group 3, (p < 0.01 vs 1 or 2).In 16 patients (four in Group 1 and 12 in Group 2) studied at catheterization, an inverse correlation (r = ?0.74, p < 0.01) was found between the aortic root slope (over a range of 30 to 73 mm./sec.) and left ventricular late diastolic chamber stiffness measured with simultaneous left ventricular echo and high-fidelity pressure recordings. No correlation was found between this slope and either left atrial size, total aortic root excursion, left ventricular pressure pre “A” wave, height of the A wave, end-diastolic pressure, or the atrial contribution to left ventricular filling. Therefore, the aortic root slope in late diastole is decreased in mitral stenosis, and in the absence of mitral stenosis, it appears to be related to late diastolic properties of the left ventricle.     

Characterization of left ventricular external wall motion in man by video dimension analyzer (Vidian)

Several investigators have described close relationships between left ventricular wall motion and physiologic cardiac events. Using an improved wall motion tracking devide (Vidian) in studies of 30 patients, we have compared the dynamics of left ventricular wall motion, recorded noninvasively, with high fidelity left ventricular and aortic pressures, intracardiac phonocardiograms, apexcardiograms, and cyclic left ventricular volume curves obtained during cardiac catheterization. Wall motion tracking signals comprised: pre-ejection outward deflection commencing with the first component of the first heart sound and coincident with the pre-ejection phase of the left ventricular pressure and apexcardiogram; a sharp descent during ejection, commencing with the ?E”? point of the apexcardiogram and with the onset of the upstroke of the aortic pressure; end ejection nadir, synchronous with the dicrotic notch of the aortic pressure; a nadir representing cessation of inward displacement, presumably reflecting slight inertial motion of the wall; a brief period of isovolumic relaxation which terminated synchronously with the ?O”? point of the apexcardiogram; rapid, then slow filling waves, coincident with those of the apexcardiogram, and demarcated by a transitional angulation synchronous with the third heart sound; and ?a”? wave, occurring simultaneously with that of the apexcardiogram. Ventricular wall motion tracking signals also corresponded to curves representing cyclic changes in left ventricular minor radius, and chamber volume derived from cineventriculograms. In 10 patients with abnormal contraction patterns detected by biplane cineventriculography, anomalous deflections were also recorded during ejection by the Vidian. Left ventricular wall motion tracking with the Vidian: 1) provides a sensitive index for timing of intracardiac events, 2) reflects cyclic changes in ventricular volumes and minor dimensions, 3) provides a convenient noninvasive technique for detection of regional asynergy involving the lateral left ventricular wall, and 4) by correlation with simultaneous ventricular pressure measurements, may provide useful information regarding left ventricular pressure/segment dimension relations.     

Relation between ionized calcium concentration and ventricular pump performance in the dog under hemodynamically controlled conditions

The effect of plasma ionized calcium concentration on left ventricular function was studied in the canine heart on right heart bypass. Stroke volume, mean arterial pressure and heart rate were controlled. Plasma ionized calcium was lowered to 0.58 ± 0.01 mM by citrate infusion and raised to 1.70 ± 0.01 mM by calcium chloride infusion in random order in each dog. Left ventricular function at each of these ionized calcium levels was compared with that in an immediately preceding normocalcemic period. At a constant stroke work (16.9 ± 0.2 g-m), sustained hypercalcemia was associated with a small decrease in left ventricular end-diastolic pressure (1.7 ± 0.7 cm H₂O, p <0.05) despite a marked increase in peak left ventricular dP/dt (first derivative of ventricular pressure) averaging 34 percent (p <0.001). Coronary blood flow, tension-time index and myocardial oxygen consumption were not significantly altered. Stroke work determined at a left ventricular end-diastolic pressure of 14 cm H₂O, by interpolation in left ventricular function curves, was 11 ± 4.4 percent above that at control normocalcemia (p <0.05).At a constant stroke work (16.9 ± 0.2 g-m), sustained hypocalcemia was associated with a marked depression of left ventricular function as demonstrated by a substantial increase (from 4.9 ± 0.3 to 12.7 ± 1.1 cm H₂O, p <0.0001) in left ventricular end-diastolic pressure (p <0.0001), decreased mean systolic ejection rate (p <0.01) and decreased peak left ventricular dP/dt (p <0.0001). Coronary blood flow increased (p <0.05) whereas myocardial oxygen consumption did not change significantly. A marked displacement of left ventricular function curves to the right (compared with curves obtained during normocalcemia) was observed, and stroke work determined at a left ventricular end-diastolic pressure of 14 cm H₂O was 52 ± 5.4 percent below control level (p <0.001).It appears that hypercalcemia, when initiated from a normal control level, provides only a small enhancement of ventricular pump performance (as indexed by the stroke work-left ventricular end-diastolic pressure relation) despite a marked increase in peak left ventricular dP/dt, whereas marked improvement of left ventricular performance may be expected when calcium infusion is initiated from an ionized calcium level that is below normal.     

Aortic valve closure and cardiac vibrations in the genesis of the second heart sound

Simultaneous M-mode echocardiograms and external phonocardiograms were recorded in 15 healthy subjects to evaluate the genesis of the second heart sound. The onset of the second sound was found synchronous with the coaptation of the aortic valve cusps and a sharp vibration on the aortic wall. The closed valve was oscillating for 30 to 45 ms after the coaptation of the cusps. Magnified echocardiographic studies of the interventricular septum revealed a consistent, momentary quiver across the septal myocardium a mean of 4 ms after the onset of the second sound. In most subjects, a transient myocardial vibration was observed in temporal association with the first heart sound as well. The present observations suggest that the aortic valve closure initiates the production of the second heart sound, the main audible component resulting, however, from vibrations in the cardiac structures after the valve closure.     

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.     

Influence of the aortic component of the second heart sound on left ventricular maximal negative dP/dt in the dog

Maximal negative left ventricular dP/dt is widely used as a measure of isovolumic muscular relaxation of the left ventricle. In the course of canine experiments designed to elucidate the hemodynamic events responsible for the aortic component of the second heart sound, high-fidelity left ventricular pressure and dP/dt signals were recorded and accelerations detected on the root of the aorta and epicardium at the cardiac apex. The second heart sound was coincident with maximal negative dP/dt and affected its magnitude to a variable and unpredictable extent. This may account for some of the unexpected variations in magnitude of maximal negative dP/dt that have been described in various disease states and in laboratory experiments where the effects of physiologic and pharmacologic interventions have been studied.     

Determinants of the amplitude of the aortic component of the second heart sound in aortic stenosis

The characteristics of the aortic component of the second heart sound in calcific and congenital noncalcific aortic stenosis were studied to determine a cause for observed differences. Intraarterial pressure and sound were measured above the aortic valve in 20 patients utilizing catheter-tip micromanometers. Ten patients had a normally functioning aortic valve, six had calcific aortic stenosis and four had congenital noncalcific aortic stenosis. As expected, the aortic sound was diminished in patients with calcific aortic stenosis compared with that in patients with a normal valve (600 ± 200 versus 2,600 ± 200 dynes/cm² (P < 0.001). In patients with congenital aortic stenosis, sound amplitude was not reduced compared with that in patients with a normal valve. Measurement of sound produced by closure of normal and stenotic valves in an in vitro model of the circulatory system yielded comparable results. In vitro high speed (2,000 frames/sec) motion pictures of the diastolic motion of the closed cusps showed vibrations of comparable magnitude in the normal porcine and the simulated congenitally stenotic valve. The calcified stenotic valve showed no noticeable diastolic vibrations. These observations indicate an association between the amplitude of the second heart sound and diastolic vibrations of the closed cusps. A calcified stenotic valve, being thick and stiff, would have a diminished ability to vibrate and would therefore produce a diminished sound. A congenitally stenotic valve, in contradistinction, if not yet damaged by degenerative changes, would not be limited in its ability to vibrate during diastole and would therefore produce a normal second sound.     

The contribution of tricuspid valve closure to the first heart sound. An intracardiac micromanometer study.

The sound-pressure correlates of the second high frequency component of a split first heart sound (S1) were investigated in 27 patients. An external phonocardiogram was recorded with high fidelity sound and pressure from the left and right atria in 21 patients, from the pulmonary artery in 14 of these, and from the central aorta in 11. In the remaining six patients, high fidelity recordings from the central aorta and right-sided chambers were obtained with an external phonocardiogram. The external component of S1 that coincided with a left atrial C wave and "internal sound" was defined as M1. In those cases where the left atrial pressure was not recorded, this component could be identified by a low frequency transient in the central aortic pressure trace. The other external high frequency component of S1 that was synchronous with a separate right atrial C wave and "internal sound" was defined as T1; with two exceptions, M1 preceded T1. The two exceptions which caused reversal of this order, so that T1 preceded M1, were due to chronic left bundle branch block and mitral stenosis. In both cases, T1 was shown to be distinctly separated from the upstroke of pressure rise in the central aorta. This finding was also demonstrated in three cases of right bundle branch block and one case with aortic valvular disease. The usual asynchrony of ventricular contraction was altered by induction of ventricular premature systoles; the separation of externally identifiable M1 and T1 components and their internal markers was predictably altered by this maneuver. The occurrence of T1 was variable in relation to the upstroke of the pulmonary artery pressure, which suggests that it is not related to pulmonic ejection. It is concluded that micromanometrically recorded right and left atrial C waves can serve as markers for externally recordable M1 and T1 components of the first heart sound. In addition, T1 is frequently an externally recordable and audible event.     

Dynamic exercise echocardiography in children with congenital heart disease affecting the left heart

Thirty-five children (male 22, female 13) with congenital heart disease resulting in volume and pressure overload of the left ventricle were investigated echocardiographically during supine bicycle exercise. The children had to follow a test-protocol with increasing workload. Left ventricular function parameters were measured from M-mode-echocardiography, electrocardiography and phonocardiograms before, during and after exercise and were expressed as fractional shortening (FS), velocity of circumferential fiber shortening (VcF) and the frequency corrected parameters: FScorr. = FS X 100/HR and VcFcorr. = VcF X 100/HR (HR = heart rate). The data of this group of children under study were compared to those obtained from 140 healthy children examined under similar conditions. In children with pressure overload, values for fractional shortening, velocity of circumferential fiber shortening and the frequency corrected parameters were significantly higher than in normals throughout exercise testing. In some children with moderate to severe aortic stenosis or coarctation the frequency corrected parameters showed a decrease at higher exercise levels instead of an increase as seen in the majority of cases. In these cases cardiac output was increased by an abnormal rise in heart rate. This was considered as a diminished left ventricular reserve. After aortic valve replacement in two cases with aortic stenosis, parameters of left ventricular function were still elevated at rest and during exercise testing. In two children with hypertrophic cardiomyopathy the almost maximally elevated rest values did not change during exercise. In children with mild volume overload (small ventricular septal defect or aortic incompetence) the left ventricular function parameters were within the normal range or slightly below.     

A case of secundum atrial septal defect combined with aortic stenosis and coronary artery disease showing a single second heart sound

We describe an extremely rare case of secundum atrial septal defect with aortic stenosis and coronary artery disease showing a single second heart sound throughout the respiratory cycle by echocardiogram with simultaneous phonocardiogram. Aortic valve closure corresponded to the single second heart sound. We were unable to detect pulmonary valve closure (PVC) on echocardiogram. Because of the presence of pulmonary hypertension, the pulmonary component of the second heart sound (P2) was presumed to be increased in intensity, and the PVC-P2 interval was thought to be abbreviated. Carotid pulse tracing showed a prolongation of the left ventricular ejection time. We concluded that the single second heart sound was due to both prolongation of left ventricular systole and pulmonary hypertension.     

The double femoral sound

A double femoral sound is described in patients with congestive heart failure of varied etiology. The factor common to all patients was a powerful atrial contraction secondary to increased right ventricular diastolic pressure or increased resistance to right ventricular filling. The first sound is produced by atrial systole transmitted by the venae cavae to the femoral veins; the second sound by left ventricular systole transmitted by the aorta to the femoral arteries.     

Left ventricular regional wall motion and velocity of shortening in chronic mitral and aortic regurgitation

Left ventricular regional wall motion (percent systolic shortening) and velocity of shortening were studied in patients with heart failure due to chronic volume overloads of mitral and aortic regurgitation. Biplane left ventriculograms were analyzed by computer and divided into four regions: anterior, inferior, posterolateral and septal. The study patients included 12 normal subjects; 21 patients with aortic regurgitation (10 asymptomatic and 11 with congestive heart failure); and 11 patients with mitral regurgitation (4 asymptomatic and 7 with congestive heart failure). No patient had coronary artery disease. With heart failure, ejection fraction was decreased (p <0.05) in both aortic and mitral regurgitation (normal 62 ± 3 percent [mean ± standard error of the mean], aortic regurgitation 48 ± 3 and mitral regurgitation 51 ± 5). In mitral regurgitation with heart failure, the percent segment shortening in anterior (normal 42 ± 2, mitral regurgitation 27 ± 5) and posterolateral (normal 23 ± 3, mitral regurgitation 16 ± 4) regions was significantly decreased (p <0.05), whereas this value in the inferior (normal 32 ± 2, mitral regurgitation 28 ± 6) and septal (normal 46 ± 4, mitral regurgitation 47 ± 5) regions was normal. In aortic regurgitation with heart failure, anterior (27 ± 2), inferior (17 ± 3) and septal (5 ± 1) segment shortening was significantly decreased, whereas posterolateral segment shortening was normal (24 ± 3).In both groups with heart failure, mean shortening velocity showed regional variations similar to those of percent shortening, whereas peak instantaneous shortening velocity was not reduced in mitral regurgitation compared with normal values. In the asymptomatic group, shortening and mean shortening velocity were normal, whereas peak instantaneous shortening velocity was increased in mitral regurgitation. In aortic and mitral regurgitation with decreased left ventricular function demonstrated by a reduced ejection fraction, there are regional wall motion abnormalities that are not caused by coronary disease.     

Pre- and postoperative hemodynamic and cineangiocardiographic assessment of left ventricular function in patients with aortic regurgitation.

Hemodynamic and angiocardiographic analysis was performed prior to and 14 months on the average following valve replacement in 11 patients with severe, isolated, pure, chronic aortic regurgitation.The aortic diastolic pressure, reduced prior to surgery, reverted to normal as did the cardiac index. Left ventricular filling pressure, elevated prior to surgery, returned to normal while aortic systolic pressure did not vary substantially. The markedly increased stroke volume returned to normal as did the net left ventricular stroke work. Left ventricular end-diastolic and end-systolic volumes, also markedly elevated, decreased but did not return to normal levels.The shape of the left ventricle, which was more spherical than normal during end-systole prior to surgery, as evidenced by the decrease in the systolic axis ratio, reverted to normal.The ejection fraction, severely reduced before surgery, increased moderately (46 ± 13 vs 51 ± 19 per cent) as did the extent of circumferential fiber shortening (δD) (21 ± 8 vs 27 ± 12 per cent). The mean velocity of fiber shortening ($\text{VCF}$) increased significantly (0.68 ± 0.2 vs 1.03 ± 0.47 circ./sec.), as did the mean left ventricular ejection rate (1.32 ± 0.48 vs 1.91 ± 0.76).Comparative analysis of the evolution of left ventricular function indices and of extramyocardial factors (end-diastolic fiber stretching and impedance to ejection) showed that whereas in some cases myocardial damage appeared to be irreversible, in others dramatic improvement sometimes occurred following surgery. It was not possible, however, to determine the threshold below which the damage was irreversible.It may therefore be concluded that in some patients with severe regurgitation attended by profound myocardial insufficiency, correction of the valvular defect could produce not only clinical and hemodynamic improvement, but also improvement in myocardial contractile status.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

Early diastolic clicks after the Fontan procedure for double inlet left ventricle: anatomical and physiological correlates.

M mode echocardiograms and simultaneous phonocardiograms were recorded in four patients with early diastolic clicks on auscultation. All had double inlet left ventricle and had undergone the Fontan procedure with closure of the right atrioventricular valve orifice by an artificial patch. The phonocardiogram confirmed a high frequency sound occurring 60-90 ms after aortic valve closure and coinciding with the time of maximal excursion of the atrioventricular valve patch towards the ventricular mass. One patient had coexisting congenital complete heart block. The M mode echocardiogram showed "reversed" motion of the patch towards the right atrium during atrial contraction. Doppler flow studies showed that coincident with this motion there was forward flow in the pulmonary artery with augmentation when atrial contraction coincided with ventricular systole. The early diastolic click in these patients was explained by abrupt cessation of the motion of the atrioventricular valve patch towards the ventricular mass in early diastole. In one patient atrial contraction led to a reversal of this motion and was associated with forward flow in the pulmonary artery.     

Hypertrophic remodeling: gender differences in the early response to left ventricular pressure overload

Objectives. To identify gender differences in left ventricular remodeling, hypertrophy, and function in response to pressure overload due to ascending aortic banding in rats.Background. Gender may influence the adaptation to pressure overload, as women with aortic stenosis have greater degrees of left ventricular hypertrophy and better left ventricular function than men.Methods. Fifty-two weanling rats underwent ascending aortic banding (16 males, 18 females), or sham surgery (9 males, 9 females). At 6 and 20 weeks, rats underwent transthoracic echo Doppler studies, and closed-chest left ventricular pressures with direct left ventricular puncture. Perfusion-fixed tissues from eight rats were examined morphometrically for myocyte cross-sectional area and percent collagen volume.Results. At 6 weeks after aortic banding, left ventricular remodeling, extent of hypertrophy, and function appeared similar in male and female rats. At 20 weeks, male but not female rats showed an early transition to heart failure, with onset of cavity dilatation (left ventricular diameter = 155% vs. 121% of same-sex sham), loss of concentric remodeling (relative wall thickness = 102% vs. 139% of sham), elevated wall stress (systolic stress = 266% vs. 154% of sham), and diastolic dysfunction (deceleration of rapid filling = 251% vs. 190% of sham). Left ventricular systolic pressures were higher in female compared with male rats (186 ± 20 vs. 139 ± 13 mm Hg), while diastolic pressures tended to be lower (14 ± 4 vs. 17 ± 4 mm Hg).Conclusions. Gender significantly influences the evolution of the early response to pressure overload, including the transition to heart failure in rats with aortic stenosis.