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不整脈の頻度は加齢とともに増加する.老年者の不整脈で高頻度なものは期外収縮と心房細動である.一方, 不整脈の基盤となる刺激伝導系の組織学的変化をみると, 高齢者における洞房結節では膠原線維, 細網線維および弾性線維の増加があり, 結節内とその周囲に脂肪の浸潤がみられる.著明な結節細胞の減少や結節周囲の線維症, 脂肪化は洞不全症候群 (SSS) をきたす.老年者の洞不全症候群22例 (男性8例, 女性14例; 平均78歳) の検討では半数は著明な洞結節細胞の減数を示し, 残りの半数は結節周囲の線維症や脂肪浸潤が関与していた.また房室伝導系では, 房室結節やヒス東貫通部は軽度の線維症を時にみるが, ヒス束分岐部, 左脚後枝は中等度の線維症を示すことが多く, 右脚にも線維症をみる.老年者の高度ないし完全房室ブロック35例 (男性17例, 女性18例; 平均79歳) の検討では, 障害部位としては補充調律QRS幅の正常群ではヒス束貫通部や分岐部内の障害が目立ち, 補充調律QRS幅の広い群ではヒス束分岐部や左右脚の線維症によるものが多かった.最もよく心臓の加齢変化と性差を示している僧帽弁輪石灰化 (MAC) は高齢女性に有意に高頻度で, これが心室中隔頂上部や中心線維体に及ぶと房室結節やヒス束を圧迫して高度の房室ブロックをきたすことがある.MACを合併した高度ないし完全房室ブロック12例 (男性4例, 女性8例; 平均86歳) につき刺激伝導系の組織学的検討を行った.その半数がMACによる房室プロックで, それらの伝導系障害部位はヒス束貫通部であった.またMACによる伝導障害と対比するために石灰化大動脈弁狭窄症 (Calc AS) 10例 (男性5例, 女性5例; 平均80歳) で刺激伝導系所見を検討した.このうち4例に高度ないし完全房室プロックがみられたが, 2例はヒス束 (貫通部と分岐部とも) と両脚の高度線維症, ほかの2例はヒス束分岐部と両脚の高度線維化を示した.なお4例中3例は, 大動脈弁バルサルバ洞底部から心室中隔頂上部にまで伸びた巨大石灰化による伝導系組織への圧排が原因であった.

Although blood pressure (BP) is a major determinant of pulse wave velocity (PWV), some treatments have independent effects on BP and arterial stiffness. Although both ambulatory BP (ABP) and self-measured BP at home (HBP) have become important measures for the diagnosis and management of hypertension, single day recordings may be insufficient for a proper diagnosis of hypertension or the evaluation of treatment efficacy. To evaluate weekly variations in BP using 7-day HBP and 7-day ABP monitoring and to determine the relation between arterial stiffness and BP measurements in community-dwelling patients with hypertension. We enrolled 68 community-dwelling hypertensive subjects in this study. Significant weekly variations in systolic blood pressure (SBP) and diastolic blood pressure (DBP) were found in the awake ABP data (p.01, respectively), while no significant weekly variations in the asleep ABP or the morning and evening HBP data were observed. In untreated subjects, significant correlations were obtained between the brachial-ankle PWV and the average awake SBP, the average asleep SBP and the average SBP measured by HBP in the evening. In treated subjects, only the average SBP measured by HBP in the morning was significantly correlated with the baPWV. Differences in the weekly variations in BP were observed between HBP and ABP monitoring. In addition, the morning systolic HBP was not correlated with arterial stiffness in untreated subjects with hypertension but was correlated in treated subjects. Relations between the morning HBP and arterial stiffness might be attributed to morning surges in BP and/or trough levels of antihypertensive drugs.

Background Although weekly variations with a peak on Monday have been reported in the incidence of cardiovascular events, few studies have investigated weekly variations in blood pressure (BP). Methods One hundred and thirty-five community-dwelling subjects had 24-h ambulatory BP monitoring for 7 days. We calculated the mean awake, asleep, morning (during the first 3 h after awaking) BP, and morning BP surge (mean morning systolic BP minus mean asleep systolic BP) for each day. Results Monday surge in BP was found in the awake and morning BP (awake BP: 128.8 ± 15.4/79.1 ± 9.2 v 131.5 ± 16.3/80.7 ± 10.0 mm Hg, P < 0.01, respectively; morning BP: 127.3 ± 17.8/78.8 ± 11.4 v 132.5 ± 18.2/81.2 ± 10.0 mm Hg, P < 0.01, respectively) but was not found in the asleep BP (112.7 ± 18.3/68.4 ± 10.7 v 113.1 ± 17.6/68.7 ± 10.5 mm Hg, P = NS, respectively). The morning BP surge on Monday was higher than on the other days of the week except for Tuesday (Monday: 19.7 ± 13.3 mm Hg v Friday: 16.4 ± 12.9 mm Hg, P < 0.05; v Saturday: 14.7 ± 13.3 mm Hg, P < 0.01 v Sunday: 13.7 ± 12.0 mm Hg, P < 0.01; v Wednesday: 15.5 ± 14.3 mm Hg, P < 0.01). Conclusion Morning BP surge was the greatest on Monday in a community-dwelling population. This may be in accord with clinical evidence that cardiovascular events more frequently occur in the morning on Monday.

症例は71歳,男性で,平成元年(60歳時)に心不全で当院内科に入院した.心房細動,僧帽弁閉鎖不全および三尖弁閉鎖不全の診断で内服治療を開始した.その後も心不全,脳梗塞,肺炎で計13回の入退院をくり返していた.平成12年2月(71歳),心エコー,心臓カテーテル検査の結果,手術適応となり当科紹介となり,同年3月,僧帽弁置換術および三尖弁輪形成術を施行した.僧帽弁は前,後尖とも中等度に肥厚し,腱索も肥厚と癒合が認められた.さらに,前側乳頭筋より僧帽弁前尖の弁基部に直接付着する乳頭筋がみられ,前尖の可動性を制限していた.病理組織所見では,古いリウマチ性と思われる変化に加えて,1ヵ所に横紋筋組織(乳頭筋)が前尖の弁基部へ走行していた.臨床的に乳頭筋前尖接合が僧帽弁閉鎖不全に関与したとする症例報告はこれまで少ないことから,若干の文献的考察を加えて報告した.

The purpose of this study was to examine complicated lesions of saccular aneurysm and dissection. We investigated the ascending aortae in 5865 consecutive elderly autopsy cases, and 5 cases (0.085%) of aortic saccular aneurysms associated with dissection at the edges were selected. Their edges characteristically protruded like a shelf, which histologically consisted of an inner part of the dissected media. All patients were female and their mean age was 76.8 (67-89) years. The aneurysmal walls at the center showed severe fragmentation and disappearance of the elastic lamellae of the remaining outer media. Thus, partial sections of these lesions were not sufficient but cross-sections of the whole diseased regions including the edges were essential for diagnosis. One patient had 3 saccular aneurysms and an adjacent shallow depression, which we called “healed microscopic dissection”. Histologically, it showed disappearance of the inner media and was replaced by fibrosis in continuation from the intima. This lesion showed no findings of intramural hemorrhage or thrombus, and thus it will differ from organized thrombi in the dissected false lumen. Another patient presented had an aneurysmal rupture which resulted in cardiac tamponade. This case implies the need for surgical treatment of this entity.

To clarify the clinical features and to select optimal treatment of hepatocellular carcinoma (HCC) in the elderly, 163 patients were divided into the following three groups and retrospectively evaluated: Group O (> or = 70 years of age, 47 cases), Group IM ( or = 60 years, 70 cases) and Group Y (< 60 years, 46 cases). There were fewer HBsAg-positive cases and those in clinical stage III in Group O than in Group Y (p < 0.05). Although the percentage of women and small HCCs in Group O were somewhat higher than those in other groups, there were no significant differences among the three groups with regard to sex, size of nodule and time after blood transfusion. Most of the alcohol-abuser were in Group Y (p < 0.05). Some active treatment was possible in 76.6% of the elderly individuals, in 87.1% of the patients of Group IM, and in 78.3% of the Group Y, while few underwent hepatic resections (Group O, 4.3% vs. Group IM, 8.5% vs. Group Y, 8.6%) or PMCT (4.3% vs. 11.4% vs. 8.6%). The allocation of other therapeutic modalities in the three groups were also statistically identical. The prevalence of concomitant diseases was significantly higher in the elderly patients (53%) than in their younger counterparts (Group IM; 30%, Group Y; 28.2%) (p < 0.05). Although the reasons for the paucity of treatment in Group IM and Y (9 and 10 cases) were liver-associated factors (i.e., advanced clinical stage or tumor size), attempts to apply therapeutic measures were abandoned in 11 cases in Group O because of their advanced age (2 cases) or heart failure (1 case). The 5-year survival rate was higher in Group O (55%) than those in Group IM (32%) and Y (26%) (p < 0.01). These results suggest that because of the higher incidence of concomitant diseases, less invasive therapeutic modalities, such as PEI/PMCT, should be recommended for elderly patients with HCC.

The aim of the present retrospective study was to clarify the histopathologic substrates of left ventricular myocardium with transient asynergy due to acute ischemic insult in man. Three patients who had had prolonged chest pain, new abnormal Q waves and new ST segment elevation were studied. There was no significant elevation of serum creatine phosphokinase activity in two of the three patients. Echocardiograms on admission or the next day showed severe hypokinetic or akinetic motion and thinning of the anteroseptal and apical portions of the left ventricle and regional dilatation of the same portions. Disappearance of the abnormal Q waves, ST segment elevation resolution, and early T wave inversion were observed later. Complete improvement of the echocardiographic abnormalities was confirmed after a few weeks in all patients. Manifest ischemic lesions of subendocardial scars of the anteroseptal region of the left ventricle were detected in only one of the three cases by gross examination. However, on microscopic examination, islands of necrotic myocytes were interspersed with islands of viable cells throughout the jeopardized region in one case, although the scattered necrotic foci were restricted to the subendocardium and the trabeculae. Normal myocardium and subendocardial scars were observed in the other two cases. In conclusion, left ventricular myocardium with transient asynergy, detected clinically during acute ischemic attack, consists of normal myocardium or small ischemic lesions primarily in the subendocardium.

A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied Purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.

A previously healthy 64-year-old woman attended our hospital with chest pain, facial edema, and general fatigue. A chest radiograph revealed cardiomegaly, small bilateral pleural effusions, and hilar congestion--findings that improved after early therapy with furosemide and methyldigoxin. A chest radiograph recorded 7 years earlier had revealed no dilation of cardiac shadow. There were no findings suggesting atrial septal defect (ASD) or valvular heart disease. Echocardiography revealed a tumor-like mass adhering to the posterior wall of the left atrium. Color-flow Doppler echocardiography revealed a left-to-right shunt at the atrial level. The Qp/Qs ratio as measured by cardiac catheterization was 2.0. Coronary angiography revealed abnormal dilated arteries from the atrioventricular nodal branch and several feeding arteries from the left circumflex branch. We hypothesized that the left-to-right shunt could be due to the tumor, which extended to the rim of the patent foramen ovale, or to the very small, previously unrecognized, ASD. This patient died 6 months after her first admission and an autopsy was performed. Light microscopic examination of the tumor revealed spindle-shaped fibroblast-like cells arranged in a storiform or fascicular pattern. The immunohistochemical findings were consistent with malignant fibrous histiocytoma (MFH). In the literature, left-to-right shunt at the atrial level has not been reported in patients with cardiac MFH.

Patient's reports of angina pectoris depend on cognition and communication, and on the patient's physical and mental activity. In elderly people, these functions are often impaired, and we therefore looked for evidence of myocardial ischemia in 770 consecutive autopsies. We defined the coronary stenosis index (CSI) as the sum of the stenosis scores of three coronary arteries: 0% = 1, 25% = 2, 50% = 3, 75% = 4, 90% = 4.5 95 or 100% = 5. A total score of more than 13.0 and a score of 5.0 in one vessel was assumed to have been associated with myocardial ischemia. Patients assumed to have had myocardial ischemia were classified according to the presence or absence of angina pectoris: 24 had angina pectoris and 92 were asymptomatic. As controls, 86 patients in whom the CSI was lower than 10.0 were studied. Death due to myocardial infarction was most frequent in patients with angina (67%). Acute myocardial infarction was more common in asymptomatic patients than in controls (27% vs. 1%). Small myocardial infarctions and inferior myocardial infarctions were more frequent in asymptomatic patients than in those with angina. Cerebrovascular disease, problems doing activities of daily living, and communication disturbance were more common in asymptomatic patients than in those with angina. Electrocardiographic evidence of an old myocardial infarction was found in 40.9%, 16.6%, and 2.3% of patients with angina, asymptomatic patients, and controls, respectively (p < 0.05). Morphologic details of the myocardial infarction, coexistence of cerebrovascular disease, inability to perform activities of daily living, and impaired communication are associated with asymptomatic myocardial ischemia. Patients with asymptomatic myocardial ischemia should be identified and treated because of their relatively poor prognosis. Ischemic events might be detected by careful observation and prevented by appropriate treatment.

Objectives. We sought to study the pathologic implications of restored positive T waves and persistent negative T waves in the chronic stage of Q wave myocardial infarction. Background. Some inverted T waves (coronary T waves) become positive after acute myocardial infarction: others retain their negative T wave component for a long time. The pathologic implications of the difference between restored positive T waves and persistent negative T waves in leads with Q waves has not, until now, been given much careful study. Methods. Of 17 patients with anterior or anteroseptal myocardial infarction confirmed by autopsy, 8 (group P) had positive and 9 (group N) had negative T waves in precordial leads with Q waves ≥ 1 year after the onset of myocardial infarction. The appearance and extent of the infarct area and the degree of coronary artery stenosis were evaluated in both groups. Results. At autopsy, seven of eight patients in group P had nontransmural fibrotic changes in the anteroseptal or anterior wall. However, seven of nine patients in group N had a transmural myocardial infarction consisting of only a thin fibrotic layer in the anteroseptal or anterior wall. The left anterior descending coronary artery showed 75% stenosis in 1 patient in each group but >90% stenosis in the remaining 15 patients. Conclusions. Persistent negative T waves in leads with Q waves in the chronic stage of myocardial infarction indicate the presence of a transmural infarction with a thin fibrotic layer, whereas positive T waves indicate a nontransmural infarct containing viable myocardium within the layer.

The aim of this study was to assess the incidence of myocardial infarction among persistent perfusion defects in dipyridamole-stress thallium scintigraphy by inspecting autopsied hearts and to evaluate whether the regional thallium activity of a scintigraphic defect can predict the presence of infarction. Autopsied hearts were compared with dipyridamole myocardial scintigrams undertaken during life in 27 patients (mean age 85±8 years), The time interval from stress testing until death was 428±351 days. Regional thallium uptake of delayed perfusion defect was calculated on the short axis images. The grade of regional myocardial fibrosis in autopsy specimens was also quantified to correlate with the corresponding regional thallium uptake. In 6 of 15 (40%) regions with persistent defects on the scintigram, myocardial infarction was not found at autopsy. Regional thallium-201 uptake of delayed defects

We investigated the relationship between clinic blood pressure (BP) and ambulatory blood pressure (ABP) in 297 elderly patients who underwent 24 hour ABP monitoring as a non-academic clinical references. Among 107 cases who were normotensive in office BP measurements, 33 cases (30.8%) proved to be hypertensive with more than 140 mmHg in ambulatory systolic BP. Those patients should be referred to as home hypertension or white coat normotension. On the other hand, among 187 patients who were hypertensive in the clinic, 78 cases (41.7%) turned out to be white coat hypertension with an ambulatory daytime systolic BP of less than 140 mmHg. Ambulatory systolic BP in white coat hypertension was comparable with that in the non-hypertensive group although their BP in the clinic was significantly higher than the latter (p < 0.02). Ambulatory systolic BP in the home hypertension group was significantly higher than that in the normotension but was comparable with that in true hypertension. The number of the antihypertensive drugs prescribed in the white coat hypertensive group tended to be greater than that in other groups although that in the home hypertensive group was similar to the other groups. The incidence of cerebro vascular disease in each group was similar.

Objectives. We sought to clarify the clinicopathologic characteristics of insidious or healed myocarditis in the elderly. Background. Myocarditis is the cause of unexplained congestive heart failure and dilated cardiomyopathy. However, acute myocarditis of the Fiedler type is rare, and the incidence and implication of insidious or healed myocarditis in the elderly are not yet known. Methods. In an autopsy study of 3,000 patients aged ⩾60 years, there were 12 (0.4%) with insidious or healed myocarditis, showing extensive and circumferential fibrosis and scattered lymphocytic infiltration of both ventricular walls without acute necrosis of the myocardial fibers. Results. Unexplained congestive heart failure was found in seven cases. In all cases, electrocardiography had demonstrated upward elevation of the ST segment and inverted T waves for durations ranging from 1 month to 12.7 years (mean 5.7 years). Mean (± SD) heart weight was 338 ± 81 g (range 220 to 470). In nine cases, fibrous lesions, which were scattered but extensive and circumferential, were located in the subepicardial and middle layers of the left ventricle. In the remaining three cases, the fibrous lesions were located predominantly in the subepicardial and middle layers, but the subendocardial layer was also locally involved. Fibrous lesions of the right ventricle were predominant in the subepicardial layer and involved the subendocardial layer in four cases. Scattered lymphocytic infiltration was found in the fibrous lesions. Conclusions. In more than half of the aged cases with insidious or healed myocarditis, unexplained congestive heart failure was also present. Fibrous lesions due to myocarditis were located predominantly in the subepicardial and middle layers and led to persistent upward elevation of the ST segment and inverted T waves.

To characterize slow abnormal conduction in the low right atrium, which is known to be responsible for atrial flutter, electrophysiologic findings were correlated with anatomic features in a canine model of atrial flutter with ligation of the crista terminalis in the midright atrium. Activation in the low right atrium was mapped with a patch electrode containing 52 bipolar electrodes and a multiplexing system. A particular region in the low right atrium showed atrioventricular node-like electrophysiologic properties, a rate-dependent conduction delay, and Wenckebach periodicity. This area coincided with an area responsible for slow conduction during atrial flutter and unidirectional block at its initiation. Both pilsicainide and E-4031 preferentially blocked conduction in the specific area, leading to the termination of atrial flutter. Although refractoriness could not explain the abnormal conduction, anatomic studies consistently found the specific region to be in or around a thick muscle bundle, that is, the crista terminalis, or a thick pectinate muscle branching from the crista, located perpendicular to the wavefront of the pacing impulse and atrial flutter. These electrophysiologic and anatomic findings suggest that slow abnormal and atrioventricular node-like conduction over a thick muscle bundle, which is a normal anatomic feature of the low right atrium, plays a role in the initiation, maintenance, and termination of atrial reentry.

A 77-year-old male had been noticing progressive weakness of the legs for three years. By the age of 75 he had difficulty in climbing stairs. On admission, serum level of CPK was moderately high. There were weakness and atrophy of the proximal muscles. Deep tendon reflexes were depressed. Sensation was normal. The electromyogram and the biopsy of the femoral quadriceps muscles showed nonspecific changes. In 1989, he developed difficulty in walking and had congestive heart failure. On the second admission, moist rales were heard over the chest, and pitting edema was present in the lower extremities. The chest roentgenogram showed a cardiothoracic ratio of 63% and bilateral pleural effusion. The electrocardiogram showed atrial flutter with 2:1 conduction, QS in V1-3, rS in V4, and ST depression and T inversion in V5,6. The echocardiogram revealed a thick left ventricular wall and impaired left ventricular contraction (EF 22%). Macroglossia, hepatosplenomegaly and renal dysfunction were not noted. Congestive heart failure progressed and he suddenly died of ventricular tachycardia in December 1989. At autopsy, skeletal muscle fibers varied in size and showed fiber splitting. A cellular infiltration was observed in the stroma. Amyloid deposit was positively stained with Congo red. The heart weight was 570 g with marked left ventricular hypertrophy and moderate bilateral atrial dilatation. In both atria and ventricles, extensive amyloid deposition was found around myocardial fibers as well as in perivascular spaces. Amyloid was present also in the liver, the kidneys, the gastrointestinal tracts, and the other organs.(ABSTRACT TRUNCATED AT 250 WORDS)

An autopsied 85-year-old man had suffered from a mild form of diabetes mellitus since the age of 67 and had experienced the first episode of heart failure with arapid ventricular rate of atrial fibrillation at the age of 72. He had remained socially active until he died suddenly of ventricular fibrillation, although he had complications of aortic regurgitation at the age of 76 and later mitral regurgitation at the age of 80. Chest roentgenograms showed gradual increase in the cardiothoratic ratio which reached 68.1% at the final stage. Autopsy revealedmarked left ventricular hypertrophy with a heart weight of 580 g, degeneration ofaortic valves, thickening of mitralvalve cusps and moderate coronary atherosclerosis without ischemic myocardial lesions. There were no specific lesions suggestive of primary cardiomyopathies on microscopic observations and the lesions of both aortic and mitral valves were not significant enough to explain the clinical findings of aortic and mitral regurgitation. Because the pathological examination failed to identify a single disease which was responsible for the marked cardiachypertrophy, we eventually reached the conclusion that the cardiac hypertrophy developed based on a multifactorial heart disease.

Two autopsy cases of aortitis syndrome (Takayasu's aortitis) in the elderly are presented. Case 1 was an 81-year-old woman in whom hypertension was observed at age 37, and difference of right and left arm blood pressure was pointed out at age 65. She was referred to the authors' hospital at age 72. Chest X-ray and computed tomography of the thorax indicated atypical coarctation and diffuse calcification of the aorta. Case 2 was a 69-year-old woman in whom hypertension was pointed out at age 49, and blood pressure in the arms was found to differ from that in the legs at age 63. Chest X-ray and computed tomography showed diffuse calcification and marked narrowing of the descending aorta. Pathological examination revealed marked calcification in the thickened adventitia of the aorta with mild atherosclerotic change. Irregular fibrotic changes of the adventitia and degeneration of elastic fibers of the media of the aorta were noted in both cases, and were consistent with Takayasu's aortitis. This disorder is common in young women and only a small number of elderly cases are reported although its incidence is increasing. Diffuse calcification of the aorta with an absence of inflammatory signs, which is frequent in older patients, were observed in both case. Systemic hypertension is the most important risk factor with coarctation of the aorta in Takayasu's aortitis. Bypass surgery is recommended in young patients, however in elderly patients, it is generally avoided, in favor of medical control of hypertension.

In an 82-year-old female case of endocardial cushion defect (ECD), a systolic regurgitant murmur was heard at the apex, and her ECG showed atrial fibrillation without right bundle branch block or left axis deviation. An echocardiogram demonstrated atrial septal defect (ASD) and a cleft of the anterior mitral leaflet with calcification. She died of refractory congestive heart failure. Autopsy revealed ECD (intermediate type) with mitral and tricuspid cleft, and ASD (ostium primum type, 2.0 x 1.0 cm in diameter). In addition, mitral ring calcification and calcification of the cleft mitral valve was disclosed, causing mitral stenosis in addition to mitral regurgitation due to the cleft mitral valve. This was the second oldest Japanese autopsy case of ECD. We concluded that echocardiographic examinations, including color flow imaging, in aged patients with heart murmur are necessary to confirm the diagnosis of congenital heart disease in the aged.

Immunohistochemical and biochemical analyses of several tissues were performed in two unusual cases of Fabry's disease which showed accumulation of globotriaosylceramide (Gal alpha 1-4Gal beta 1-4 Glc-Cer, Gb3Cer) only in the hearts, but no clinical signs of the disease. Immunohistochemical study revealed that the hearts from our cases (cases no. 1 and 2) contained large amounts of anti-Gb3Cer antibody-positive granules in cytoplasms as in typical Fabry's disease. The contents of accumulated Gb3Cer in the hearts from case no. 1, case no. 2, and a typical Fabry's disease case were approximately 100, 340, and 100 times higher than those from normal controls, respectively. While typical Fabry's diseased kidney and liver contained approximately 40 and 50 times higher amounts of Gb3Cer than did controls, no accumulation of Gb3Cer was observed in kidney and liver of our cases. The only exception was a slight increase of Gb3Cer in kidney of case no. 2 (about two times higher than controls), in which epithelial cells of the glomeruli but not of other types of cells were positively stained by anti-Gb3Cer antibody. Case no. 1 kidney and liver were not stained by the antibody. The glomerular endothelium and epithelium, tubular epithelium, smooth muscle of renal arteries, and several hepatocytes were Gb3Cer-positive in the typical Fabry's disease case. The involvements of our cases differed distinctly from the typical Fabry's disease case.

Seven elderly patients with hypertrophic obstructive cardiomyopathy (HOCM), who had the three following characteristics on echocardiograms 1) extremely thickened septum, 2) systolic anterior motion of the mitral valve, 3) mid systolic semi-closure of the aortic valve, were clinically evaluated. Ages ranged from 73 to 86 years old (average 78.9% yr.) and all were women. None had not a family history of hypertrophic cardiomyopathy but they had mild hypertension. Six patients showed a significant high voltage on the ST-segment and T-wave abnormalities ("strain" pattern). The left ventricular posterior wall as well as the septum was thickened in 5 and the remaining 2 showed asymmetrical septal hypertrophy (ASH) on echocardiograms. The left ventricular cavity was narrowed due to left ventricular hypertrophy and the shape of the left ventricular cavity was ovoid in all patients. The aorto-septal angles in these 7 patients were 80 degrees to 120 degrees. In addition, proximal septal bulge in all and anterior displacement of the mitral posterior leaflet due to the mitral ring calcification (MRC) in some patients contributed to the narrowing of the left ventricular outflow tract, and the mitral valve was pulled up toward the septum because of the good left ventricular systolic function (ejection fraction: 70 to 94% by echocardiography) and blood was ejected at a high velocity through a narrowed outflow tract (Venturi effect). Pressure gradients in the left ventricular outflow tract was 38 to 146 mmHg in 5 examined by cardiac catheterization. Biopsy specimens were obtained from 2 patients, showing hypertrophic myocytes (diameter: 20 to 30 micron) in 2 and mild disarray in 1.(ABSTRACT TRUNCATED AT 250 WORDS)

A case of invasive thymoma that responded well to the administration of a high-dose methylpredonisolone with cisplatin and adriamycin is reported. A 63-year-old woman was admitted to our hospital because of dyspnea, chest oppression and edema of the face. Chest CT revealed a large mass in the anterior mediastinum with the opacification of superior vena cava. Biopsy specimens from the mass revealed a spindle cell thymoma, consisting of epithelial cells and lymphoid cells. A diagnosis of invasive thymoma was made and the patient was intravenously treated with a high-dose of methylprednisolone (1000 mg on days 1-5 and 500 mg on days 6 and 7), cisplatin (80 mg/m2 on day 1) and adriamycin (40 mg/m2 on day 1). The treatment with three courses of this combined chemotherapy resulted in the improvement and regression of all clinical signs and symptoms. This case demonstrated that a high-dose methylprednisolone with cisplatin and adriamycin might be potentially effective for invasive thymoma.

We evaluated the relationship between the severity of thrombocytopenia and the serum hepatitis C virus (HCV) RNA level to investigate the mechanism of thrombocytopenia in patients with HCV infection. Patients who had chronic hepatitis without splenomegaly were divided into two groups according to the platelet count, which were 18 patients with a platelet countor =150 x 10(9)/L and 22 patients with a platelet count150 x 10(9)/L. HCV RNA, platelet-associated immunoglobulin G (PAIgG), rheumatoid factor (RF), and other immunological parameters were measured and correlations were investigated. Patients in the low platelet group had higher levels of PAIgG, Th1 cells, thrombopoietin (TPO), and RF than those in the normal platelet group (textitP0.05). Twenty-two patients completed 6 months of IFN therapy and were followed for more than 1 yr afterwards. Twelve patients who responded to IFN therapy with clearance of HCV showed an increase of the platelet count, whereas the 10 patients who did not respond to IFN showed a decrease of the platelet count. The improvement of thrombocytopenia after interferon therapy suggests a contribution of HCV infection to this condition.

Hypertrophic osteoarthropathy is an important manifestation of lung carcinoma, particularly in a non-small cell tumor, and hampers quality of life. Although removal of the primary tumor usually resolves this syndrome, effective treatment in patients with advanced lung carcinoma has not been established. Recently, an orally active, selective epidermal growth factor receptor tyrosine kinase (EGFR) inhibitor ("Gefitinib") provided clinical anti-tumor activity. We describe a 71-year-old male smoker with cough, who presented with clubbed fingers. A transbronchial lung biopsy (stage T2N3M1-IV) on a cavity lesion in the left lower lobe showed the features of adenocarcinoma, while bone scintigram revealed bilaterally symmetrical abnormal uptakes in the lower extremities, suggesting secondary hypertrophic osteoarthropathy. The serum level of growth hormone was increased to 1.42 ng/ml. Chemotherapy (cisplatin, vinorelbine) was not effective. Gefitinib, as a second-line therapy, induced disappearance of the abnormal accumulation on bone scintigraphy and decrease of the cavity in the lung and of serum growth hormone. The presented case suggests that the EGFR inhibitor might be a promising option for the treatment of hypertrophic osteoarthropathy with advanced lung adenocarcinoma.

Lewy bodies (LB) are characteristic pathological findings for idiopathic Parkinson disease, and extracranial organs have also been known to exhibit these structures. Clinically, the possible involvement of LB in cardiac dysfunction has attracted attention based on the findings of studies using [123I] metaiodobenzyl guanidine (MIBG) scintigraphy. The purpose of the present study was to investigate the possible involvement of LB in heart disease. A total of 40 autopsy cases consisting of Lewy body disease and Parkinson syndrome were examined. The former were cases with intracranial LB regardless of clinical symptoms, and the latter were cases with parkinsonism but without intracranial LB. The presence of heart disease or an atrial arrhythmia and the results of an MIBG scintigraphy study were clinically examined. The sinoatrial node was examined microscopically and immunohistochemically. The results showed that heart disease and atrial arrhythmia complications were more frequent in cases with Lewy body disease than in cases with Parkinson syndrome and that LB were frequently found in extracranial organs, especially in the sinoatrial nodal ganglion, in cases with Lewy body disease. In the current report, we hypothesized that neuronal changes involving LB in the sinoatrial nodal ganglion may cause arrhythmia and ischemic heart disease as a result of vasoconstriction.

Hepatic tuberculosis is one of the uncommon forms of extrapulmonary tuberculosis. We report a 78-year-old woman who developed tuberculous liver abscesses with splenic abscess not associated with pulmonary foci. Ultrasonography and computed tomography of the abdomen showed the low-density lesions in the liver and spleen. Histopathology of specimens obtained by percutaneous needle biopsy revealed coagulation necrosis and epithelioid cells but not tumor cells, suggesting tuberculosis infection in the liver and spleen. Systemic chemotherapy with anti-tuberculous agents led to the improvement of the lesions in the liver as well as spleen. Although tuberculous liver abscess is a very rare case, it should be included in the differential diagnosis of unknown hepatic mass lesions.

We present a case of Lemierre syndrome characterized by thrombophlebitis of the internal jugular vein with multiple metastatic foci after acute otopharyngeal infection in a 30-year-old woman. Despite treatment with tonsillectomy leading to a diagnosis of peritonsillar abscess, her condition worsened and she was admitted with high fever. Chest radiograph and CT scan of the thorax revealed multiple pulmonary cavities and pleural effusion on the right side. On neck CT, a thrombus was detected in the left internal jugular vein. She received with intravenous clindamycin (CLDM) and cefepime (CFPM) and progressively improved. Although Lemierre syndrome is a relatively uncommon disease with the potentially life-threatening complication of acute pharyngotonsillitis, this syndrome should be considered in cases of severe tonsillitis or pharyngitis.

To elucidate the role of mitogen-activated protein kinases (MAPKs) and Akt kinase in leukemogenesis caused by the breakpoint cluster region (BCR)–Abelson (ABL) tyrosine kinase oncoprotein, we examined the activities of MAPKs and Akt kinase and their roles in the action of STI571, a specific inhibitor of BCR-ABL tyrosine kinase, in chronic myelogenous leukemia (CML) cells. We found that extracellular signal-regulated kinase (ERK) 1/2 and Akt kinase are constitutively active in the chronic phase of CML, blast crisis of CML, and the CML-derived K562 cell line. Both interferon-α and STI571 suppressed ERK1/2 activity in K562 cells. In contrast, Akt kinase activity was inhibited only by STI571. K562 cell proliferation was markedly suppressed by LY294002, a specific inhibitor of PI3K/Akt kinase, and STI571 but not by PD98059, a specific inhibitor of MEK1/2. In addition, caspase-3 was activated by treatment of cells with STI571 and LY294002 but not with PD98059. These data indicate that Akt kinase may play a role in the proliferation of CML leukemia cells and the action of STI571. Primary leukemia cells from patients with CML blast crisis did not show inhibition of ERK1/2 or Akt kinase activity and were resistant to caspase-3-associated apoptosis after treatment with STI571. These findings suggest that STI571 does not effectively block signaling molecules downstream of the BCR–ABL tyrosine kinase in some cases of CML blast crisis.

A 66-year-old man was admitted to our hospital for fever on January 19, 1998. He began showing periodic high fever in June 1997 and an increased serum LDH in August 1997. His history included surgery for esophageal cancer in 1993. On admission, the patient's body temperature was 38.5 degrees C. Physical examination was negative for lymphadenopathy, hepatosplenomegaly, and skin rash. Peripheral blood revealed a hemoglobin level of 8.6 g/dl and a platelet count of 7.9 x 10(4)/microliter. Bone marrow examination showed hypocellularity with marked histiocytic hemophagocytosis. The various bacterial cultures were negative. Serum LDH was elevated to 1,606 IU/l, and ferritin was greater than 3,000 ng/ml. Antinuclear antibodies were negative. No significant elevation of viral antibody titers including that to Epstein-Barr virus was found. Hemophagocytic syndrome (HPS) was diagnosed, but no underlying diseases was identified. The patient's condition was complicated by interstitial pneumonia and pleural effusion. gamma-globulin and pulse methylprednisolone both proved ineffective for the HPS; however, complete remission was achieved with cyclic intravenous administration of etoposide (VP-16, 150 mg/day). Interestingly, the interstitial pneumonia resolved promptly with etoposide therapy. The patient relapsed, in July 2001, exhibiting high fever, cytopenia, and marrow hemophagocytosis. His condition was ameliorated by administration of etoposide. This was a rare case of chronic and recurrent HPS of unknown etiology accompanied by interstitial pneumonia. Etoposide should be considered as a primary therapy for HPS and its complications in cases such as our patients.

Background Although heart rate variability (HRV) has been found to be associated with increased mortality in the elderly, the association of HRV and cognitive function and activity of daily living (ADL) capacity in the very elderly are not clear. Methods A sample of very elderly people (N = 138), aged 75 years and older, living in Urausu, Hokkaido, participated in this study. Participants were classified into three groups: normal, borderline, and dementia. Time and frequency domain measures of HRV were compared with behavioral and cognitive functions. Results HRV components, except for the LF/HF ratio, did not correlate with age in the very elderly. The LF component showed a statistically significant correlation with all the variables of behavioral functions. Most HRV components showed statistically significant and positive correlations with the flexibility of the back. The LF and LF/HF ratio were significantly lower in the dementia group than in the normal group. Conclusion Although the meaning of the LF component is still controversial, we foundadefinite relationship between the LF component and behavioral functions. A positive relationship between most HRV components and the flexibility of the back may suggest that reduced flexibility leads to deteriorated cardiopulmonary function and reduced HRV. A further prospective study is needed to examine whether HRV and neurobehavioral functions are independent predictors of morbidity and mortality in very elderly people.

A Japanese man who died at age 85 had been followed since the age of 59, when he first presented. He had hypertension of 162/102 mmHg and a loud systolic murmur on his first visit. He had had an active daily life without any medication for the next 10 years. At the age of 72 he complained of mild chest discomfort on exercise. Although electrocardiography showed no abnormalities, echocardiogram showed calcified bicuspid aortic valve with mild stenosis. At the age of 81 the dyspnea and chest oppression were exacerbated, associated with marked ST depression on exercise electrocardiogram and restriction of aortic valve opening on echocardiograms. In the following years a gradual increase in QRS voltage and ST depression with T wave inversion were recorded on resting electrocardiograms and sharp increases in both left ventricular end-diastolic diameter and flow velocity at the aortic root were observed on echocardiograms. At the age of 85 he died of intractable heart failure with massive pleural effusion. Autopsy revealed marked hypertrophy and moderate dilatation of the heart (weight: 580 g). The bicuspid aortic valve had anterior-posterior cusps with a raphe on the anterior cusp. The mobility of the cusps was almost lost because of severe calcification and thickening. Severe stenosis was found near the orifice of the right coronary artery, but there were no significant ischemic myocardial lesions.

The present study undertook an extensive analysis of the histopathological findings of the atrioventricular conduction system in 14 elderly patients treated with permanent pacemakers for sick sinus syndrome (SSS). Special attention was given to the lowest Wenckebach block points of atrioventricular conduction during rapid atrial pacing, and ventricular rate or duration of ventricular pause during chronic atrial fibrillation. An electrophysiological study (EPS) was conducted under sinus rhythm in 13 patients and under junctional escape rhythm in 1 patient. Three of the 14 cases showed a lower Wenckebach block point of 130 beats/min or less. Two of these 3 cases showed excessive fatty infiltration around the atrionodal junction area and into the atrophic atrioventricular node (AVN) itself. Of the 6 patients who had chronic atrial fibrillation after pacemaker implantation, 2 cases showed a slow ventricular response of less than 60 beats/min and/or a long ventricular pause of 3.3 s. One of the 2 cases showed a lower Wenckebach block point of 130 beats/min at the time of EPS. The other, who later progressed to idiopathic atriomegaly, also showed marked fatty infiltration around the AVN. This fatty lesion was closely associated with diffuse disruption of the muscular fibers connecting the atrophic AVN with the atrium. In addition, most of the remaining cases also had an atrophic AVN. In conclusion, a sparse or absent atrionodal connection and an atrophic AVN due to excessive fatty infiltration in the atrionodal transitional area should be investigated in atrioventricular conduction disturbances in the elderly with SSS.

A 61-year-old female who had shown Raynaud's phenomenon and articular swelling for 10 years, was admitted to hospital because of fever of unknown origin (FUO) and dry cough. She was diagnosed by skin biopsy to have a collagen disease or overlap syndrome. Anemia developed rapidly and FUO persisted, but blood culture was negative. Although indomethacin and prednisolone were administered for the progression of clinical signs and symptoms, severe dyspnea developed, resulting in bradycardia, followed by recurrent episodes of ventricular tachycardia. In spite of extensive treatment for her arrhythmia she died on the 9th hospital day. An autopsy revealed generalized Wegener's granulomatosis with extensive cardiac involvement. Necrotizing angitis and severe granulomatous inflammatory foci affected characteristically the common bundle of His and right bundle branch in addition to the ordinary myocardium.

The relationship between dipyridamole thallium-201 myocardial single-photon emission computed tomography and clinical findings during stress testing was investigated in 57 patients (mean age 72 years), including 11 patients with normal coronary arteries. Systolic blood pressure decreased from 138.2 +/- 19.7 to 119.8 +/- 20.1 mmHg (mean: -13.8 +/- 6.6%) after dipyridamole infusion (0.568 mg/kg/4 min). Scintigraphic sensitivity for the diagnosis of coronary artery disease was higher in 30 patients with a systolic blood pressure decrease above the average value than in 27 patients with a blood pressure reduction of less than 14% (88% vs. 60%, p < 0.005). Reversible perfusion defects among stenosed coronary arteries were more frequent in the former group (73% vs. 27%, p < 0.001) with no difference in other clinical findings. In conclusion, systolic blood pressure change during stress testing was significantly correlated with dipyridamole-induced perfusion defects and detectability of coronary stenosis.

Ninety-five patients aged 60 years or over with a permanent pacemaker implanted for sick sinus syndrome were divided into two groups: 32 patients with physiological pacing (group P) and 63 patients with ventricular pacing (group V). The mean follow-up period was 45.0 +/- 36.6 months in group P and 50.3 +/- 37.8 months in group V. Paroxysmal atrial fibrillation (Af) occurred in 28% of group P and 71% of group V (p < 0.05). The incidence of stable Af was also lower in group P than in group V (9% vs. 30%, p < 0.05). None of group P with only bradyarrhythmia had stable Af. However, 6 of 21 patients (29%) in group V with bradyarrhythmia showed stable Af. There was no significant difference in stable Af between group P with bradycardia-tachycardia syndrome (BTS) and group V with BTS (19% vs. 31%). A lower incidence of embolic events was also observed in group P (3% vs. 25%, p < 0.05). Nine of 16 patients with embolic events in group V died of complications following embolism (8 patients; cerebral embolism, one patients: renal and superior mesenteric arterial embolism). The survival rates at 5 and 10 years were 80% and 69%, respectively, for group P and 56% and 33% for group V (p < 0.01). Thus, with regard to permanent pacing for patients with sick sinus syndrome, physiological pacing should be selected for control of morbidity and total mortality.

An electrophysiologic study was performed in a 95-year-old man with bifascicular block (right bundle branch block and left anterior hemiblock). During sinus rhythm (AA interval = 980 ms), every sinus beat was conducted to the ventricle. The AH interval was 130 ms and HV interval was 50 ms. A programmed premature atrial stimulation was performed after 8 paced beats at a slightly shorter cycle length than the sinus cycle length (900 ms). As the atrial coupling interval was shortened, the H1H2 interval also shortened. At an H1H2 interval of 680 ms the premature atrial beat was blocked distal to the recording site of the His potential. The block persisted up to an H1H2 interval of 560 ms. AV conduction resumed paradoxically when the H1H2 interval was further shortened to intervals lasting 540-490 ms. During this period the H2V2 interval was 50 ms. At still shorter H1H2 intervals, H2 was again blocked. The H2V2 intervals during this phase of improved conduction were unchanged compared with those of other conducted beats. Therefore normalization due to the gap phenomenon could be ruled out, and the improved conduction could be explained by a phenomenon of supernormal conduction in the posterior division of left bundle branch.

A morphological examination of aging was performed on 141 normal hearts selected from a total of 972 consecutive autopsies on persons aged 60 years or over. The average heart weight was 270 ± 41 g. The circumference of the valvular ring was 99 ± 10 mm in the tricuspid valve, 68 ± 8 mm in the pulmonic valve, 83 ± 10 mm in the mitral valve, and 73 ± 7 mm in the aortic valve. The thickness of the tricuspid valve (anterior leaflet) was 0.9 ± 0.3 mm, pulmonic (anterior cusp) 0.4 ± 0.3 mm, mitral (anterior leaflet) 1.3 ± 0.6 mm, and aortic (posterior cusp) 1.0 ± 0.6 mm. Cardiac chamber volumes were as follows: 40 ± 14 mL in the right atrium, 22 ± 7 mL in the right ventricle, 37 ± 12 mL in the left atrium, and 7.3 ± 3.4 mL in the left ventricle. The circumference of the tricuspid ring was the largest. Left-sided valves were thicker than right-sides valves, and atrioventricular valves were thicker than semilunar valves. Cardiac chamber volumes were generally larger on the right side. Because this study was limited to hearts from persons aged 60 years or over, age-related changes were observed in only four parameters: (i) the circumference of the aortic valvular ring, (ii) the thickness of the aortic posterior cusp, (iii) the thickness of the pulmonic anterior cusp, and (iv) the volume of the left ventricle. With increasing age the aortic valvular ring dilated, the aortic posterior cusp and the pulmonic anterior cusp thickened, and the left ventricular volume diminished.

In order to evaluate the role of calcium regulating hormones in the pathogenesis of mitral ring calcification, we have studied the serum levels of PTH and vitamin D metabolites in aged females both with and without mitral ring calcification (MRC). In the patients with MRC (n = 17), significantly lower levels of serum total protein (6.6 +/- 0.2 in the MRC group vs 7.1 +/- 0.1 g/dl in the control group, mean +/- SEM), BUN (15.7 +/- 0.9 vs 18.3 +/- 0.9 mg/dl), creatinine (0.7 +/- 0.02 vs 0.9 +/- 0.02 mg/dl) and calcium (8.4 +/- 0.1 vs 9.2 +/- 0.1 mg/ml) were observed as compared with those in the controls (n = 32). Significantly higher PTH levels (0.57 +/- 0.07 vs 0.38 +/- 0.04 ng/ml) were found in the MRC group. Levels of all three vitamin D metabolites in the MRC group were significantly lower than those in the control group (25-OHD; 11.2 +/- 1.4 vs 19.6 +/- 1.2 ng/ml, 24,25(OH)2D; 0.7 +/- 0.1 vs 1.3 +/- 0.1 ng/ml and 1,25(OH)2D; 12.5 +/- 2.4 vs 43.0 +/- 3.5 pg/ml). The correlation coefficient between PTH and 1,25(OH) 2D was -0.382(n = 49, p less than 0.01). Thus, the significantly higher PTH levels in the MRC group might result in hypovitaminosis D. In conclusion, evidence of hypovitaminosis D in the patients with mitral ring calcification was demonstrated.

Diagnosis of disseminated intravascular coagulation (DIC) was made in 64 cases (16.2%) among a total of 395 autopsy cases. There were 31 men and 33 women. Their ages ranged from 31 to 91 years (mean 76.3). Underlying diseases were mainly malignancy and sepsis. Fresh cardiac lesions were found in 40 cases (62.5%). Coronary thrombosis was found in 13 cases (20.3%) and myocardial necrosis in 24 cases (37.5%), with acute myocardial infarction in 9 and focal necrosis in 15. Nonbacterial thrombotic endocarditis was found in 17 cases (26.6%), mural thrombi in 11 (17.2%), and bleeding of the heart in 11 (17.2%). Platelet count, fibrinogen and euglobulin lysis time were not correlated with myocardial necrosis nor coronary thrombosis. Increase of fibrin degradation products correlated with the presence of coronary thrombosis with or without myocardial necrosis. DIC was found with a high incidence in the aged, and many of them were complicated with fresh cardiac lesions. Development of acute myocardial infarction depends on the small thrombi in the severe stenosis of the main coronary arteries or on the multiple microthrombi in the peripheral coronary branches.

To evaluate lesions of the left main coronary artery (LM) in the aged, a pathologic study was performed on a total of 972 consecutive autopsy cases over 60 years of age. The study population consisted of 503 men and 469 women with an average age at death of 79.0 years. In this study the degree of narrowing and length of the LM were evaluated in all cases (T), and the 141 cases with normal hearts (N) were compared with the 202 cases with myocardial infarction (MI). The following results were obtained: (1) the average coronary stenotic index (CSI) was 9.1/15 in T, 5.8/15 in N and 11.2/15 in MI (N less than MI, p less than 0.001), (2) the grade of narrowing in the LM (LMG), when 100% obstruction of the LM is counted as 5, was 1.8 +/- 0.9 in T, 1.3 +/- 0.6 in N and 2.3 +/- 1.1 in MI (N less than MI, p less than 0.001). Cases showing more than 75% narrowing of the LM were found in 58 (6%), of which 35 cases belonged to MI, but development of MI directly due to lesions in the LM was found in only 9 patients (4.5% among MI), (3) the average length of the LM (LML) was 9.4 +/- 4.4 mm in T, 9.0 +/- 4.2 mm in N and 9.3 +/- 3.8 mm in MI (N vs MI; n.s.). Cases presenting left coronary artery dominance (n = 82) or a balanced type (n = 159) showed shorter LML than those with right coronary artery dominance (n = 729) (8.5 +/- 4.0 mm, 8.8 +/- 4.6 mm and 9.7 +/- 4.4 mm, respectively, p less than 0.05), (4) in T there was a correlation between the LMG and CSI, but not between the LML and CSI. In conclusion, lesions of the LM in the aged were generally mild and the LMG showed a positive correlation with CSI and the narrowing of each coronary branch, while no relationship was noted between the LML and CSI.

老年者の血管内凝固症候群 (DIC) に合併する急性心筋梗塞 (AMI) の頻度とその臨床的特徴を明らかにするため, 老年者連続剖検例中その急性期を観察し, かつ剖検によりAMIを確認しえた53例 (男28, 女25, 年齢66～93歳, 平均78.2歳) を, 凝血学的にDIC所見を呈したI群と, 同所見を認めなかったII群に分け, 両群について臨床所見, 経過ならびに死因などを比較検討した.成績は以下の如くであった. 1) 症例数はI群 (DIC群) 12例 (22.6%), II群 (非DIC群) 41例 (77.4%) であり, 両群の年齢分布はほぼ同様であった. 2) AMIの初発症状の出現頻度は, 胸痛を訴えた例がI群33.3%, II群46.7%であったが, 無痛性梗塞例については, 呼吸困難 (I群8.3%: II群15.6%, 以下同様に示す). 低血圧ないしショック (16.6%:13.3%), 中枢神経系症状 (8.3%:4.4%), 不整脈 (0:4.4%), 無症状ないし症状不明例 (33.3%:15.6%) であり, I群において初発症状の非典型例が多い傾向がみられた. 3) 血清酵素値の典型的上昇を認めた例はI群16.6%, II群57.6%で, I群において酵素値上昇が非典型的である例を多く認めた (p

In a series of 1,000 consecutive autopsy cases, we evaluated the clinical utility of thallium-201 (Tl-201) myocardial scintigraphy and electrocardiography (ECG) in 101 patients who had been studied while alive. Fifty-five cases had myocardial infarctions (MI) at autopsy. The Tl-201 scintigram and ECG in diagnosis of MI showed sensitivities of 68% and 60%, specificities of 87% and 83%, and diagnostic accuracies of 76% and 70%, respectively. The sensitivity of the Tl-201 scintigram was 70% in anterior MI, 80% in postero-inferior MI, 25% in lateral and subendocardial infarction. The sensitivity was 88% for large massive MI, but was low in scattered (50%) or middle-sized MI (17%). The diagnostic limit of the resolution of Tl-201 scintigrams was 4.5 cm in long diameter. All 8 cases with MI of less than 4 cm could not be diagnosed with the technique. There were 48 cases of large MI (more than 5 cm), but 8 cases could not be diagnosed by scintigraphy because of non-transmural or scattered MI. A comparison of the Tl-201 scintigram and ECG showed that 27 cases out of 60 cases were diagnosed by both methods, 14 only by the Tl-201 scintigram, 9 only by ECG and 10 by neither method.

The incidence, the size of mitral ring calcification (MRC) and its relation to the mitral valve disease were examined in a total of 600 consecutive autopsy cases of over 60 years of age. (1) The incidence of MRC was 10% (60 cases among 600), and the sex difference was statistically significant with 6.7% in male and 13.3% in female (p less than 0.01). The age was 82 years in average, and an increase of its incidence with aging was significant only in female (p less than 0.005). (2) MRC was found in the annulus of the posterior mitral leaflet. The length of MRC was 12.5 +/- 10.3 mm in male, and 31.8 +/- 23.5 mm in female (p less than 0.01). Large MRC more than 30 mm were found in 1 man and 19 women. (3) The relationship between the length and cross sectional diameter of the MRC showed a positive correlation (r=0.75). Three cases of mitral stenosis or combined stenosis and regurgitation belonged to the extremely large MRC group. (4) There were 27 cases with systolic murmur; 3 holosystolic and 24 ejection type. In large and small MRC groups, systolic murmurs were found in 70% and 33% (p less than 0.05), MRC extending to the anterior leaflet in 65% and 2.5% (p less than 0.005), moderate to severe calcification of the aortic valve in 40% and 20% (n.s.), respectively. (5) X-ray films were examined retrospectively, and large MRC was diagnosed in 85%, and incidence of calcification in the other soft tissues (trachea, bronchi, costal cartilage, aortic arch, thoracic and abdominal aorta) was higher in large MRC group than in the control group (87 cases) without MRC (p less than 0.005).