Satoshi Nakatani

Assessment of mitral annular dynamics during diastole by Doppler tissue imaging : Comparison with mitral Doppler inflow in subjects without heart disease and in patients with left ventricular hypertrophy

The purpose of this study was to determine the normal pattern and magnitude of mitral annular velocities in diastole by Doppler tissue imaging (DTI) and to assess whether this is altered in patients with left ventricular hypertrophy. Mitral annulus velocities were measured by DTI. Peak and time-velocity integral were measured from the DTI tracings and the timing of the velocities in relation to electrocardiogram. DTI was compared with M-mode echo of the annulus and mitral inflow Doppler velocities. Integrated annular velocities by DTI correlated with the annular displacement. Early diastolic velocities decreased with age and in patients with left ventricular hypertrophy. In the hypertrophy group, early diastolic velocities were significantly lower than normal even after correcting for age. Patients with left ventricular hypertrophy also showed a delay in peak early diastolic mitral annular velocity (5.5 +/- 21 msec after the E wave). In conclusion, mitral annular velocity in diastole is readily recorded by DTI. The magnitude and the pattern of these velocities are significantly altered by age and by left ventricular hypertrophy. This method provides a new insight into diastolic filling events and may prove useful in detecting abnormal diastolic function.

Mechanism of Mitral Regurgitation in Hypertrophic Cardiomyopathy Mismatch of Posterior to Anterior Leaflet Length and Mobility

BACKGROUND In hypertrophic cardiomyopathy, a spectrum of mitral leaflet abnormalities has been related to the mechanism of mitral systolic anterior motion (SAM), which causes both subaortic obstruction and mitral regurgitation. In the individual patient, SAM and regurgitation vary in parallel; clinically, however, great interindividual differences in mitral regurgitation can occur for comparable degrees of SAM. We hypothesized that these differences relate to variations in posterior leaflet length and mobility, restricting its ability to follow the anterior leaflet (participate in SAM) and coapt effectively. METHODS AND RESULTS Different mitral geometries produced surgically in porcine valves were studied in vitro. Comparable degrees of SAM resulted in more severe mitral regurgitation for geometries characterized by limited posterior leaflet excursion. Mitral geometry was also analyzed in 23 patients with hypertrophic cardiomyopathy by intraoperative transesophageal echocardiography. All had typical anterior leaflet SAM with significant outflow tract gradients but considerably more variable mitral regurgitation; therefore, regurgitation did not correlate with obstruction. In contrast, mitral regurgitation correlated inversely with the length over which the leaflets coapted (r= -0.89), the most severe regurgitation occurring with a visible gap. Regurgitation increased with increasing mismatch of anterior to posterior leaflet length (r=0.77) and decreasing posterior leaflet mobility (r= -0.79). CONCLUSIONS SAM produces greater mitral regurgitation if the posterior leaflet is limited in its ability to move anteriorly, participate in SAM, and coapt effectively. This can explain interindividual differences in regurgitation for comparable degrees of SAM. Thus, the spectrum of leaflet length and mobility that affects subaortic obstruction also influences mitral regurgitation in patients with SAM.

Resting echocardiographic features of latent left ventricular outflow obstruction in hypertrophic cardiomyopathy.

We determined resting echocardiographic features predictive of latent left ventricular (LV) outflow obstruction in 50 consecutive patients with nonobstructive hypertrophic cardiomyopathy (26 provocable, 24 nonprovocable with amyl nitrite inhalation) to have a better understanding of the pathophysiology of this condition and to identify such patients without pharmacologic provocation. Measurements included wall thickness, type of hypertrophy, LV outflow tract diameter, degree of mitral systolic anterior motion, outflow pressure gradient, and ventricular volume. The direction of the ejection streamline was measured to assess the magnitude of the drag force acting on the mitral valve. Thirteen of 16 patients (81%) with proximal septal bulge were provocable, whereas only 3 of 8 patients (38%) with asymmetric septal hypertrophy and 10 of 26 (38%) with concentric hypertrophy were provocable (p < 0.05). LV outflow tract was significantly narrower and the angle between the ejection flow and the mitral valve was larger in provocable patients. The sensitivity for predicting provocable patients by a combination of a narrow outflow tract (< or = 2 cm) and a large angle (> or = 35 degrees) was 65%, with a specificity of 80% and a positive predictive value of 79%. When these criteria were combined with the presence of septal bulge, the sensitivity was 35%, but the specificity and the positive predictive value were both 100%. Patients with nonobstructive hypertrophic cardiomyopathy with proximal septal bulge, a narrow LV outflow tract, and an oblique angle between the ejection flow and the mitral valve appeared to be predisposed for latent outflow obstruction. These features are consistent with the presence of the large Venturi and drag forces. Thus, the left ventricle, which is capable of increasing both the Venturi and the drog forces on the basis of the morphologic change, contributes to the development of outflow obstruction with amyl nitrite inhalation.

Noninvasive assessment of left atrial maximum dP/dt by a combination of transmitral and pulmonary venous flow

OBJECTIVES The study assessed whether hemodynamic parameters of left atrial (LA) systolic function could be estimated noninvasively using Doppler echocardiography. BACKGROUND Left atrial systolic function is an important aspect of cardiac function. Doppler echocardiography can measure changes in LA volume, but has not been shown to relate to hemodynamic parameters such as the maximal value of the first derivative of the pressure (LA dP/dt(max)). METHODS Eighteen patients in sinus rhythm were studied immediately before and after open heart surgery using simultaneous LA pressure measurements and intraoperative transesophageal echocardiography. Left atrial pressure was measured with a micromanometer catheter, and LA dP/dt(max) during atrial contraction was obtained. Transmitral and pulmonary venous flow were recorded by pulsed Doppler echocardiography. Peak velocity, and mean acceleration and deceleration, and the time-velocity integral of each flow during atrial contraction was measured. The initial eight patients served as the study group to derive a multilinear regression equation to estimate LA dP/dt(max) from Doppler parameters, and the latter 10 patients served as the test group to validate the equation. A previously validated numeric model was used to confirm these results. RESULTS In the study group, LA dP/dt(max) showed a linear relation with LA pressure before atrial contraction (r = 0.80, p < 0.005), confirming the presence of the Frank-Starling mechanism in the LA. Among transmitral flow parameters, mean acceleration showed the strongest correlation with LA dP/dt(max) (r = 0.78, p < 0.001). Among pulmonary venous flow parameters, no single parameter was sufficient to estimate LA dP/dt(max) with an r2 > 0.30. By stepwise and multiple linear regression analysis, LA dP/dt(max) was best described as follows: LA dP/dt(max) = 0.1 M-AC +/- 1.8 P-V - 4.1; r = 0.88, p < 0.0001, where M-AC is the mean acceleration of transmitral flow and P-V is the peak velocity of pulmonary venous flow during atrial contraction. This equation was tested in the latter 10 patients of the test group. Predicted and measured LA dP/dt(max) correlated well (r = 0.90, p < 0.0001). Numerical simulation verified that this relationship held across a wide range of atrial elastance, ventricular relaxation and systolic function, with LA dP/dt(max) predicted by the above equation with r = 0.94. CONCLUSIONS A combination of transmitral and pulmonary venous flow parameters can provide a hemodynamic assessment of LA systolic function.

Plasma Volume and Its Regulatory Factors in Congestive Heart Failure After Implantation of Long-term Left Ventricular Assist Devices

BACKGROUND Congestive heart failure is associated with blood volume expansion caused by stimulation of the renin-aldosterone system and arginine vasopressin. The use of left ventricular assist devices as bridges to heart transplantation has improved the survival of patients during this critical period. In studying heart failure physiology on support devices, we hypothesized that improvement of cardiac function by a left ventricular assist device is associated with normalization of volume load secondary to normalization of its regulatory substances. METHODS AND RESULTS We studied 15 patients (13 men, 2 women: age 51 +/- 8 years) with end-stage heart failure who were cardiac transplant candidates eligible for HeartMate implantation. We measured plasma volume and plasma levels of atrial natriuretic peptide, aldosterone, renin, and arginine vasopressin sequentially before HeartMate implantation (baseline), after HeartMate implantation (weeks 4 and 8), and after transplantation. Baseline plasma volume was 123 +/- 20% of normal; it was 122 +/- 22% at week 4 and decreased to 115 +/- 14% at week 8. Atrial natriuretic peptide was 359 +/- 380 pg/mL at baseline, 245 +/- 175 pg/mL at week 4, and 151 +/- 66 pg/mL at week 8. Plasma aldosterone fell from 68 +/- 59 ng/dL at baseline to 17 +/- 16 ng/dL at week 4 (P < .05 versus baseline) and was 32 +/- 50 ng/dL at week 8. Plasma renin activity decreased from 80 +/- 88 ng/dL at baseline to 11 +/- 12 ng/dL at week 4 and was 16 +/- 38 ng/dL at week 8 (both P < .05 versus baseline). Arginine vasopressin fell from 5.0 +/- 4.8 fmol/mL at baseline to 1.1 +/- 0.7 fmol/mL at week 4 and 1.2+/-0.8 fmol/mL at week 8 (both P < .05 versus baseline). CONCLUSIONS The reduction of plasma renin activity, plasma aldosterone, and arginine vasopressin occurred earlier than the reduction of plasma volume and atrial natriuretic peptide after HeartMate implantation, possibly because of decreased pulmonary congestion and improved renal perfusion. The reduction of atrial natriuretic peptide cannot be responsible for the lack of adequate decrease of plasma volume; its reduction can be taken as a marker of improved cardiac pump function and decreased atrial stretch.

New insights into the reduction of mitral valve systolic anterior motion after ventricular septal myectomy in hypertrophic obstructive cardiomyopathy

To determine the mechanism of reduction of mitral valve systolic anterior motion by myectomy, we examined 33 patients with hypertrophic obstructive cardiomyopathy echocardiographically before and after myectomy. Measurements included outflow tract diameter, the direction of ejection streamline (the angle between the ejection flow and the mitral valve), midventricular fractional area change, and papillary muscle inward excursion in the short-axis image. After myectomy, the outflow tract was enlarged (from 1.2 +/- 0.3 cm to 2.1 +/- 0.4 cm; p < 0.001), and the ejection flow became more parallel to mitral leaflets (from 51 +/- 10 degrees to 28 +/- 8 degrees; p < 0.001), whereas hyperdynamic midventricular fractional area change was reduced (81% +/- 14% to 62% +/- 14%; p < 0.001), and papillary muscle excursion decreased (1.3 +/- 0.3 cm to 0.8 +/- 0.3 cm; p < 0.001). Outflow enlargement and reduced ventricular contraction would decrease the Venturi force. Change of ejection streamline and reduced contraction would decrease the drag force onto the mitral leaflets. Blunted papillary motion would increase the mitral leaflet tension and decrease the effect of drag force on both leaflets. Thus myectomy decreases Venturi and drag forces and appears to reduce systolic anterior motion of the mitral valve.

Dynamic magnetic resonance imaging assessment of the effect of ventricular wall curvature on regional function in hypertrophic cardiomyopathy

We hypothesized that contraction within the ventricular septum in hypertrophic cardiomyopathy (HC) may be related to its abnormal morphology because ventricular wall stress is related to wall curvature by the Laplace equation. To test this, we studied 17 HC patients with various septal morphologies using dynamic magnetic resonance imaging techniques. Short- and long-axis curvatures of the basal septal and basal lateral walls were determined on cine images as the reciprocal of the radius of the arc best fit to the endocardial contour, which was negative if the wall was convex to the cavity of the left ventricle. Endocardial and epicardial intramyocardial circumferential shortening (% circumferential shortening) was measured in the septal and lateral walls on basal short-axis myocardial tagging images. Septal walls were flatter in the short-axis plane and more convex toward the left ventricular cavity in the long-axis plane than lateral walls, as indicated by smaller short- and long-axis curvatures. Septal percent circumferential shortening was significantly lower than the lateral percent circumferential shortening, suggesting reduced septal contraction. Endocardial and epicardial percent circumferential shortening showed significant positive correlations with wall curvatures. Multiple stepwise linear regression analysis revealed that both short- and long-axis curvatures significantly contributed to percent circumferential shortening (r=0.87 for endocardial and r=0.70 for epicardial, both p<0.0001). In conclusion, wall curvature is related to wall function in HC; the more convex toward the left ventricular cavity the wall is, the less it contracts. Reduced contraction of the septum in HC may be partly due to its abnormal curvature.