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The clinical usefulness of catheter fragmentation and aspiration therapy was studied in 8 patients with acute pulmonary embolism who received thrombolytic therapy using urokinase or tissue-type plasminogen activator (t-PA) (thrombolysis group) and 8 patients who underwent catheter fragmentation and aspiration therapy using a percutaneous transluminal coronary angioplasty (PTCA) guide catheter (catheter group). The patients were selected from 20 patients with a definite diagnosis of acute pulmonary embolism based on pulmonary arteriography and nuclear imaging. Urokinase (48 x 10(4) to 96 x 10(4) unit/day) or t-PA (12 x 10(6) unit/day) was administered intravenously for mean 4 days in the thrombolysis group. Pulmonary artery pressure was first measured using a Swan-Ganz catheter via the jugular vein or the femoral vein in the catheter group. Then, a PTCA guide catheter was advanced into the pulmonary artery, and the thrombus was disrupted repeatedly using a Radifocus wire, followed by manual aspiration. Subsequent treatment consisted of intravenous infusion of heparin (10,000 to 15,000 unit/day) and urokinase (24 x 10(4) to 48 x 10(4) unit/day) for mean 6 days. Partial revascularization was achieved in all patients in both groups. Five patients in the thrombolysis group died within 1 month due to respiratory failure, re-embolization, and/or hemorrhagic complications. One patient in the catheter group died of hemorrhagic shock. Pulmonary artery systolic pressure in the catheter group was significantly reduced from 47.4 to 26.5 mmHg (p < 0.01). Catheter treatment of acute pulmonary embolism associated with acute circulatory failure such as shock can lead to rapid hemodynamic improvement. In contrast, thrombolysis is an effective treatment, but bleeding problems are common and caution is required. Catheter fragmentation and aspiration therapy is effective for acute pulmonary embolism, is minimally invasive, and should be considered the treatment of first choice.

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Hemodynamic changes associated with the lowering of total cholesterol (TC) by the water-soluble HMG-COA reductase inhibitor pravastatin were investigated in 59 patients with hypercholesterolemia (TC level at least 220 mg/dl) who received pravastatin therapy for 6 months. The patients were divided into two groups according to the reduction in TC: a > or = 15% reduction group and a < 15% reduction group. The changes in hemodynamics were compared before and after pravastatin treatment. No changes in blood pressure, heart rate or aortic damping factor were found in either group. However, significant decreases in pulse wave velocity and total peripheral resistance, and increase in cardiac output were seen in the > or = 15% reduction group. All these hemodynamic parameters remained unchanged in the < 15% reduction group. The 12 patients with a clear pravastatin-induced reduction in TC maintained over a 5-year period showed no changes in blood pressure, heart rate or aortic damping factor, but the reductions in pulse wave velocity and total peripheral resistance, and increase in cardiac output were maintained. These changes in hemodynamics were not dependent on aortic elasticity, and appeared to result from improved peripheral hemodynamics. Lowering of TC levels by pravastatin results in improvement in the peripheral endothelium-dependent vasodilation disorder associated with hypercholesterolemia.

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OBJECTIVE: This study was performed to investigate whether it is possible to use saliva instead of blood usually used for therapeutic drug monitoring (TDM) of disopyramide. METHODS: Six healthy male volunteers ingested 200 mg of disopyramide base, and the disopyramide concentrations in saliva and plasma (total and unbound) were determined by the HPLC. RESULTS: Disopyramide concentration-time profiles for the saliva were nearly equal to those for the plasma unbound concentrations. A large variation for absorption time of the drug was observed among the subjects. Disopyramide concentrations (Cs) in saliva did not correlated well with plasma total concentrations (Cp), r = 0.799, but did well with unbound concentrations (Cpu), r = 0.969, for the 3-12 h period on the elimination phase. The mean ratio of disopyramide concentrations in the saliva against the plasma unbound concentrations was almost constant (1.02(0.10), CV = 9.7%) for the period. The pharmacokinetic parameters (tmax, t1/2, AUC, AUMC and MRT values) for disopyramide calculated from the saliva data were nearly equal to those from the unbound data. CONCLUSION: Disopyramide concentrations in saliva correlated well with plasma unbound concentrations on the elimination phase.

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Dentistry has lacked an effective indicator of the impact of dental problems on a person's daily life. Subjective factors in dental health need to be included in order to improve current indicators. The purpose of this research was to develop a new type of indicator recorded from a questionnaire which takes account of subjective factors in dental health. The indicator we constructed has the following advantages. 1. Calculation process is simple in practice. 2. The indicator values range from 0 to 100, with values closer to 100 indicating a more favorable condition for the individual. 3. The distribution of indicator values is similar to the normal distribution. 4. The score of each item is reflected on the indicator, suggesting the individual's characteristics in terms of dental health. 5. Although it is principally an indicator for individuals, it can also be applied to groups. This study will also provide a model for the preparation of a dental health indicator.

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The purpose of this study was to examine the association between site-specific periodontal conditions assessed by CPITN and BANA test results. A total of 161 Japanese company employees aged 18-59 were examined for their periodontal conditions at mesio-buccal and mid-lingual sites of the maxillary right and mandibular left first molars using CPITN. Code 2 (calculus) was divided into Code 2+ and Code 2- by the presence or absence of bleeding. Plaque samples were collected from the examined sites with a scaler and placed on BANA reagent cards. The results indicated a close relationship between site-specific CPITN Codes and the BANA test results except at sites designated Code 2-. The proportion of sites with strong-positive reactions were 19.0% for Code 0, 21.4% for Code 2-, 29.9% for Code 1, 37.0% for Code 2+ and 50.0% for Code 3. These data indicated that the teeth given higher CPITN Codes tend to have higher risks for periodontal disease. From these results, it was concluded that the site-specific CPITN score is a good indicator of periodontal disease activity and that a higher priority for treatment should be given to the sites with pocket formation (Code 3 and Code 4) and/or gingival bleeding (Code 1 and Code 2+).

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To contribute for making early diagnosis and treatment of acute pulmonary embolism (APE), we investigated on clinical pictures of 225 patients with APE. Common underlying factors were heart disease, prolonged bed rest, post-surgical state, thrombophlebitis, malignant tumor and post-catheterization state in this order. Dyspnea, chest pain, tachycardia and shock were frequently seen as initial symptoms and signs. Blood screening showed leukocytosis, hypoxemia, hypocapnia and elevated serum LDH. Electrocardiographic findings highly demonstrated were ST.T abnormalities, such as T inversion with ST elevation in V1-3, ST depression in V4-6 and sinus tachycardia. Chest X-rays showed diminished pulmonary vascular marking and pulmonary artery dilation. Right ventricular dilatation were frequently seen on 2-dimensional echocardiograms. Pulmonary artery pressure were elevated up to 49/20 (30) mmHg. Twenty-five percent of the patients died, and the recurrence was seen in 4%. Thus, as soon as APE is suspected by above clinical findings, definitive diagnosis should be obtained by the lung perfusion scan and pulmonary arteriography, then oxygen and thrombolytic agents should be given immediately to prevent the fatal outcome.

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Using transmitral flow velocity and left ventricular ejection flow velocity, we measured left ventricular inflow volume (LVIV) and left ventricular outflow volume (LVOV) by pulsed Doppler echocardiography in 73 patients who had mitral valve regurgitation (MR), aortic valve regurgitation (AR), or no valvular regurgitation. Doppler-determined regurgitant volume (DOPRV), Doppler-determined regurgitant fraction (DOPRF), total stoke volume, and forward stroke volume were calculated to compare the severity assessed by angiographic scoring and the regurgitant fraction determined by radionuclide angiography (RIRF). In 17 patients with MR, LVIV (84.4 +/- 20.4 ml) was significantly greater (p less than 0.01) than LVOV (52.5 +/- 15.7 ml). LVOV, which is equivalent to forward stroke volume, was lower in patients with MR (52.2 +/- 15.7 ml) than in normal subjects (67.0 +/- 15.7 ml). In 15 patients with AR, LVOV (121.7 +/- 61.1 ml) was significantly greater (p less than 0.01) than LVIV (75.1 +/- 28.1 ml) and LVOV, which is equivalent to total stroke volume, was greater in patients with AR (121.7 +/- 61.1 ml) than in normal subjects (64.0 +/- 14.4 ml). DOPRF correlated with RIRF (r = 0.79, p less than 0.01, n = 11). DOPRV (mild: 10.5 +/- 8.5 ml; moderate: 28.8 +/- 13.6 ml; severe: 74.5 +/- 36.7 ml) and DOPRF (mild: 13.7% +/- 11.5%; moderate: 33.1% +/- 14.2%; severe: 52.6% +/- 15.3%) increased markedly with the severity of regurgitation as assessed by cineangiography. In AR, total stroke volume influenced both forward stroke volume and regurgitant volume, and in MR, regurgitant volume influenced both total stroke volume and forward stroke volume. Total stroke volume in AR and regurgitant volume in MR may play a key role in valvular regurgitation.

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Calcium ionophore, A23187, is known to be a comitogen, but it activates a suicide process characterized by DNA fragmentation at linker regions in mouse immature thymocytes. It did not induce DNA fragmentation in T lymphocytes prepared from lymph node and spleen cells. Induction of DNA fragmentation by A23187 depends on protein phosphorylation and synthesis of mRNA and protein, because an inhibitor of protein kinase, 1-(5-isoquinolinesulfonyl)-2-methyl-piperazine dihydrochloride (H-7), actinomycin D, and cycloheximide, respectively, inhibits the DNA fragmentation and cell death. Studies adding the inhibitors at various times show that protein phosphorylation and mRNA synthesis occur within a few hours after incubation with A23187 followed by the protein synthesis responsible for inducing DNA fragmentation. Phorbol esters, 12-O-tetradecanoyl 13-acetate (TPA) and phorbol 12,13-dibutyrate (PBD), which are capable of activating protein kinase C, also induced similar DNA fragmentation in immature thymocytes, followed by cell death. PBD committed the suicide process after 6 h of incubation, because the DNA fragmentation above the control level was not induced when PDB was removed from the medium before 6 h of incubation. A23187 or a phorbol ester alone induced DNA fragmentation followed by cell death, whereas the addition of TPA at low concentration inhibited the DNA fragmentation induced by A23187 accompanied with an increase in DNA synthesis. The result suggests that TPA switched a suicide process induced by A23187 to an opposite process: stimulation of DNA synthesis. Physiologic factors and mechanisms which regulate cell proliferation and death in the thymus are not known at present, but the signals by protein kinases and calcium ions may regulate both cell proliferation and death, independently, synergistically or antagonistically.

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Left ventricular inflow volume (LVIV) and outflow volume (LVOV) were determined by pulsed Doppler echocardiography, and the ratio of pulmonary to systemic flow (Qp/Qs) was estimated as a ratio of LVIV to LVOV (LVIV/LVOV). Seventy-seven patients were studied, 47 control subjects and 30 patients with ventricular septal defect (VSD). LVOV was calculated from the left ventricular ejection flow velocity and left ventricular outflow tract diameter; LVIV was calculated from the transmitral flow velocity and mitral valve motion as traced by M-mode echocardiography. Cardiac input (COin) and cardiac output (COout) were calculated as the product of LVIV or LVOV and heart rate. Cardiac output was also determined by the dye dilution method (COdye) in control subjects. A close correlation was observed between COdye and COin (y = 1.18x - 243, r = 0.85, p less than 0.005, SEE = 1026 ml/min) and COdye and COout (y = 1.16x - 323, r = 0.90, p less than 0.005, SEE = 639 ml/min). LVIV and LVOV were highly correlated in control subjects (y = 0.95x + 5.3, r = 0.94, p less than 0.005, SEE = 6.6 ml). LVIV/LVOV was 0.97 +/- 0.1 (mean +/- SD) in control subjects, whereas LVIV/LVOV (1.87 +/- 0.88) was significantly higher in patients with VSD (p less than 0.01). In patients with VSD, LVIV/LVOV correlated with Qp/Qs determined invasively (y = 0.97, SEE = 0.23, n = 16). Thus with our method LVIV and COin can be accurately determined, and we suggest that Doppler-determined LVIV/LVOV is clinically useful for evaluating the shunt flow magnitude in VSD.

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New criteria for the diagnosis of right ventricular hypertrophy (RVH) using a point scoring system were developed after analyzing standard 12-lead ECGs in 155 patients with mitral stenosis verified by cardiac catheterization and 155 age and sex-matched apparently normal healthy subjects. ECGs were evaluated to identify criteria that provided maximum sensitivity and at least a 95% specificity: (1) the R wave magnitude in V1 had to be greater than 0.7 mV; (2) the S wave magnitude in V6 had to be greater than 0.3 mV; (3) the S wave magnitude in V1 less than 0.5 mV; (4) the R wave magnitude in V1 plus the S wave magnitude in V6 minus the S wave magnitude in V1 must be greater than 0 mV; and (5) the degree of frontal QRS axis had to be greater than 90 degrees. Application of these criteria achieved 25% (39 of 155) sensitivity in patients with RVH, significantly better (p less than 0.01) than the 17% sensitivity (17 of 155) of Bonner's criteria for the automated ECG. The specificity of the proposed criteria was 98% (152 of 155), significantly better (p less than 0.01) than the 90% specificity (139 of 155) of Mortara's criteria. Thus, it was evident that the accuracy of the proposed criteria was the highest among those criteria used in a point scoring system including the currently used automated ECG criteria for the diagnosis of RVH.

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Using pulsed Doppler echocardiography, left ventricular inflow flow volume (LVIV) and outflow flow volume (LVOV) were noninvasively determined, and the ratio of pulmonary to systemic flow (Qp/Qs) was evaluated as the ratio of LVIV to LVOV (LVIV/LVOV). Thirty patients with ventricular septal defect (VSD) were studied, and 47 cardiac patients without aortic or mitral valve disease or intracardiac shunt served as controls. LVOV was derived from the left ventricular ejection flow velocity and the outflow tract diameter immediately proximal to the aortic valve ring. LVIV was derived from the transmitral flow velocity and the M-mode tracing of mitral valve motion. Doppler-determined cardiac outputs (COin and COout) were calculated as the products of LVIV or LVOV as and heart rates. Cardiac outputs were also determined by the dye dilution method (COdye) references for comparison with Doppler-determined cardiac outputs. There were good correlations between COdye and COin (y = 1.18x-243, r = 0.85, p less than 0.005, SEE = 1026 ml/min) and between COdye and COout (y = 1.16x-323, r = 0.90, p less than 0.005, SEE = 639 ml/min). LVIV and LVOV correlated well in the controls (y = 0.95x + 5.3, r = 0.94, p less than 0.005, SEE = 6.6 ml). LVIV/LVOV was 0.97 +/- 0.1 (mean +/- SD) in the controls; whereas LVIV/LVOV (1.86 +/- 0.90) was significantly higher in patients with VSD (p less than 0.01) and this ratio correlated well with Qp/Qs by an oximetry (r = 0.98, SEE = 0.20, n = 14), including patients associated with pulmonary regurgitation. These findings indicate that our method permits determination of LVIV with a high degree of accuracy and that the Doppler-determined LVIV/LVOV is clinically useful to evaluate accurately the magnitude of shunt flows in patients with VSD.

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