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We undertook a retrospective study of elderly patients with stage III non-small cell lung cancer who had been treated solely with radiotherapy during the period 1986 to 1995. Our study was designed to assess the influence of age on survival and malnutrition in patients aged 75 years or older (elderly group) and patients aged 74 years or younger (younger group). Radiotherapy alone resulted in a median survival period of 11.5 months in the younger group and 6.3 months in the elderly group (p = 0.0043). With the Cox multivariate model, good performance status, age less than 75 years, and good response were significant favorable independent predictors. Furthermore, the elderly group patients more frequently died of respiratory infections and had lower prognostic nutritional indexes than the younger group patients before and after radiotherapy. These findings suggested elderly patients with stage III non-small cell lung cancer who had been treated with radiotherapy alone had a poor prognosis and that malnutrition caused by radiotherapy was a factor contributing to the risk of death from respiratory infection in such patients.

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.

To improve the quality of life in patients with malignant diseases at the near-terminal stage, we established a system for home infusion therapy (HIT) in Osaka Prefectural Habikino Hospital in 1994. Thirty-three patients were taken care of at home using the HIT system from January, 1995 to May, 1996. Their average age was 70 years old. The duration of HIT varied from 1 to 105 days (mean:25.5 days). Twenty-four cases received parenteral nutrition. The others received agents for brain edema (4 cases), morphine hydrochloride (2 cases), and anti-fungal agents (3 case). Additionally, 63% of these patients required home oxygen therapy (HOT) with HIT. Questionnaires to their families revealed that they were afraid of the progress of the disease in patients and their physical burden became heavier after the start of HIT. However, they were quite satisfied with the results of HIT.

Patients with unresectable non small-cell lung cancer were treated to evaluate the toxicity and efficacy of high-dose thoracic irradiation (RT) combined with concurrent daily cisplatin plus vindesine. Fourteen evaluable patients with unresectable stage III non small-cell lung cancer treated with continuous-course RT (70 Gy in 35 fractions of 2 Gy once daily) and concurrent daily intravenous cisplatin (6 mg/m2) plus vindesine (3 mg/m2 on day 1 and day 8). The objective response rate was 86%, and two patients achieved a radiographic complete response. Leukocytopenia was the severe toxicity, but there were no episodes of discontinuation of treatment. Only one patient had grade 3 acute radiation esophagitis. Ten patients experienced late radiation pneumonitis and nine of those had grade 1 or grade 2. There was only one life-threatening case of toxicity (grade 5 pneumonitis). We concluded that the regimen of high-dose thoracic RT combined with concurrent daily cisplatin plus vindesine obtained a high response rate. Further testing on late toxicities and survival time is required.

A 68-year-old male presented with choroid plexus carcinoma in the left lateral ventricle manifesting as dysarthria and gait disturbance. Magnetic resonance imaging showed a homogeneously enhanced mass in the trigone of the left lateral ventricle. Selective left posterior cerebral arteriography showed the tumor was fed by the left medial posterior choroidal artery. Detailed examinations found no evidence of an extraneural primary focus. He underwent partial removal of the tumor followed by local Lineac irradiation (50 Gy). After irradiation, the serum level of carcinoembryonic antigen decreased and the size of the residual tumor was reduced.

Six cases of severe epistaxis were treated with the super-selective intraarterial embolization of the internal maxillary artery. Tens of fragments of Gelfoam were delivered into the distal internal maxillary artery and, additionally, embolized by several pieces of the coils. In a case with cerebral infraction, catheter was inserted via the superficial temporal artery. There were no complications due to these procedures in all cases of this study. It is considered that therapeutic intraarterial embolization of the internal maxillary artery is an effective therapy for severe epistaxis and the superficial temporal artery approach is useful for selected cases.

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.

Successful removal of a cardiac fibroma of the left ventricular free wall in a 76-year-old male is reported. The rarity of this tumor in the elderly and diagnostic clues are discussed.

Left ventricular hypertrophy is caused by a wide variety of cardiovascular conditions, including systemic hypertension, aortic valvular disease, and hypertrophic cardiomyopathy. This paper describes a case of diffuse hypoplasia of the aorta in left ventricular hypertrophy. This condition has not previously been well documented. We emphasize the need for evaluation of aortic dimension when systolic hypertension and vascular bruits are observed in association with myocardial hypertrophy.

To clarify the clinical significance of a small heart; i.e., a small cardiac silhouette on chest radiography, an echocardiographic study was performed. Sixty persons with small heart according to cardiothoracic ratios less than or equal to 40%, and 23 age- and sex-matched normal controls (42% less than cardiothoracic ratio less than or equal to 50%) received two-dimensional and M-mode echocardiography. The body weights and body surface areas (BSA) in the small heart group were significantly less than those in the control group. On the lateral chest radiographs, numerous cases with small heart had straight spines and chests with decreased anteroposterior diameters. More than half of the small heart group had a variety of cardiovascular complaints, including chest pain, palpitation, dyspnea, and dizziness. Echocardiographic measurements were performed and hemodynamic indices were calculated. The results were as follows: Left ventricular dimension at end-diastole (LVDd), left ventricular dimension at end-systole (LVDs), left atrial dimension (LAD), and left ventricular mass (LV mass) of the small heart group were significantly less than those of the control group. There were, however, no differences in the values corrected by BSA (LVDd/BSA, LVDs/BSA, LAD/BSA and LV mass/BSA) between the two groups. We found no differences in hemodynamic indices (heart rate, stroke volume, ejection fraction, and cardiac output) at rest between the small heart and control groups. Nineteen cases (32%) had mitral valve prolapse (MVP) on echocardiography in the small heart group. Characteristic phonocardiographic findings were found in 11 cases with MVP (systolic click in four, mitral regurgitant murmur in three, and both in four).(ABSTRACT TRUNCATED AT 250 WORDS)

In view of the fact that stable echocardiograms are easily obtained during atrial pacing, pacing echocardiography was performed to evaluate the usefulness for detecting regional wall motion abnormalities during pacing-induced ischemia and to investigate the relationship between changes in the R wave and left ventricular dimension. The patients were 12 cases of angina pectoris (10 of coronary artery disease; CAD, and 2 of coronary patent aortic valvular disease; AVD) and 6 control cases. Simultaneous recording of two-dimensional and M-mode echocardiograms and electrocardiograms was done before, during and after the atrial pacing at increasing heart rate until angina appeared or the heart rate of at least 140/min was reached. In 12 angina cases, angina and ST depression were induced in 10 and 11, respectively. Excursion of the interventricular septum (IVS) decreased during pacing-induced ischemia in 6 of 7 CAD cases, in which the left anterior descending coronary artery was significantly stenosed (more than 75%). Excursion of the left ventricular posterior wall (LVPW) decreased during pacing-induced ischemia in 4 of 7 CAD cases, in which the vessels giving rise to posterior descending coronary artery were significantly stenosed (more than 75%). In 2 AVD cases, excursion of both IVS and LVPW decreased during ischemia. Left ventricular end-diastolic dimension (LVEDD) increased in only 2 angina cases, although R wave amplitude increased in 6 angina cases.

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.

Summary This paper reports 10 years experience of 31 patients with asymmetric apical hypertrophy, in whom left ventricular hypertrophy involved the apex exclusively and giant T wave inversion in the left precordial leads was the characteristic finding. This type of hypertrophic cardiomyopathy was observed predominantly in men over 40 years of age. Family history was negative and patients usually had no complaints. Left ventricular hypertrophy was evident by physical examination as in other forms of hypertrophic cardiomyopathy, but a systolic murmur was faint or absent and the second heart sound was frequently split. Electrocardiographic signs may fluctuate, and occasionally progression or regression occurs. Echocardiography including the two-dimensional method was essential for the diagnosis and left ventriculography was helpful for confirmation. To date complications have been infrequent and the prognosis seems good. The relation of asymmetric apical hypertrophy to other forms of hypertrophic cardiomyopathy is under investigation.

To investigate whether coronary artery disease is detected noninvasively, we correlated calcification on computed tomography (CT) with coronary angiographic (CAG) findings in 90 consecutive patients including 48 with angina pectoris or myocardial infarction. The mean age was 52.2 years and 83% were men. CT scans without contrast enhancement (3 sec scan time) were obtained at 1 cm thickness from the ascending aorta to cardiac apex to identify calcification in coronary arteries. Results; CAG revealed of 50 patients, and stenosis was present more often at calcified vessels on CT. (table; see text) Calcification occurred more often in 2 or 3 vessel disease. However, stenotic segments were not always calcified. We conclude that CT is sensitive for the detection of calcification and an important method for the diagnosis of coronary artery disease.

The records of 2,000 consecutive patients who had been examined by auscultation, phonocardiography (PCG), two-dimensional echocardiography and pulsed Doppler echocardiography (PDE) were reviewed to assess the clinical significance of apical systolic murmurs which cease well before the aortic closure sound. Fifty-five patients were verified to have early or mid-systolic apical murmurs. Mitral regurgitation (MR) was detected in 32 patients by PDE (29/32) and/or PCG with methoxamine test (27/32). The degree of MR was judged to be mild by PDE in all cases. Apical systolic murmurs due to MR began mainly with the first heart sound (27/32), were confined to the apex (27/32), and high-pitched (25/32). Their intensity was grade III/VI or less in all cases. Mitral valve prolapse (12 patients) was the most common cause of MR. Other causes were rheumatic mitral involvement in seven patients, dilated or ischemic cardiomyopathy in five, mitral annular calcification in three, and hypertrophic cardiomyopathy in two. The causes of the MR in the remaining three patients could not be identified. Thus, early or mid-systolic apical murmurs are mainly attributable to mild MR which can be diagnosed by careful auscultation, PDE and/or PCG with the methoxamine test.

A case was reported in which generalized lentigo was associated with hypertrophic cardiomyopathy and right ventricular outflow tract obstruction. A 34-year-old man was admitted to our hospital for cardiac evaluation. He had been noted to have a heart murmur since his childhood and had had a diagnosis of pulmonary stenosis in his high school age. Physical examination revealed precordial murmurs and numerous lentigines over his whole body surface including palms and soles. Two-dimensional and M-mode echocardiography disclosed asymmetric septal hypertrophy, systolic anterior motion of the mitral valve (SAM) and systolic semiclosure of both semilunar valves. A systolic turbulent flow was recorded at the outflow tracts of both ventricles by pulsed Doppler technique. Cardiac catheterization demonstrated a pressure gradient of 13 mmHg across the right ventricular outflow tract. We considered that the present case was an atypical LEOPARD syndrome with predominant right ventricular outflow tract obstruction which was precisely evaluated by noninvasive techniques.

The high-frequency vibrations of the first heart sound (S1) have been reported to be associated with the closure of atrioventricular valves. However, the genesis of the low-frequency component (LFC) preceding S1 remains controversial. In order to investigate the genesis of the production of this LFC, we recorded phonocardiograms simultaneously with M-mode echocardiograms in 10 healthy subjects and 26 patients with various diseases including mitral valve replacement. The apical phonocardiograms were recorded using a 100 Hz/12 dB high-pass filter and a commercially available acceleration microphone. Patients with rheumatic mitral valve disease and bundle branch block were excluded from this study. The electrocardiograms demonstrated sinus rhythm in 23, atrial fibrillation in nine, complete atrioventricular block in two and atrial flutter in two. The P-R interval in sinus rhythm ranged from 130 to 200 msec. The LFC occurred an average of 24 msec after the QRS complex, but 38 msec before the first high-frequency component of S1. The final fast closing movement of the mitral valve echogram started following the onset of LFC in sinus rhythm or the arrhythmias. Coaptation of the mitral valve leaflets was coincident with the first high-frequency S1. In 23 cases with the visible tricuspid valve, the valve closure occurred 28 msec after that of the mitral valve. The onset of the LFC was almost synchronous in timing with, or very close (10 msec or less) to the initial upstroke of apex cardiograms simultaneously recorded in 10 cases. The amplitude of the LFC was constantly smaller than that of S1 in all cases, but it was variable in atrial fibrillation or complete atrioventricular block. The LFC became loudest after a short RR interval and then ventricular systole was coincided in time with the rapid filling of the left ventricle, or when atrial systole was very close in time to an expected time of ventricular systole. It is certain that antegrade mitral blood flow was decelerated at that time, though the mitral valve was in the rapidly closing process. We conclude that the LFC is produced by the vibration of cardiohemic system, or the acceleration of the left ventricular mass plus the deceleration of blood flow, and that atrial activity and atrioventricular valve tension are not prerequisite to the production of this soft apical vibration preceding S1.

To determine the usefulness of pulsed Doppler echocardiography (PDE) in diagnosing aortic regurgitation (AR), the following two studies were performed. PDE and phonocardiography (PCG) were evaluated for the diagnosis of AR in 36 patients for whom angiography was performed. In 24 patients with grade 2 to 4 by Sellers' classification, all PDE studies were positive for AR (sensitivity of 100%) and PCG studies were positive in 21 patients (sensitivity of 88%). Among 10 patients of grade 1, PDE studies were positive for eight (sensitivity of 80%) and PCG studies were positive for seven (sensitivity of 70%). Angiography was negative for AR in two PCG-proven cases, and PDE also proved AR in one of these. Thus, in all patients, the sensitivity of PDE and PCG were 94 and 82%, respectively. These results indicate that AR may be missed during auscultation, or even when using the latest type PCG. The ability of detecting silent AR was studied in 160 consecutive patients with AR. PDE was positive for AR in 156 of 160 consecutive patients who were diagnosed as having AR by PDE or PCG. In the remaining four patients, three were diagnosed by PCG alone and one by pharmacodynamic phonocardiography using methoxamine (ME-PCG). On the other hand, in 137 of 160, Ar was proven by PCG, and the remaining 23 were so-called "silent AR". ME-PCG was performed for 11 cases of silent AR, but an unequivocal AR murmur was detected in only five. Therefore, the sensitivity of PDE in diagnosing silent AR was 96 percent, while that of ME-PCG was only 45 percent. Thus, compared to PCG and even pharmacodynamic PCG, PDE is a much more sensitive method of diagnosing AR. However, in mild AR cases, angiography, PDE and PCG, all have some limitations in diagnosing AR.

Cardiac involvement of mucopolysaccharidosis has not been well characterized by echocardiography. In this paper, we reported a case of Hunter syndrome with special reference to the noninvasive diagnosis of cardiac anomalies. A 21-year-old male of Hunter syndrome was referred to our noninvasive laboratory for the evaluation of his heart murmurs. He was strikingly dwarfed, 115 cm in height and 28 kg in weight, and had apparently Gargoyle-like facial appearance. Physical examination disclosed a mild funnel chest and a loud systolic murmur. Blood pressure was 98/56 mmHg and regular pulse rate was 100/min. The chest X-ray film revealed a shift of the heart to the left with a prominent pulmonary artery segment. There were no signs of pulmonary congestion. The electrocardiogram demonstrated right axis deviation, clockwise rotation and left atrial overload. In phonocardiograms, a basal ejection and an apical scratchy systolic murmurs were recorded. The latter was associated with a presystolic murmur and a loud first heart sound. A loud pulmonary second heart sound was also present. Outstanding findings were observed in the two-dimensional and M-mode echocardiograms, which showed remarkable thickening of both mitral valve leaflets with reduced opening. There was also generalized thickening of tricuspid and aortic valves, and endocardium of the free ventricular wall. Two leaflets of the tricuspid valve were visualized to prolapse, but the aortic valve motion appeared intact. In addition, echocardiograms revealed the dilatation of right-sided cardiac chambers and pulmonary artery, but the size of the left ventricle was rather small. Pulsed Doppler echocardiography demonstrated systolic turbulence in the right atrium in the vicinity of the tricuspid valve orifice. Stenotic turbulence was also recorded in the inflow tract of the left ventricle during diastole. Thus, the final diagnosis of predominant mitral stenosis associated with tricuspid valve prolapse and pulmonary hypertension was obtained. In conclusion, cardiac involvements in Hunter syndrome were precisely evaluated by noninvasive methods. Hunter syndrome may be considered as one of the etiologies producing mitral stenosis.

A case of a leiomyosarcoma of the duodenum is reported. A 52-year-old man with a duodenal submucosal tumor underwent a pancreatico-duodenectomy. Histologically, the resected tumor revealed moderate cellular atypism and moderate pleomorphism, but revealed no mitotic figures. The histological diagnosis was leiomyoma. Nine years after operation, the tumor showed a recurrence and metastasis in the liver. Thus, the patient underwent a lobectomy of the liver. The resected liver tumor showed similar histological features seen in the primary duodenal tumor but with high mitotic activity. Histologically, the patient was diagnosed as having a metastatic leiomyosarcoma. This history suggests that a smooth muscle tumor of potential malignancy, as seen in this case, should be followed continuously, even though mitoses may not be recognized.

To investigate the potential of a new method for detecting coronary sinus (CS), two-dimensional (2-D) echocardiography was satisfactorily performed on 80 consecutive cases, of which the coronary sinus was detected in 74 by adopting parasternal three-chamber approach. These 74 cases were classified into four groups; 25 normal individuals, 7 patients with atrial septal defect (ASD) but without tricuspid insufficiency (TI), 13 with TI and 29 with other cardiac diseases. We measured diastolic maximum diameter of CS on 2-D echocardiograms. The mean diameter of the CS was significantly increased in ASD (9.0 mm) and TI (12.4 mm) comparing with normal control (6.7 mm). The enlargement of CS seemed to correlate with right-sided volume overload. Although there were three exceptional cases, we could observe the CS during the whole cardiac cycle only in patients with TI. We conclude that CS is excellently detected in over 90% of cases by a new parasternal approach and that the diameter of CS would be a new screening index of right-sided volume overload.

Mucocutaneous lymph node syndrome (MCLS) in the young has been known to have coronary aneurysms, and then it has been recently suspected as a cause of premature atherosclerosis and cardiomyopathy. Thirty-three schoolchildren who suffered from MCLS were studied to evaluate cardiac involvements and left ventricular function using two-dimensional (2-D) echocardiograms and submaximal stress test. Fifteen normal schoolchildren were studied as normal control. All these MCLS children were asymptomatic and had no significant findings in routine chest X-ray and electrocardiographic examinations. According to submaximal stress test, 8 cases showed a J type ST depression of only 0.5--1.0 mm, and there were no positive cases. Using 2-D echocardiograms, the left coronary artery was detected in 85% and the right coronary in 27%. One case showed an aneurysm of the left coronary artery. However, none of them showed abnormal left ventricular wall motion or the wall motion abnormality compatible with cardiomyopathy. There were no significant differences between MCLS and normal control in ejection fraction, mean VCF, diastolic descent rate of the anterior mitral valve, D/S ratio of the left ventricular wall, and Weissler's index (PEP/ET). These findings suggested that 1) most of MCLS schoolchildren do not have obvious cardiac involvement and their left ventricular function is within normal limits, 2) because of its low sensitivity, submaximal stress test is not so useful in screening coronary lesions, and 3) the 2-D echocardiogram works not only in detecting coronary aneurysms but also in evaluating left ventricular function.

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 IIIIV) 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.

Musical murmurs are probably related to the vibrations of some structures in the cardiovascular system, and this may be reflected in the characteristic stripes which are recorded by the fast Fourier transformation (FFT) of the pulsed Doppler echocardiography (so-called FFT stripe). In the present study, we demonstrated new stripes by color Doppler echocardiography, which were composed of multiple warm and cold color bands which we termed color Doppler stripes (CD stripe). An experiment was performed to obtain Doppler signals from the surface of a vibrating tonometer at a frequency of 128 Hz. When the CD stripe was obtained, a similar FFT stripe was also recorded from the same sampling site. Fourteen patients with musical murmurs were selected from 2,000 consecutive phonocardiographic records made during the last one and a half years. The CD stripe was obtained in three and the FFT stripe in six. When both stripes were obtained, the FFT stripe was always obtained if we set carefully the sample site in the CD stripe, and these two were consistent in timing. We concluded that, in view of the close correlation between the CD stripe and the FFT stripe, the newly observed CD stripe is also a characteristic finding reflecting a regularly vibrating structure. The technical feasibility of color Doppler echocardiography to detect fine movements of structures may be helpful in the study of musical murmurs.

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)

M-mode and two-dimensional echocardiography were performed to investigate the motion of the interventricular septum (IVS) and posterior wall (PW) in cases with pure mitral (MI) or aortic (AI) insufficiency. Subjects were classified into four groups; 15 cases with chorda rupture or floppy mitral valve (acute MI), four with AI of acute onset (acute AI), 17 with chronic MI including rheumatic MI, mitral valve prolapse syndrome, and 11 with chronic AI. There wee no differences of left ventricular dimension (LVDI), stroke volume (SV), ejection fraction (EF) and cardiac output (CI) between acute and chronic MI, and between acute and chronic AI, although LVDI and CI were increased in all groups. The ratio of the amplitude of IVS to PW excursion was significantly increased in cases with LV dilation due to acute MI or AI, compared with that in chronic MI or AI. This ratio had a linear relationship with LVDI in acute volume overload, but in chronic volume overload, it was constantly 1.0 or less. The mechanism of the increased septal motion in acute MI or AI is still unknown, but it appears to reflect the intact and contractile septum which adapts to volume overload more readily than the posterior wall. It is probably because the posterior wall is prevented from distension by the pericardium. On the other hand, in chronic MI or AI, vigorous septal motion would not be observed because of the occasional presence of relative tricuspid insufficiency, the effects of the long standing burden on the septal myocardium, and compensatory distension of the posterior wall and pericardium.

Two-dimensional echocardiographic studies were performed for 22 patients with asymmetric septal hypertrophy and systolic anterior motion (SAM) of the mitral valve to clarify the mechanism of SAM and left ventricular outflow obstruction. The long-axis view of the left ventricle showed that a distal portion of the anterior mitral leaflet became surplus when the mitral valve was closed in 15 of 16 patients with SAM-septal contact and in four of six patients without it. In these patients, the mitral leaflet coaptation was displaced anteriorly, and/or the anterior leaflet was elongated, showing an anterior motion. In an unusual patient with SAM-septal contact, a distal portion of the long posterior mitral leaflet was surplus. The remaining two patients without SAM-septal contact had a rather widely coapted portion of the mitral leaflets. The distal surplus portion and the coapted portion of the mitral valve were displaced anteriorly prior to the onset of ejection, and moved forward and protruded into the outflow tract more rapidly and more excessively than the papillary muscles during early to mid systole in all patients. Then, the distal mitral valve and the chordae tendineae adopted the configuration of an inverted V in mid systole. The tip of the surplus leaflet contacted the interventricular septum in patients with SAM-septal contacts. In the short-axis view of the left ventricle, the central portion of the distal mitral valve moved forward excessively and bent like an inverted U during early to mid systole. Therefore, SAM of the distal mitral valve is thought to be caused by the hydrodynamic force generated by the ejection flow. This force is supposed to be not only due to the Venturi effect, but is more properly understood as a "pushing force". Left ventricular outflow obstruction is considered to be formed by the protruding distal mitral valve and the hypertrophied septum.

This investigation was performed to determine the presence of unilateral or bilateral pulsus alternans in the systemic and pulmonary circulations in heart failure and to estimate the prevalence of pulsus alternans in congestive cardiomyopathy. The subjects were 36 adult patients in heart failure due to a variety of cardiopulmonary diseases. We measured left- and right-sided systolic time intervals from simultaneous dual echocardiograms of both semilunar valves. The alternans was left-sided in seven patients, right-sided in one patient and bilateral in six patients. Pulsus alternans was induced by ventricular premature complexes (VPCs), except in one patient with bilateral and persistent alternans. For a VPC to precipitate alternans, the early beat itself must be associated with an abbreviated ejection time. Echophonocardiographic records of 100 patients with congestive cardiomyopathy were reviewed for evidence of pulsus alternans. We found persistent alternans in 10 patients and VPC-induced alternans in seven patients. We could not measure any difference in severity of disease in patients with pulsus alternans compared with those without.

A family in which the five members including the identical twins had a mitral valve prolapse was described. None of these members had any known stigmata of Marfan syndrome and their auscultatory findings were different each other. M-mode echocardiograms disclosed a midsystolic buckling of the mitral valve in the identical twins, their parents and the mother's brother, but all were asymptomatic. Electrocardiograms revealed a wandering pacemaker in two members. The index case was a 13-year-old girl whose apical late systolic murmur was detected incidentally by the mass screening examination for cardiac diseases. Both the inhalation of amyl nitrite and injection of methoxamine induced the augmentation of this murmur and made it holosystolic. The identical twin of the index case had multiple apical non-ejection clicks. However, a mitral regurgitant murmur was not induced by pharmacological provocations. Two-dimensional echocardiograms revealed prolapse of both the anterior and posterior mitral valve leaflets in both of them. Their mother had a late systolic click and the mother's brother had a cardiopulmonary murmur. The abnormal auscultatory findings were not observed in their father. This familial study suggested the genetic background and the various clinical manifestations of mitral valve prolapse.

To investigate the clinical significance of mitral valve prolapse (MVP) in patients with atrial septal defect, we investigated 90 patients using various techniques including phonocardiography, mechanocardiography and echocardiography. The examinations were repeated pre- and post-operative periods, and the particular attention was paid on the behavior of the mitral valve motion after surgery. Post-operatively, the incidence of MVP was 56% (50 of 90 patients) compared with the preoperative incidence of 78%. Improvement of MVP was only 24%, and there was no case in which MVP newly developed after surgery. Clinical and laboratory data indicated that the cases with MVP after surgery had larger Qp/Qs, higher pulmonary pressures and larger right ventricular dimension pre-operatively, but had no relationship to the age of surgery and the deformity index of the left ventricle. MVP after surgery was not associated with significant mitral regurgitation.