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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.

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.

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.

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 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.

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.

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.

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.