[Emergency CABG for evolving myocardial infarction following PTCA].
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Aged↗
Biomedical subjects
M Kashida
Publications and source records attributed to M Kashida.
[PTCA in patients undergoing coronary bypass surgery and its potential availability: when can PTCA be an alternative to coronary artery bypass grafting?].
The potential availability of percutaneous transluminal coronary angioplasty (PTCA) was retrospectively evaluated for the responsible lesions among grafted vessels of 149 patients who underwent coronary artery bypass grafting (CABG). The lesions suitable for PTCA were defined as discrete, segmental, subtotal and noncalcific, in proximal or middle portions of the major coronary arteries. Patients with left main trunk lesions, those with obstruction of two major coronary arteries, and those with lesions in donor arteries of jeopardized collaterals were excluded. Ninety-seven (31%) of a total of 308 grafted lesions were appropriate for PTCA. These included 38% of left anterior descending artery (LAD) lesions, 39% of left circumflex artery (CX) lesions, and 14% of right coronary artery (RCA) lesions. At least one lesion of 77 (52%) of 149 patients was suitable for PTCA. These included 66% of single vessel graft candidates, 54% of double vessel graft candidates, and 38% of triple or more vessel graft candidates. Ideal candidates for PTCA were 34 patients (23%) in whom all lesions in the grafted vessels were thought to be appropriate for PTCA, and these included 25 (LAD: 23, CX: 1, RCA: 1) of 38 single vessel graft candidates and nine (LAD + RCA: 6, LAD + CX: 2, CX + RCA: 1) of 111 multivessel graft candidates. There was no significant difference between the clinical characteristics of the patients ideally suited for PTCA and the remaining patients. Additional 25 candidates for multivessel grafting, whose lesions were appropriate for PTCA except that of the LAD, were considered limited candidates for PTCA.(ABSTRACT TRUNCATED AT 250 WORDS)
Angioplasty, Balloon↗
[Mitral regurgitation due to abnormal reinsertion of chordae tendineae (looping) of the posterior mitral leaflet: clinical and echocardiographic features].
Two-dimensional (2D) echocardiographic and clinical characteristics of patients with mitral regurgitation (MR) due to abnormal reinsertion of chordae tendineae (looping) in the middle scallop of the posterior leaflet were described and compared with those of patients with chordal rupture of the posterior leaflet. Twenty-five patients with posterior mitral valve prolapse who underwent mitral valve replacement were studied. They were categorized in three groups; 14 patients with MR due to ruptured chordae tendineae (RCT) of the posterior leaflet (RCT group); three patients with looping of the chordae tendineae in the middle scallop of the posterior leaflet (looping group); and eight patients with both RCT and looping (looping + RCT group). It was difficult to distinguish the looping group from the other two groups by their 2D echocardiographic findings, which were characteristic of those of RCT. However, the following findings were more frequently encountered in the patients with looping than in those without: 1) aberrant or absent systolic coaptation with salient arc of the posterior leaflet, observed in six of the RCT group (43%), two in the looping group (67%) and seven in the looping + RCT group (88%); 2) with thickened edges of the posterior leaflet, shown in three of the RCT group (21%), two of the looping group (67%) and five of the looping + RCT group (63%) in the long-axis view, and also noticed in four of the RCT group (29%), two of the looping group (67%) and six of the looping + RCT group (75%) in the short-axis view. In the clinical history, the onset of a heart murmur, congestive heart failure and surgical treatment occurred at significantly younger ages in the looping group than in the RCT group. As for hemodynamic parameters, pulmonary hypertension was significantly milder in the looping group than in the RCT group. In conclusion, although 2D echocardiographic findings of patients with looping were similar to those of patients with RCT, it seemed possible to differentiate the looping group from the RCT group by the 2D finding of a prolapsed posterior mitral valve with a salient arc and a thickened edge. It was also suggested that the looping of chordae tendineae in the middle scallop of the posterior leaflet was congenital in origin.
Adolescent↗
[Biochemical assessment of the effects of coronary thrombolysis by serum cardiac myosin light chain levels].
To establish the method of biochemical assessment of effects of intracoronary thrombolysis after acute myocardial infarction (MI), the relationships between plasma creatine kinase (CK) or serum cardiac myosin light chain (LC) I levels and changes in left ventricular (LV) wall motion were evaluated. Twenty-seven cases with acute MI without previous infarction were included in this study. Intracoronary thrombolysis was successful within seven hours after onset of MI in 13 patients (reperfusion group), and 14 patients were treated in a conventional manner (control group). Peak levels of CK reached earlier in the reperfusion group (11.3 +/- 2.9 hours) than in the control group (20.9 +/- 5.3 hours). The peak appearance time of CK in the reperfusion group was significantly related to the time between the onset of MI and achievement of coronary reperfusion (r = 0.76). The relationship between total CK release and LV ejection fraction determined by cineangiography one month after onset was not good (r = -0.42). Peak levels of CK were not related to LV ejection fraction. Peak levels of LC appeared about four days after onset in both groups. Peak levels of LC were closely related to LV ejection fraction (r = -0.72). Twenty-four-hour and four-day levels of LC were also related to LV ejection fraction (r = -0.62 and -0.73, respectively). Peak levels of LC were related to asynergic area determined by biplane cineangiography.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[Metastatic thyroid cancer to the right ventricle causing obstruction of the right ventricular outflow tract and associated with disseminated intravascular coagulopathy: a case report].
A case of thyroid cancer causing right ventricular outflow tract obstruction is described. A 72-year-old woman was admitted because of shortness of breath, some ecchymoses, and marked anasarca. Her liver was palpable four fingerbreadths below her costal margin. Laboratory findings included leukocytosis, marked thrombocytopenia, and an increase in fibrinogen degradation products due to disseminated intravascular coagulopathy. Two-dimensional echocardiography demonstrated a solid mass in the right ventricle, which protruded into the right atrium and main pulmonary artery. Right ventricular outflow tract obstruction and tricuspid regurgitation were demonstrated by contrast echocardiography. These findings were confirmed by CT scans, RI angiography, and contrast angiography. The mass was partially resected from her right ventricle and her tricuspid valve was replaced successfully, but she died of sepsis three weeks after surgery. At autopsy, undifferentiated thyroid cancer and cardiac metastasis were verified. To date, only eight cases with initial symptoms of congestive heart failure due to right ventricular outflow tract obstruction caused by metastatic intracavitary tumors have been reported. Very rarely have cardiac tumors resulted in disseminated intravascular coagulopathy.
Aged↗
[Mitral regurgitation due to ruptured chordae tendineae: sensitivity and specificity of the diagnostic criteria by two-dimensional echocardiography].
The sensitivity and specificity of the two-dimensional (2D) echocardiographic criteria for diagnosing ruptured mitral chordae tendineae (RCT) were assessed in 52 cases with non-rheumatic mitral regurgitation undergoing mitral valve prostheses. At surgery, chordal rupture was confirmed in 38 cases (RCT group), but not in 14 cases (non-RCT group). Four presumptive and three definite findings for diagnosing mitral chordal rupture using 2D echo were evaluated. Mitral valve prolapse with incomplete coaptation of the mitral leaflets in the long-axis view was observed in 32 cases in the RCT group and in four cases in the non-RCT group (sensitivity 84%, specificity 80%). In the short-axis view at the level of the mitral orifice, delayed closure of the involved mitral leaflet was observed in four cases in the RCT group but in none of the non-RCT group (sensitivity 11%, specificity 100%), delayed protodiastolic opening of the involved leaflet in 15 cases of the RCT group and in one of the non-RCT group (sensitivity 39%, specificity 92%), and finally, increased excursion of the involved valve in 27 cases of the RCT group and in three cases of the non-RCT group (sensitivity 71%, specificity 79%). The following three echocardiographic findings were regarded as direct evidence of mitral chordal rupture: Fine echoes with abnormally rapid transverse and/or oblique motion around the mitral orifice in the short-axis view were observed in 13 cases of the RCT group (sensitivity 34%, specificity 100%); echoes with abnormal whip-like motion in the long-axis view in 10 cases (sensitivity 26%, specificity 100%).(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
[Two-dimensional echocardiographic measurement of the surgical aortic ring: its clinical significance in non-rheumatic regurgitation and in predicting the sizes of prosthetic valves].
The purpose of the present study was to determine the usefulness of two-dimensional echocardiographic measurements of the surgical aortic ring diameters (ARDs) in predicting correct sizes of the prosthetic valves and in determining the mechanisms of aortic regurgitation. Forty patients with aortic regurgitation who underwent prosthetic valve surgery, and 20 normal controls were selected for the study. The 40 patients consisted of 21 with rheumatic aortic regurgitation (RHD group), and 19 with non-rheumatic non-inflammatory aortic regurgitation (non-RHD group). Aortic regurgitation due to annuloaortic ectasia with or without the stigmata of Marfan's syndrome and bicuspid aortic valves were excluded from the non-RHD group. Echocardiographic estimates of the ARDs proved to be useful for predicting prosthetic valve sizes considering the good correlation between the echocardiographic and direct measurements (r = 0.814), despite a slight tendency to echocardiographic underestimation. The ARDs was 24.7 +/- 3 mm in the RHD group, 28.8 +/- 2.9 mm in the non-RHD group and 21.8 +/- 1.7 mm in the normal controls. The ARDs in the RHD group was significantly larger than that of the normal controls (p less than 0.001), and the ARDs of the non-RHD group was significantly larger than that of the RHD group (p less than 0.001). There were loose correlations between the ARDs and left ventricular end-diastolic dimension, and between the ARDs and left ventricular end-systolic dimension in the RHD group (r = 0.549 and r = 0.455, respectively), but there were no correlations between these two parameters in the non-RHD group. In four patients with aortic regurgitation in the non-RHD group, mitral regurgitation coexisted. Both the ARDs and the mitral ring dimension were markedly increased in these patients. It is concluded that in the non-RHD group, marked dilatation of the ARDs appears to be one of the cause of aortic regurgitation.
Adult↗
[Pulmonary regurgitation with special reference to the shape of the pulmonary valve ring: a pulsed Doppler and angiographic study].
Using pulsed Doppler echocardiography and cineangiography, the significance of pulmonic valve ring dimensions in the genesis of pulmonic regurgitation (PR) was studied in 40 patients, including 12 with valvular disease, 19 with coronary artery disease and nine with the normal heart. In nine of the 40 subjects, pulmonary hypertension (mean pulmonary artery pressure greater than or equal to 20 mmHg) was observed. The criterion for diagnosing PR was disturbed flow patterns recorded just below the pulmonic valve which spanned more than 40% of diastole, exceeding 1.5 KHz in peak frequency (corresponding to a flow velocity of about 50 cm/sec). Sagittal and transverse diameters of the pulmonic valve ring (PRDs, PRDt) at the upper edge of the pulmonary sinus, and the sagittal diameter of the pulmonary sinus (PSD) at the level of its maximal bulging were measured using pulmonary angiography. PR was detected in 15 subjects (37.5%). The prevalence of PR among three groups regardless of the absence or presence of pulmonary hypertension was not significantly different. The peak frequency of the regurgitant flow signals as well as the farthest point of the signals detected did not differ among the three groups irrespective of pulmonary hypertension. The ratio of the PRDs to the PRDt (PRDs/PRDt) was greater in patients with PR than in those without PR (p less than 0.001), but no correlation was established between PRDs/PRDt and mean pulmonary artery pressure. The PRDt index and PRDs index (normalized by body surface area) correlated well with the mean pulmonary artery pressure (r = 0.70, p less than 0.001 and r = 0.62, p less than 0.001, respectively). PSD also correlated with the mean pulmonary artery pressure (r = 0.49, p less than 0.01), whereas, PSD/PRDs correlated inversely with the mean pulmonary artery pressure (r = 0.40, p less than 0.01), indicating a relatively more prominent dilatation of the PRDs than of the PSD in cases with pulmonary hypertension. These results suggest that the etiology of PR in our series of patients was primarily attributable to the distortion of the pulmonic valve ring. The wide-spread concept that pulmonary hypertension dilates the pulmonic valve ring, leading to the development of PR, should be criticized.
Blood Pressure↗
[Hemodynamic determinants of late systolic reversed flow in the main pulmonary artery in pulmonary hypertension: a pulsed Doppler echocardiographic study].
Pulsed Doppler echocardiograms of the main pulmonary artery were evaluated in 46 cases including 23 cases with valvular heart disease, 13 with an intracardiac shunt, two with severe right ventricular failure and low cardiac output state, and eight healthy normals. In each Doppler echocardiogram the sample volume was placed at well defined nine locations within the main pulmonary artery. Among 23 cases with valvular heart disease, 10 cases with pulmonary hypertension showed a late systolic reversed flow ("rebound" pattern : type B) in all nine sample volumes examined. This pattern was neither detected in any cases with normal pulmonary arterial pressure, cases with an intracardiac shunt, cases with low cardiac output state, nor healthy normals. A comparative study of 10 cases with "rebound" pattern (type B) and 13 cases without it disclosed that the former had a significantly increased pulmonary arterial pressure (30.9 + 15.1 mmHg vs 17.8 +/- 9.0 mmHg, p less than 0.001), an increased total pulmonary resistance (789 +/- 496 dynes X cm X sec-5 vs 285 +/- 170 dynes X cm X sec-5, p less than 0.001) and a decreased pulmonary arterial compliance expressed as stroke volume divided by pulmonary arterial pulse pressure (1.75 +/- 0.94 ml/mmHg vs 3.80 +/- 1.65 ml/mmHg, p less than 0.01). Mean acceleration of the pulmonary ejection expressed as peak flow velocity divided by acceleration period was also significantly larger in cases with "rebound" pattern (type B) than in cases with "normal" pattern (938 + 255 cm X sec2 vs 675 +/- 160 cm X sec2, p less than 0.01). In conclusion, "rebound" pattern (type B) in pulmonary hypertension is not simple swirl formation, but a totally reversed late systolic flow in the main pulmonary artery, which is caused by sudden interruption of the distal run-off due to markedly elevated total pulmonary resistance under normal right ventricular ejection.
Adolescent↗
[Case of "brown bowel syndrome" with posterior column degeneration, probably due to vitamin E deficiency].
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Adult↗
[Effects of beta-blockers and Ca antagonists on diastolic function of the hypertrophied left ventricle: an echocardiographic study].
Left ventricular (LV) relaxation was studied in patients with hypertensive heart disease with LV hypertrophy (HHD, n = 25) and hypertrophic cardiomyopathy (HCM, n = 9), and these data were compared with that of normal controls (n = 20). The effects of oral administration of propranolol (n = 11), pindolol (n = 3), nifedipine (n = 6) and diltiazem (n = 5) in patients with HHD and that of propranolol (n = 9) in patients with HCM were also studied. Isovolumic relaxation time (IRT) was measured using dual M-mode echocardiography and peak normalized rate of change of the LV cavity in early diastole (peak dD/dt/D) was calculated by M-mode echocardiography using a digitizer and microcomputer system. IRT was significantly longer in HHD (112 +/- 24 msec, p less than 0.001) and in HCM (85 +/- 40 msec, p less than 0.05) compared with that of normal subjects (64 +/- 24 msec). The normal value of peak dD/dt/D was 3.8 +/- 0.7 sec-1, and it was significantly lower in HHD (2.7 +/- 0.8 sec-1, p less than 0.001). It was also lower in HCM (3.2 +/- 0.8 sec-1), but without a statistical significance. In HHD there was a significant relationship (r = -0.611, p less than 0.01) between peak dD/dt/D and wall thickness of the LV (interventricular septum + LV posterior wall). There was no significant change in IRT before and after the administration of beta-blockers and calcium antagonists except nifedipine in HHD (before: 116 +/- 28 msec, after: 80 +/- 14 msec, p less than 0.005). It was probably due to the effect of an accompanied decrease in heart rate. However, peak dD/dt/D was significantly increased in both HHD and HCM groups after the administration of propranolol, pindolol, nifedipine and diltiazem. These data show that LV relaxation is abnormal in the hypertrophied LV. Although the genesis of this abnormality is not clear, there seems to be a close relationship between the relaxation abnormality and increased LV mass in HHD. Oral administration of propranolol, pindolol and diltiazem for patients with HHD and propranolol for patients with HCM seems to improve the abnormal LV relaxation of each disease.
Adrenergic beta-Antagonists↗
[Evaluation of left ventricular asynergy by parasternal and subcostal M-mode echocardiography].
In 47 patients with old myocardial infarction (MI), parasternal and subcostal M-mode echocardiograms (M-mode) guided by the two-dimensional echocardiogram (2D) were recorded to evaluate left ventricular asynergy quantitatively, and were compared with 2D findings. By placing the transducer at the left sternal border, the short-axis views of the left ventricle (LV) by 2D at the level of the chorda tendineae and papillary muscle were recorded. The LV wall was divided into 4 segments; including (1) anterior wall (AW) and anterior septum (AS), (2) lateral wall (LW), (3) posterior wall (PW), and (0) inferior wall (IW) and posterior septum (PS), and asynergy was analyzed on moving images. The AS and PW were recorded by parasternal M-mode, and the PS and LW were recorded by subcostal approach. Asynergy by M-mode was defined when septal amplitude was less than 3 mm, LW or PW amplitude was less than 9 mm, % systolic thickening (% ST) of the septum was less than 17%, and % ST of the LW or PW was less than 25%. Of 25 patients with anterior MI, asynergy of the AW and AS wass s present in 19, LW asynergy in 10, PW asynergy in 2, and IW and PS asynergy in 1 by 2D, meanwhile, M-mode detected asynergy of AS in 21, and LW asynergy in 15. Of 15 patients with inferior MI, asynergy of the PW and PS was present in 4 and 7, respectively by 2D, but by M-mode asynergy was present in 11 and 14, respectively. In 31 patients underwent left ventricular cineangiography, detection rate of asynergy by angiography was compared with that by echocardiography. In 124 segments by cineangiography, wall motion characteristics were correctly identified in 83% by 2D and 91% by M-mode. Of 25 patients with anterior MI, amplitude of the AS was 3 approximately -5 mm in 19, and %ST of the AS wa 0 approximately 6% in 2, but amplitude of the PS was within normal range in 24. Of 15 patients with inferior MI, amplitude of the AS was within normal range in all, and amplitude of PS was 3 approximately -8 mm in 13 and %ST of PS was 10% in 1. This study shows that combined use of parasternal and subcostal M-mode detects asynergy more sensitively than 2D alone even in its quantitative sense, and therefore, not only 2D but M-mode in essential for evaluation of LV asynergy. Asynergy of PS was present in inferior MI, and this segment was not injured in anterior MI, while AS asynergy was present in anterior MI. When analysing asynergy of the interventricular septum, it should be subdivided into two parts including AS and PS. Subcostal M-mode detected PS asynergy that was not visualized by routine cineangiography. In inferior MI, subcostal M-mode is recommended for detection of PS asynergy.
Adult↗