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Background and Purpose: To assess effects of long-term anemia management on left ventricular hypertrophy in patients with chronic kidney disease (CKD) not on dialysis, we performed secondary outcome analyses of a randomized controlled study that evaluated effects of anemia management with erythropoiesis stimulating agents in this population., Methods and Subjects: Subjects [hemoglobin (Hb)<10.0 g/dL, 2.0 ≤ serum creatinine<6.0mg/dL] were randomized either to high Hb (11.0 ≤ target Hb ≤ 13.0 g/dL with darbepoetin alfa), or to low Hb group (9.0 ≤ target Hb ≤ 11.0 g/dL with recombinant human erythropoietin), and followed up to 48 weeks. Data from echocardiographic evaluation and values of neurohumoral factors associated with heart failure were assessed in subjects whose data were evaluable both at the baseline and at the end point., Results: The high Hb group achieved target range Hb levels (12.1 ± 1.1g/dL, at 32 weeks, N=111), which was significantly higher (p<0.001) than the low Hb group (N=95). Though blood pressure and renal function changes were similar between the groups, left ventricular diastolic dimension was significantly decreased only in the high Hb group (p < 0.001), and the change in left ventricular mass index (LVMI) correlated coarsely but significantly with the achieved Hb levels (r = 0.147, p = 0.032). The higher Hb levels were associated with greater reduction in LVMI and left ventricular wall thickness, and the lower Hb levels with the greater increase in human arterial- or brain natriuretic polypeptide levels., Conclusions: Anemia correction targeting modestly higher Hb levels better preserves cardiac function in CKD patients not on dialysis., (Copyright © 2013 Japanese College of Cardiology. Published by Elsevier Ltd. All rights reserved.)

A 15-year-old girl developed subacute constrictive pericarditis following successful surgical repair of double-chambered right ventricle. Two weeks after surgery, the patient had massive pericardial effusion, which acutely progressed to constrictive pericarditis with the symptoms of cardiac tamponade. Further surgery was necessary to resect the parietal pericardium. No blood transfusion was required for this patient, who was a Jehovah's Witness. She was doing well 9 months after the second operation, with residual pericardium of normal thickness.

Apical pulsed Doppler tissue imaging can be used to assess the function of regional myocardium. We hypothesized that septal dysfunction might be clarified in the hypertrophic cardiomyopathy (asymmetric septal hypertrophy) by this method. Twenty-one patients with asymmetric septal hypertrophy (mean age 54.8 +/- 11 years) and age-matched 24 normal subjects (52.4 +/- 8 years) were studied. The E/A ratio measured by mitral inflow Doppler was not different between the groups (1.1 vs 1.2). E wave velocities of the septum were significantly decreased in the hypertrophy group compared to the control group (4.0 +/- 1.5 vs 8.1 +/- 2.2 cm/sec), and A wave velocities were increased in the hypertrophic septum, resulting in a significantly lower E/A ratio (0.5 +/- 0.3) compared to the E/A ratio (0.9 +/- 0.3) of the normal septum. Deceleration time of the E wave and isovolumic relaxation time were significantly prolonged in the thick septum compared to the normal septum (136 +/- 51 vs 107 +/- 28 msec, 91 +/- 36 vs 63 +/- 19 msec, respectively). In conclusion, asymmetric septal hypertrophy was characterized by diastolic dysfunction of the thickened septum. Intramyocardial pulsed Doppler echocardiography can detect regional myocardial dysfunction earlier than the mitral inflow Doppler method.

A 66-year-old man presented with Ebstein's anomaly associated with left ventricular dysfunction. He had been followed since 40 years of age for cardiomegaly and arrhythmia, and experienced episodes of orthopnea at the age of 64. He was referred to our hospital in April 1997 because of lower extremity edema. Physical examination revealed dilated external jugular vein, tenderness of the right hypocondorium, and lower extremity edema. Electrocardiography confirmed atrial fibrillation. Transthoracic echocardiography revealed bilateral atrial and ventricular dilation, and paradoxical septal movement. The apical four-chamber view demonstrated 15 mm apical displacement of the septal leaflet. Color Doppler echocardiography revealed moderate tricuspid regurgitation. Transesophageal echocardiography revealed low echoic and hypoplastic tricuspid valve. Left ventriculography showed diffuse hypokinesis, and the ejection fraction was 49%. The coronary artery was normal. Atrial septal defect was not detected. Diffuse fibrosis, which may be found in the hearts of patients with Ebstein's anomaly at autopsy may have been responsible for the left ventricular depressed systolic function in this patient.

Doppler tissue imaging-guided pulsed Doppler echocardiography can record velocities of the regional ventricular wall, but the potential clinical applications have not yet been investigated. To propose a new modality for assessment of left ventricular wall dynamics, we investigated the longitudinal and latitudinal motions of the normal left ventricular wall with intramyocardial pulsed Doppler echocardiography under tissue imaging guidance, and characterized the velocity patterns in 31 normal subjects or normal volunteers (mean age 38 +/- 18 years old). Velocity patterns of the septal and posterior walls were recorded and compared using the parasternal and apical approaches. The apical approach showed that the entire left ventricle moved, coded in red, toward the transducer during systole, and moved away, coded in blue, during diastole. Pulsed Doppler echocardiography recorded the systolic S, early diastolic E and presystolic A waves from both windows. All three waves had higher velocities in the apical compared to the parasternal approach, and the velocities of S and E waves were increased more in the posterior wall than in the septum. Thus, the A/E ratio was significantly lower in the posterior compared to the septal wall (0.63 +/- 0.3 and 0.77 +/- 0.3, respectively, in the apical approach) and the A/E ratio of transmitral inflow was between those of the walls. Apical intramyocardial pulsed Doppler echocardiography can accurately evaluate septal and posterior wall dynamics. The present study provides important basic data for assessing regional myocardial function.

Cardiothoracic ratio has been a useful index of cardiac dilatation, and a value of 50% is generally considered to indicate the upper limit of normal cardiac size. However, this value is not always correct and increases the number of false-positive results, especially in obese or older subjects who may have a misdiagnosis of cardiac enlargement. The maximal transverse diameter of the cardiac shadow of chest X-ray film consists mainly of the diameters of the left ventricle and the right atrium as shown by X-ray computed tomography, but this ratio is influenced by many factors; not only left ventricular dilatation or hypertrophy, but also dilatation of the other cardiac chambers and the aorta, rotation and shift of the heart, respiratory phase, body posture, and measurement errors. In contrast, echocardiography is an accurate method for the diagnosis of cardiac dilatation. This study correlated left ventricular dimension with cardiothoracic ratio in 80 consecutive subjects with normal physical, ECG and Doppler echocardiography examinations. There was no relationship between left ventricular end-diastolic dimension and the cardiothoracic ratio. Chest X-ray is mandatory for initial cardiac examination. However, we must be careful about roentgenographic diagnosis of cardiac dilatation. Cardiac enlargement should be diagnosed by echocardiography, but follow-up and management can be based on chest X-ray films.

To assess the patency of coronary artery bypass grafts, we tested the capability of X-ray computed tomography (CT) with and without contrast enhancement. This procedure was used on 63 grafts (30 in the LAD; 20 in the LCX; 13 in the RCA) in 32 patients with a mean age of 56 +/- 8 years, all of whom were referred to our department for postoperative management or evaluation. The CT scanner used was Toshiba TCT-60A with a scan time of 3 sec, 5 mm thick slices, and 512 x 512 pixels. CT scans without contrast enhancement were obtained from the level of the aortic arch to the left ventricle. Eight sec after 30 ml of contrast media was injected at a rate of 3 ml/sec into an antecubital vein, 5 scans were made at the same level of the pulmonary artery truncus. After positioning the regions of interests on the ascending aorta and grafts, we obtained time-density curves (TDCs) and compared the data with those recorded from an intraoperative electromagnetic flow meter (EMF). Fifty grafts were angiographically patent. The appearance time, build-up time, peak time, disappearance time and peak densities obtained from TDCs of grafts did not correlate with the flow volumes measured by EMF. Patent grafts were easily identified visually, without contrast enhancement (sensitivity; 88%, specificity; 100%, accuracy; 91%). Occluded grafts were not imaged on CT, either with or without contrast enhancement. We concluded that the TDCs of grafts obtained by CT are of no value for predicting the graft flow, and that plain CT without contrast enhancement is sufficiently useful for assessing the patency of such grafts.

Twenty-five patients with main and peripheral pulmonary artery stenosis were studied to determine the most frequently observed diagnostic sign of this abnormality regardless of the underlying etiologies, such as intrinsic or extrinsic narrowing of the pulmonary artery due to tumor, fibromuscular dysplasia, thromboembolism, angitis including the aortitis syndrome (Takayasu arteritis) and a variety of other disease entities. Among a variety of signs and symptoms, we emphasized the importance of cardiac auscultation and phonocardiography, which were often the initial diagnostic clues. The diagnostic features included a systolic murmur of pulmonary arterial origin and the behavior of the splitting of the second heart sound. The systolic murmur was often trans-systolic or continuous. In cases with left-sided cardiac murmurs (Takayasu arteritis, etc), the pulmonary systolic murmurs were not identified by auscultation alone and required phonocardiographic confirmation. In many cases the second heart sound was split and this was sometimes the first clue to the diagnosis. The split intervals varied, but were more marked in cases with pulmonary hypertension, and were accompanied by the accentuated pulmonic component (IIP). Phonocardiographic analysis disclosed that wide splitting was caused by the delayed appearance of IIP as well as the concomitant early appearance of the aortic component (IIA). It was concluded that, although the final etiological diagnosis is not identified, auscultation and phonocardiography provide important clues for further diagnostic and etiological studies of pulmonary artery stenosis.

To evaluate the prevalence, causes and clinical significance of mitral valve prolapse (MVP) associated with surgically-closed atrial septal defect (ASD), 90 patients (M: 41, F: 49) were studied using two-dimensional and color-coded Doppler echocardiography. Among the 90 patients, preoperative echocardiograms were available in 27. MVP was found in 21 of the 27 patients (78%) preoperatively, but it was found in 59% (16/27) postoperatively. In total, MVP was detected in 50 of the 90 patients (56%) postoperatively. The postoperative MVP group had higher pulmonary-to-systemic flow ratios (3.6 +/- 1.9 vs 2.8 +/- 1.1, p less than 0.05) and higher mean pulmonary arterial pressures (21 +/- 11 vs 13 +/- 5 mmHg, p less than 0.01) at the time of surgery. Between the two groups with or without MVP postoperatively, there was no difference (p less than 0.05) in age at surgery, the postoperative duration and left ventricular (LV) deformity index both in pre- and postoperative states. A mitral regurgitant (MR) murmur was recorded in seven patients postoperatively. However, only two had clinically severe MR. It was concluded that MVP is frequently detected in patients with closure of ASD and it is related neither to degree of the LV deformity nor to age at operation; rather, it is related to the severity of the preoperative hemodynamic state. Clinically significant MR is rare in the postoperative period.

Left ventricular short-axis images were obtained by ECG-gated magnetic resonance imaging (MRI) in nine patients with hypertrophic cardiomyopathy and seven patients with chest pain, all of whom had diagnostic cardiac catheterization including angiography. The accuracy and usefulness of the short-axis image in MRI for measuring wall thickness and dimension and for calculating ejection fraction were evaluated. All patients were examined on an examination couch in the right anterior oblique position in optimal positions to obtain the left ventricular long-axis images in the Z-X plane (conventional coronal plane). Next, the paraxial mode was used to obtain the short-axis images by rotating the Y-Z plane (conventional sagittal plane) around the Y axis. The intervals between the trigger on the middle point of the upstroke of the R wave and the 90 degree pulse of saturation recovery spin echo sequence were 40 msec and 340 msec with a 34 msec echo delay time for the end-diastolic and end-systolic images, respectively. Short-axis images in MRI in end-diastole were utilized to measure wall thickness and dimension in patients with hypertrophic cardiomyopathy and the measurements obtained were compared with those of echocardiography. As for calculating ejection fraction in patients with chest pain, the length of the left ventricular long axis (L) was measured using the MRI long-axis image. The intraventricular sectional area at four levels (S1, S2, S3, S4) were measured using the MRI short-axis image in end-diastole and in end-systole. Left ventricular end-diastolic and end-systolic volumes were calculated using the following formula: V = 1/2 X (L -4.5) X S1 + 1.5 X (S1 + S2 + S3) + 1/3 X 1/2 X (L -4.5) X S4. Ejection fraction by MRI was compared with that by cardiac catheterization (single plane, area-length method). The measurements of wall thickness and dimension by MRI correlated well with those by echocardiography (r = 0.97, p less than 0.01). Ejection fraction calculated by MRI correlated significantly with that by cardiac catheterization (r = 0.82, p less than 0.05). We concluded that the left ventricular short-axis image in MRI is satisfactorily accurate for measuring wall thickness and dimension, and useful for evaluating the left ventricular ejection fraction.

The prevalence of Still's murmur was examined by phonocardiographic study, and the clinical significance of this murmur was investigated using pharmacodynamic phonocardiography and echocardiography. Still's murmur was present in 224 of 9,478 cases (2.4%) in school children. Its prevalence was 143 in 4,524 (3.2%) in elementary school children and this was significantly greater than that in middle school youngsters who numbered 81 among 4,954 (1.6%) (p less than 0.001). There were neither abnormal findings on two-dimensional echocardiography, nor pathological regurgitant signals on pulsed Doppler examination. After the inhalation of amyl nitrite, Still's murmur was accentuated by 5.3 +/- 3.0 dB, and was louder in the expiratory than in the inspiratory phase by 4.7 +/- 3.5 dB.

Our previous study of mitral regurgitation in obstructive hypertrophic cardiomyopathy suggested that left ventricular outflow obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet may hydrodynamically induce mid-systolic mitral regurgitation. To test this hypothesis, we examined whether drug-induced left ventricular outflow obstruction in dogs might cause mitral regurgitation. Dobutamine, 20-60 micrograms/kg/min, induced the obstruction due to mitral systolic anterior motion with mitral-septal contact in 11 of 18 dogs. Pulsed Doppler and contrast echocardiography demonstrated that mitral regurgitation was concomitantly induced in the 11 dogs. The regurgitation was prominent during mid-systole from the onset to the end of mitral-septal contact. Two-dimensional echocardiography showed reduction of the mitral annular dimension and anterior shifts of the mitral valve coaptation during drug infusion in the 11 dogs. Accordingly, the distal portion of the mitral valve, especially of its anterior leaflet, became residual, and moved anteriorly in early systole and protruded into the outflow tract during mid-systole. Catheter-tip pressure recordings simultaneous with two-dimensional echocardiographic observation revealed that the outflow pressure gradient occurred across the protruding distal residual mitral valve. The onset and the end of the pressure gradient were nearly simultaneous with those of the mitral-septal contact. After cessation of the infusion, the mid-systolic mitral regurgitation disappeared together with the obstruction. These results indicate a close relationship between left ventricular outflow obstruction and mid-systolic mitral regurgitation, and strongly support the hypothesis that the obstruction due to systolic anterior motion of the distal residual anterior mitral leaflet is responsible for mitral regurgitation.

To assess the prevalence of mitral valve prolapse (MVP) in patients with premature ventricular contractions (PVCs), 109 patients with PVCs (M: 69, F: 40, 42 +/- 20 years; mean +/- SD) and 50 control subjects (M: 38, F: 12, 47 +/- 10 years) were studied by echocardiography. MVP was diagnosed by two-dimensional echocardiography. The criterion for mitral valve prolapse by two-dimensional echocardiography is extension of the mitral leaflet to the left atrial side beyond the plane of the mitral annulus. In addition, 60 patients with PVCs were examined by 24-hour Holter ECG and scored by the Lown's classification. Results were as follows: 1) MVP was detected more frequently in patients with PVCs than in the control subjects (22/109, 20% vs 3/50, 6%, p less than 0.05) by echocardiography. 2) PVC patients with MVP were significantly younger than patients without MVP (34 +/- 14 vs 47 +/- 21 yrs, p less than 0.05), but there were no significant differences between these two groups as to sex, left atrial diameter and left ventricular dimension. 3) The 24-hour Holter ECG revealed that the high grade PVCs (Lown grade III & IV) was more closely related to the absence of MVP (20/45, 44% vs 4/11, 36%), though this trend did not reach statistical significance. It was suggested that MVP is not a major determinant of PVC, and life-threatening arrhythmias are more likely related to cases without MVP.

Aortic regurgitation (AR) in patients with hypertrophic cardiomyopathy (HCM) has rarely been reported. Using color Doppler echocardiography, we assessed the incidence and the cause of AR in patients with HCM. There were 86 patients with HCM (M:F = 66: 20, 57 +/- 12 years, mean +/- SD) and 43 control subjects (M: F = 33: 10, 57 +/- 8 years). HCM was diagnosed by echocardiography; the thickness of the interventricular septum (IVS) was more than 15 mm and the ratio to the thickness of the left ventricular free wall (LVPW) was more than 1.3. The rate and degree of aortic regurgitation were observed by color Doppler echocardiography, and aortic regurgitant murmurs were recorded by phonocardiography. Echocardiographic measurements were made using standard techniques. In the M-mode echocardiograms, the aortic diameter, the thicknesses of the IVS and LVPW were measured. In the 2DE, calcification of the aortic valve and systolic anterior movement of the mitral valve (SAM) were evaluated. In the early systolic 2DE image, the distance from the point of the greatest bulging of the upper IVS to the aortic root (D1) and the distance from the point of the greatest bulging to the line which is parallel to the long axis of the aorta (D2) were measured. Results were as follows: 1. Color Doppler echocardiography revealed aortic regurgitation in 17 (21%) patients with HCM; whereas it was observed in only three (7%) of the control subjects. 2. The aortic regurgitant signals were limited to the left ventricular outflow tract both in patients with HCM and in the control subjects. 3. Aortic regurgitant murmurs were recorded in only two patients with HCM and in none of the control subjects. 4. There was no difference between the patients with and without AR as to age (59 vs 56 years), blood pressure (141/84 vs 136/80 mmHg), aortic diameter (34 vs 33 mm), aortic valve calcification (12% vs 9%) and SAM (53% vs 52%). 5. In the patients with HCM, D1 was shorter (9.9 vs 14 mm, p less than 0.001) and D2 was longer (16 vs 10 mm, p less than 0.001) in the patients with AR than in those without AR. That is, the basal septum of the patients with AR protruded more deeply into the outflow tract, and the distance to the aortic valve was significantly shorter than in those without AR.(ABSTRACT TRUNCATED AT 400 WORDS)