Evaluation of left atrial function by the functional volume change curve derived from Doppler flow spectra.

The objective of this study was to clarify the left atrial (LA) reservoir and booster pump function in patients with left ventricular (LV) diastolic dysfunction. To determine LA reservoir and booster pump function, a new algorithm to determine LA functional volume change curve (FVC) was developed from Doppler flow spectra of pulmonary venous flow and LV inflow by transthoracic echocardiography in 110 patients. Patients were classified into normal (N), and abnormal (AB) and pseudonormal (PN) groups on the basis of their Doppler flow patterns. From the indices of FVC, atrial reservoir volume (ARV), passive emptying volume (PEV) and active emptying volume (AEV) were obtained. ARV/stroke volume (SV) was increased in the AB group, but decreased in the PN group compared with N (N, 0.61+/-0.09; AB, 0.73+/-0.10; PN, 0.52+/-0.13, p<0.05). PEV/SV was significantly decreased in AB, but increased in PN compared with N (N, 0.27+/-0.07; AB, 0.19+/-0.07; PN, 0.31+/-0.18, p<0.05). AEV/SV was significantly increased in AB, but decreased in PN compared with N (N, 0.41+/-0.08; AB, 0.56+/-0.10; PN, 0.26+/-0.19, p<0.05). Thus, in patients with an abnormal relaxation pattern, the LA reservoir and booster pump function are augmented, but in patients with a pseudonormal pattern, both LA reservoir and booster pump function are deteriorated, suggesting a vulnerability to pulmonary congestion.

Effect of low-intensity warfarin therapy on left atrial thrombus resolution in patients with nonvalvular atrial fibrillation: a transesophageal echocardiographic study.

The presence of left atrial thrombus (LAT) is associated with an increased risk of embolic stroke. However, it has yet to be established definitively whether low-intensity warfarin therapy (INR: 1.5-2.0) can prevent LAT formation in patients with nonvalvular atrial fibrillation (NVAF). The present study analyzed the clinical and transesophageal echocardiography (TEE) features of 123 such patients to identify risk factors for LAT formation and the efficacy of prophylactic low-intensity warfarin therapy. Left atrial thrombi were found in 35 patients (28%) in whom systemic hypertension (49% vs 23%; p<0.01) and ischemic heart disease (17% vs 3%; p<0.01) were more frequent. Left ventricular ejection fraction (54+/-14% vs 60+/-11%; p<0.05), left ventricular end-diastolic dimension (51+/-7 mm vs 48+/-5 mm; p<0.05), spontaneous echo contrast (2.2+/-0.7 vs 1.4+/-0.9; p<0.01), left atrial diameter (50+/-6 mm vs 43+/-7 mm; p<0.01), left atrial appendage blood velocity (22.3+/-8.7 cm/s vs 37.2+/-21.5 cm/s; p<0.01) and the incidence of left ventricular hypertrophy (37% vs 15%; p<0.01) were also significantly different between the groups. Fourteen patients received continuous warfarin therapy (target INR: 1.5-2.0) and on the follow-up TEE study the left atrial thrombus resolved in 10 (71%). There were no thromboembolic events or major hemorrhagic complications in these patients, so it was concluded that low-intensity warfarin therapy is efficacious in treating LAT formation in patients with NVAF.

Improvement of atherosclerosis and stiffness of the thoracic descending aorta with cholesterol-lowering therapies in familial hypercholesterolemia.

The thoracic aorta is frequently involved in atherosclerotic lesions associated with familial hypercholesterolemia (FH). Transesophageal echocardiography (TEE) allows quantitative evaluation of the wall properties of the thoracic aorta. Using TEE, we tested whether atherosclerosis of the thoracic aorta in FH could be improved by cholesterol-lowering therapies. The subjects investigated were 22 FH patients and 22 age-matched normal subjects. The descending aorta (DA) was divided into four longitudinal portions of equal length. Atheromatous lesions of each portion of the DA were scored by character and extension of lesions by biplane two-dimensional TEE. The scores of atheromatous lesions from all four portions of the DA were added together to give the total atheromatous score (TAS). We also measured instantaneous dimensional changes of the DA in a cardiac cycle by M-mode TEE and blood pressure by a cuff method and calculated the stiffness parameter beta (In[SBP/DBP]/[Dmax-Dmin]/Dmin), where SBP is the systolic arterial blood pressure, DBP is the diastolic arterial blood pressure, Dmax is the maximum aortic dimension during the ejection period, and Dmin is the minimum aortic dimension during the preejection period. TAS was higher in FH (3.70 +/- 1.32) than normal (0.62 +/- 0.54, P < .0001) subjects. Beta in FH (10.35 +/- 4.87) was greater than in normal (5.10 +/- 1.25, P < .0001) subjects, but there were no significant differences of DA dimensions between the groups. In both normal subjects and FH patients, beta correlated with age (r = .52, P < .02 and r = .59, P < .005, respectively). In FH patients, beta and TAS correlated well with pretreatment total cholesterol levels (r = .43, P < .05 and r = .60, P < .005, respectively). In 12 of 22 FH patients, strict cholesterol-lowering therapies with diet and cholesterol-lowering drugs (pravastatin and probucol) were undertaken for 13 months. Cholesterol levels were significantly decreased from 333 +/- 45 to 219 +/- 39 mg/dL (P < .0001); this was associated with significant decreases in beta and TAS (from 9.88 +/- 5.03 to 7.88 +/- 3.92, P < .005, and from 3.61 +/- 1.50 to 2.94 +/- 1.22, P < .0005, respectively). In FH patients, the incidence and severity of morphological and physiological atherosclerosis of the DA were significantly higher than in age-matched normal subjects. A significant regression of atherosclerosis was achieved by strict cholesterol-lowering therapies in relatively young FH patients.

Effects of nifedipine on mechanical properties of the normal and atherosclerotic descending aorta assessed by transesophageal echocardiography.

We assessed the effects of calcium ion (Ca++) entry blockade (nifedipine) on the static elastic properties of the thoracic descending aorta in 60 subjects classified into 4 groups according to age and complications. The stiffness index (beta), which expresses the mechanical properties of the arterial wall, was calculated from the dimensional changes of the thoracic aorta by transesophageal echocardiography and blood pressure was determined by conventional cuff method. After administration of nifedipine, beta was significantly decreased in all groups. There was a significant correlation between beta at rest and the value of a decrease in beta after nifedipine in the relatively younger and the older groups with complications, but no significant correlation was observed in the older group without complications. Nifedipine directly reduces the stiffness of the descending aorta. The effect is stronger in relatively younger subjects, especially in subjects with risk factors of atherosclerosis and stiff descending aorta at rest. These results suggest that there may be a reversible sclerotic property of the descending aorta, probably caused by high smooth muscle tone before an irreversible atherosclerosis occurs in patients with risk factors promoting atherosclerosis.

Assessment of flow profile of left anterior descending coronary artery in hypertrophic cardiomyopathy by transesophageal pulsed Doppler echocardiography.

This study assessed the flow velocity profiles of the left anterior descending coronary artery (LAD) in 7 patients with nonobstructive hypertrophic cardiomyopathy (HC) and in 6 normal subjects by transesophageal pulsed Doppler echocardiography, and evaluated their characteristics and the hemodynamic determinants. Systolic peak flow velocity of the LAD (7 +/- 30 cm/sec) was significantly lower in patients with HC than in normal subjects (34 +/- 11 cm/s, p < 0.05), and there was a significant inverse correlation between systolic peak flow velocity and the thickness of the ventricular septum (r = 0.81, p < 0.01). In 2 cases of HC with ventricular septal thickness of > 20 mm, a remarkable systolic reverse flow was observed in the LAD. However, there was no significant difference in diastolic peak flow velocity between HC and normal subjects. During early diastole, the acceleration time of LAD flow velocity was significantly prolonged (210 +/- 67 vs 95 +/- 15 ms, p < 0.01) and the acceleration rate was significantly decreased (3.6 +/- 2.0 vs 6.6 +/- 1.8 m/s2, p < 0.02) in patients with HC. The time constant of the left ventricular pressure decay was significantly prolonged in patients with HC (55 +/- 6 ms) compared with normal subjects (39 +/- 2 ms, p < 0.001). In HC, increased intramural perivascular pressure of the thickened ventricular septum during systole may be attributed to systolic LAD flow pattern. However, the early and mid-diastolic LAD flow pattern may be affected by impaired left ventricular relaxation.

[Blood flow dynamics and dimensions of the descending thoracic aorta in patients with intra-aortic swirling echoes: assessment by biplane transesophageal echocardiography].

To examine the blood flow dynamics in the descending thoracic aorta (DAo) where intra-aortic swirling echo contrast was observed, we analyzed the flow velocity patterns (FVP) in DAo and the DAo dimensions by biplane transesophageal echocardiography (TEE) in 9 patients with intraortic swirling echo contrast and in 25 control subjects (N). We recorded sampling volumes with pulsed Doppler echocardiograms at 3 sites: median, central, and lateral sites on longitudinal scan images and on the DAo at the level of the mitral valve. We measured systolic peak flow velocity (Vp), time from the onset of the systolic flow to Vp (acceleration time: AT), deceleration time (DT) of the systolic flow, and AT/(AT + DT) for each sampling volume in the DAo. From the M-mode echogram of DAo, we measured the maximum dimension of the aorta, which usually coincided with the mid to late systolic phase. In the normal controls, the systolic forward flow was followed by a small reversal flow in early diastole and then by a small forward flow during holodiastole. Vp was highest at the center (64 +/- 10 cm/sec), then at the median (60 +/- 11 cm/sec) and lowest in the lateral (56 +/- 9 cm/sec; p < 0.01 vs center) sites in the DAo. AT was 70 +/- 13 msec and DT 215 +/- 26 msec. This flow velocity profile in the DAo was observed in both the control and patient groups. In patients with intra-aortic swirling echoes, Vp was markedly low (33 +/- 7 cm/sec; p < 0.001 vs N) and dimension of the DAo (13 +/- 2 mm/m2 in N) was significantly enlarged (21 +/- 7 mm/m2; p < 0.001 vs N), which might be related to swirling echoes and mural thrombi at the lateral portion in the DAo. Thus, we concluded that intra-aortic swirling echoes closely related to the production of mural thrombi observed mainly at the lateral site of the significantly dilated DAo.

[Assessment of atherosclerotic lesions and distensibility of the thoracic aorta in familial hypercholesterolemia by biplane transesophageal echocardiography].

Atherosclerosis involving the thoracic aorta frequently occurs in patients with familial hypercholesterolemia (FH). In this study, we employed two-dimensional (2-D) transesophageal echocardiography (TEE: 5 MHz) to assess atherosclerotic lesions of the thoracic aorta in 9 patients with FH (47.8 +/- 10.3 yrs) and 11 age-matched normal control subjects. Biplane TEE probe (i.e., transverse or sagittal scan transducer) was used to permit direct imaging of the distal half of the ascending aorta. The atherosclerotic lesions were classified based on the severity of the aortic wall sclerosis as intimal thickening (I.), atheromatous plaque, (II.) and calcification (III.). In all of the patients with FH, atherosclerotic lesions of grade I. or greater were observed particularly in the aortic arch and descending aorta, while, lesions more severe than grade I. in the thoracic aorta were not observed in any of the control subjects. In 6 FH patients (67%), atherosclerotic lesions more severe than grade II. were frequently observed, which were more frequent in the aortic arch and descending aorta than in the ascending aorta.

[Estimation of atherosclerotic lesions in the thoracic aorta by transesophageal echocardiography].

The thoracic aorta is one of the portions frequently involved with atherosclerotic lesions. We estimated atherosclerotic lesions in the thoracic aorta in consecutive 137 patients (59 +/- 10 years old) using transesophageal echocardiography. The study population consisted of 60 with coronary artery disease (CAD), 36 with hypertension (HT), 28 with hypercholesterolemia (HC, total cholesterol greater than or equal to 230 mg/dl), eight with dissecting aneurysm, nine with true aneurysm and two with aortitis syndrome. We used a single transverse scan-plane probe with ultrasound frequency of 5 MHz. We could obtain satisfactory echograms of whole thoracic aorta except upper portion of the ascending aorta. We defined atherosclerotic lesions as an increased echo-density of the intima, protruded plaque, ulceration or aneurysm. Atherosclerotic lesions were observed in 71 of 137 patients (52%). High incidence of the atherosclerotic lesions was seen in patients with HT (72%), HC (57%) and CAD (57%), whereas incidence of atherosclerotic lesions was low (15%) in patients without HT, HC, CAD or aortic aneurysm. Atherosclerotic lesions were observed more frequently in patients aged greater than or equal to 60 years (69% vs 34%, p less than 0.001). In patients with HT or HC, atherosclerotic lesions were frequently observed even in patients younger than 60 years old (HT: 58%, HC: 53%). We concluded that HT, HC and aging were important risk factors for the atherosclerotic process in the thoracic aorta, and transesophageal echocardiography was a useful approach for the detailed estimation of atherosclerotic lesions in the thoracic aorta.