The evaluation method for evapotranspiration and its application to the actual area of pyroclastic deposit on the south-western slope of Mt. Merapi volcano are presented in this paper. In the study sites (Gunung site at an altitude of 960m and Pusung Malang that of 1200m), it can be assumed that the amount of evapotranspiration can be evaluated by two processes. One depends on the transpiration by plants which is related to the water absorbed from the soil through their roots, the other is due to direct evaporation from the ground surface. We can evaluate the water balance for a soil layer by adding; the amount of water which infiltrates from the ground surface during rainfall, gravitational water moving down and passing through the layer, evaporation water through the ground surface and transpiration water by plant leaves. On the basis of this idea, an unsaturated water flow simulation is carried out to evaluate the amount of evapotranspiration by using soil suctions observed at two sites. The results show that the annual amount of evapotranspiration from August 1992 to July 1993 is about 1600mm at Gunung , and the seasonal amount from August to November 1992 is about 500mm at Pusung Malang.

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Hypertrophic cardiomyopathy (HCM) is the most common cause of sudden cardiac death (SCD) in young people, including trained athletes. It is now 30 years since the introduction of implantable cardioverter-defibrillators (ICDs) to clinical cardiovascular practice and coronary artery disease, and now device therapy represents the most significant therapeutic innovation and the only definitive strategy for prolonging the life of HCM patients. ICDs have proved effective in preventing SCD in young HCM patients with appropriate intervention rates of 11% for secondary and 4% for primary prevention, despite massive left ventricular (LV) hypertrophy, LV outflow obstruction, diastolic dysfunction or microvascular ischemia. Targeting candidates for prophylactic ICD therapy can be complex, compounded by the unpredictability of the arrhythmogenic substrate, the absence of a dominant risk factor, and difficulty in assembling randomized trials. However, a single major risk factor is often sufficient to justify an ICD, although additional markers and other disease features can resolve ambiguous decision-making. Nevertheless, the absence of all risk factors does not convey absolute immunity to SCD. The current risk factor algorithm, when combined with a measure of individual physician judgment (and patient autonomy considerations), is an effective guide to identifying high-risk HCM patients. ICDs have altered the natural history of HCM for many patients and provided an opportunity to achieve many decades of productive life, and the potential for normal or near-normal longevity. Indeed, prevention of SCD has now become a new paradigm in the management of HCM. (Circ J 2010; 74: 2271-2282)

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The underlying pathophysiology of hypertrophic cardiomyopathy (HCM) is still unclear. Positron emission tomography is a suitable and promising technique for the detection of possible metabolic consequences of the disease. To assess regional myocardial blood flow and metabolism, 19 asymptomatic or only mildly symptomatic patients with HCM and 10 normal control subjects were studied using carbon-11 acetate and fluorine-18-labelled deoxyglucose (FDG) as tracers of myocardial blood flow (Ao), oxygen consumption (k), and exogenous glucose utilization. In the patients, regional Ao in the hypertrophied septum and apex (H) was similar to that in the nonhypertrophied free wall (N) (91.3±3.9% vs 92.9±3.1%; p=NS). However, the k values were significantly lower in H than in N (0.044±0.012 vs 0.060±0.016/min, p<0.0001). The k value in N and normal control subjects (0.062 ±0.013) was similar. Postprandial FDG uptake was lower in H than in N (70±16 vs 91±7%; p<0.0001) in 16 patients and slightly higher in 3 patients, Fasting FDG study showed increased FDG uptake in H in 3 out of 13 patients, suggesting a disorder of the myocardial microvascular circulation. A relative decrease in hypertrophied septal and apical oxidative metabolism and glucose utilization without any corresponding perfusion defect could reflect abnormal regional aerobic metabolism in the disproportionately thickened myocardium in patients with HCM. This suggests that a primary myocardial metabolic defect might be present in patients with HCM. (Jpn Circ J 1997; 61: 201 -210)

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We have shown that myocardial glucose metabolism is heterogeneous in patients with hypertrophic cardiomyopathy. It is not known, however, whether glucose metabolism is impaired in patients with apical hypertrophic cardiomyopathy, which is fairly common in Japan. We studied 7 patients with apical hypertrophic cardiomyopathy and 5 normal subjects using nuoro-18 2-deoxyglucose (FDG) and positron emission tomography (PET). We calculated regional FDG fractional uptake and the inter-regional coefficient of variation (CV) of FDG fractional uptake in the interventricular septal, anteroapical, and posterolateral regions. The regional FDG fractional uptake was similar in the 2 groups and among the 3 different segments within each group. However, the inter-regional CV of FDG fractional uptake was increased in the anteroapical wall segment of the patient group compared with the control group and also with the other 2 regions in the patient group. The results did not differ when we studied another 5 patients and 6 normal control subjects with a PET scanner with higher spatial resolution. These data suggest that myocardial glucose metabolism may be impaired in the anteroapical wall segment of patients with apical hypertrophic cardiomyopathy. (Jpn Circ J 1997; 61: 223 - 230)

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　心臓震盪が心停止の原因と考えられる症例（25例）を集積し，その発症状況，年齢，予後を調査した。衝撃の原因は野球のボールが10例と最も多く北米例と同一傾向であるが，北米では報告がないサッカーボールや交通事故による胸部打撲などの発生例がみられた。年齢分布は北米と同様で，22例が18歳以下であった。予後は，社会復帰が9例，脳障害が残存したものが1例，死亡が15例であった。心電図が確認できた症例は16例あり，14例が心室細動，1例が心室頻拍，1例が心静止であった。心室細動の14例で電気的除細動が実施され，8例が社会復帰した。もう1例はbystander CPRのみで自己心拍が出現し，社会復帰できた。社会復帰例はいずれもbystander CPRがなされており，bystander CPRと電気的除細動の重要性を示している。

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The beneficial effects of Acanthopanax divaricatus var. albeofructus (ADA) extracts have been assessed by mutagenic and anti-mutagenic activities by Ames test. Mutation of Salmonella typhimurium strains TA 98, TA 100, TA1535, TA1537, and Escherichia coli WP2 uvr A was assayed in duplicates by the procedure of and Ames in the presence or absence of S9 mix. As a result, ADA extracts were not mutagenic for S. typhimurium strains TA 98, TA 100, TA1535, TA1537, and E. coli by the Ames assay. Anti-mutagenic activity was assayed by the Ames mutagenicity assay using histidine mutant of S. typhimurium strains TA 98 and TA 100, using the plate-incorporation method. 2-Aminoanthrancene (2-AA), 2-(2-furyl)-3-(5-nitro-2-furyl) acrylamide (AF-2), and sodium azide (NaN₃) were used as the mutagens. ADA extracts showed a strong anti-mutagenic activity against 2-AA-induced mutagenesis which requires liver-metabolizing enzymes, and the same extract exhibited inhibitory effects on AF-2 and NaN₃-induced mutagenesis in the absence of liver-metabolizing enzymes. The data indicate that ADA extracts contain anti-mutagenic activities against typical mutagens. The anti-mutagenic property of ADA provides additional health supplemental value to the other claimed therapeutic properties of the plant.

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A 71-year-old woman had hypertrophic cardiomyopathy associated with midventricular obstruction and an apical aneurysm in the left ventricle. She had had abnormal electrocardiograms for more than 30 years and for the past year had been suffering from occasional attacks of dizziness and low systemic blood pressure. Holter 24-h electrocardiographic monitoring revealed ventricular paroxysmal contractions (676/day) with nonsustained ventricular tachycardia. Doppler echocardiography revealed paradoxical jet flow from the apical aneurysm to the left ventricular outflow during early diastole. Magnetic resonance imaging depicted midventricular hypertrophy and a dyskinetic thin apical wall, which were confirmed by angiography. Coronary angiograms showed no narrowing of the major extramural coronary arteries, but there was compression of aberrant coronary arteries apparently feeding the hypertrophic portion of the left ventricular wall. Stress thallium-201 myocardial imaging showed a persistent severe defect in the left ventricular apex. A hemodynamic study revealed low cardiac output and an intraventricular pressure gradient (approximately 90 mmHg) between the left ventricular apical high-pressure chamber and the subaortic low-pressure chamber. The present case represents a rare combination of hypertrophic cardiomyopathy, midventricular obstruction, and an apical aneurysm in an elderly woman. Myocardial ischemia may have played an important role in the genesis of the apical aneurysm. (Jpn Circ J 2001; 65: 915 - 919)

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After a volcanic eruption, in situations where pyroclastic material generates thick ground cover, even small amounts of rainfall can trigger lahars; this effect sometimes continues for many years. For hazard mitigation against lahar disasters after an eruption, it is essential to evaluate the current risk of occurrence and estimate any possible temporal changes for the future. Putih River is one of the rivers where lahars occurred frequently after the 1984 eruption of Mt. Merapi. In this study, the characteristics of lahars and floods in the Putih River after the 1984 eruption and their change over the years were analyzed, focusing on the runoff characteristics of lahars. Irrelevant rainfall and discharge data for analyzing runoff characteristics of lahars were excluded in preprocessing. The magnitude and occurrences of lahars decreased annually during the four years following the eruption. The maximum runoff rate of lahars was approximately 12 during the 1984–1985 rainy season and decreased yearly after this. A judgement graph was employed to track the temporal changes of lahar- triggering rainfall characteristics. For the 1984–1985 and 1985–1986 rainy seasons discriminant lines, which discriminate between rainfall events triggering lahar flow with peak discharge > 900 m³/s and other rainfall events, were drawn on the judgement graph.

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Stroke volume (SV), cardiac output (CO) and systolic blood pressure (SBP) were measured during maximal symptom-limited bicycle exercise testing in 13 young patients (age, 11-26 years) with nonobstructive hypertrophic cardiomyopathy (HCM). SV was measured by impedance plethysmocardiography; %SV_end, %CO_end, and %SBP_end represent the ratio of the value at termination of the exercise to the respective value at rest. In all patients of HCM-I (the Cardiac Event Group, 3 patients) and 3 of HCM-II (the Non-Cardiac Event Group, 10 patients), the %SV_end was less than 100%. The %SV_end of HCM-I was significantly lower than the respective values of the HCM-II and Control groups. The %CO_end values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. The %SBP_end values of the HCM-I and HCM-II groups were each significantly lower than that of the Control. Among the HCM patients, the %SV_end value was positively correlated with the %SBP_end value. The patients who had more severe HCM had poorer exercise-induced increases in SV and SBP. These results suggest that sudden cardiac death in young HCM patients is associated with inhibition of the increase in SV upon exercise. (Jpn Circ J 2001; 65: 300 - 304)

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Reactive oxygen species (ROS) have long been viewed as deleterious chemicals that lead to oxidative stress. More recently, ROS, especially the stable ROS hydrogen peroxide (H₂O₂), have been shown to have roles in normal physiological responses in vascular cells. Endothelial nitric oxide synthase (eNOS) is dynamically targeted to plasmalemmal caveolae, and represents the principal enzymatic source of nitric oxide (NO^•) in the vascular wall. eNOS maintains normal vascular tone and inhibits the clinical expression of many cardiovascular diseases. Increases in oxidative stress are associated with eNOS dysfunction. In a paradigm shift in the conceptual framework linking redox biochemistry and vascular function, H₂O₂ has been established as a physiological mediator in signaling pathways, yet the intracellular sources of H₂O₂ and their regulation remain incompletely understood. The subcellular distributions of ROS and of ROS-modified proteins critically influence the redox-sensitive regulation of eNOS-dependent pathways. ROS localization in specific subcellular compartments can lead to selective oxidative modifications of eNOS and eNOS-associated proteins. Likewise, the dynamic targeting of eNOS and other signaling proteins influences their interactions with reactive nitrogen species and ROS that are also differentially distributed within the cell. Thus, the subcellular distribution both of eNOS and redox-active biomolecules serves as a critical basis for the control of the “redox switch” that influences NO^•- and oxidant-regulated signaling pathways. Here we discuss the biochemical factors, cellular determinants, and molecular mechanisms that modulate redox-sensitive regulation of eNOS and NO^• signaling under normal and pathological conditions.  (Circ J 2012; 76: 2497–2512)

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The present study investigated gender differences among adult patients with obstructive hypertrophic cardiomyopathy (OHCM) and resting gradient. Using outflow gradients >10 mmHg and the presence of asymmetrical septal hypertrophy of the left ventricle as inclusion criteria, 122 patients were identified among patients referred for echocardiographic examinations between May 1990 and October 1996. Clinical, echocardiographical and follow-up data were compared between male and female patients. The female patients were significantly older than male patients (mean age ± SD 66.7±10.5 vs 54.8±12.5 years). The female patients had a smaller interventricular septal wall thickness, less frequent systolic anterior movement of the mitral valve, more frequent association with hypertension, and less frequent association with ischemic heart disease (IHD) and giant T wave inversion. In this study population, adult female patients presented with OHCM 12 years later than males. Whether this represents female patients' reluctance to seek medical attention early, a different disease process that affects predominantly elderly females, or a gender-specific end organ response to aging, hypertension, IHD and other processes, or the protective effects of estrogen remains to be determined. (Jpn Circ J 1999; 63: 859 - 864)

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We describe a family in which five members had hypertrophic cardiomyopathy (HCM) with a similar distribution of left ventricular (LV) hypertrophy and LV filling pattern. All five family members had myocardial hypertrophy localized between the anterior LV wall and ventricular septum, in addition to having a triphasic transmitral flow (TMF) velocity pattern with a mid-diastolic wave. The HCM patients with this TMF velocity pattern exhibit decreased LV compliance and delayed LV relaxation, suggesting that the features of diastolic failure may be specific. Thus, these findings may provide an important clue to elucidating the relationship between the pathophysiology and mode of inheritance in patients with HCM.

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　若年者の突然死は，肥大型心筋症や冠動脈奇形，心筋炎などを基礎に持つ人のスポーツ中に多いとされている。ところが，1980年代の北米において，心臓病がない健康な子どもが，胸に比較的軽い鈍的外力を受けた直後に突然死する事例が続けて報告された。1995年，

ら1）はこういった事例を心臓震盪として報告した。本邦においては，2002年に堀2）がスポーツ中の突然死として心臓震盪を紹介し，著者3）4）は国内例をまとめて報告している。ここでは，本邦における発症状況を北米例と比較して提示し，発症のメカニズム，予後について文献的考察を含め示す。尚，ここで示す本邦での1997年から2019年における49例のデータは，著者自身の症例に加え，救急隊員，学会報告，文献などから得た情報をもとにしたデータであり，著者が把握できていない症例もあることをご理解いただきたい。

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To examine the mechanism of myocardial ischemia in hypertrophic cardiomyopathy (HCM), coronary flow velocity was measured in the left anterior descending coronary artery (LAD) using a Doppler guide wire in 11 patients with HCM and in 8 normal controls. The average peak velocity (APV), percent increase of APV (%APV), and APV during systole (Vs) and diastole (Vd) were calculated at rest and during rapid atrial pacing. The APV in HCM reached a peak value at a heart rate of 90 beats/min, while in the controls the APV increased continuously until the heart rate reached 130 beats/min [%APV (130 beats/min); 103±30% in HCM vs 139±23% in controls, p<0.04]. During rapid atrial pacing, Vs in the controls increased, whereas Vs in HCM decreased further. During high-rate pacing, Vd in HCM reached a peak value at a heart rate of 90 beats/min, whereas in the controls, Vd increased continuously until the heart rate reached 130 beats/min. The acceleration rate of early diastolic flow was significantly lower in HCM than in the controls (1.85±0.66 vs 3.18±1.62 m/s², p<0.03). This abnormal response might be due to an increase in the reverse systolic flow and a decrease in the diastolic flow, probably caused by a slow acceleration of early diastolic flow velocity in the LAD. (Jpn Circ J 1999; 63: 350 - 356)

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The clinical outcome and the incidence of ischemic strokes in patients with hypertrophic cardiomyopathy (HCM) with and without atrial fibrillation (AF) were examined. Eighty-three patients with HCM, complicated by AF in 19 patients, and 131 patients with AF but without HCM were studied retrospectively. Primary endpoints (ischemic strokes or cardiac death, whichever occurred first) and ischemic strokes were examined by Kaplan-Meier curves. In the patients with HCM, the primary endpoints occurred more frequently in those with AF than in those without AF (event rate at 5 years 23.0% vs 12.3%, p<0.01). Similarly, the frequency of ischemic strokes in HCM was also much higher with AF than without AF (23.0% vs 5.9% at 5 years, p<0.01). According to multivariate Cox analysis, the strong independent risk factor for ischemic strokes in HCM was AF (p<0.01), whereas in patients with AF they were HCM (p<0.01) and age (p <0.01). These results suggest that incidence of ischemic strokes in HCM is markedly increased if complicated by AF as compared with that in patients with AF alone. (Jpn Circ J 1997; 61: 673 - 681)

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To evaluate the relationship between the distribution of hypertrophy and the electrocardiographic findings in patients with hypertrophic cardiomyopathy (HCM), 54 HCM patients were studied using magnetic resonance imaging. The patients were divided into 4 groups according to hypertrophic patterns: (i) hypertrophy only at the apex (group I, n=12); (ii) hypertrophy in both the apex and base (group II, n=20); (iii) hypertrophy only at the base with asymmetric septal hypertrophy (ASH) (group IIIa, n=17); and (iv) hypertrophy only at the base without ASH (group IIIb, n=5). Abnormal Q waves in leads II, III and aV_F were found in 1/12, 3/20, 10/17 and 0/5, respectively, and in leads I and aV_L they were found in 1/12, 8/20, 4/17 and 1/5, respectively. The largest negative T waves (mm) were found in group I (group I vs group II vs group IIIa vs group IIIb: 15.2±5.3, 8.2±6.1, 1.6±2.0, 0.8±1.3, respectively). The largest positive T waves (mm) were identified in group IIIb (3.8±3.0, 6.8±3.2, 5.8±3.6, 9.3±2.1, respectively). The presence of abnormal Q waves reflected regional hypertrophy in HCM patients but the configuration of T waves represented the difference in the localization of hypertrophy between the basal and apical segments. (Jpn Circ J 1998; 62: 483 - 488)

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Hypertrophic cardiomyopathy (HCM) was simulated with a computer heart model having a realistic shape and rotating fiber orientation in order to elucidate possible mechanisms for abnormal ECG findings. The disarray of myocardial muscle in HCM was simulated by assigning random fiber direction and isotropic electrophysiologic properties to abnormal hypertrophic regions, in contrast to the anisotropic modeling for normal myocardium. With these models, main ECG features including abnormal Q wave and QS pattern were reproduced and were comparable with clinical findings. This study suggests that the change in anisotropy in the hypertrophic myocardium is likely to be the main factor responsible to the ECG features of HCM.

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This report describes an adult patient with Noonan syndrome accompanied by biventricular hypertrophic cardiomyopathy causing isolated right ventricular outflow tract obstruction. Biventricular hypertrophic cardiomyopathy causing right- and/or left-side outflow tract obstruction, as well as valvular pulmonary stenosis, is relatively common in infants with Noonan syndrome. However, this condition without a dysplastic pulmonary valve, or indeed any polyvalvular dysplasia, is rare in adults with Noonan syndrome. Treatment with a β-adrenergic receptor blocking agent improved the patient's symptoms. Because neither the etiologic and prognostic relationship nor the genetic linkage between hypertrophic cardiomyopathy associated with Noonan syndrome and non-syndromic hypertrophic cardiomyopathy is clearly defined, clinicopathological findings and further follow-up may provide important evidence for the pathogenesis of hypertrophic cardiomyopathy. (Jpn Circ J 2001; 65: 132 - 135)

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