Intraoperative Doppler echocardiography in hypertrophic cardiomyopathy: correlations with the obstructive gradient

Although significant pressure gradients can be recorded across the left ventricular outflow tract in patients with hypertrophic cardiomyopathy, controversy exists regarding the presence or absence of true obstruction. Ten patients with hypertrophic cardiomyopathy were studied at the time of septal myectomy. A sterile continuous wave Doppler transducer was placed on the ascending aorta and directed toward the left ventricular outflow tract to measure velocity simultaneously with invasive gradient measured using solid-state hub transducers by direct puncture of the left ventricle and aorta. Simultaneous Doppler velocity and invasive gradient measurements (n = 33) were made at rest, before and after myectomy and during interventions with isoproterenol, volume loading and phenylephrine. High velocity flow with a characteristic contour was recorded in patients with a significant gradient. Using the modified Bernoulli equation (gradient = 4 X velocity), a good correlation was found between the Doppler-derived gradient and the peak instantaneous gradient measured invasively (r = 0.93, y = 0.89X + 12, p = 0.0001). Changes in gradient and velocity due to interventions also correlated well (r = 0.96, y = 0.91X - 3, p = 0.0001). Continuous wave Doppler echocardiography can accurately estimate the outflow tract gradient. The magnitude, timing and contour of these high velocity flow signals support the hypothesis that true obstruction is present in patients with hypertrophic cardiomyopathy who have a significant gradient.     

Adverse effect of nifedipine on left ventricular obstruction detected by pulsed Doppler echocardiography

The effect of nifedipine on the ejection flow pattern in the left ventricular outflow tract was observed using pulsed Doppler echocardiography in 6 patients with hypertrophic cardiomyopathy. After sublingual administration of nifedipine (10 mg) to 1 patient, the turbulent ejection flow pattern became more marked and increased in duration compared with the initial state. An increase in turbulence in the left ventricular outflow tract may increase the pressure gradient between the left ventricle and the aorta. Nifedipine appeared to have the potential of adverse action on left ventricular outflow obstruction.     

A case of hypertrophic cardiomyopathy with right ventricular outflow obstruction manifested during three-year follow-up study

A case is reported of a 55-year-old female with idiopathic hypertrophic cardiomyopathy, which was accompanied with outflow obstruction in the right ventricle developed during the previous 3 years without lesion of the left ventricle. In 1984, she was admitted to our hospital to be examined for cardiac murmurs and abnormal electrocardiogram including ST depression and inverted T. The findings of echocardiography and cardiac catheterization revealed non-obstructive hypertrophic cardiomyopathy. She had been treated with sympathetic beta-blockade and calcium antagonist for 3 years until she complained of dyspnea on exertion, and she was readmitted to our hospital in 1987. Echocardiographic findings showed protrusion of the ventricular septum toward the right ventricle and systolic turbulent flow along the right ventricular outflow tract (by pulsed Doppler technique). A pressure gradient of 20 mmHg across the protrusion was detected by the examination of the cardiac catheter. However, neither protrusion nor pressure gradient was observed in the left ventricular outflow tract as well as that in 1984. Idiopathic hypertrophic cardiomyopathy has been described as involving both ventricles, and outflow obstruction is the usual hemodynamic finding in the left ventricle. However, right ventricular outflow obstruction is the usual hemodynamic finding in the left ventricle. However, right ventricular outflow obstruction with the left ventricular outflow tract intact has been very rare. In addition, in this case, the change of hemodynamic characteristics from non-obstructive to obstructive hypertrophic cardiomyopathy, and the development of these changes only in the right ventricle were observed during the last 3 years.     

Echocardiographic assessment of right ventricular obstruction in hypertrophic cardiomyopathy.

Echocardiography was used to evaluate the incidence, flow dynamics and morphological characteristics of right ventricular obstruction in 91 patients with hypertrophic cardiomyopathy. Color flow mapping was used to define the sites of obstruction in the left and right ventricles. Ventricular obstruction was considered to be present if the flow velocity was less than 2.0 m/s as measured by continuous wave Doppler. The thickness of both the right ventricular free wall and anterior ventricular septum was measured to assess the magnitude and extent of hypertrophy. Right ventricular obstruction was present in 14 patients of whom 6 (43%) had left ventricular obstruction also. The right ventricular obstructions were found in the outflow tract (9 patients), mid-base septal bulge (2 patients) and apical trabecular region (3 patients). Doppler waveform was confined to systole in all patients with obstruction in the outflow tract and in one of the patients with mid-base septal bulge. Moreover, the flow wave persisted into early diastole in 4 patients, including 2 with apical trabecular obstruction. The thickness of both the right ventricular free wall and anterior ventricular septum suggested that these hypertrophied regions were the sites of right ventricular obstruction. Thus, echocardiography was useful in evaluating right ventricular obstruction in hypertrophic cardiomyopathy.     

Doppler color flow mapping studies of jet formation and spatial orientation in obstructive hypertrophic cardiomyopathy

To help clarify the mechanism of outflow tract obstruction and systolic anterior motion of the anterior leaflet of the mitral valve and their relation to the geometry of the left ventricle, we studied left ventricular outflow tract flow in 20 patients with hypertrophic cardiomyopathy (HCM) using two-dimensional Doppler flow mapping. We compared our results with outflow tract flow in 10 patients with isolated valvular aortic stenosis, (AS) and with those in 10 healthy volunteers. In HCM, a 94- to 145-degree angle (mean 111.4 +/- 11.9 degrees) developed between the direction of left ventricular outflow tract flow acceleration and aortic valve outflow, resulting in posterolaterally directed left ventricular outflow jets. The angle of the outflow jet and the peak velocity of the jet measured with continuous wave Doppler (as an indicator of the severity of obstruction) correlated well (r = -0.81, SEE = 7.8 degrees). Jet narrowing during ejection measured just proximal to the point of systolic anterior motion was 42 +/- 11% in HCM and was weakly correlated with peak jet velocity (r = 0.61, SEE = 8.9 degrees). Aliasing of left ventricular outflow occurred proximal to systolic anterior motion of the mitral valve, and color M-mode demonstrated temporal and spatial flow acceleration proximal to systolic anterior motion, providing evidence for obstruction at that site. In AS, left ventricular outflow tract jets were more parallel to the axis of aortic outflow (129 to 153 degree, 138.4 +/- 8.1 degrees). Jet narrowing was only 8 +/- 5% compared to HCM (both p less than 0.05), and flow acceleration occurred proximal to the stenotic valve.(ABSTRACT TRUNCATED AT 250 WORDS)     

Left Ventricular Outflow Tract Obstruction Following Mitral Valve Replacement with Carpentier-Edwards Prosthesis

Left ventricular outflow tract (LVOT) obstruction is a rare complication of mitral valve replacement. In this article, we describe three patients in whom left ventricular outflow tract obstruction occurred following Carpentier-Edwards porcine mitral valve replacement. All three patients presented with symptomatic mitral regurgitation (angiographic grade 3–4) requiring mitral valve replacement. Preoperatively there was no evidence of hypertrophic obstructive cardiomyopathy by physical exam, echocardiography, or by cardiac catheterization. At the time of surgery all three were shown to have severe mitral valve prolapse. The native anterior mitral leaflet was left intact and pledgeted to the mitral annulus. Following surgery a new systolic murmur was appreciated. Echocardiographic exam visualized obstruction of the left ventricular outflow tract by the prosthetic strut in two cases and by a flail anterior leaflet in one case. Continuous-wave Doppler measured a calculated peak gradient of 72 to 81 mmHg across the left ventricular outflow tract. In one case simultaneous Doppler and cardiac catheterization confirmed the diagnosis and severity of left ventricular outflow tract obstruction. Mechanisms of left ventricular outflow tract obstruction following Carpentier-Edwards porcine mitral valve replacement are discussed. These three cases highlight the importance of echo-Doppler techniques in understanding the mechanism of newly detected systolic murmurs following mitral valve replacement.     

Accuracy of combined two-dimensional echocardiography and continuous wave Doppler recordings in the estimation of pressure gradient in right ventricular outlet obstruction

Fifteen patients (median age 8.5 years) with fixed right ventricular outflow tract obstruction were evaluated by two-dimensional echocardiographically directed continuous wave Doppler ultrasound within 24 hours of cardiac catheterization. Pulmonary artery blood velocity measurements were determined from a real time spectral display of pulmonary artery flow profile and converted to pressure drop utilizing a modified Bernoulli equation. Use of both parasternal and subcostal imaging permitted more accurate detection of maximal flow velocity than did use of either approach alone. Gradients estimated from Doppler recordings correlated well with those measured at cardiac catheterization (correlation coefficient = 0.95, standard error of the estimate = 7.9 mm Hg) with a trend to slight underestimation of gradient in more severe obstruction. In three patients with combined valvular and subvalvular stenosis and one patient with right ventricular outlet obstruction due totally to a ventricular septal aneurysm, Doppler estimation of gradient provided an accurate assessment of total right ventricular-pulmonary artery gradient. Thus, continuous wave Doppler ultrasound combined with two-dimensional echocardiography provides a reliable noninvasive method of estimating pressure gradient in patients with right ventricular outflow tract obstruction.     

Left ventricular remodeling in patients with hypertrophic obstructive cardiomyopathy treated with percutaneous alcohol septal ablation: an echocardiographic study

INTRODUCTION: In patients with hypertrophic obstructive cardiomyopathy, obstruction in the left ventricular outflow tract may generate more hypertrophy. Our aim was to evaluate the impact of reducing ventricular outflow tract obstruction on left ventricular hypertrophy and remodeling after alcohol septal ablation. PATIENTS AND METHOD: 20 patients with hypertrophic obstructive cardiomyopathy who underwent alcohol septal ablation were included. Doppler echocardiography was performed in all patients at baseline, immediately after alcohol septal ablation, and at 3 and 12 months' follow-up. Left ventricular diameters and wall thickness and pressure gradients in the ventricular outflow tract were determined. RESULTS: Immediately after alcohol septal ablation, ventricular outflow tract pressure gradient decreased from 63.0 27.7 to 28.2 24.7 mmHg (p < 0.001), without significant changes in left ventricular dimensions. However, after 12 months we observed an increase in left ventricular end-diastolic (from 47.1 4.9 to 50.8 4.5 mm) and end-systolic diameter (from 27.1 3.0 to 33.7 4.6 mm), as well as a reduction in septal (from 19.5 4.0 to 15.5 2.7 mm) and posterior wall thickness (from 14.0 2.2 to 12.9 1.3 mm) (p < 0.01 in all cases). Left ventricular end-diastolic and end-systolic volumes increased (from 106.4 26.9 to 123.1 28.7 ml and from 50.2 17.3 to 56.7 18.3 ml, respectively, p < 0.01 in both cases), without changes in left ventricular ejection fraction. The reduction in ventricular outflow tract pressure gradient at 12 months' follow-up correlated significantly with the increase in left ventricular end-systolic diameter (r = 0.63; p < 0.01). CONCLUSIONS: In patients with hypertrophic obstructive cardiomyopathy who underwent alcohol septal ablation, relief of ventricular outflow tract obstruction is associated with an increase in left ventricular chamber diameters and volume. These findings suggest that middle- and long-term ventricular remodeling and regression of hypertrophy occur in these patients, which may contribute to their clinical improvement.     

Significance of left ventricular outflow tract cross-sectional area in hypertrophic cardiomyopathy: a two-dimensional echocardiographic assessment

The morphologic determinants of subaortic obstruction in patients with hypertrophic cardiomyopathy are not completely understood. To define the relation between left ventricular outflow tract orifice size and presence or absence of subaortic obstruction, we studied 65 patients with hypertrophic cardiomyopathy and 16 normal controls by quantitative two-dimensional echocardiography. Left ventricular outflow tract area was measured at the onset of systole in the short-axis view in the stop-frame mode. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy and subaortic obstruction (2.6 +/- 0.7 cm2) than in patients without obstruction (5.9 +/- 1.6 cm2, p less than 0.001). Twenty of 21 patients with obstruction had a left ventricular outflow tract area smaller than 4.0 cm2, whereas 28 of 30 patients without obstruction had a left ventricular outflow tract area of 4.0 cm2 or greater. The outflow tract area in patients with provocable obstruction (4.6 +/- 1.6 cm2) was intermediate between the areas of patients with and without obstruction. Left ventricular outflow tract area was significantly smaller in patients with hypertrophic cardiomyopathy (4.6 +/- 2.0 cm2) than in normal subjects (10.4 +/- 1.2 cm2, p less than 0.001). We conclude that the cross-sectional outflow tract area is closely related to the presence or absence of subaortic obstruction in patients with hypertrophic cardiomyopathy. Hence, the size of the outflow tract at the level of the mitral valve appears to be of major pathophysiologic significance in producing obstruction in these patients.     

Intraventricular flow dynamics in hypertrophic cardiomyopathy with midventricular obstruction investigated by Doppler echocardiography

Seven patients with hypertrophic cardiomyopathy having midventricular obstruction (MVO) were examined using two-dimensional, conventional Doppler and color Doppler echocardiography to investigate intraventricular flow conditions. The controls were 35 patients with hypertrophic cardiomyopathy without MVO. All MVO patients had "hour-glass" LV cavities during systole, resulting from either hypertrophy at the midventricular level or hypertrophied papillary muscles, where systolic mosaic signals originated. Systolic peak flow velocities at the midventricle ranged from 2.5 to 4.2 m/s, proving the presence of a pressure gradient between the apex and the base of the LV. In fact, a pressure drop of 15-30 mmHg was demonstrated in four patients who underwent cardiac catheterization. These high velocity jet flows were not detectable at the midventricle in the control subjects. Peak ejection velocities in the outflow tracts were significantly lower in patients with MVO compared to those with hypertrophic cardiomyopathy and subaortic stenosis (129 +/- 29 vs 384 +/- 111 cm/s; p less than 0.001). As midventricular obliteration became severe, systolic jets at the midventricle increased in velocity. Waveforms changed from single- to double-peaked, and lasted until the isovolumic relaxation or the rapid filling phase beyond the second heart sound. Consequently, isovolumic relaxation waveforms at the midventricle using the apical approach changed the direction; from "the base to apex" to "the apex to base". An isovolumic signal away from the transducer was only observed in two patients without MVO. Diastolic color reversal and mosaic signals at the midventricle were also seen in five of the seven patients with MVO. Peak flow velocities in the rapid filling phase were significantly higher at the papillary muscle level than at the mitral valve level, indicating that MVO continues up to early diastole. It was suggested that MVO disturbs intraventricular flow dynamics during both systole and diastole. Color Doppler echocardiography is particularly useful in determining the site of obstruction and allows further evaluation by pulsed and continuous wave Doppler techniques to precisely measure pressure gradients. With routine, careful use of Doppler echocardiography, MVO may prove to be a more common entity than was previously believed.     

Transient Hypertrophic Obstructive Cardiomyopathy During Pregnancy

Hypertrophic obstructive cardiomyopathy (HOCM) is a primary myocardial disease with typical echocardiography features of asymmetric septal hypertrophy and evidence of left ventricular outflow tract obstruction. The natural history of HOCM is characterized by a slow progression of symptoms and a significant annual mortality rate. We report an unusual case of transient HOCM during pregnancy with evidence of total resolution postpartum.
hypertrophic cardiomyopathy, pregnancy, idiopathic hypertrophic subaortic stenosis, two-dimensional echocardiography, Doppler echocardiography     

Left ventricular filling in hypertrophic cardiomyopathy: a pulsed Doppler echocardiographic study

Abnormal left ventricular diastolic properties have been described in patients with hypertrophic cardiomyopathy. To evaluate the diastolic filling characteristics of the left ventricle in patients with this disease, pulsed Doppler echocardiography was used to study mitral flow velocity in 17 patients with hypertrophic cardiomyopathy (11 with and 6 without systolic anterior motion of the mitral valve) and 16 age-matched normal subjects. There were no statistically significant differences between patients with hypertrophic cardiomyopathy with and without systolic anterior motion with regard to ventricular septal thickness, left ventricular posterior wall thickness, left ventricular internal dimensions or the extent of hypertrophy evaluated by two-dimensional echocardiography. Mitral regurgitation was detected by Doppler echocardiography in all 11 patients with and in 2 (33%) of the 6 patients without systolic anterior motion of the mitral valve. Early and late diastolic peak flow velocity, the ratio of late to early diastolic peak flow velocity and deceleration of early diastolic flow were measured from Doppler mitral flow velocity recordings. There were no statistically significant differences in these four indexes between the patients with systolic anterior motion and normal subjects. In contrast, the patients with hypertrophic cardiomyopathy without systolic anterior motion showed lower early diastolic peak flow velocity, higher ratio of late to early diastolic peak flow velocity and lower deceleration of early diastolic flow compared with the patients with systolic anterior motion and normal subjects, suggesting impaired left ventricular diastolic filling.(ABSTRACT TRUNCATED AT 250 WORDS)     

Doppler echocardiographic determination of the pressure gradient in hypertrophic cardiomyopathy

The continuous wave Doppler ultrasound signal across the left ventricular outflow tract in hypertrophic cardiomyopathy has a characteristic pattern that is in keeping with the dynamic nature of the pressure gradient in this condition. To determine the accuracy and reliability of the peak Doppler flow velocity signal for measuring the peak pressure gradient in this condition, 340 beats were analyzed from five consecutive patients studied with simultaneous continuous wave Doppler ultrasound and dual catheter pressure recordings across the left ventricular outflow tract. Each patient was studied at steady state and during physiologic and pharmacologic manipulations of the pressure gradient. Peak velocity and calculated peak gradient were determined by two independent observers who did not know the catheter measurements. In addition, 18 beats with well defined flow velocity envelopes were digitized for analysis of the magnitude, timing and contour of the instantaneous Doppler ultrasound and catheter gradients throughout systole. Peak catheter gradient in the 340 beats ranged from 12 to 245 mm Hg. The correlations between the Doppler-derived and catheter peak gradients were close (r = 0.96, SEE = 4 mm Hg for Observer 1 and r = 0.97, SEE = 11 mm Hg for Observer 2). Interobserver variability for measurement of peak flow velocity was small (mean +/- SD 0.16 +/- 0.15 m/s). An interobserver difference greater than 0.3 m/s occurred in 25 of the 340 beats analyzed. By retrospective analysis, this was due to contamination of the outflow tract signal by mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)     

应用Doppler超声观察肥厚性心肌病患者左心室内血流速度的改变

本文应用 Doppler 超声及实时二维 Doppler 彩色血流显象(CDFI)法观察了19例肥厚性心肌病(HCM)患者左心室内收缩期血流速度及左室收缩状态,结果示,不论有无左室流出道狭窄,HCM 患者左室内(包括左室流出道、室中及心尖部)收缩期血流峰值速度均明显增高,在左室流出道内可呈高速的湍流,于 CDFI 上表现为严重的 Aliasing 现象及轻度 Mosaic 现象,说明 HCM 患者左心室呈高动力型收缩状态。应用 CDFI 技术可指导脉冲波(PW)及连续波(CW)Doppler 对异常血流的采样,提高对 HCM 患者左室内高速血流速度测定的准确性。     

Mid-systolic septal deceleration. A new sign of left ventricular outflow tract obstruction obtained by color-coded tissue Doppler echocardiography

Hypertrophic obstructive cardiomyopathy (HOCM) is characterized by the presence of a dynamic left ventricular outflow tract gradient. We studied septal longitudinal motion by color coded tissue Doppler echocardiography in a 69-year old HOCM patient during and after catheter based treatment by trans coronary alcohol ablation of septal hypertrophy. The presence of dynamic left ventricular outflow tract obstruction was associated with a characteristic abrupt mid-systolic septal deceleration pattern in the tissue Doppler velocity trace. Five weeks after treatment, this pattern was no longer visible at rest.     

Pitfalls in the echo-Doppler diagnosis of hypertrophic cardiomyopathy

While Doppler echocardiography has become the gold standard for the diagnosis of hypertrophic cardiomyopathy, there are many pitfalls in its use. Some of these pitfalls are technical in nature resulting from inadequate image quality, incorrect transducer angulation, and improper equipment settings. Other pitfalls relate to the diversity and heterogeneity in defining hypertrophic cardiomyopathy and to the host of disorders that may mimic it by echocardiography. The pattern and extent of ventricular hypertrophy, systolic anterior motion of the mitral valve, and Doppler determination of left ventricular outflow tract obstruction, diastolic dysfunction, and mitral regurgitation are discussed, as are wall-motion abnormalities and myocardial echo reflectivity. While these echocardiographic features of hypertrophic cardiomyopathy are nonspecific when seen in isolation, their combined presence in the appropriate clinical setting makes the diagnosis likely.     

Noninvasive assessment of left ventricular diastolic function by pulsed Doppler echocardiography in patients with hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy is a primary myocardial disease in which symptoms may frequently result from impaired left ventricular relaxation, filling and compliance. In the present investigation, Doppler echocardiography was utilized to measure transmitral flow velocity and thereby assess left ventricular diastolic performance noninvasively in a group of 111 patients representative of the broad clinical spectrum of hypertrophic cardiomyopathy. In patients with hypertrophic cardiomyopathy, all Doppler indexes of diastolic relaxation and filling differed significantly (p less than 0.001) from those obtained in 86 control subjects without heart disease, namely, prolongation of isovolumic relaxation (94 +/- 24 versus 78 +/- 12 ms) and of the early diastolic peak of flow velocity (244 +/- 55 versus 220 +/- 28 ms), as well as slower deceleration (3.4 +/- 1.4 versus 4.9 +/- 1.3 m/s2) and reduced maximal flow velocity in early diastole (0.5 +/- 0.2 versus 0.6 +/- 0.1 m/s). As an apparent compensation for impaired relaxation and early diastolic filling, the atrial contribution to left ventricular filling was increased, as shown by increased late diastolic flow velocity (0.4 +/- 0.3 versus 0.3 +/- 0.1 m/s) and reduced ratio of maximal flow velocity in early diastole to that in late diastole (1.4 +/- 0.8 versus 2.1 +/- 0.9). The vast majority of patients with hypertrophic cardiomyopathy (91 [82%] of 111) showed evidence of impaired left ventricular diastolic performance, as assessed from the Doppler waveform. Abnormal Doppler diastolic indexes were identified with similar frequency in patients with (78%) or without (83%) left ventricular outflow obstruction, as well as in patients with (84%) or without (80%) cardiac symptoms. However, patients with nonobstructive hypertrophic cardiomyopathy showed more severe alterations in the Doppler indexes of diastolic function than did patients with obstruction. Thus, abnormal diastolic performance as assessed by Doppler echocardiography was apparent in the vast majority of the study patients with hypertrophic cardiomyopathy, independent of the presence or absence of cardiac symptoms or a subaortic pressure gradient. The high frequency with which diastolic abnormalities are identified in asymptomatic patients with hypertrophic cardiomyopathy suggests that impaired diastolic performance may be present at a time in the natural history of the disease when functional limitation is not yet evident.     

Prediction of the site and severity of obstruction in hypertrophic cardiomyopathy by color flow mapping and continuous wave Doppler echocardiography.

OBJECTIVE. We investigated whether the site and severity of an obstruction in hypertrophic cardiomyopathy can be accurately predicted by the combined use of color-coded and continuous wave Doppler echocardiography. BACKGROUND. Predicting the site of obstruction by end-systolic cavity shape is not reliable. Therefore, hemodynamic localization of the obstruction is required before surgery is performed. Such localization should be possible with color flow imaging, which provides two-dimensional velocity mapping reflecting the distribution of pressures within the left ventricle. Discrepancies in assessment of the pressure gradient by Doppler echocardiography and cardiac catheterization (which are usually not performed simultaneously) may be due to spontaneous variation of the dynamic obstruction in addition to technical factors related to both methods. METHODS. Twenty consecutive patients with hypertrophic cardiomyopathy were examined 1 day before transseptal left heart catheterization. The obstruction site was defined by color flow mapping. The pressure gradient was determined by continuous wave Doppler echocardiography. Measurements were also performed simultaneously in 10 patients during cardiac catheterization. RESULTS. Midventricular obstruction was correctly identified in 4 patients and subvalvular obstruction in 15 patients. One patient had no obstruction at rest. Invasively and noninvasively determined pressure gradients correlated well (r = 0.89, SEE = 16.3 mm Hg). Multiple single-beat analysis in 10 patients, also simultaneously examined with Doppler echocardiography and catheterization, yielded an excellent correlation (r = 0.97, SEE = 13.1 mm Hg). Comparing the simultaneous (r = 0.96, SEE = 12.5 mm Hg) and nonsimultaneous (r = 0.81, SEE = 23.8 mm Hg) recordings in these patients, we found that the spontaneous variation of the dynamic obstruction mainly accounted for discrepancies (p less than 0.05). CONCLUSION. The combined use of color-coded and continuous wave Doppler echocardiography provides the relevant hemodynamic information required for decision-making in patients with hypertrophic cardiomyopathy who are considered for transaortic myectomy.     

Utility of continuous wave Doppler echocardiography in the noninvasive assessment of left ventricular outflow tract pressure gradient in patients with hypertrophic cardiomyopathy.

Subaortic obstruction is an important determinant of the clinical presentation of and therapeutic approach to patients with hypertrophic cardiomyopathy. Therefore, assessment of the presence and magnitude of the intraventricular pressure gradient is paramount in the clinical evaluation of these patients. To establish the utility of continuous wave Doppler echocardiography in assessing the pressure gradient in hypertrophic cardiomyopathy, 28 patients representing the wide hemodynamic spectrum of this disease underwent simultaneous determination of the subaortic gradient by continuous wave Doppler ultrasound and cardiac catheterization. With use of the modified Bernoulli equation, the Doppler-estimated gradient showed a strong correlation with the maximal instantaneous pressure difference measured at catheterization, both under basal conditions (r = 0.93; p less than 0.0001) and during provocative maneuvers (r = 0.89; p less than 0.0001). In 26 of the 28 patients, all assessments of the subaortic gradient were in agreement within 15 mm Hg (average difference 5 +/- 3 mm Hg). In the other two patients there were substantial differences between these measurements (under basal conditions in one patient and after provocation in another), although the Doppler technique predicted the presence of marked subaortic obstruction in each. In both patients the erroneous interpretation was due to superimposition of the mitral regurgitation signal on that of left ventricular outflow. Doppler waveforms from the left ventricular outflow tract showed variability in contour among different patients and in individual patients. Hence, continuous wave Doppler echocardiography is a useful noninvasive method for estimating the subaortic gradient in patients with hypertrophic cardiomyopathy. However, technical factors such as contamination of the outflow tract jet with that of mitral regurgitation and variability in waveform configuration may importantly influence such assessments of the subaortic gradient.     

Left ventricular diastolic reserve during acute pressure loading in hypertrophic cardiomyopathy and dilated cardiomyopathy

To evaluate left ventricular diastolic reserve during acute pressure loading, changes in mitral flow velocity patterns before and after the elevation of blood pressure were analyzed by pulsed Doppler echocardiography in 11 cases of hypertrophic cardiomyopathy (HCM), nine cases of dilated cardiomyopathy (DCM), and 11 control subjects. Systolic blood pressure was elevated 25% above basal values by methoxamine infusion (0.01 mg/kg/min). Before and after methoxamine, left ventricular dimension and mitral flow velocity pattern were obtained by M-mode and pulsed Doppler echocardiography, respectively. The peak velocity in the rapid filling and atrial contraction phases and time-velocity integrals were measured from the flow pattern. After methoxamine, left ventricular diastolic dimension was significantly increased in all groups, from 43.8 +/- 4.7 mm to 47.4 +/- 4.9 mm in the control subjects, from 43.7 +/- 6.3 mm to 47.2 +/- 6.0 mm in HCM, and from 57.9 +/- 6.4 mm to 60.6 +/- 5.9 mm in DCM. Left ventricular systolic dimension was significantly increased from 48.6 +/- 8.4 mm to 52.8 +/- 8.3 mm in DCM, but not in the control subjects or HCM. The peak velocity in the rapid filling phase was significantly increased from 60 +/- 16 cm/sec to 69 +/- 14 cm/sec in the control subjects and tended to be increased from 44 +/- 13 cm/sec to 52 +/- 12 cm/sec in HCM. The extent of this increase tended to be less in HCM. However, the peak velocity in the rapid filling phase tended to decrease in DCM. There were no consistent trends of changes in the peak velocity in the atrial contraction phase in any groups. The mitral velocity integral increased from 502 Hz-sec to 621 Hz-sec in the controls and from 525 Hz-sec to 613 Hz-sec in HCM, but it did not increase in DCM. These findings suggest that there is impaired diastolic reserve during acute pressure loading in HCM and DCM and that the diastolic disturbance might be reflected in the early diastolic phase, rather than in the late diastolic phase.