In patients with acute myocardial infarction, reocclusion after achievement of coronary reperfusion by thrombolytic therapy using urokinase (UK) or tissue plasminogen activator (tPA) has become a problem. The causes of reocclusion may include rethrombosis as well as activation of platelets and coagulation factors by thrombolytic agents. To elucidate the mechanism of reocclusion involved, thrombin generation was measured. Coagulation of platelet-rich plasma was induced by CaCl_2. Each sample was reacted with S-2238 to determine the thrombin generation. UK or tPA was added to this system and the thrombin generation was assessed. The clotting time was shortened by UK and tPA when compared with control. Thrombin generation was increased by UK and tPA. Stimulation of thrombin generation by thrombolytic agents may contribute to reocclusion.

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Clinical features of 54 patients with crescentic glomerulonephritis (CrGN), experienced from 1980 to 1999 at Kyorin University Hospital, were analyzed. CrGN measuring serum anti-neutrophil cytoplasmic antibody (ANCA) and anti-glomerular basement membrane (GBM) antibody were classified into three patterns, linear, granular and pauci-immune CrGN by glomerular immunfluorescent staining pattern of immunogloburin deposit. The results were as follows: (1) Twenty eight patients (51.9%) had pauci-immune pattern CrGN, 21 patients (38.9%) had granular pattern CrGN and 5 patients (9.3%) had linear pattern CrGN. Average age of patients with pauci-immune pattern CrGN was significantly higher than that of granular pattern CrGN (pauci-immune pattern CrGN : 60.3±14.3, granular pattern CrGN : 45.4±15.1). Average age of patients with linear pattern CrGN was 55.8 (55.8±12.1). (2) Numbers of patients with CrGN, especially with pauci-immune CrGN, increased during recent 10 years compared with the previous decade. (3) Main risk factors of mortality were high age onset (over 60 years old), sepsis, rapidly progressive glomerulonephritic syndrome (RPGN), severe renal failure requiring hemodialysis and alveolar hemorrhage. (4) ANCA was detected in 31 of 54 (31/54:57.4%) patients with CrGN. Twenty nine had myeloperoxidase (MPO)-ANCA and 2 had proteinase 3 (PR3)-ANCA. ANCA was detected in 25 of 28 patients (89.3%) with pauci-immune CrGN (MPO-ANCA:25 patients, PR3-ANCA:3 patients), 4 of 17 patients (23.5%) with granular pattern CrGN and 2 of 5 patients (40%) with linear pattern CrGN. ANCA titer values in pauci-immune pattern CrGN were significantly higher than those in granular pattern CrGN. A linear pattern CrGN patient with high ANCA titer had ANCA related alveolar hemorrhage at the time of negative anti-GBM antibody. (5) High frequency of extra-renal vasculitic symptoms associated with CrGN, especially with pauci-immune CrGN, indicated that CrGN might be renal manifestation of systemic vasculitis. (6) In relationship between serum creatinine level at the start of treatment and prognosis, patients with serum creatinine below 2.2mg/dl had better prognosis than those with serum creatinine over 2.3mg/dl.

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The criteria usually used for the diagnosis of inferoposterior myocardial infarction (MI) are an R/S ratio ≥1.0 in lead V1 or V2 and electro-cardiographic (ECG) findings indicative of an inferior MI. However, no studies have investigated whether the amplitude of the QRS complex in the right precordial leads obtained before the onset of MI (baseline ECGs) affects the ECG-based diagnosis of inferoposterior MI. We studied 78 patients who had had ECGs recorded within 6 months before MI, 53 with an inferior MI and 25 with an inferoposterior MI. The two groups were compared in relation to ECG findings and regional wall motion shown by two-dimensional echocardiography. The baseline R-wave amplitude and R/S ratio in leads V1 and V2 were significantly greater in patients with inferoposterior MI than in those with inferior MI. Two-dimensional echocardiography revealed abnormal posterior wall motion in 44% of patients with inferoposterior MI but in 2% of the patients with inferior MI. When abnormal posterior wall motion was used to define posterior MI, the conventional ECG criteria for inferoposterior MI had a sensitivity of 92%, a specificity of 78%, a positive predictive value of 44%, and an accuracy of 81%. Using new diagnostic criteria in which inferoposterior MI was diagnosed by the difference between the R/S ratios in lead V1 from the baseline and post-infarction ECGs ≥0.3 and findings indicative of inferior MI, the sensitivity was 83%, the specificity was 91%, the positive predictive value was 63%, and the accuracy was 90%. Conventional diagnostic criteria for inferoposterior MI are affected by variability in the amplitude of the QRS complex in the right chest leads on the baseline ECG. Using the baseline ECG, we established new criteria with higher accuracy for diagnosing inferoposterior MI.

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Abnormal Q waves resulting from myocardial infarction (MI) may regress, or disappear, after MI. However, the clinical significance of the disappearance of Q waves after MI remains unknown. The purpose of this study was to evaluate the clinical significance of the disappearance of Q waves within 1 month after MI. The study included 285 consecutive patients with their first anteroseptal MI (mean age: 63±12 yrs, 221 men, 64 women) who had electrocardiograms recorded on the onset day, on the 7th day and 1 month after MI. In addition, the patients underwent 2-dimensional echocardiography on the onset day and 1 month after MI, radionuclide angiography in the acute phase and 1 month after MI, and coronary angiography on the onset day. Twenty patients (7%) showed disappearance of Q waves in the precordial leads on the 7th day, and 48 patients (17%) showed disappearance of Q waves 1 month after MI. Logistic multivariate regression analysis demonstrated that the left ventricular ejection fraction (LVEF) during acute phase was the only independent factor associated with the disappearance of Q waves 1 month after MI. In patients with ≧4 precordial leads with Q waves on the onset day patients with ≦2 precordial leads with Q waves on the 7th day had significantly higher LVEF than patients with 4 precordial leads with Q waves on the 7th day (51.9±13.2% vs. 43.7±14.3%, p<0.05; 51.9±13.2% vs. 42.3±9.3%, p<0.01). In the same group, there were no significant differences in LVEF between patients with ≧4 precordial leads with Q waves on the onset day and patients with ≦2 precordial leads with Q waves 1 month after MI. In patients with 3 precordial leads with Q waves on admission, patients with ≦2 precordial leads with Q waves had a significantly higher LVEF than patients with 3 precordial leads with Q waves on the 7th day (55.4±11.6% vs. 45.6±14.0%, p<0.05). In the same group, there was no significant difference in LVEF between patients with 3 precordial leads with Q waves on the onset day and patients with ≦2 precordial leads with Q waves 1 month after MI. I conclude that the LVEF is the only independent factor associated with the disappearance of Q waves and that the disappearance of Q waves on the 7th day is a predictor of a satisfactory LVEF 1 month after MI.

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Cardiogenic shock in the setting of an acute myocardial infarction (MI) with left ventricular (LV) failure is associated with an extensive infarct and a poor prognosis. It also occurs due to hemodynamic deterioration from severe right ventricular (RV) dysfunction in RVMI, and adversely affects the prognosis of acute inferior MI. We evaluated the outcomes of patients with acute inferior MI and cardiogenic shock with respect to the presence or absence of RVMI. Subjects consisted of 504 consecutive patients with acute inferior MI. On admission, 159 of the 504 patients were diagnosed as having an RVMI. Of these, 69 developed cardiogenic shock in the acute phase (RVMI (+)/shock (+)), while 90 did not (RVMI (+)/shock (-)). Of the 345 patients without RVMI, 99 developed cardiogenic shock in the acute phase (RVMI (-)/shock (+)), while 246 did not (RVMI (-)/shock (-)). Compared with RVMI (+)/shock (+) patients, patients in the RVMI (-)/shock (+) group had a significantly increased LV dimension (p<0.01) and total wall motion index (p<0.01) and significantly reduced values for LV ejection fraction, RV dimension, right atrial pressure, and the rate of primary coronary angioplasty (all p<0.05). RVMI (-)/shock (+) patients exhibited increased in-hospital mortality (p<0.01) and reduced long-term survival (p<0.01) compared to the RVMI (+)/shock (+) group. Multiple logistic-regression analysis revealed cardiogenic shock, but not RVMI, to be a significant, independent marker for the prediction of long-term prognosis (odds ratio, 3.57 ; 95% confidence interval 2.05-6.22 ;p<0.01). In acute inferior MI, cardiogenic shock is an important predictor of worse in-hospital and long-term outcomes. Development of cardiogenic shock following acute inferior MI is associated with a poor prognosis, even in the absence of RVMI.

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Regarding our primary study about the abnormalities in the autonomic nervous system of autistic patients, we tried another evaluation of them with thermography. It is known that the variance of the skin temperature is influenced by the peripheral blood flow and the sweat transpiration. Therefore, we examined the changes of the facial skin temperature to investigate the alteration of physical functions following exercise loading, using thermography in infantile autistic patients. Five squares (tip of nose, lips, forehead, left cheek and right cheek) of facial skin temperature were compared before and just after the loading. Marked decrease of temperature was observed in control subjects but not in patients with autism. Skin temperature of the forehead and the lips in autistic patients did not change significantly during thermographic measurements though significant decrease was observed in controls. These results indicated the possibility that the autistic patients have the dysfunction of autonomic nervous system associated with peripheral vasomotor system or sweat regulation. Furthermore, it was suggested that the estimation of the facial skin temperature with thermographic technique is useful as means of investigation of autonomic nervous function in autistic patients.

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