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The clinical significance of reverse redistribution of technetium-99m sestamibi (MIBI) was investigated in 36 patients with acute myocardial infarction and angiographically confirmed single-vessel disease, but without previous infarction using resting MIBI myocardial single photon emission computed tomography (SPECT) and exercise-reinjection thallium-201 (Tl) myocardial SPECT. MIBI myocardial SPECT was performed 90 min and 300 min after injection of MIBI 370 MBq at rest. Four hours after exercise Tl imaging was completed, reinjection imaging was obtained. Wall motion abnormalities on left ventriculograms were analyzed at the onset of infarction and 1 month later. The severity scores on the MIBI early image, MIBI delayed image and Tl reinjection image were 98 +/- 18, 170 +/- 22 and 90 +/- 18, respectively. The reverse redistribution of MIBI was marked in acute infarction. A significant correlation of severity score was found between the MIBI early image and Tl reinjection image (r = 0.89). In 18 patients with significant stenosis of an infarct-related artery, there was a significant correlation between the degree of reverse redistribution and that of Tl redistribution (r = 0.826). A good correlation was found between the severity score on the MIBI early image and wall motion abnormality at 1 month after infarction (r = 0.816). There was a significant correlation between the degree of reverse redistribution and wall motion improvement (r = 0.782). Despite stenosis of the infarct-related artery, the wall motion abnormality was less in 22 patients with marked reverse redistribution (defect score on the MIBI delayed image was double that on the early image) than the other 14 patients. In conclusion, the MIBI early image may reflect myocardial viability and the reverse redistribution of MIBI was observed frequently in patients with acute myocardial infarction. Marked reverse redistribution was observed in patients with preserved left ventricular function. Because of the close correlation of reverse redistribution with Tl redistribution and wall motion improvement, reverse redistribution of MIBI is considered to occur in areas at risk for acute myocardial infarction.

Resting 99mTc sestamibi (MIBI) SPECT and exercise-reinjection thallium-201 (T1) SPECT were performed in fourteen patients with acute myocardial infarction (AMI). MIBI SPECT were obtained 90 min (MIBI-90) and 300 min (MIBI-300) after injection of 370 MBq of MIBI at rest. MIBI-90 and MIBI-300 were compared with exercise T1 imaging (T1-EX) and T1 reinjection imaging (REINJ). Each SPECT image was divided into 22 segments and myocardial uptake was scored visually. Abnormal perfusion defects were observed in 94 myocardial regions. Worsening of the score was observed in 79 segments (84%) on MIBI-300 compared with MIBI-90. Total MIBI-300 uptake score per person was significantly greater than that at MIBI-90 (14.8 +/- 8.6 vs. 7.7 +/- 7.9, p = 0.001). The concordance rate of defect score between MIBI-90 and REINJ was significantly higher than that between MIBI-300 and REINJ (55% vs. 17%, p = 0.001). In nine patients without recanalization of an infarct-related artery, perfusion defects were seen in 74 segments. The concordance rate of defect scores between MIBI-300 and T1-EX was significantly higher than that between MIBI-90 and T1-EX (45% vs. 16%, p = 0.001). In conclusion, rapid clearance of MIBI was observed frequently in patients with AMI. MIBI-90 and MIBI-300 may reflect myocardial viability and areas at risk for AMI, respectively.

Adenosine triphosphate (ATP) is an alternative to dipyridamole or adenosine in thallium-201 myocardial scintigraphy. However, the optimal dose of ATP has not been determined. A Doppler guide wire study showed the coronary flow velocity at a dose of 0.15 mg/kg of ATP was equal or higher than that at 0.14 mg/kg of adenosine or 0.56 mg/kg of dipyridamole. ATP was given intravenously to 67 patients with coronary artery disease at 0.15 mg/kg/min for 6 min. Thallium-201 was injected at 3 min, followed by immediate and delayed (3 hrs) tomographic imaging. There was no serious side effect during examination, although chest pain (26%), dyspnea (17%), and flushing (33%) were common. The sensitivity and specificity to detect coronary artery disease were 98 and 100%, respectively. The sensitivity to detect left anterior descending artery, left circumflex artery, and right coronary artery lesions was 94, 59 and 77%, respectively. ATP loading thallium-201 scintigraphy provides an accurate diagnosis of coronary artery disease. The optimal dose of ATP is 0.15 mg/kg/min for 6 min.

Diagnosis of sinus venosus atrial septal defect based on transthoracic color Doppler and two-dimensional echocardiography is often difficult. We recently experienced two cases of sinus venosus atrial septal defect which were correctly diagnosed using transesophageal color Doppler and two-dimensional echocardiography. Transthoracic color Doppler flow imaging did not demonstrate the atrial septal defect or the shunt flow across the defect in either case. Transesophageal two-dimensional echocardiography visualized a defect in the upper most portion of the interatrial septum in one case, and transesophageal color Doppler flow mapping detected a left-to-right shunt across the defect in both cases. Transesophageal color Doppler flow mapping also demonstrated the flow signal of the right upper pulmonary vein into the right atrium near its junction with the superior vena cava in each case. The diagnoses of sinus venosus atrial septal defect and combined partial anomalous pulmonary venous return were confirmed by surgery in both cases. Transesophageal color Doppler and two-dimensional echocardiography are very useful in diagnosing sinus venosus atrial septal defect and combined partial anomalous pulmonary venous return.

Factors indicating changes in mitral valve area after single-balloon percutaneous transvenous mitral commissurotomy (PTMC) were evaluated in 53 patients receiving PTMC by follow up for 3-48 months (mean 18 +/- 12 months) using serial transthoracic echocardiography to measure mitral valve area by planimetry. The echocardiographic scores of the mitral commissures and mitral valve, and other clinical variables were assessed. Mitral valve area showed an immediate increase from 1.1 +/- 0.3 to 1.8 +/- 0.3 cm2 (p0.01). There was a small but significant decrease in mitral valve area at follow-up to 1.6 +/- 0.4 cm2 (p0.01). Restenosis (a decrease in mitral valve area of more than 25% from immediately after PTMC to follow-up) occurred in nine patients (17%). There was no significant correlation between clinical or echocardiographic features and an increase in mitral valve area immediately after PTMC. The total echocardiographic score of the mitral commissures correlated with the decrease in mitral valve area at follow-up (r = 0.42, p = 0.002). Multiple regression analysis showed the total echocardiographic score of the mitral commissures was the best indicator of a decrease in mitral valve area at follow-up (p = 0.0059). Six of nine patients with restenosis had a commissure score of more than 3, while only five of 44 patients without restenosis had a commissure score of more than 3 (p0.01). Mitral valve area increases significantly immediately after PTMC, and decreases significantly at follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

To investigate the serum levels of myosin light chain 1 (MLC1) during the acute phase of myocardial infarction, the MLC1 and creatine kinase (CK) levels were measured in samples from 59 consecutive patients with acute myocardial infarction. The serum concentration of MLC1 increased rapidly, reaching an early peak in 22 of the 59 patients (the MLP + group). Fifteen patients showed rapid increases in MLC1 levels without an early peak (the MLP - group). Serum MLC1 levels remained within normal limits (the MLN group) 10 hours after the onset of symptoms in the remaining 22 patients (but in eight of these serum MLC1 levels were abnormal 16-39 hours after the onset of symptoms). Serum level curves of CK showed a single episode of acute myocardial infarction in all patients. The patterns of MLC1 levels correlated with the washout phenomenon of CK (p0.001) and the maximum MLC1 level (p0.05). The ratio of serum MLC1 level during the early phase to the maximum level (EMR) decreased in the order of groups MLP+, MLP-, MLN (0.54 +/- 0.28, 0.31 +/- 0.22, 0.13 +/- 0.09, respectively). The EMR was correlated with the washout phenomenon of CK (p0.001), but not with the maximum MLC1 level which might reflect the size of the infarction. The patterns of neither MLC1 nor EMR were correlated with the administration of urokinase or the patency of the infarct-related artery at the early phase (within 10 hours of onset).(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of percutaneous transvenous mitral commissurotomy (PTMC) and open mitral commissurotomy (OMC) were evaluated in 18 patients who underwent PTMC and 16 patients who underwent OMC, before and within one month of the procedure, using two-dimensional and color Doppler echocardiography. There was no significant difference between the two groups in the mitral valve area, the severity of mitral stenosis, or cardiac function before the procedure. The mitral valve area after PTMC as measured by two-dimensional echocardiography and continuous wave Doppler echocardiography increased from 1.07 +/- 0.24 cm2 to 2.01 +/- 0.42 cm2 (p0.001), and from 0.99 +/- 0.26 cm2 to 1.76 +/- 0.23 cm2 (p0.001), respectively. The mitral valve area after OMC measured by two-dimensional echocardiography and continuous wave Doppler echocardiography increased from 1.04 +/- 0.24 cm2 to 1.78 +/- 0.41 cm2 (p0.001), and from 0.95 +/- 0.32 cm2 to 1.62 +/- 0.46 cm2 (p0.001), respectively. The mitral valve areas after PTMC did not differ significantly from those after OMC by either method.

To assess left ventricular shape and contraction pattern under the condition of the narrowed mitral orifice, 41 patients with mitral stenosis were studied by cross-sectional and M-mode echocardiography. Abnormal left ventricular configuration and asynergy were observed in 23 patients (56%). The change in configuration persisted during the cardiac cycle and was mainly due to a straightening and abnormal motion of the interventricular septum. Furthermore, hypokinesis or akinesis of the posterior left ventricular wall contributed to the change of left ventricular shape. Consequently the left ventricular shape became from circular to half moon- or pear-like configuration. Of these 23 patients, 19 had a severe degree of subvalvular lesion, whereas such a lesion was noted in only 6 of the 18 patients with normal left ventricular shape and contraction pattern. It is considered that a rigid mitral complex immobilizes the posterior wall of the left ventricle in patients with mitral stenosis. In addition, tricuspid regurgitation, which was frequently observed in our patients, may play an important role in abnormal septal motion. This study showed that abnormal left ventricular shape and asynergy in the posterior wall are not rare in patients with mitral stenosis and are due to a rigid mitral complex and associated tricuspid regurgitation.

A patient with a double-chambered right ventricle and cor triatriatum dexter was presented. The non-invasive diagnosis of cor triatriatum dexter was stressed. A plate-like echo was imaged in the right atrium using two-dimensional echocardiography. It divided the atrium into two chambers. Contrast echocardiography revealed delayed filling of the lower portion of the atrium. Pulsed Doppler echocardiography demonstrated systolic turbulence in the lower portion of the atrium, indicating that the plate-like structure produced a stenosis in the right atrium. We conclude that non-invasive methods including contrast echocardiography and pulsed Doppler echocardiography, are effective in identifying stenoses in the right atrium.

The detection of regional myocardial dysfunction due to acute ischemic event has been limited almost entirely to experimental animal models. In human subjects, it has been limited to the observations during spontaneously-occurring or exercise-induced ischemic events. Recently, percutaneous transluminal coronary angioplasty (PTCA) provides an opportunity to study such dysfunction as the result of repeated interruptions of coronary blood flow. Echocardiograms and electrocardiograms were simultaneously recorded immediately before, during, and after 21 episodes of complete interruptions of coronary blood flow by PTCA in 11 patients. No patient had asynergy of the left ventricle either by two-dimensional echocardiography (2DE) or angiography. All patients had isolated single coronary artery stenosis including the left anterior descending artery in nine, left circumflex artery in one and right coronary artery in one. Recordings of M-mode and 2DE were successfully obtained in 10 patients. After balloon inflation, regional asynergy in the distribution of the instrumented coronary artery appeared in all 10 patients. Hypokinesis developed 9 +/- 3 (means +/- SD) sec after balloon inflation and progressed rapidly to akinesis or dyskinesis. At the same time, decreased systolic thickening of the left ventricular wall appeared in some patients in relation to the development of regional asynergy. However, systolic thinning of the left ventricular wall was not noted in all. The regional asynergy preceded ischemic electrocardiographic changes and had no relation to chest pain. Left ventricular wall motion began to normalize 12 +/- 3 sec after balloon deflation. Thereafter, transient hyperkinesis of the left ventricle developed. The first ischemic electrocardiographic change was a negative U wave which appeared 13 +/- 7 sec after coronary occlusion and remained 3 to 4 sec. Tall T waves were recorded at 28 +/- 12 sec and significant ST elevations developed 31 +/- 11 sec, after balloon inflation. These electrocardiographic changes invariably occurred only after the onset of wall motion abnormalities. Normalization of T waves was recognized at 17 +/- 16 sec and ST segment deviation were no longer present at 18 +/- 10 sec, after reperfusion. These electrocardiographic changes also preceded normalization of regional myocardial dysfunction. In conclusion, left ventricular wall motion abnormalities after coronary occlusion invariably precede the electrocardiographic changes, and begin to normalize after reperfusion prior to the electrocardiographic recovery.

Our criteria for the diagnosis of prolapsed mitral valve were proposed in this paper. With this abnormality, the principal alterations in the mitral valve consist of an abnormal systolic leaflet motion and mitral regurgitation with or without systolic clicks. Our criteria include: (1) auscultatory or phonocardiographic findings suggestive of mitral regurgitation or mitral complex abnormality, (2) a posterior displacement of the mitral valve throughout the latter half of systole by M-mode echocardiography, and (3) a systolic bulging or an apparent systolic ballooning of the mitral valve by two-dimensional echocardiography. A diagnosis of prolapsed mitral valve is justified in a given case if (1) plus one or two other findings are present. Several confusing M-mode and two-dimensional echocardiographic findings for the diagnosis of this condition are neglected in this criteria. We believe that the diagnosis of prolapsed mitral valve, as a rule, should depend on the presence of significant auscultatory or phonocardiographic finding which is a major manifestation of our criteria. However, our criteria seem to be inadequate for the diagnosis of a systolic ballooning of the mitral valve toward the left atrium which is frequently associated with atrial septal defect, since an apical systolic murmur is often absent. The mitral valve ballooning in atrial septal defect, however, is of functional origin, and should be differentiated from an organic prolapsed mitral valve. Thus, to be significant of prolapsed mitral valve, an apical auscultatory or phonocardiographic findings should be unequivocal.

It is well known that right ventriculography has unavoidable disadvantages as a method for diagnosing tricuspid regurgitation. In this study, inferior vena caval angiography (IVC angiography) was tested as a new method for quantitatively diagnosing tricuspid regurgitation. With this method, no catheter passes through the tricuspid valve, and only a small amount (10 ml) of contrast material injected into the upper portion of the inferior vena cava visualizes the entire right atrium, and tricuspid regurgitation is manifested by turbulence or a negative jet in the right atrium. With respect to the degree, tricuspid regurgitation was graded as absent (0), mild (1+), moderate (2+) and severe (3+) using the criteria shown in Fig. 1. Mild tricuspid regurgitation was diagnosed when systolic turbulence was observed in the right atrium and did not reach the right atrial wall. Moderate tricuspid regurgitation was diagnosed when systolic turbulence reached the right atrial wall. Severe tricuspid regurgitation was diagnosed when systolic turbulence entered the inferior vena cava. Sixty-four patients with valvular heart disease and four having coronary heart disease were studied using IVC angiography and pulsed Doppler echocardiography. Using Doppler, the severity of tricuspid regurgitation was determined according to the distribution of the regurgitant signal in the right atrium. The degree of tricuspid regurgitation by IVC angiography correlated well with that by Doppler. All patients with severe (3+) regurgitation and 15 of 22 patients with moderate (2+) regurgitation required surgery, but all with no (0) regurgitation and 12 of 14 with only mild (1+) regurgitation required no surgical correction of the tricuspid valve.(ABSTRACT TRUNCATED AT 250 WORDS)

This report describes a case of left ventricular pseudoaneurysm examined by phonocardiography, two-dimensional echocardiography, Doppler color flow mapping, continuous wave and conventional pulsed Doppler echocardiography. The patient had early systolic and early diastolic murmurs. The pseudoaneurysm sac and the site of left ventricular rupture were identified by two-dimensional echocardiography. The flow between the left ventricle and the pseudoaneurysm were imaged by Doppler color flow mapping. Two jets from the left ventricle were directed toward the aneurysm during systole, and from the aneurysm toward the left ventricle in early diastole. Continuous wave Doppler and high pulse repetition frequency Doppler echocardiography demonstrated the maximum flow velocity in systole to be 3 m/sec and in early diastole, 1.7 m/sec. Those flow patterns between the left ventricle and the pseudoaneurysm could have been closely related to the murmur. Doppler echocardiography thus proved useful for detecting specific flow patterns related to a left ventricular pseudoaneurysm.

Twenty-seven patients in cardiogenic shock or medically refractory left ventricular failure due to acute myocardial infarction were treated with intraaortic balloon counterpulsation. Twenty-one of them were treated with counterpulsation alone; the remaining six underwent surgery. Thirteen patients were benefited by counterpulsation alone. Three of the patients treated with counterpulsation and surgery survived and were discharged from the hospital. Thus, 16 of the 27 patients (59%) survived. Four patients in medically refractory left ventricular failure or shock due to acute myocarditis were treated with counterpulsation. All patients were weaned easily from circulatory assist and were discharged from the hospital. This study shows that intraaortic balloon counterpulsation is a very useful adjunct to currently existing medical measures for the treatment of cardiogenic shock or for medically refractory left ventricular failure in both myocardial infarction and myocarditis.

To assess the timing and duration of mitral regurgitation (MR) in patients with mitral valve prolapse (MVP), 20 subjects with mid-systolic click(s) and/or a late systolic murmur were studied using phonocardiography, two-dimensional echocardiography (2DE) and Doppler techniques including pulsed Doppler (PD), high pulse repetition frequency Doppler (HPRF), continuous wave Doppler (CW) and M-mode color Doppler (MD) methods and two-dimensional Doppler color flow mapping (2DD). The results were compared with those of 16 patients with a pansystolic murmur having late systolic accentuation. MVP with MR was observed in 15 of the 20 patients with mid-systolic clicks and/or a late systolic murmur and in all of the 16 patients with a pansystolic murmur. Using MD, MR signals were seen throughout systole and isovolumic relaxation period in all but one of these patients, and they were not related to the patterns of the systolic murmur. In only one, an MR signal was recorded just after the click. Five patients with a mid-systolic click lacked the findings of MVP, but two of them had MR signal only in early systole. Using PD and HPRF techniques, the timing and duration of MR signals in patients with mid-systolic clicks and/or a late systolic murmur were varied by changing the sites of the sample volume. Similarly, the timing and duration of MR signals in these patients were dependent on the ultrasonic beam direction by the CW method. In most patients with a pansystolic murmur having late systolic accentuation, however, MR signals throughout systole and the isovolumic relaxation period were demonstrated by each Doppler method. Therefore, PD, HPRF, and CW were not so efficiently sensitive or adequate techniques for investigating the timing and duration of MR, especially in patients with mid-systolic clicks and/or a late systolic murmur, who had mild or eccentric MR jets. In conclusion, 1) MR in MVP involves the entire systole and isovolumic relaxation period, 2) PD, HPRF and CW methods are not adequate for detecting mild or eccentric MR jets in patients with mid-systolic clicks and/or a late systolic murmur, and 3) MD is useful for the time analysis of MR in these patients.

To assess the frequency, characteristics and relation to systemic embolization of mobile left ventricular thrombi, 154 patients with myocardial infarction were studied by cross-sectional echocardiography. In 5 (3%) a mobile left ventricular thrombus was detected. The electrocardiograms of all these patients showed anterior wall myocardial infarction pattern. One had cerebral embolism and two died suddenly. The cause of sudden death was not known, but it may be related to the presence of mobile left ventricular thrombi. In the remaining 149 patients, only 3 (2%) had cerebral or peripheral embolism. Mobile left ventricular thrombi was shown as rotating abnormal echoes arising from the left ventricular wall (infarcted area) by cross-sectional echocardiography. The size of thrombus was variable in each case. We concluded that cross-sectional echocardiography was useful in detecting mobile left ventricular thrombi, and that mobile left ventricular thrombi may be related to cerebral or peripheral emboli secondary to myocardial infraction.

To assess the incidence of valvular regurgitation, 180 patients more than 40 years of age without cardiac symptoms were studied by pulsed Doppler echocardiography. The 180 patients were categorized by age as group 1, 40 to 49 years; group 2, 50 to 59 years; group 3, 60 to 69 years; group 4, 70 to 79 years; and group 5, more than 80 years of age. The incidence of valvular regurgitant flow signals increased significantly with age. Multivalvular regurgitation were often detected in groups 4 and 5. Furthermore, acoustically silent regurgitation at each valve was frequently noted (71 of 85 cases with valvular regurgitant flow signal: 84%). Mitral valve prolapse was diagnosed by two-dimensional echocardiography in 27 patients, but a mid-systolic click or pansystolic murmur with late-systolic accentuation was not noted. In conclusion, valvular regurgitations were common in the aged who lacked auscultatory findings.

Collapse of the right ventricle and right and left atria is observed in cardiac tamponade. To assess the diagnostic value of each collapse component in identifying cardiac tamponade, two-dimensional and M-mode echocardiograms were recorded simultaneously with the measurement of intrapericardial pressure in five patients as they underwent pericardiocentesis. Before pericardiocentesis, each patient had evidence of right ventricular and right atrial collapse. In addition, left atrial collapse was observed in four patients. During pericardiocentesis, left atrial collapse initially resolved accompanied by a drop in pressure in the pericardial sac. Continuous drainage of pericardial effusion resulted in significant symptomatic improvement and the cessation of paradoxical pulse at the point of resolution of right ventricular collapse. However, right atrial collapse persisted after resolution of right ventricular collapse, but it was absent when pericardiocentesis was completed. Injection of saline solution with heparin into the pericardial sac for cleansing initially caused right atrial collapse, while right ventricular collapse developed with the appearance of cardiac tamponade. In one patient, the simultaneous recording of right ventricular and intrapericardial pressures and two-dimensional echocardiograms demonstrated that right ventricular collapse occurred early in diastole, when intrapericardial pressure exceeded right ventricular pressure. In conclusion, right ventricular collapse is the most reliable sign of cardiac tamponade. Right atrial collapse occurs in the early stage of cardiac tamponade. Left atrial collapse appears very late in the course of hemodynamic deterioration due to cardiac tamponade.

To assess the usefulness of two-dimensional echocardiography (2DE) in diagnosing ventricular free wall rupture following acute myocardial infarction, we studied the 2DE findings and the clinical pictures of seven consecutive patients with ventricular free wall rupture confirmed at the time of surgery or autopsy. Three patients had acute rupture; four, subacute rupture. All patients apparently had circulatory collapse despite continuing electrical activity at the onset of cardiac rupture. Four patients with subacute rupture recovered. In all patients, mild pericardial effusion was imaged by 2DE; however, this was not characteristic for cardiac rupture. In the patients with acute rupture, active left ventricular contractions were not observed after each QRS complex of the electrocardiogram. However, weak mitral valve motion was recorded at the time of cardiopulmonary resuscitation. The interesting and constant finding in acute rupture was the right ventricular collapse observed throughout the cardiac cycle. Diastolic right ventricular collapse was consistently observed in patients with subacute rupture, immediately after recovery from cardiogenic shock. Subacute cardiac rupture is a potentially curable lesion, and the clinical features and quick 2DE confirmation of cardiac tamponade allowed immediate surgery which saved two of the four patients.

To assess the diagnostic performance of two-dimensional echocardiography in the diagnosis of dissecting aneurysm, 12 patients (7 women and 5 men with a mean age of 51 years) with clinically suspected dissecting aneurysm were investigated. The diagnosis was confirmed by angiography or operation or autopsy in all patients. Eight had a dissecting aneurysm and the remaining 4 had a saccular aneurysm. The intimal flap echo was observed in 7 of the 8 patients with dissecting aneurysm. The intimal flap motion in these patients showed a fluctuating motion. The site or spread of this echo corresponded well with the anatomical lesion. On the other hand, an intra-aortic abnormal linear echo was observed in three of the 4 patients with saccular aneurysm. However, this linear echo showed little motion. The sensitivity, specificity and predictive value of the intimal flap echo in association with its fluctuating motion in the diagnosis of dissecting aneurysm were all 100%, although the efficiency remained at 69%. It was concluded that the real-time two-dimensional echogram is useful in the diagnosis of acute dissecting aneurysm.

To investigate the normal configuration of the tricuspid valve and the normal size of the tricuspid valve ring, 17 normals, 20 patients with atrial septal defect, 4 patients with tricuspid valve prolapse, and 41 patients with various diseased conditions were studied by cross-sectional echocardiography. The tricuspid valve ring diameter in atrial septal defect was judged to be increased in comparison with that of normals. All the patients with tricuspid valve prolapse exhibited an excessive systolic ballooning of the leaflets toward the right atrium. However, a systolic ballooning of the leaflets alone was frequently observed in normals and many other conditions. Therefore, we conclude that cross-sectional echocardiography has some clinical limitations in the differential diagnosis between tricuspid valve prolapse and normals.

To evaluate the clinical value of various Doppler techniques in detecting valvular regurgitation, we compared the sensitivity, timing and duration of regurgitation, and the peak velocity of regurgitant signals among conventional pulsed Doppler, color Doppler, continuous wave Doppler and HPRF Doppler echocardiography. 1. Sensitivity of Doppler techniques in detecting mitral regurgitation: Among fifty patients with mitral regurgitation confirmed by left ventriculography, mitral regurgitation was detected in 48 (96%) using color Doppler and pulsed Doppler echocardiography; in 41 (82%) by HPRF Doppler; and in 37 (74%) by continuous wave Doppler echocardiography. In 103 consecutive normal volunteers, mitral regurgitant signals were detected in 46 (45%) by color Doppler, in 39 (38%) by pulsed Doppler, in 16 (16%) by HPRF Doppler, and in 8 (8%) by continuous wave Doppler echocardiography. 2. Timing and duration of regurgitant signals: To assess the timing and duration of regurgitant signals, 43 patients with regurgitant signals of short duration during systole or diastole were studied using M-mode color Doppler echocardiography. Using the latter method, regurgitant signals throughout systole and the isovolumic relaxation period could be demonstrated in all but four patients who had regurgitant signals of short duration during systole, but suggesting mitral or tricuspid regurgitation. In all patients with regurgitant signals of short duration during diastole, aortic or pulmonary regurgitant signals throughout diastole could be demonstrated with M-mode color Doppler echocardiography. Thus, this technique is superior to conventional pulsed Doppler echocardiography for detecting accurate timing and duration of valvular regurgitation. 3. Peak velocity of regurgitant flow: To compare the peak velocity of regurgitant flow by continuous wave Doppler and by HPRF Doppler echocardiography, 20 patients with mitral regurgitation and 22 patients with tricuspid regurgitation were examined using the both methods. In patients with severe mitral regurgitation, the peak velocity detected by HPRF Doppler echocardiography correlated well (r = 0.96) with that detected by continuous wave Doppler echocardiography. However, in patients with mild mitral regurgitation, the peak velocity detected by HPRF Doppler echocardiography was higher than that detected by continuous wave Doppler echocardiography. In patients with severe tricuspid regurgitation, the peak velocity had a close correlation (r = 0.99) with the both techniques. In patients with mild tricuspid regurgitation, the peak velocity was higher by HPRF than by continuous wave Doppler echocardiography. In conclusion, color or pulsed Doppler echocardiography should be used for detecting valvular regurgitation. M-mode color Doppler echocardiography is superior to conventional pulsed Doppler echocardiography for detecting timing and duration of valvular regurgitation.(ABSTRACT TRUNCATED AT 400 WORDS)

To assess a possible mechanism of abnormal interventricular septal motion following cardiac surgery, 16 patients were studied during cardiac surgery by M-mode and two-dimensional echocardiography. All 16 patients underwent open heart surgery using cardiopulmonary bypass. M-mode echocardiogram and short-axis views of the left ventricle by two-dimensional echocardiography were obtained before and after pericardiotomy, and before and after the closure of the pericardium. Interventricular septal motion did not change after pericardiotomy. Interventricular septal motion just after cardiac surgery was variable and dependent on each underlying condition. In all the 16 patients, interventricular septal motion became abnormal after the closure of pericardium. The abnormal septal motion persisted following the chest closure. We conclude that pericardial closure is responsible for post-operative abnormal septal motion.

A young female with aortitis syndrome (Takayasu's arteritis) and angina pectoris due to severe narrowing of the right and left coronary arterial ostia was presented. The thoracic and abdominal aorta and the distal coronary arteries were not involved. The exercise electrocardiogram and thallium-201 scanning were indicative of myocardial ischemia. Two-dimensional echocardiography did not disclose the stenosis of the ostia of the right and left coronary arteries. The final diagnosis was made by arteriography and coronary angiography. At the time of coronary arterial bypass graft operation, the ascending aorta in the vicinity of the coronary ostia was confirmed to be markedly thickened. Severe stenosis of the coronary ostia appeared to be due to proliferation of the aortic intima. Microscopic examination of the ascending thoracic aorta demonstrated lymphatic cell infiltrate and collagen fiber destruction in the adventitia and media. Angina pectoris may be the first symptom of the disease, when the coronary ostia are involved and the thoracic and abdominal aorta are not affected by arteritis. Both exercise electrocardiography and thallium-201 scanning prior to coronary angiography are recommended in evaluating this condition.

Sixty-eight patients with severe tricuspid regurgitation proven by right ventriculography were examined using pulsed and continuous wave Doppler echocardiography and color Doppler flow imaging. Among the 68 patients, there was no tricuspid regurgitant murmur in 16 (24%) in whom laminar regurgitant flow signals were demonstrated by pulsed Doppler echocardiography. The area in which laminar flow was detected ranged from 8 to 46 mm2 (mean 19.5 +/- 9.8 mm2). The peak velocities in patients without regurgitant murmurs as measured by continuous wave Doppler echocardiography ranged from 1.1 to 1.9 m/sec (mean: 1.61 +/- 0.21 m/sec). Laminar regurgitant flow signals were obtained in six; and turbulent regurgitant flow signals in 46 of 52 patients with tricuspid regurgitant murmurs, and their peak velocities ranged from 1.7 to 5.1 m/sec (2.80 +/- 0.78 m/sec). The peak velocities of the regurgitant flow signals in patients without tricuspid regurgitant murmurs were significantly lower than those in patients with regurgitant murmurs (p less than 0.01). In six patients with laminar regurgitant flow signals and regurgitant murmurs, the areas of laminar flow signals ranged from 3 to 12 mm2 (mean 7.0 +/- 3.5 mm2) and were smaller than those of patients without regurgitant murmurs (p less than 0.001). A characteristic candle flame pattern of regurgitant flow signals was observed in all patients without murmurs. Thus, the absence of a tricuspid regurgitant murmur results from laminar regurgitant flow signals of low velocity and this is characterized by a candle flame pattern using color Doppler flow imaging.

A 36-year-old male with left ventricular myxoma was presented. The patient had no significant cardiac symptoms except for premature ventricular contractions. The diagnosis was made by two-dimensional echocardiography and cineangiography. The both visualized a tumor of 1.5 cm in diameter which was mobile in the anterior portion of the left ventricle at the level of the chordae tendineae. The accuracy of these techniques was confirmed at the time of operation. In the diagnosis of this lesion, two-dimensional echocardiography was superior to angiography because the stalk connecting the tumor with the anterior left ventricular wall was well visualized. M-mode echocardiography visualized an abnormal echo behind the interventricular septum, but failed to demonstrate the shape, size, mobility and stalk of the tumor. The tumor was not visualized by computerized tomography and RI angiography. The importance of two-dimensional echocardiography was emphasized in the diagnosis of a left ventricular myxoma, even if it is small.

An unusual mid-diastolic musical murmur developed soon after cardiac catheterization of a 55-year-old man with mitral stenosis. His physical findings consisted of an accentuated first heart sound, an opening snap and a grade 3/6 mid-diastolic rumbling murmur. No early diastolic murmur was audible. However, soon after cardiac catheterization, a mid-diastolic "cooing" murmur at a frequency of 200 cycles/sec developed. This murmur resolved with the patient in the sitting position, or by leg raising. With Valsalva or Müller maneuvers this murmur was abolished transiently, and it disappeared on administering either amyl nitrite or methoxamine. Echocardiography revealed early diastolic vibrations in the aortic valve. Pulsed Doppler echocardiograms revealed harmonic signals of the aortic cusp at a fundamental frequency of 200 cycles/sec. These harmonic signals could be recorded only in mid-diastole. The frequency patterns of the murmur and the Doppler signals were identical; therefore, the murmur was judged to be produced by aortic valve vibrations. Furthermore, resonance of cardiac structures which accentuate the murmur might be related to the occurrence of this murmur. Pulsed Doppler echocardiography is helpful in identifying the site of origin of this musical murmur.

In a previous report, we showed that pericardium closure is responsible for post-operative abnormal septal motion. To elucidate this hypothesis, we performed additional clinical and experimental studies. Twenty-six patients were studied during cardiac surgery. We also studied five dogs during cardiopulmonary bypass using M-mode and two-dimensional echocardiography. M-mode echograms and short-axis views of the left ventricle were obtained before and after pericardiotomy, and before and after pericardium closure. In the clinical study, the patients were divided into three groups according to pre-operative septal motion: Group 1 included six patients with atrial septal defect showing paradoxical motion, Group 2 included thirteen patients with aortic or mitral regurgitation of hyperdynamic motion, and Group 3 consisted of seven patients with ventricular septal defects or mitral stenosis showing normal systolic motion. In Group 1, septal motion became normal after closure of atrial septal defect and then, became abnormal just after pericardium closure. Again in Group 2, septal motion became normal following surgical repair, but abnormal motion appeared immediately after pericardium closure. In Group 3, normal septal motion persisted until just prior to closure of the pericardium. Abnormal septal motion in all groups persisted following chest closure. In all dogs, paradoxical septal motion resulted from pericardium closure after cardio-pulmonary bypass. We conclude that both pericardium closure and cardio-pulmonary bypass are responsible for post-operative abnormal septal motion.

The analysis of systolic time intervals (STI) has provided an indirect method of assessing left ventricular performance in man (1–4). These intervals are conveniently derived from the simultaneous recording of the electrocardiogram, the indirect carotid pulse tracing, and the phonocardiogram. Noninvasive measurement of right ventricular STI, however, has not been possible because of the inability to define the onset of right ventricular ejection. Recently echocardiography has been used to determine right as well as left ventricular STI (5–7).

M-mode and cross-sectional echocardiograms of 3 cases with vegetative endocarditis in the right-sided heart were reported. The location of vegetative lesions was the tricuspid valve in one, the parietal band of the right ventricle and chordae tendinae in one, and the pulmonary artery wall in the remaining patient. Ruptured chordae tendinae were observed in the patient with tricuspid valve vegetation. M-mode echocardiography detected vegetative lesions in all patients. However, the precise size and location of these lesions, and a complication of the destructive process were not evaluated by M-mode echocardiography. On the other hand, cross-sectional echocardiography not only documented the presence but also assessed the morphologic characteristics of the lesions, since this technique provides spatial orientation concerning moving structures. Furthermore, ruptured chordae tendineae in the patient with tricuspid valve vegetation was correctly estimated. However, the lesions should be differentiated from other conditions including a localized calcified lesion, abscess and thrombus. In conclusion, cross-sectional echocardiography in combination with M-mode echocardiography is recommended in diagnosing vegetative lesions in the right-sided heart.

It is well known that a small amount of regurgitation occurs through Björk-Shiley valves. Obviously, this functional regurgitation is related to the construction of the Björk-Shiley valve, wherein the disc does not overlap the ring, but fits within its orifice, leaving a minimal space between the edge of the disc and the ring. The aim of this study was to evaluate the clinical significance of regurgitation in patients having Björk-Shiley valves in the aortic position by pulsed Doppler echocardiography. The study group consisted of 46 patients with normally functioning valves and five patients with malfunctioning valves. Valve dysfunction resulted from paravalvular regurgitation in three, and thrombosed valves in two (confirmed by surgery and angiography). Using pulsed Doppler echocardiography, aortic regurgitation was observed in 29 of the 46 normally functioning Björk-Shiley aortic valves. Among these, regurgitant flow signals were constantly located in the vicinity of the valve ring in the left ventricular outflow tract. Therefore, these regurgitant flow signals were considered to represent functional regurgitation of the Björk-Shiley valve. Aortography was performed for 11 of the 46 normally functioning Björk-Shiley valves, and there was minimal transvalvular regurgitation in all. In all of the five malfunctioning Björk-Shiley aortic valves, aortic regurgitant flow signals were detected by pulsed Doppler echocardiography, and the maximal distance of the regurgitant flow signals from the Björk-Shiley valve ring was more than 0.5 cm. However, it was difficult to differentiate transvalvular regurgitation from paravalvular regurgitation using pulsed Doppler technique alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Hepatic vein flow can be reliably measured because Doppler sampling volumes are easily oriented parallel with the course of the hepatic vein. In this study, the relationship between the Doppler signal in the hepatic vein and the external jugular vein pulse was evaluated, and the contribution of the Doppler echocardiography to the quantitative diagnosis of tricuspid regurgitation was also assessed. The subjects consisted of five healthy persons, four patients with lone atrial fibrillation, 27 patients who underwent cardiac surgery, and 34 patients with tricuspid regurgitation. The severity of the regurgitation was judged by right ventriculography and inferior caval angiography. The pattern of the Doppler hepatic vein flow mimicked that of the jugular phlebogram in each patient. The normal hepatic vein flow consisted of two forward flows toward the heart; one in systole; the other, in diastole, and one retrograde flow toward the liver during atrial contraction. In patients with lone atrial fibrillation, a systolic backward flow toward the liver or a decrease in the systolic forward flow was observed, though there was no tricuspid regurgitation. In patients who had cardiac surgery, a systolic backward flow toward the liver or a decrease in the systolic forward flow was usual. However, a prominent systolic backward flow toward the liver was observed in patients with severe tricuspid regurgitation, and a decreased systolic forward flow toward the heart was observed in patients with moderate tricuspid regurgitation in sinus rhythm. We concluded that Doppler measurement of hepatic vein flow does not contribute to the diagnosis of tricuspid regurgitation in the presence of atrial fibrillation or in postoperative conditions, but that it is useful in identifying severe tricuspid regurgitation.

The efficacy of two-dimensional echocardiography in diagnosing the localization of myocardial infarction (MI) was studied by comparing the echocardiographic and pathological findings of 28 patients having MI. The ventricular wall was divided into 18 segments including three segments of the right ventricular wall. The regional wall motion abnormalities for each of the 504 segments were diagnosed by visual assessment. The echocardiographic recordings were reviewed individually by four examiners using the same protocol to assess the interobserver's variation. The receiver operating characteristics (ROC) curves differed by examiners. However, when the subjects were limited to anterior MI patients, the ROC curves established by the echo-trained physicians did not differ significantly. It was concluded that the echocardiographic diagnosis of regional wall motion by visual assessment has universal validity. Individual differences are thought mainly to depend on the sites of infarction. Sensitivities for detecting transmural (TM), non-transmural (non-TM) infarcted segments and intact segments were 90, 70 and 70%, respectively. Most of the underestimated TM or overestimated intact segments corresponded to the sites adjacent to MI. As the unexpectedly misdiagnosed segments, the mimic inward motion of the inferior wall drawn by the intact anteroapical wall was observed in a inferior MI patient, or the mimic anterior motion of the anteroapical wall by a swinging motion of the heart, or the paradoxical motion of the interventricular septum was observed in a right ventricular MI case. In the two third of the overestimated non-TM segments, it was considered that the wall motion was affected by the myocardial ischemia, which was not revealed by pathological examination. The underestimated non-TM segments located adjacent to the intact segments or opposite to the severely ischemic segments. From the echocardiographic viewpoint, nearly 90% of segments showing akinetic or dyskinetic motion had MI. However, one third of segments diagnosed as normal were actually MI segments.

Non-invasive techniques were assessed for their capabilities of detecting prosthetic valve malfunctions in 70 consecutive patients with angiographically-documented or surgically-proven prosthetic valve dysfunction. Their 74 dysfunctioning valves were studied using phonocardiography, M-mode and two-dimensional echocardiography and Doppler methods, including pulsed and continuous wave (CW) Doppler echocardiography and two-dimensional Doppler color flow mapping (2DD). These results were compared among the examinations, and also compared between 43 patients with 44 dysfunctioning mechanical valves and 27 patients with 30 dysfunctioning bioprosthetic valves. Symptoms related to valve malfunction were recognized in all patients with prosthetic valve endocarditis and in all patients but one with stenotic condition. In patients with valvular regurgitation, however, symptoms were observed in only six of the 21 patients with mechanical prostheses and in 12 of the 25 patients with bioprosthetic valves (p less than 0.01). Among 43 patients with 44 mechanical valve dysfunctions, the sensitivities of phonocardiography, M-mode and two-dimensional echocardiography and Doppler techniques were 85, 65 and 86 percent, respectively, in 20 patients with stenosis; 100, 57 and 80 percent in seven patients with transvalvular regurgitation; and 100, 50 and 100 percent in 14 patients with paravalvular regurgitation. Similarly, among 27 patients with bioprosthetic valve dysfunctions, the sensitivities of phonocardiography, M-mode and two-dimensional echocardiography and Doppler methods were 67, 100 and 100 percent, respectively, in three patients with stenotic condition; 85, 65 and 100 percent in 20 patients with transvalvular regurgitation; and 60, 40 and 100 percent in five patients with paravalvular regurgitation. Furthermore, 26 of the 27 patients with malfunctioning mechanical valves and 20 of the 24 patients with malfunctioning bioprostheses had abnormal findings using more than two techniques. In addition, each patient had at least one abnormal finding. In conclusion, malfunctioning mechanical or bioprosthetic prostheses could be detected using non-invasive techniques. The combined use of phonocardiography, M-mode and two-dimensional echocardiography and Doppler techniques is most helpful in detecting malfunctioning prostheses.