Kazuyo Manabe

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 Aging on Systolic Left Ventricular Wall Motion Velocities Along the Long and Short Axes in Clinically Normal Patients Determined by Pulsed Tissue Doppler Imaging

Our objective was to evaluate the influence of aging on left ventricular (LV) regional systolic function along the long and short axes in clinically normal patients. We recorded LV wall motion velocity patterns at the mid-wall portion of the middle of the LV posterior wall in the parasternal long-axis view (short-axis direction) and at the endocardial portion of the middle of the LV posterior wall in the apical long-axis view (long-axis direction) with pulsed tissue Doppler imaging in 80 normal patients (age range 15 to 78 years). In all patients the LV pressure curve and its first derivative (dP/dt) were recorded. The systolic wave of the LV posterior wall motion velocity pattern exhibited 2 peaks, the first (Sw(1)) and second (Sw(2)) systolic waves. No significant changes were seen with aging in the percent LV fractional shortening determined by M-mode echocardiography, LV ejection fraction determined by left ventriculography, the peak Sw(1) and Sw(2) along the short axis, the peak Sw(2) along the long axis, and the peak dP/dt. The peak Sw(1) along the long axis correlated inversely with age (P <.0001) but did not correlate significantly with the peak dP/dt. These results suggest that shortening of the longitudinal fibers in early systole is impaired with increased age in healthy individuals. This impairment results in insufficient spherical change in the LV cavity, although global LV pump function and myocardial contractility are maintained.

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.

Evaluation of left atrial appendage function by measurement of changes in flow velocity patterns after electrical cardioversion in patients with isolated atrial fibrillation

We investigated temporary changes in left atrial appendage (LAA) flow velocity patterns in patients undergoing electrical cardioversion for chronic isolated atrial fibrillation, and evaluated the role of active LAA contraction in directing blood flow to the left atrial main chamber and left ventricle. The study consisted of 26 patients with chronic isolated atrial fibrillation treated with electrical cardioversion and 20 normal controls in sinus rhythm. Using transthoracic and transesophageal Doppler echocardiography, we recorded transmitral, pulmonary venous, and LAA flow velocity patterns before, 24 hours, and 1 week after cardioversion in all subjects. In the 15 patients who underwent successful cardioversion, the maximal LAA area 24 hours after cardioversion was smaller than the area before cardioversion, whereas LAA ejection fraction during atrial systole and peak atrial systolic emptying velocity of the LAA flow were lower 24 hours after cardioversion than those in the control group. One week after cardioversion, maximal LAA area and LAA peak atrial systolic emptying velocity were restored to levels approximately equivalent to those in the control group, although LAA ejection fraction was lower than in the control group. Maximal LAA area and LAA peak atrial systolic emptying velocity correlated negatively and positively with LAA ejection fraction, respectively, 24 hours and 1 week after cardioversion. These results suggest that LAA and the left atrial main chamber show stunning 24 hours after cardioversion, and the atrial systolic emptying wave of LAA flow is generated by active LAA contraction.

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.

Cross sectional echocardiographic demonstration of the mechanisms of abnormal interventricular septal motion in congenital total absence of the left pericardium.

OBJECTIVE: To investigate the influence of the absence of the pericardium on the left ventricular wall, particularly on interventricular septal motion, using M mode and cross sectional short axis echocardiography in patients with congenital total absence of the left pericardium. METHODS: 21 patients with, congenital total absence of the left pericardium were divided into three groups according to the interventricular septal motion; systolic type (n = 6) with paradoxical motion during systole, diastolic type (n = 11) with abnormal posterior motion during mid to late diastole, and mixed type (n = 4) with paradoxical motion during systole and abnormal posterior motion during diastole. RESULTS: On cross sectional short axis echocardiograms of the left ventricle, in the diastolic type the degree of angular displacement of the papillary muscles during end diastole to end systole showed excessive anticlockwise rotation about the long axis of the left ventricle without marked anteroposterior displacement. In the systolic type, there was shift of the left ventricle towards the anteromedial portion in systole and towards the posterolateral portion in diastole without significant rotation. There was a significantly positive correlation between the degree of angular displacement and the amplitude of diastolic interventricular septal motion during mid to late diastole in all patients. CONCLUSIONS: There was abnormal interventricular septal motion during systole and diastole in patients with total absence of the left pericardium. Abnormal systolic motion was induced by anteroposterior displacement of the left ventricle, and abnormal diastolic motion by left ventricular rotation about the long axis of the heart during the cardiac cycle. Analysis using cross sectional echocardiography was useful for elucidating the mechanisms of abnormal interventricular septal motion.