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A 68-year-old woman was admitted to our hospital with congestive heart failure. She had been diagnosed with hypertrophic cardiomyopathy 12 years ago in another hospital. She had received irradiation therapy for left breast cancer 33 years ago after resection of her left breast. Echocardiography revealed left ventricular hypertrophy and wall motion hypokinesis, and multiple cavities in the myocardium of the left ventricle, interventricular septum, and anterior wall. Some cavities were observed to connect to the left ventricular cavity and Doppler echocardiography showed slow velocity flows in them different from that of the coronary artery. The pathologic diagnosis was severe sclerosis of the left coronary artery, especially the left descending artery and its branch, which was the area with irradiation. Histopathology revealed sclerotic changes of the coronary artery causing acute and chronic myocardial infarction, and incomplete regeneration and hypertrophy of cardiac cells. There was no sign of hypertrophic cardiomyopathy. Myocardial degeneration and deciduation were present next to the cavities connected to left ventricle-like fistulas.

Atrial fibrillation is one of the most common arrhythmias which is associated with various organic heart diseases or systemic disorders. Although a pathological basis for atrial fibrillation has not been clarified, an anatomical substrate corresponding to long-term atrial fibrillation has been recently demonstrated. Age-related changes of the atrial myocardium were frequently observed in healthy people. Quantitative histological study of the sinoatrial node revealed no difference in the reduction of the nodal cells between 12 patients with atrial fibrillation and 21 age-matched controls. The pathological findings of the myocardium including atrial preferential pathways in patients with long-term atrial fibrillation showed depletion of the muscular bundles, fibrosis and fatty metamorphosis of the atrial myocytes. These findings suggest that atrial fibrillation might be related to reentry in the residual muscular bundles including circumferential muscular bundles in the right atrium.

Single photon emission computed tomography (SPECT) using I-123 metaiodobenzylguanidine (MIBG) was evaluated for the detection of doxorubicin (DXR) cardiomyopathy in seven patients with malignant lymphoma receiving DXR doses ranging from 70 to 530 mg (DXR group), and 20 normal subjects without hypertension, diabetes mellitus or electrocardiographic abnormalities (control group). The ratio of the heart to mediastinal counts (H/M) and the washout rate (WR) in MIBG SPECT images were compared between the two groups. Correlation of total doses of DXR with H/M and the relationship of H/M to WR were investigated. The H/M of the DXR group was lower than that of the control group (3.00 +/- 0.97 vs 4.90 +/- 1.08, p < 0.001). The WR of the DXR group was higher than that of the control group (30.9 +/- 10.5% vs 16.5 +/- 9.1%, p < 0.001). Total DXR doses were inversely correlated with H/M (r = -0.86), H/M correlated inversely with the WR (r = -0.83) only in the DXR group. Pathological findings of one patient, who died of DXR cardiomyopathy, showed atrophic and fibrotic nerve fibers in the apical inferior segment of the left ventricle where MIBG uptake was reduced markedly. DXR cardiomyopathy can be detected with MIBG SPECT as cardiac sympathetic nervous dysinnervation. The pathological findings correspond to the MIBG SPECT findings.

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 (p < 0.01). There was a small but significant decrease in mitral valve area at follow-up to 1.6 +/- 0.4 cm2 (p < 0.01). 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 (p < 0.01). 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 (p < 0.001) and the maximum MLC1 level (p < 0.05). 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 (p < 0.001), 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 (p < 0.001), and from 0.99 +/- 0.26 cm2 to 1.76 +/- 0.23 cm2 (p < 0.001), 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 (p < 0.001), and from 0.95 +/- 0.32 cm2 to 1.62 +/- 0.46 cm2 (p < 0.001), respectively. The mitral valve areas after PTMC did not differ significantly from those after OMC by either method.

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.

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 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.

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.

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.

Spontaneous echocardiographic contrast is caused by increased ultrasonic density in the cardiac chambers or great vessels, or both, with the characteristic flow pattern of blood, but in the absence of any intravascular injections. This study demonstrated the clinical features and characteristics of the echocardiographic findings of eight patients with spontaneous contrast echoes. Spontaneous contrast echoes were observed in the right heart in five patients, and in the left heart in two. In one patient spontaneous contrast echoes were observed in the right and left heart. All six patients with spontaneous contrast echoes in the right heart had impaired liver function. In these patients, we observed that spontaneous contrast reaching the heart via the hepatic vein on two-dimensional echocardiography. In one patient with atrial septal defect, these contrast echoes were also recognized in the superior mesenteric vein and portal vein. Since capillary beds normally remove ultrasound contrast, the failure of this function suggests porta-systemic shunting in or around the liver. All three patients with spontaneous contrast echoes in the left heart had prosthetic valve dysfunction including paravalvular or transvalvular regurgitation, and consequent hemolysis. Under these conditions, water-vapor bubbles may be formed because of an exhaust pressure decrease due to the Bernoulli effect, or gases may be released from erythrocytes during hemolysis. These water-vapor bubbles or gases could be the cause of spontaneous contrast echoes in the left heart. In conclusion, spontaneous contrast echoes in the right heart are produced by gas absorbed from the intestine because of porta-systemic shunting. The cause of spontaneous left-sided heart echo contrast may be related to prosthetic valve regurgitation, and consequently to hemolysis.

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)