To evaluate the relationship between maximum venous outflow (MVO) of the leg and development of deep vein thrombosis (DVT), venous occlusion plethysmography (VOP) using a Mercury strain gauge was carried out in 56 unilateral DVT patients. The data from these patients were compared with those obtained from several control groups. Then, the relationship between plethysmographic and 9 clinical variables was statistically analysed in the normal legs of these patients. The mean MVO of the normal legs of these patients was significantly higher than that of the affected legs, but it was significantly lower than those of normal controls and patients with mild congestive heart disease. However, it was similar to those in patients with lymphedema and obese men. A decrease in the MVO of the normal legs of these patients was noted in older females with femoral vein obstruction of the left leg, with a shorter number of days from the onset of symptoms or with higher values for the obesity index and calf circumference. Significant correlations between the MVO and the obesity index (r=-0.59), venous capacitance (VC, r=0.49) and the number of days from the onset of symptoms (r=0.40) were found in the normal right legs of these patients (n=40). In the normal left legs (n=16), on the other hand, significant correlations were found between the MVO and the VC (r=0.65) and the MVO and age (r=-0.65). The MVO of the normal legs of these patients was predicted from clinical variables by multivariate analysis, and a multiple correlation coefficient of 0.64 was achieved using 4 variables (F-value>2); i.e. the obesity index, the side of venous obstruction, the number of days from the onset of symptoms and calf circumference. From these results, we concluded that in the normal right legs of these patients, the MVO was more closely related to the obesity index than to the VC or the number of days from the onset of symptoms. In the normal left legs, however, the MVO was influenced by another factor; i.e. the iliac compression syndrome, which might become more apparent with age. Finally, it was concluded that a decrease in the MVO of the normal legs could increase the occurrence of DVT.

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Using newly developed ring-type emission computed tomography (SPECT), we investigated the washout ratio (WR) of Tl-201 in the myocardium quantitatively with fast dynamic scanning after infusion of dipyridamole (0.57mg/kg), and assessed the feasibility of early WR as a marker to detect coronary artery disease. Twenty-three patients with and 8 patients without coronary aryery disease had serial SPECT images obtained every 5 min for 45 min and at 180 min after dipyridamole and subsequent Tl-201 injection. The best appropriate transaxial slice was selected for WR analysis. Most appropriate diagnostic time was 25 min after infusion of Tl-201 (WR-25). Normal WR-25 was 7.1±4.0%. 5.9±3. 1% and 7.1±2.3%, at the septum, anterior and lateral wall, respectively. Sensitivity, specificity and accuracy to identify coronary stenosis > 50% with a usage of abnormal WR-25, defined as WR-25 < (mean of normals - 1 SD) in each region of inferest of the left ventricle (LV), were 96%. 100% and 97%. respectively. These results were better than those achieved by visual analysis (sensitivity 78%, specificity 100%, accuracy 84%). In patients with single as well as multivessel disease, the regional accuracy in assessing stenosis of more than 50% in the left anterior descending artery (LAD) and left circumflex artery (LCX) by WR-25 was 940/c and 83%, respectively, which was significant-ly better than using visual methods (LAD 72% and LCX 50%; p<0.05). Thus, evaluation of early washout ratios (WR-25) after dipyridamole injection is a valuable method to increase sensitivity in assessing regional myocardial perfu-sion abnormality and is helpful in detection of ischemic heart disease, even with multivessel disease.

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Left ventricular (LV) systolic function was assessed in patients with hypertensive heart disease (HHD, n=30), hypertrophic cardiomyopathy (HCM, n=27), dilated cardiomyopathy (DCM, n=25), volume overload heart (VOH, n=31) and normal subjects (NS, n=32) in the two-dimensional framework of force-length (end-systolic stress-end-systolic volume index) and stress-shortening (mid-systolic stress-ejection fraction). Quadratic discriminant analysis revealed that the ellipses of confidence of HHD and normal subjects were in the same place with regard to both force-length and stress-shortening, while all other groups were well-discriminated. Three subgroups of patients, those with DCM with mild heart failure and those with VOH (with and without heart failure). were easily distinguishable on the basis of stress-shortening, but not on the basis of force-length measurements. It is concluded that LV systolic function and afterload are maintained within the normal range under pressure and volume overload until symptoms of heart failure appear via the mechanism of compensatory hypertrophy. Stress-shortening appears to be a more useful parameter than force-length for the analysis of LV systolic function in clinical practice.

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The clinical features of acute myocardial infarction patients in whom abnormal Q wave disappeared were analyzed. Of 201 patients. 40 (20%) (Group A) showed disappearance of Q wave in serial electrocardiograms. Regional ejection fraction of the infarcted portion improved significantly (from 24±2 to 34±40%, p<0.001) during chronic phase in Group A, but no such improvement was present in Group B patients who showed no change in the Q wave. Global ejection fraction was greater and percent akinetic segment was smaller in Group A than in Group B at chronic phase. Coronary occlusion occured more often at segment 7 in Group A; in Group B, occlusion occurred more frequently up-stream at segment 6, suggesting Group A had a smaller area of risk. Spontaneous recanalization was more often (57%) and complete occlusion was less frequent in Group A. These indicate that Group A is characterized by a smaller area of risk, smaller infarct size, earlier reperfusion, and greater improvement in wall motion. Twenty-eight patients (70%) of Group A lost Q wave within one month and 12 patients (30%), after 3 months or more. Electrical stunning of the myocardium may be a possible mechanism for the early disappearance of Q waves. and anatomical healing for the late disappearance of Q waves.

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Changes in the pattern of the global left ventricular (LV) time-activity curve with increasing pacing rates were evaluated using radionuclide ventriculography in 15 patients with chronically implanted right ventricular VVI pacemakers. The variables obtained were correlated with the conventional systolic time intervals recorded immediately after radionuclide ventriculography in 8 of the 15 patients. Increasing the pacing rate from 50 to 110 beats per minute (bpm) altered the pattern and timing of LV contraction and filling dramatically. It produced progressive delay and reduction of LV contraction, thus shortening the LV diastolic filling time, and sometimes resulting in LV filling even during early systole. Despite these profound alterations, relative cardiac output in-creased progressively, peaking at a pacing rate of 110 bpm in most patients. In paced patients, filling parameters and diastolic timing intervals require careful attention, since they may be difficult to determine from the altered LV time-activity curve at higher pacing rates.

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To evaluate the responsible factors for left atrial ejection, the left atrial pre-ejection period (LAPEP), i.e., the time interval between atrial pacing pulse and onset of atrial ejection, and left atrial ejection time (LAET), i.e., the duration of atrial ejection, were determined from mitral inflow velocity patterns in 35 patients with various heart diseases using pulsed Doppler echocardiography. LAPEP ranged from 75 to 157 (mean 110±18) msec and LAET from 80 to 169 (mean 124±19) msec. The left atrial dimension before atrial contraction showed no significant correlation with LAPEP or LAET. Peak velocity during atrial contraction was negatively correlated with LAPEP (r=-0.42, p<0.05) and positively with LAET (r=0.56, p<0.01). Left ventricular end-diastolic pressure (LVEDP) indicated a significant negative linear correlation with LAET (r=-0.44, p<0.05). LAPEP showed no significant linear correlation with LVEDP, but a significant curvilinear relationship was observed between them (LAPEP=169-9·LVEDP+0.28·LVEDP², r=0.63, p<0.001). Mean pulmonary capillary wedge pressure (mPCWP) was curvilinearly related to LAPEP (LAPEP=168-11·mPCWP+0.42·mPCWP², r=0.72, p<0.001) and LAET (111+4.1·mPCWP-0.22·mPCWP², r=0.63, p<0.001). Although LAPEP decreased and LAET increased with increase in mPCWP up to about 15mmHg, the reverse situation was noted for greater mPCWP. Thus, the major determinants of left atrial systolic time intervals are left atrial and ventricular pressures, and peak velocity during atrial contraction.

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A leftward shift of the interventricular septum (IVS) of the heart is observed in patients with right ventricular pressure overload (RVPO). We simulated the leftward displacement of IVS in a modified ellipsoidal model on the assumption that the IVS generates the same tension as the left ventricular (LV) free-wall in acute RVPO, and derived the relational equations between ventricular pressures (RVP. LVP) and eccentricity index (EI=LVAPD/LVSLD, LVAPD: left ventricular anterior-posterior diameter, LVSLD: left ventricular septal-lateral diameter). The equations indicate that RVP/LVP correlates with simultaneous El, independent of the absolute LV wall tensions and the LV size. To confirm this result, we undertook recurrent pulmonary embolizations in anesthetized open-chest dogs, and analyzed the relationship between RVP/LVP and EI at four phases in systole through the course of RVPO and shock. The advance of RVPO shifted the peak of RVP toward late-systole and made the values of RVP/LVP and EI significantly greater at late-systole than at early-systole. There were significant linear relationships between instantaneous EI and RVP/LVP at each phase, expect for the early systole in the shock stage, and the regression lines on all phases were similar to one another. These results are consistent with our theoretical ones. Therefore we conclude that it is reason-able to predict RVP by using EI, theoretically and experimentally.

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Intravenous administrations of 2000×10⁴IU (33mg) (rt-PA2) and 3000×10⁴IU (50 mg) (rt-PA3) of a new recombinant tissue plasminogen activator (rt-PA : TD-2061) derived from uterine endotherial cells and urokinase (UK) 96×10⁴IU were compared in a double blind, randomized trial of 198 patients with evolving myocardial infarction. All patients entered the trial within 6 h of the onset of symptoms and underwent baseline coronary angiography of the infarct-related coronary artery before thrombolytic therapy was instituted. Sixty minutes following thrombolytic therapy occluded infarct-related arteries were successfully reperfused in 41.5% of 66 patients in the UK, 76.4% of 72 patients in the rt-PA2, and 74.6% of 59 patients in the rt-PA3 group. Statistically significant differences were observed between the UK and rt-PA groups (p<0.01). Serum fibrinogen levels declined in all 3 groups at 60 min post-therapy by averages of 35.9±3.1% in the UK, 16.8±4.8% in the rt-PA2 and 17.5±4.5% in the rt-PA3 group. The difference between the UK and the rt-PA groups was statistically significant (p<0.01). Plasma plasminogen and α2-plasmin inhibitor levels showed the same tendencies. Bleeding was the most commonly observed complication and was most commonly seen at the catheterization site. There was no difference in the incidence among the 3 groups. Hospital deaths occurred in 5.3%, 6.3%, and 4.7% of the cases in the UK, rt-PA2 and rt-PA3 groups, respectively. We conclude, therefore, that rt-PA achieves a significantly higher rate of recanalization with less extensive systemic fibrinogenolysis at the dose employed than does UK. The optimum intravenous dose of rt-PA for Japanese patients is considered to be 2000×10⁴IU (33mg).

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To investigate the possibility of estimating the right ventricular volume overload in atrial septal defect (ASD) by body surface mapping (BSM), 45 children with ASD were included in the present study. The breakthrough minimum (BTM) appeared later and more leftward in ASD subjects than in the normal controls. Neither the length of the delay in the appearance of the BTM nor the extent of its leftward deviation was significantly correlated with the pulmonary and systemic flow volume ratio (Qp/Qs), obtained by cardiac catheterization. Therefore neither could be used as the parameter of the right ventricular volume overload. ΣR. Rmax (D3+D4)+ | S | max (H4+H5) and "T dep", the sum of the absolute values of the departure indices (DIs) in the G4. G5. H4 and H5 leads, and the DIs in the J5. J6, K5, and K6 leads in T departure Map, correlated with the Qp/Qs significantly (r=0.62, 0.68, 0.69, respectively). Accordingly, they might be useful for estimating the right ventricular volume overload. The subjects were divided into 3 groups according to their Qp/Qs. Discriminant analysis between these 3 groups was then performed, using Rmax (D3), | S | max (H4), and T dep as the variables. The accuracy of this discrimination was 82.2%. The result suggests the possibility of estimating the severity of ASD by BSM.

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In the present study. we examined the difference in hemodynamic responses between groups of canine lung lobes which received latex particles of different sizes (50μm and 300μm in diameter). We also assayed prostaglandin I₂ (PGI₂) and thromboxane A₂ in the effluent blood of the lobes. Reversible pressor response was clear in embolization by 50μm particles whereas it was not in that by 300μm. No difference in PGI₂ between two embolizations was seen. We conclude that a local contractile mechanism exists in the pulmonary arterial wall of about 50 pm in diameter whereas participation of the same mechanism is mininal in 300μm, and that this difference cannot be explained from the change in PGI₂.

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Acute left main coronary artery (LMCA) occlusion is rare and typically fatal. According to the recent literature, only three cases have been reported surviving emergent coronary artery bypass grafting (CABG) for acute myocardial infarction (AMI) caused by total LMCA occlusion. We report the case of a 52-year-old man presenting with total occlusion of the LMCA associated with acute anterolateral myocardial infarction and cardiogenic shock. The patient's dominant right coronary artery did not supply the collaterals to the left coronary system. After ineffective thrombolysis the patient underwent successful emergent CABG for the management of uncontrollable cardiogenic shock. Emergent CABG, though controversial, appears to be a feasible approach for patients with AMI in life-threatening situations, when other attempts at reperfusion have been unsuccessful.

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To explore the etiology of paroxysmal atrial fibrillation (AF) in the Wolff-Parkinson-White (WPW) syndrome, we examined the rates of AF episodes and performed electrophysiologic studies in 58 patients with WPW syndrome. They were classified into three patient groups depending on the property of antegrade conduction over accessory pathways: manifest WPW, intermittent WPW, and concealed WPW. Atrial vulnerability was defined as the inducibility of AF or repetitive atrial responses. The three groups were: 24 patients in manifest WPW, aged 42±15 yrs. 38% with AF; 12 patients in intermittent WPW, aged 40±15 yrs, 25% with AF; 22 patients in concealed WPW, aged 44±16 yrs. 9% with AF. There were no significant differences in the mean age between the groups. The incidences of atrial vulnerability detected in electrophysiologic studies in each group were 54%, 42%, and 27% respectively. The incidence of AF was well correlated with that of atrial vulnerability (p<0.01). The effective refractory periods (ERP) of the atrium and the retrograde ERP of the accessory pathway did not differ significantly between the three groups. Atrial conduction delay was more prominent in manifest WPW than in concealed WPW. The incidence of AF and atrial vulnerability was highest in the manifest WPW group, intermediate in the intermittent WPW group, and lowest in those patients with concealed WPW. The difference in incidence between the manifest WPW group and the concealed WPW group was significant (p<0.05). There-fore, the property of antegrade conduction over accessory pathways may be replated to the genesis of AF in the WPW syndrome.

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We encountered a 31-year-old female patient with mild valvular pulmonary stenosis who had no abnormality in the electrocardiogram but pulmonary dilatation in the chest radiograph. Two-dimensional echocardiography and magnetic resonance imaging demonstrated two small protrusions at the interventricular septum indicating diverticula. Large perfusion defects were observed at the anterior wall in the thallium-201 myocardial tomograms. Short axial and vertical long axial images by ECG-gated blood pool tomography revealed an out-pouching best seen during diastole and a good contraction during systole in the corresponding areas. These findings suggested the presence of thin but normal myocardium in the anterior wall, i.e.a muscular type of left ventricular diverticulum. The presence of the muscular type of left ventricular diverticulum at the anterior and septal walls was confirmed by contrast left ventriculography. A congenital diverticulum at the anterior and septal walls with pulmonary stenosis is very rare. Furthermore, its scintigraphic images were quite characteristic and useful for its diagnosis.

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