Journal of cardiography最新文献

The clinical usefulness of thallium-201 myocardial emission computed tomography (ECT) for evaluating left ventricular myocardial fibrosis was assessed in 47 patients with Duchenne (MD), facioscapulo-humeral (FSH), limb-girdle (LG) and myotonic (MT) dystrophy. Trans-, long- and short-axial images were interpreted quantitatively by circumferential profile analysis, and the extent of fibrotic tissue (%FIB) was estimated by integrating hypoperfused areas in six to eight consecutive short-axial slices. Lung/mediastinum count ratio (L/M ratio), LV cavity dilatation, aneurysm formation and cardiac malrotation were also assessed with ECT. Distinct ECT defects were demonstrated in 95 of a total of 235 LV segments (40%) and in 37 of 47 cases (85% of DMD, 71% of FSH, 50% of MT and 60% of LG). They were observed specifically in the posterior wall (82%) and the apex (65%) in DMD, and were scattered in all LV wall segments in FSH, LG, and MT. There was a significant correlation between %FIB and the L/M ratio (r = 0.79, p less than 0.001), and the L/M ratio was significantly higher in DMD than in MT (0.67 +/- 0.36 vs 0.34 +/- 0.25, p less than 0.05). ECT showed marked LV dilatation in seven (15%), apical aneurysm in five (11%) and vertical heart in 12 (26%) of the 47 patients. There were no significant correlations between age or clinical stage scores and numbers of defect segments or %FIB in each group. During the one-year follow-up period of these patients, a DMD boy with the largest %FIB (54%) and the highest L/M ratio (1.4) together with LV dilatation had complications of refractory heart failure and he died eight months following the ECT examination. Thallium-201 planar imaging and standard 12-lead ECG underestimated the perfusion defects which were evaluated with ECT.

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

The influence of exercise training on left ventricular performance was investigated by exercise two-dimensional echocardiography in 12 top-ranking Japanese volleyball players and 10 untrained subjects. Left ventricular wall thickness and dimension were greater in the athletes than in the nonathletes. The left ventricular wall thickness-internal radius ratio, however, was nearly the same in both groups. At rest, heart rate, the stroke area index, % fractional area and the cardiac index were significantly lower in the athletes than in the nonathletes. During exercise, heart rate was slower in the athletes at every exercise stress stage. The stroke area index, % fractional area and the cardiac index increased linearly in the athletes, although these indices of the nonathletes reached a plateau at the moderate exercise stage. The double product at the last stage was greater in the athletes than in the nonathletes. Both groups did not differ as to segmental fractional area change of left ventricular contraction at rest and during exercise. Serum norepinephrine concentration was significantly lower in the athletes than in the nonathletes at rest. After exercise, however, the difference between the two groups was not apparent. It is suspected that exercise training increased the exercise capacity due to an increase in the left ventricular systolic function reserve, the increment of cardiac VO2 max, and the change of blood flow distribution, and generalized aerobic metabolism in various organs.

Although the frequencies of transmural involvements of Q wave and non-Q wave myocardial infarction (MI) are similar, their clinical features are different in many aspects. In the present study, the wall motion abnormalities of 34 patients with Q wave MI and eight patients with non-Q wave MI, all with isolated left anterior descending artery (LAD) lesion, were compared using left ventriculography and two-dimensional echocardiography. This study clearly demonstrated that the severity and distribution of asynergy were significantly greater in patients with Q wave MI than in those with non-Q wave MI. Akinesis or dyskinesis was observed in all 34 patients (100%) (151 of 544 segments) with Q wave MI, and in four of eight patients (50%) (eight of 128 segments) with non-Q wave MI (p less than 0.05). Apical aneurysm occurred exclusively in patients with Q wave MI. In non-Q wave MI, asynergy was localized at the papillary muscle level or the apex. At the chordal level, asynergy was observed in only one of eight cases with non-Q wave MI, and in 24 of 34 cases with Q wave MI (p less than 0.05). These results suggest that the infarct size may be smaller in non-Q wave MI than in Q wave MI in patients with isolated LAD lesion.

Echocardiography was performed to compare pre- and postoperative findings and to evaluate the postoperative state in 109 patients with mitral stenosis (MS) including 22 who underwent closed mitral commissurotomy (CMC) (34.3 +/- 6.9 y.o.); 71, open mitral commissurotomy (OMC) (42.9 +/- 8.7 y.o.); and 16, mitral valve replacement (MVR) (44.5 +/- 8.9 y.o.). Echocardiographic examinations were performed using a Toshiba SSL-51H with a mechanical sector scanner or an SSH-11A with a phased-array electronic sector scanner, one or two weeks before and about one month after surgery, and were reviewed yearly. The results were as follows: The E-F slope of the anterior mitral leaflet (AML) and mitral valve orifice area (MVA) were significantly increased after cardiac surgery in both the CMC and OMC groups. The amplitude of the mitral valve was slightly increased in the CMC group, but was unchanged in the OMC group. Before surgery, the left atrial dimension (LAD) was larger in the MVR group than in the other two groups, and it was significantly decreased after surgical intervention in all three groups. The aortic dimension (AOD) was slightly increased in the majority of patients, and the ratio of the aortic dimension to the sum of the aortic and left atrial dimensions [AOD/(AOD + LAD)] was significantly increased after cardiac surgery due to the improvement of cardiac function and the resolution of the left atrial enlargement. Repeated echocardiography facilitated follow-up of the state of the mitral valve and of cardiac performance, and is considered useful in determining indication for reoperation.

To evaluate the effects of left ventricular (LV) distortion on its pump function, the LV cavity shape was analyzed by two-dimensional echocardiography in normal subjects and in patients with right ventricular (RV) volume or pressure overload. The functional significance of LV distortion in the short-axis sections was evaluated by an index of the efficiency of ejection (E) of endocardial circumferential fiber length (ECL) shortening in reducing LV cavity area during systole; E = measured systolic area reduction/ideal systolic area reduction X 100 (%), where an ideal area at end-diastole or end-systole was computed for the measured ECL, assuming its shape to be perfectly circular (ideal area = ECL2/4 pi), and then an ideal systolic area reduction was determined. E at the chordal level was termed Ech. In patients with atrial septal defect (ASD), the LV cavity was distorted at end-diastole and became more circular at end-systole. Since this characteristic change during systole diminished the E, and the values of E at the chordal level (Ech) were significantly lower in ASD than those in normal subjects (89.4 +/- 4.4% vs 98.3 +/- 0.8%, p less than 0.001), strongly suggesting impairment of the efficiency of LV pump function in ASD. In patients with pulmonary hypertension, the LV cavity was more distorted at systole, and a decrease in cavity area at end-systole with the distorted LV contributed to increased systolic area reduction. Thus, the values of Ech in this group exceeded 100% in five of nine patients (103.8 +/- 12.3%). In other words, when marked RV systolic overload exists, an increase in LV systolic area reduction due to progressive LV compression will occur against LV systolic pressure. This phenomenon suggests the existence of "cardiac massage on the LV by the RV with elevated pressure". In conclusion, it was strongly suggested that the efficiency of LV pump function is modulated by RV overload through dynamic changes in the LV shape.

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.

A case of so-called pseudoaneurysm of the left ventricle without pericardial adhesion, serially demonstrated by two-dimensional echocardiography, was reported. A 76-year-old man developed congestive heart failure 10 hours after gastrectomy, and was diagnosed as having acute myocardial infarction. Two-dimensional echocardiography on the 21st day after onset revealed moderate pericardial effusion and an echo-free space in the posterolateral myocardium of the left ventricle. The echo-free space gradually expanded exteriorly and formed an aneurysm, which remained unchanged after the resolution of the pericardial effusion. Clinical diagnosis of pseudoaneurysm of the left ventricle was made by left ventriculography and coronary angiography. At autopsy, there was an aneurysm measuring 2.3 X 3.0 X 5.0 cm which communicated with the left ventricle via two small ostia, 5 mm each in diameter. There was a loose fibrous adhesion between the pericardium and the epicardium. The wall of the aneurysm consisted of organized fibrous tissue without any elements of the myocardium. Both myocardium and fibrous tissue were located at the junction of the left ventricular wall and the aneurysm. It is surmised that dissection of the infarcted myocardium expanded so greatly as to form an aneurysmal cavity, resulting in the formation of a so-called pseudoaneurysm of the left ventricle after fibrous changes of the outer wall in the infarcted myocardium. Therefore, this aneurysm might be termed a "dissecting" aneurysm of the left ventricle. The hypothesis that a pseudoaneurysm is derived from a localized hemopericardium should be reconsidered.

Factor analysis was applied to multigated cardiac pool scintigraphy to evaluate its ability to detect left ventricular wall motion abnormalities in 35 patients with old myocardial infarction (MI), and in 12 control cases with normal left ventriculography. All cases were also evaluated by conventional Fourier analysis. In most cases with normal left ventriculography, the ventricular and atrial factors were extracted by factor analysis. In cases with MI, the third factor was obtained in the left ventricle corresponding to wall motion abnormality. Each case was scored according to the coincidence of findings of ventriculography and those of factor analysis or Fourier analysis. Scores were recorded for three items; the existence, location, and degree of asynergy. In cases of MI, the detection rate of asynergy was 94% by factor analysis, 83% by Fourier analysis, and the agreement in respect to location was 71% and 66%, respectively. Factor analysis had higher scores than Fourier analysis, but this was not significant. The interobserver error of factor analysis was less than that of Fourier analysis. Factor analysis can display locations and dynamic motion curves of asynergy, and it is regarded as a useful method for detecting and evaluating left ventricular wall motion abnormalities.

To elucidate the useful indices for differentiating cardiac hypertrophy due to essential hypertension (EH) from that due to hypertrophic cardiomyopathy (HCM), we examined standard 12-lead ECGs, chest radiographs and echocardiograms (Echo) in 66 EH and 46 HCM cases. Body surface isopotential mappings (MAPs) were recorded in 16 cases of EH and 18 of HCM. The thickness of the interventricular septum (IVST) and the IVST/PWT ratio (PWT = the thickness of the posterior wall) were greater and left ventricular diastolic diameter (LVDd) was smaller in the HCM group than in the EH group. The septal activation time (SAT), the time interval during which the maximum positive potential moves from the mid-sternal line or the left sternal border to the left mid-clavicular line in the QRS complex, correlated directly with the IVST (r = 0.55, p less than 0.005) and the IVST/PWT ratio (r = 0.61, p less than 0.005). When the SAT was longer than 30 msec, the IVST was over 25 mm and the IVST/PWT ratio was over 2.0, all cases belonged to the HCM category. When subjects were limited to patients with IVST less than 25 mm, the SAT of the HCM group was significantly greater than that of the EH group. These data suggest that the SAT may reflect the etiological differences between the septal hypertrophy of the EH group and that of the HCM group, and that these parameters of MAPs may be helpful to distinguish cardiac hypertrophy due to EH from that due to HCM.