Miwa Sasaki

Relationship between the angiotensin converting enzyme gene polymorphism and the effects of enalapril on left ventricular hypertrophy and impaired diastolic filling in essential hypertension: M-mode and pulsed Doppler echocardiographic studies.

Objective To investigate the relationship between the angiotensin converting enzyme (ACE) gene polymorphism and the effects of the ACE inhibitor enalapril on left ventricular hypertrophy and impaired diastolic filling. Design and methods Enalapril (5-10 mg/day) was administered for 12 months to 60 previously untreated patients with essential hypertension. M-mode and pulsed Doppler echocardiography were performed before and after treatment, and changes in various parameters after treatment with enalapril were examined. ACE gene polymorphism was examined by the polymerase chain reaction method and the patients were classified as having the 490 bp deletion homozygous (DD) genotype, the 490 bp insertion homozygous (II) genotype or the 490 bp insertion 190bp deletion heterozygous (ID) genotype. Results No The DD genotype was observed in 10 patients (17%), the ID genotype in 24 patients (40%) and the II genotype in 26 patients (43%). Plasma ACE activity before treatment with enalapril was significantly higher in seven patients with DD genotype than it was in 18 patients with ID genotype and in 14 patients with II genotype. In all of the 60 patients, the left ventricular mass index, the peak atrial systolic velocity:early diastolic velocity ratio and the deceleration time from the peak of the early diastolic wave to the baseline in transmitral flow velocity were decreased significantly after treatment with enalapril. The changes in left ventricular mass index and atrial systolic velocity:early diastolic velocity ratio after enalapril administration were significantly greater in the DD genotype group than they were in the other two genotype groups. Conclusion Enalapril-induced regression of left ventricular hypertrophy and improvement in left ventricular impaired diastolic filling were significantly greater in the DD genotype group than they were in the ID and II genotype groups, suggesting that the circulating and tissue renin-angiotensin systems, particularly the former system, are most active in hypertensive patients with the DD genotype.

Influence of left atrial pressure on left atrial appendage flow velocity patterns in patients in sinus rhythm

To examine changes in left atrial appendage flow velocity patterns in relation to left atrial pressures during sinus rhythm, transesophageal echocardiography and cardiac catheterization were performed in 31 patients with myocardial diseases in sinus rhythm and 20 control subjects without cardiovascular disease. The 31 patients were divided into two groups according to mean pulmonary capillary wedge pressure: the group with high wedge pressure (19.9 +/- 5.8 mmHg) and the group with low wedge pressure (8.6 +/- 2.9 mmHg). The left atrial appendage peak early emptying velocity was decreased significantly in the groups with both high and low wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity was significantly greater in the group with low wedge pressure compared with the control group, whereas it was decreased significantly in the group, with high wedge pressure compared with the control group. The left atrial appendage peak late emptying velocity had a significant negative correlation with wedge pressure. The maximum left atrial appendage area at end systole in the group with high wedge pressure was significantly greater than that in both the group with low wedge pressure and the control group. There was a significant positive correlation between the maximum left atrial appendage area and the wedge pressure, as well as a significant negative correlation between the left atrial appendage ejection fraction during atrial contraction and the wedge pressure. In the group with high wedge pressure, one patient had evidence of left atrial appendage thrombi and two had spontaneous echo contrast. These results suggest that even in patients in sinus rhythm, a marked elevation in the left atrial pressure is likely to reduce the left atrial appendage peak early and late emptying velocities. These changes may be accompanied by an increased incidence of thrombus formation in the left atrial appendage compared with individuals with normal or only slightly elevated left atrial pressures.

Influence of Aging on Left Atrial Appendage Flow Velocity Patterns in Normal Subjects

Transesophageal pulsed Doppler echocardiography was performed to examine changes with age in the left atrial appendage flow velocity patterns in 50 normal subjects (15 to 80 years) in sinus rhythm. There was a significant negative correlation between the peak early diastolic forward and backward left atrial appendage flow velocities and age, as well as a significant positive correlation between the peak early diastolic forward left atrial appendage flow velocity and the peak early diastolic transmitral and pulmonary venous flow velocities. Although there was a significant positive correlation between the peak atrial systolic transmitral flow velocity and age, there was a negative correlation between the peak atrial systolic forward and backward left atrial appendage flow velocities and age. There was a positive correlation between both the maximum left atrial diameter and the amplitude of the interatrial septal motion during atrial systole and age. There was a significant negative correlation between the left atrial appendage ejection fraction during atrial systole and age. Left atrial appendage thrombi and spontaneous echo contrast were detected in two subjects with low peak early diastolic and atrial systolic left atrial appendage flow velocities. In conclusion, both peak early diastolic and atrial systolic left atrial appendage flow velocities decreased with age. A decrease in the peak atrial systolic flow velocity appeared to be an important sign of left atrial appendage thrombus formation even in normal elderly subjects in sinus rhythm.

Changes in transmitral and pulmonary venous flow velocity patterns after cardioversion of atrial fibrillation

To examine the recovery time of left atrial mechanical function after electrical cardioversion of atrial fibrillation, we recorded transmitral flow, pulmonary venous flow velocities, and interatrial septal motion during atrial systole within 24 hours (16 +/- 5 hours) and 10 days after cardioversion in 25 patients with atrial fibrillation, including 6 patients with hypertension, 4 with ischemic heart disease, 2 with alcoholic heart disease, 5 with dilated cardiomyopathy, and 8 with no evidence of underlying heart disease. With the exception of the five patients with dilated cardiomyopathy, the peak atrial systolic transmitral and pulmonary venous flow velocities, peak first systolic velocity of pulmonary venous flow, duration of both atrial systolic waves, and amplitude of the interatrial septal motion during atrial systole decreased markedly within 24 hours after cardioversion and increased 10 days after cardioversion. These results suggest that active atrial systolic and relaxant variables obtained from transmitral and pulmonary venous flow velocities may reflect left atrial mechanical function after cardioversion of atrial fibrillation.

Predisposing factors for severe mitral regurgitation in idiopathic mitral valve prolapse

To elucidate predisposing factors for severe mitral regurgitation (MR) in idiopathic mitral valve prolapse (MVP), 124 MVP patients were classified into the following categories: 55 with isolated clicks (click group), 35 with a late-systolic murmur (late-SM group), and 34 with a holosystolic murmur (holo-SM group). Their clinical and echocardiographic findings were compared with those of 26 patients with spontaneous chordal rupture (rupture group). In 22 patients in the click group, 24 in the late-SM group, and 22 in the holo-SM group, follow-up studies were performed for a mean of 4.5 years (range 1 to 13.5). The mean age was youngest in the click group and oldest in the rupture group. The click and late-SM groups showed a female predominance, but the holo-SM and rupture groups showed a male predominance. There was no difference in the incidence of systemic hypertension among the 4 groups. Most patients in the click and late-SM groups had anterior leaflet prolapse. In the holo-SM and rupture groups, however, the incidence of posterior leaflet involvement was significantly increased. The incidence of thickened mitral valve increased in order of the click (8%), late-SM (21%), holo-SM (38%), and rupture (50%) groups. Six patients in the holo-SM group developed chordal rupture with severe MR during the follow-up period. In the click and late-SM groups, however, there were no complications and no development into a holo-SM. Thus, aging, male sex, posterior leaflet prolapse, thickened mitral valve, and holo-SM were found to be important predisposing factors for severe MR in idiopathic MVP.

Left atrial systolic performance in the presence of elevated left ventricular end-diastolic pressure: evaluation by transesophageal pulsed Doppler echocardiography of left ventricular inflow and pulmonary venous flow velocities

We recorded left ventricular inflow (LVIF) and pulmonary venous flow (PVF) velocities by trans‐esophageal pulsed Doppler echocardiography in 25 patients with a ratio of peak atrial systolic to early diastolic LVIF velocity of < 1 and a left ventricular end‐diastolic pressure (LVEDP) of 15 mmHg or greater, as well as in 30 normal subjects. The group consisted of 14 patients with prior myocardial infarction, 7 with dilated cardiomyopathy, and 4 with cardiac amyloidosis, and were divided into: (1) group A (n = 7): peak atrial systolic LVIF velocity of 40 cm/sec or greater; (2) group B (n = 7): peak atrial systolic LVIF velocity of < 40 cm/sec and peak atrial systolic PVF velocity of 30 cm/sec or greater; and (3) group C (n = 11): peak atrial systolic LVIF velocity of < 40 cm/sec and peak atrial systolic PVF velocity of < 30 cm/sec. Although LVEDPs in groups B and C were significantly greater than in group A, there was no difference between groups B and C. The mean pulmonary capillary wedge pressure (mPCWP) in group C was significantly greater than in groups A and B, but there was no difference between groups A and B. The difference between LVEDP and mPCWP (LVEDP — mPCWP) in group B was significantly higher than in groups A and C. Dilatation of the left atrium (LA) was seen in all three groups, particularly in groups B and C. There were no differences in peak atrial systolic LVIF velocity and LA volume change during atrial contraction between group A and the control group, and there were no differences in LA volume change and peak second systolic PVF velocity between groups A and B. LA volume change and peak second systolic PVF velocity were significantly less in group C than in groups A and B. Among the four patients whose courses could be observed after medical treatment with diuretic and vasodilator, one changed from group B to A, one from group B to C, one from group C to A, and one remained in group C. Thus, recording of peak atrial systolic LVIF and PVF by transesophageal pulsed Doppler echocardiography permits detailed evaluation of LA systolic performance in the presence of elevated LVEDP. These two variables provide important information for less invasive differentiation of LA afterload mismatch from LA myocardial failure.

Pulmonary and systemic venous flow patterns assessed by transesophageal Doppler echocardiography in congenital absence of the pericardium

In conclusion, alterations in venous return are more marked in the right side of the heart than in the left side of the heart in patients with complete absence of the left pericardium.

Transesophageal Pulsed Doppler Echocardiographic Study of Pulmonary Venous Flow in Mitral Stenosis

For evaluation of pulmonary venous flow (PVF) in mitral stenosis, transthoracic and transesophageal echocardiography were performed in 33 patients with mitral stenosis and 20 normal controls. The peak systolic flow velocity of the PVF was significantly lower in patients with mitral stenosis and atrial fibrillation. The peak diastolic flow velocity of the PVF was significantly lower in the patients with mitral stenosis than in normal controls. The diastolic wave recorded as laminar flow in the mitral stenosis group showed a peak in the rapid filling phase with a gradually descending slope of velocity during mid to late diastole. There was a significant negative correlation between the peak diastolic flow velocity of the PVF and the pressure half time from transmitral flow obtained by continuous wave Doppler in the mitral stenosis group. These results demonstrate that evaluation of the PVF is helpful in understanding hemodynamic events between the left atrium and left ventricle in patients with mitral stenosis.

Assessment of Right-to-Left Shunt Flow in Atrial Septal Defect by Transesophageal Color and Pulsed Doppler Echocardiography

To investigate the clinical significance and problems of right-to-left (R-L) shunt flow dynamics in atrial septal defects, we performed transesophageal color and pulsed Doppler echocardiography in 30 patients with atrial septal defects of the ostium secundum type. The 30 patients consisted of 20 with a pulmonary artery systolic pressure of less than 40 mm Hg, four with a pressure of 40 to 60 mm Hg, three with a pressure of 90 mm Hg or more, two patients with pulmonic stenosis, and one patient with Ebsteins anomaly. R-L shunting was determined by the presence of a shunt flow signal across the defect during each cardiac cycle. The time of R-L shunt flow was compared with the various parameters obtained by echocardiography and cardiac catheterization. R-L shunt flow signals were detected at the following times: (1) at the onset of ventricular contraction or the closing phase of the tricuspid valve in five patients with isolated atrial septal defect. These patients showed an increase of mean right atrial pressure but had no severe pulmonary hypertension; (2) during ventricular systole in five of 26 patients with tricuspid regurgitation and one patient with Ebsteins anomaly. The tricuspid regurgitant signal was directed toward the ostium of the defect in three patients and was massive in the other patients; (3) during middiastole in three patients without pulmonary hypertension. These patients showed massive left-to-right shunt flow from end systole to early diastole; and (4) during atrial systole in three patients with severe pulmonary hypertension and two patients with pulmonic stenosis. The former, in particular, showed the aliasing signal as a high-speed shunt flow. In two of the three patients with severe pulmonary hypertension, R-L shunting continued from atrial systole to early ventricular systole and was also observed in early diastole. R-L shunt flow was detected in patients with atrial septal defects not only with pulmonary hypertension but also without pulmonary hypertension and was influenced by the right atrial pressure in the phase of tricuspid valve closing, the volume or direction of tricuspid regurgitation, rebound flow caused by massive left-to-right shunt flow, the grade of right ventricular distensibility or the complication of pulmonary hypertension, and complications with other cardiac anomalies. Thus R-L shunt flow in patients with atrial septal defects was detected easily by transesophageal color and pulsed Doppler echocardiography because of the high efficiency of this method for its detection.

Transesophageal echocardiographic evaluation of mitral regurgitation in hypertrophic cardiomyopathy: Contributions of eccentric left ventricular hypertrophy and related abnormalities of the mitral complex

This study was designed to evaluate the contribution of eccentric left ventricular hypertrophy and its related organic and spatial abnormalities of the mitral complex to the occurrence of mitral regurgitation in patients with hypertrophic cardiomyopathy We selected 45 consecutive patients with systolic mitral regurgitation by color Doppler echocardiography and performed transesophageal echocardiography in all patients. Eighteen patients were in the obstructive group and 27 patients were in the nonobstructive group of hypertrophic cardiomyopathy with asymmetric septal hypertrophy. Twenty subjects without any cardiac disorders served as the control group. The maximum area of mitral regurgitation was significantly greater in the obstructive group than in the nonobstructive group. Mitral regurgitation appeared more frequently during pansystole in the two groups with hypertrophic cardiomyopathy, particularly in the obstructive group. Mitral valve prolapse was observed in 20 (44%) of the 45 patients with hypertrophic cardiomyopathy. Distances between the posterior papillary muscle and anterior or posterior mitral anulus were significantly smaller in the two groups with hypertrophic cardiomyopathy than in the normal control group. In the obstructive group, the length of the anterior mitral leaflet and the thickness of the rough zone of the anterior mitral leaflet at mid-diastole were significantly greater than in the other groups. Systolic anterior motion was observed in all patients with obstructive cardiomyopathy and contact between the interventricular septum and the anterior mitral leaflet during early diastole was observed in 17 of the 18 patients in the obstructive group.(ABSTRACT TRUNCATED AT 250 WORDS)