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Biomedical subjects

K Shimamoto

Publications and source records attributed to K Shimamoto.

At least 145 records · Page 8Linked to original sources
PubMed1998

Interobserver agreement in sonographic diagnosis of breast tumors.

OBJECTIVE: To evaluate interobserver agreement in the interpretation of breast ultrasonography. METHODS: 55 breast masses (30 benign, 24 malignant) were interpreted by seven radiologists using a CRT viewing station. US criteria for differentiating between benign and malignant lesions included shape, border, boundary echoes, internal echoes, posterior echoes, and bilateral shadows. Each criterion and the observers' final impression was scored using the 5-point rating scales. For analyzing interobserver agreement, the kappa (kappa) values were employed. RESULTS: The kappa values of shape and posterior echoes were significantly higher than those of the other four criteria (P<0.05). Agreement was intermediate in border and internal echoes, and was low in boundary echoes and bilateral shadows. Agreement in the senior group (four observers) was relatively higher than that in the junior group (three observers) for all criteria but for internal echoes. Easily-diagnosed cases showed significantly higher kappa values compared with more ambiguous cases (P<0.05). CONCLUSION: Interobserver agreement in shape and posterior echoes was significantly higher than those of the other four criteria. Agreement was significantly dependent on case difficulty.

Breast Diseases↗
PubMed1998

Aberrant jugular bulb vein obstructing approach to intracanalicular vestibular schwannoma.

In cases of jugular bulb anomalies, such as a high jugular bulb, troublesome bleeding may occur during surgery. We report an unusual case with a vestibular schwannoma, in which we recognized an additional branch arising from the jugular bulb. Three-dimensional computed tomography (3-D CT) revealed this anomaly beforehand, enabling us to avert excessive bleeding upon resection of the tumour. The abnormal vein was thought to be a remnant of the petrosquamosal sinus in the embryonic stage.

Female↗
PubMed1998

Time window for the contribution of the delta-opioid receptor to cardioprotection by ischemic preconditioning in the rat heart.

The present study aimed to examine (1) whether the role of the opioid receptor in ischemic preconditioning (PC) is consistent regardless of the duration of ischemic insult and (2) which opioid receptor subtype contributes to PC. In the first series of experiments, the effects of PC, a nonselective opioid receptor antagonist (naloxone), and their combination on the infarct size after various durations of ischemia were assessed. In anesthetized, open-chest rats, the coronary artery was occluded for 20, 30, or 40 minutes to induce infarction and was reperfused for 3 hours, PC was performed with two cycles of 5-minute ischemia followed by 5-minute reperfusion before the sustained ischemia. At 25 minutes before the ischemia, naloxone was injected alone or in combination with subsequent PC. Infarct size was determined by tetrazolium staining and was expressed as a percentage of the risk area size (%IS/RA). In the second series of experiments, the effects of a delta-receptor-selective antagonist, naltrindole (NTI), and a kappa-receptor selective antagonist, nor-binaltrophimine (nor-BNI), on PC before 30-minute coronary occlusion were assessed. In untreated controls, %IS/RA was 53.1 +/- 3.2 after 20 minutes, 67.9 +/- 3.9 after 30 minutes, and 87.8 +/- 2.0 after 40 minutes of ischemia, respectively. PC significantly reduced %IS/RA after 20, 30, and 40 minutes of ischemia to 3.1 +/- 0.8, 12.8 +/- 1.1, and 42.1 +/- 4.3, respectively (P < 0.05 vs. each control). Naloxone (6 mg/kg) partially attenuated the protection afforded by PC when the sustained ischemia was 30 minutes (%IS/RA = 27.4 +/- 4.5; P < 0.05 vs. PC), but this inhibitory effect of naloxone was not detected when the duration of the ischemia was 20 or 40 minutes. NTI (10 mg/kg) also attenuated infarct size limitation by PC after 30 minutes of ischemia (%IS/RA = 25.6 +/- 3.7), but nor-BNI (10 mg/kg) failed to modify infarct size limitation by PC (%IS/RA = 13.3 +/- 3.2). The present results suggest that activation of the opioid delta-receptor partly contributes to preconditioning against infarction in the rat and that there may be a time window (at around 30 minutes after the onset of ischemia) for this opioid receptor-mediated protective mechanism.

Animals↗
PubMed1998

A naturally occurring functional allele of the rice waxy locus has a GT to TT mutation at the 5' splice site of the first intron.

In cultivated rice two wild-type alleles, Wxa and Wxb, predominate at the waxy locus, which encodes granule-bound starch synthase. The activity of Wxa is 10-fold higher than that of Wxb at the level of both protein and mRNA. Wxb has a +1G to T mutation at the 5' splice site of the first intron. Sequence analysis of Wxb transcripts revealed that splicing occurs at the mutant AG/UU site and at two cryptic sites: the first is A/GUU, one base upstream of the original site and the second is AG/GU found approximately 100 bases upstream of the mutant splice site. We introduced single base mutations to the 5' splice sites of both Wxa and Wxb, fused with the gus reporter gene and introduced them into rice protoplasts. Analysis of GUS activities and transcripts indicated that a G to T mutation in Wxa reduced GUS activity and the level of spliced RNA. Conversely, a T to G mutation of Wxb restored GUS activity and the level of spliced RNA to that of wild-type Wxa. These results demonstrated that the low level expression of Wxb results from a single base mutation at the 5' splice site of the first intron. It is of interest that the Wxb allele of rice carrying the G to T mutation of intron 1 has been conserved in the history of rice cultivation because there is a low amylose content of the seed caused by this mutation.

Alleles↗
PubMed1998

Infarct-size limitation by preconditioning is enhanced by dipyridamole administered before but not after preconditioning: evidence for the role of interstitial adenosine level during preconditioning as a primary determinant of cardioprotection.

Although the importance of adenosine (Ado)-receptor activation in preconditioning (PC) has been established, it is unclear whether cardioprotection afforded by PC is determined by the Ado level during PC ischemia or by that during sustained ischemia. Accordingly, we tested whether the PC effect is modified by augmenting the increase in the interstitial Ado level during PC or by that during sustained ischemia. In the first series of experiments, the effect of 0.25 mg/kg dipyridamole (DIP) on the interstitial Ado level was assessed by in vivo microdialysis in the rabbit heart. Dialysate Ado during 2-min ischemia was 70% higher in the heart pretreated with 0.25 mg/kg of DIP than in the untreated controls, indicating that DIP was capable of enhancing an ischemia-induced increase of interstitial Ado. In the second series of experiments, myocardial infarction was induced in the rabbit by 30-min coronary artery occlusion and 3-h reperfusion. Infarct size was determined by tetrazolium staining and expressed as percentage of area at risk (%IS/AR). Rabbits were subjected to one of nine treatments before the 30-min ischemia: no treatment, DIP (0.25 mg/kg, i.v.), PC with 2-min ischemia, DIP before 2-min PC, DIP after 2-min PC, PC with 3-min ischemia, DIP before 3-min PC, DIP after 3-min PC, or 8-sulfophenyltheophylline (SPT) after 3-min PC. DIP alone did not modify %IS/AR (38.8 +/- 5.8% vs. 41.2 +/- 4.7%), but administration of DIP before 2-min PC significantly enhanced the infarct size-limiting effect (14.6 +/- 2.1% with DIP vs. 32.1 +/- 4.7% without DIP). Although the 3-min PC per se could achieve significant infarct limitation, the effect of DIP on 3-min PC was not significant (14.7 +/- 1.9% with DIP vs. 20.5 +/- 1.8% without DIP). On the other hand, the effect of DIP administered after PC was very slight (only 7% reduction of %IS/AR) and statistically insignificant, regardless of the duration of PC ischemia. However, infarct limitation by 3-min PC was inhibited by SPT given after the PC (%IS/AR = 34.5 +/- 3.2), as reported previously. These results suggest that the interstitial Ado level during PC ischemia, not the level during sustained ischemia, is a primary determinant of the extent of cardioprotection by PC and that the threshold for Ado-receptor activation required during sustained ischemia is much lower than that for triggering PC.

Adenosine↗
PubMed1998

Suppression of reperfusion arrhythmias by preconditioning is inhibited by an ATP-sensitive potassium channel blocker, 5-hydroxydecanoate, but not by protein kinase C blockers in the rat.

It has been suggested that preconditioning (PC) against infarction in the rat heart is mediated by opening of ATP-sensitive potassium (KATP) channels, which may be induced by receptor-triggered activation of protein kinase C (PKC). However, the mechanism of suppression of reperfusion arrhythmias by PC remains unclear. This study first examined whether suppression of reperfusion arrhythmias by PC requires the activation of KATP channels, PKC, and opioid receptors. In anesthetized rats, reperfusion arrhythmias were induced by occluding the left main coronary artery for 5 min and subsequent reperfusion. In untreated control rats, the incidence of reperfusion ventricular tachycardia (VT) was 100%, and 80% of the VT deteriorated to ventricular fibrillation (VF). PC with 2-min ischemia/5-min reperfusion reduced the incidences of VT and VF to 30% and 0, respectively. Although a KATP channel blocker, 5-hydroxydecanoate (5-HD), alone caused no significant effect on the incidence of reperfusion VT, this agent blocked the suppression of reperfusion VT by PC (VT incidence, 91%). The incidence of reperfusion VF in the 5-HD-treated rats tended to be lower than that in the untreated controls and was not different between preconditioned and nonpreconditioned groups (30 vs. 27%). PKC inhibitors staurosporine and calphostin C modified neither reperfusion arrhythmias nor the antiarrhythmic effect of PC on reperfusion VT and VF. Naloxone (6 mg/kg, i.v.) did not alter the incidence or duration of VT in the nonpreconditioned heart. However, suppression of reperfusion VT by PC was prevented by naloxone (VT incidence, 70%). The incidence of reperfusion VF was similarly low in the naloxone-treated rats in both nonpreconditioned and preconditioned groups (20% vs. 0). In the second series of experiments, the effect of 5-HD on repetitive PC was assessed. Repetitive PC was performed with three cycles of 2-min ischemia/5-min reperfusion, which totally abolished reperfusion VT and VF. This antiarrhythmic effect of repetitive PC was not inhibited by 5-HD. These results suggest that KATP channels and opioid receptors may be partly involved in suppression of reperfusion arrhythmias, although their roles may be compensated for by other antiarrhythmic mechanisms in repetitive PC. In contrast with PC against infarction, PKC is unlikely to play a major role in PC against reperfusion arrhythmias in the rat.

Adenosine Triphosphate↗
PubMed1998

DL-threo-beta-benzyloxyaspartate, a potent blocker of excitatory amino acid transporters.

DL-threo-beta-Benzyloxyaspartate (DL-TBOA), a novel derivative of DL-threo-beta-hydroxyaspartate, was synthesized and examined as an inhibitor of sodium-dependent glutamate/aspartate (excitatory amino acid) transporters. DL-TBOA inhibited the uptake of [14C]glutamate in COS-1 cells expressing the human excitatory amino acid transporter-1 (EAAT1) (Ki = 42 microM) with almost the same potency as DL-threo-beta-hydroxyaspartate (Ki = 58 microM). With regard to the human excitatory amino acid transporter-2 (EAAT2), the inhibitory effect of DL-TBOA (Ki = 5.7 microM) was much more potent than that of dihydrokainate (Ki = 79 microM), which is well known as a selective blocker of this subtype. Electrophysiologically, DL-TBOA induced no detectable inward currents in Xenopus laevis oocytes expressing human EAAT1 or EAAT2. However, it significantly reduced the glutamate-induced currents, indicating the prevention of transport. The dose-response curve of glutamate was shifted by adding DL-TBOA without a significant change in the maximum current. The Kb values for human EAAT1 and EAAT2 expressed in X. laevis oocytes were 9.0 microM and 116 nM, respectively. These results demonstrated that DL-TBOA is, so far, the most potent competitive blocker of glutamate transporters. DL-TBOA did not show any significant effects on either the ionotropic or metabotropic glutamate receptors. Moreover, DL-TBOA is chemically much more stable than its benzoyl analog, a previously reported blocker of excitatory amino acid transporters; therefore, DL-TBOA should be a useful tool for investigating the physiological roles of transporters.

ATP-Binding Cassette Transporters↗
PubMed1998

Ecto-5'-nucleotidase is not required for ischemic preconditioning in rabbit myocardium in situ.

This study tested the hypothesis that cardiac ecto-5'-nucleotidase (ecto-5'-NT) activity during ischemic preconditioning (PC) contributes to augmented tolerance against ischemia, thereby reducing infarct size in the rabbit heart in situ. The effects of alpha,beta-methylene-adenosine diphosphate (AOPCP), a selective inhibitor of ecto-5'-NT, on cardiovascular responses to AMP were measured to establish in vivo activities of the enzyme and its inhibitor. Left atrial infusion of AOPCP (0.75 mg . kg-1 . min-1) raised AOPCP plasma levels to 138 microM; under these conditions negative chronotropic and inotropic effects of AMP were blocked, demonstrating essentially full inhibition of ecto-5'-NT in the heart in situ. This AOPCP-blocked heart in situ model was used to examine the proposed contribution of ecto-5'-NT in ischemic PC. Myocardial infarction caused by 30-min ischemia was followed by 3-h reperfusion. Infarct size (IS) was measured and expressed as a percentage of the size of the area at risk (%IS/AR). In untreated controls, %IS/AR was 38.1 +/- 3.8%; PC (5-min ischemia, 5-min reperfusion) markedly reduced %IS/AR to 10.0 +/- 2.0%. Essentially identical IS reductions by PC were observed in AOPCP-blocked animals (%IS/AR = 13.8 +/- 2.2 and 13.3 +/- 1.8% in rabbits receiving AOPCP at 0.75 and 1.50 mg . kg-1 . min-1, respectively); here plasma AOPCP levels were established before and during PC but not during the subsequent prolonged ischemia. As expected, AOPCP also did not affect %IS/AR in non-PC controls (%IS/AR = 35.5 +/- 3.7%). In contrast but as predicted, adenosine-receptor blockade by 8-phenyltheophylline (10 mg/kg iv) substantially attenuated IS reduction by PC in both AOPCP-blocked and control hearts (%IS/AR = 25.2 +/- 4.3 and 21.8 +/- 2.2%, respectively; P < 0.05 vs. PC alone). The results demonstrate that cardiac ecto-5'-NT is not required for ischemic PC against infarction in the rabbit.

5'-Nucleotidase↗
PubMed1998

Ischemic and non-ischemic myocyte damage and antimyosin monoclonal imaging.

Antimyosin monoclonal antibody is a specific marker of impaired sarcolemmal integrity resulting not only from ischemia but also from non-ischemic myocardial injury, such as infection, inflammatory, or immunologic reactions, and alcohol or drug intoxication. In addition, antimyosin accumulation has been demonstrated in some forms of cardiomyopathy with unknown as well as known etiologies. Antimyosin positivity appears to indicate precisely the extent of myocardial necrosis and to reflect cardiac dysfunction in an acute stage of active myocardial damage caused by ischemia and inflammation. However, the correlation is not necessarily good in the chronic stages of the disease or in idiopathic cardiomyopathic hearts; in other words, cardiac antimyosin uptake can be detected even in myocardial tissue with a normal histologic appearance independent of the presence of inflammatory responses, myocyte necrosis, or functional or morphologic deterioration. Thus, antimyosin is useful not only for detecting and quantifying acute myocardial necrosis but also for specifically identifying ongoing or latently progressing myocardial degeneration and sarcolemmal disruption, which will certainly lead to myocardial necrosis. These characteristics may contribute to the early detection of myocardial damage and lead to the investigation of pathophysiologic mechanisms. Further progress in immunologic and radiolabeling techniques is necessary for better specificity and less antigenicity against humans in antimyosin monoclonal antibody imaging.

Animals↗
PubMed1998

Endogenous immunoreactive ouabain-like and digoxin-like factors in reduced renal mass hypertensive rats.

We evaluated the urinary excretion of immunoreactive endogenous ouabain-like factor (OLF) and digoxin-like factor (DLF) to investigate their pathophysiological roles in sodium metabolism and blood pressure in 5/6-reduced renal mass rats, a model of volume-expanded hypertension. About five-sixths of the kidney mass (5/6 RRM, n = 9) was removed from male Sprague-Dawley rats, or the rats were sham operated (control, n = 10). Both groups were fed regular diets with tap water for 1 wk as a control period, followed by 1% saline solution for 4 wk. Systolic blood pressure (SBP), urine volume (UV), urinary sodium excretion (UNaV), DLF, and OLF were measured on the last 2 d of every week throughout the experimental period. SBP and UNaV were significantly higher in 5/6 RRM rats than in control rats. Urinary DLF significantly increased, reaching peak value in the first week, while OLF increased continuously, reaching peak value in the fourth week. In the first week, there were a significant positive correlations between the change in DLF and the changes in UNaV and SBP. However, the change in OLF was not correlated with changes in either UNaV or SBP. Both SBP and UNaV showed a significant positive correlation with OLF (p<0.001, r=0.547, p<0.001, r=0.658, respectively), whereas DLF significantly correlated with UNaV (p< 0.001, r= 0.584) but not with SBP in 5/6 RRM. These findings suggest that endogenous OLF and DLF coexist in rat urine and that an increased level of OLF, but not DLF, may contribute to the development and maintenance of hypertension. DLF may contribute to renal sodium excretion in this volume-expanded hypertensive rat model.

Animals↗
PubMed1998

Association of insulin resistance and hyperinsulinemia with disturbed lipid metabolism in patients with essential hypertension.

To clarify the association of insulin resistance and hyperinsulinemia with lipid metabolism in patients with essential hypertension (EHT), we used the euglycemic hyperinsulinemic glucose clamp technique (GC) and the 75-g oral glucose tolerance test (OGTT) to compare the characteristics of glucose and lipid metabolism in insulin-resistant patients with essential hypertension (EHT-R) with those in insulin-non-resistant patients with essential hypertension (EHT-N) and normotensive subjects (NT). Twenty-eight NT and 42 EHT whose body mass index (BMI) was less than 28 kg/m2 were studied to eliminate the effects of obesity on insulin sensitivity and lipid metabolism. Insulin sensitivity was evaluated by GC and expressed as metabolic clearance rate of glucose (M value, mg/m2/min). Mean -ISD of the M value in NT (145.0 mg/m2/min) was chosen as the cutoff point for insulin resistance. On the basis of this value, 33.3% of the EHT were EHT-R. There was no significant difference in age or BMI among the three groups. Blood samples were collected before GC to measure levels of total cholesterol (TC), triglyceride (TG), free fatty acid (FFA), and HDL cholesterol (HDL-C). EHT-R had significantly higher levels of fasting blood sugar, fasting immunoreactive insulin, insulin at 120 min (IRI-120), and summation of insulin or blood sugar (BS) during the OGTT, as compared with NT and EHT-N. EHT-R also had significantly higher FFA and TG than the other two groups, while there was no difference in FFA or TG between EHT-N and NT. TC and HDL-C were similar in the three groups. There was either a significant negative correlation, or a trend toward negative correlation, between M value and FFA (r= -0.50, p < 0.05) or TG (r= -0.24, p < 0.1). There were significant positive correlations between IRI-120 and FFA (r=0.35, p< 0.05) or TG (r=0.29, p< 0.05). There was a positive correlation (r= -0.36, p< 0.01) between sigma BS and FFA, while no other significant relation was found between sigma BS and serum lipids. In summary, (i) 33.3% of EHT were found to be insulin resistant, when insulin resistance was defined as M value < 145.0 mg/m2/min, i.e., mean -ISD of the M value of NT; (ii) these EHT-R had higher levels of BS, insulin, FFA, and TG than did NT and EHT-N; (iii) EHT-N showed no difference in the levels of BS, insulin, or lipid, as compared with NT; and (iv) the levels of FFA and of TG correlated negatively with insulin sensitivity and positively with the insulin level during the OGTT. These results suggest that disturbances of glucose and lipid metabolism in EHT may be related to both insulin resistance and compensatory hyperinsulinemia, and that EHT-R may have more risk factors for arteriosclerotic complications than EHT-N.

Blood Glucose↗
PubMed1998

Rheumatoid arthritis associated with renal amyloidosis and crescentic glomerulonephritis.

A 43-year-old woman with rheumatoid arthritis (RA), renal amyloidosis and crescentic glomerulonephritis had severe abdominal pain, melena and progressive renal failure. Autopsy findings revealed vasculitis of small and middle size of vessels and there was a deposition of amyloid in the small intestines. Although there were no findings of vasculitis in the kidney, amyloid deposition was noticed and 70-80% of glomeruli showed a crescentic formation. No immunological abnormality was found in glomeruli. Although the immunological mechanisms of crescentic glomerulonephritis were not necessarily eliminated, amyloid deposition may play a role in crescent formation.

Acute Kidney Injury↗
PubMed1998

[Significance of accumulation of arteriosclerotic risk factors in elderly people: from a study conducted in Tanno-Sobetsz].

Data from an 18-year prospective study were used to investigate the effect of accumulation of arteriosclerotic risk factors in elderly people on cerebrovascular and cardiovascular disease mortality rates. Risk factors include smoking, hypertension, diabetes mellitus, hyperlipidemia, and obesity. We compared survival rates between a group with few risk factors (< two risk factors) and a group with many risk factors (> or = two risk factors) in four groups of subjects: middle-aged men (< 61-years-old) and middle-aged women and elderly men (> or = 61-years-old) and elderly women. In the elderly male group, the survival rate was lower in subjects with many risk factors than in those with few risk factors. In the middle-aged male group, however, there was no difference between the two risk groups. On the other hand, in the middle-aged female group, the survival rate was lower in subjects with many risk factors than in those with few risk factors, while no difference was found between the two risk groups in the elderly female group. The results indicated that the effects of an accumulation of risk factors are different in men and women and greater in elderly men than in elderly women.

Adult↗
PubMed1998

[Role of impaired glucose tolerance in the progression of hypertension].

The present report describes the relationship between the glucose tolerance and hypertension surveyed in a ten-year longitudinal epidemiological study in two rural communities in Hokkaido, Japan. The 1972 subjects (928 men and 1044 women, aged 40-64, mean 51.1 +/- 7.0 years) were randomly selected in 1977 and 1978, underwent a 50-g oral glucose tolerance test (GTT) at the first year. The prevalences of borderline hypertension (BHT) and of hypertension (HT) were highest in those with diabetes mellitus (DM), followed by those with borderline diabetes (BDM) and those normal glucose tolerance (NGT). Systolic and diastolic blood pressure were significantly and positively correlated with plasma glucose levels during fasting (FPG), 60 min. after GTT (60G), and 120 min. after GTT (120G), and were ordered as follows: NGT < BDM < DM. The FPG, 60G and 120G plasma glucose levels were all significantly higher in BHT and HT than in NT. The prevalences of the progression to hypertension from non-hypertension over the ten-year follow-up period were ordered as follows: NGT < BDM < DM. Glucose levels in progression group were higher than those in non-progression group. Multiple logistic regression analysis indicated that age, glucose intolerance, systolic blood pressure, and obesity index were significant predictors of the progression to hypertension. These results indicate that impaired glucose tolerance may be associated with hypertension, and might play a role in the development of hypertension.

Adult↗
PubMed1998

[Prevalence of glucose intolerance in Japan--from the National Circulatory Disorders Basic Survey, 1990].

The prevalence of glucose intolerance was surveyed in 8,063 people over 30 years old from the general population of Japan. The data used in the analysis were from the Fourth National Circulatory Disorders Basic Survey, which was conducted in 1990. Survey items included history of diabetes mellitus, body mass index (BMI) and daily life activity. Blood and urine were also examined, and the blood glucose levels, presence or absence of sugar in urine, and levels of glycohemoglobin (HbA1c) were determined. Glucose intolerance was identified from the blood glucose level, HbA1c level and history of diabetes mellitus. The frequency of glucose intolerance was 8.6% in all subjects (11.9% in men and 6.3% in women). The frequency was higher in older people: 1.7 times higher in men over 65 years old and 2.5 times higher in women over 65 years old. Among people over 40 years old, glucose intolerance was significantly more prevalent in men than in women. It was also significantly more prevalent in men living in big cities than in men living in rural areas. Among obese male subjects and men with a low level of activity in daily life, the frequency of glucose intolerance was higher than in normal male subjects. The level of activity in daily life tended to be lower for people living in big cities than for those in rural areas. The results suggest that the prevalence of glucose intolerance depends on the environment in which people live. The results also indicate that raising the level of activities in daily life might help prevent diabetes mellitus.

Activities of Daily Living↗
PubMed1998

[Incidence rate of acute myocardial infarction in Hokkaido, Japan].

A survey of acute myocardial infarctions (AMI) that occurred from October 1990 through September 1993 in Obihiro City, Hokkaido, was conducted. A total of 114 new cases of AMI was registered over the 3-year period. The incidence rate of AMI was 33.4 cases per 100,000 men per year and 137 cases per 100,000 women per year (total, 23.2 cases). The mean age at which AMI occurred was 11 years higher in women (71.1 +/- 9.4 years) than in men (60.0 +/- 11.8 years). In men, AMI was most common during the eighth decade of life, while in women the incidence of AMI increased after menopause. The ratio of cases of AMI to cases of stroke in the same period was 1:4.5. These results did not differ from the results of other surveys done over the same period in seven other area of Japan. To study risk factors for myocardial infarction, the data were grouped according to the results of medical examinations. Hypertension, diabetes, obesity and smoking were common among people with AMI. The incidence rate of hypercholesterolemia did not differ between those with AMI and those without, and only a relatively small number of people with AMI drank alcohol. Past reports have pointed out changes in the 'structure' of cardiovascular disease in Japan, which have accompanied changes in diet and lifestyle. This study has shows that aging hypertension, diabetes, obesity, and smoking are risk factors for myocardial infarction. Proper management, including early detection of these factors, will help to prevent of ischemic heart disease in Japan.

Adult↗
PubMed1998

Outcome significance of thallium-201 and iodine-123-BMIPP perfusion-metabolism mismatch in preinfarction angina.

UNLABELLED: The relevance of brief antecedent ischemia to preservation of myocyte viability and cardiac function is still controversial in humans. Dysfunctioning but viable myocardium shows impaired fatty acid metabolism despite restored coronary perfusion. We asked whether preinfarction angina might be related to preservation of cell viability and better functional recovery in comparison with impaired fatty acid metabolism. METHODS: Tomographic imagings with thallium and beta-methyl-p-iodophenyl penta-decanoic acid (BMIPP) were performed in 32 patients with first acute myocardial infarction who received primary coronary angioplasty: 20 patients with preexisting angina before infarction (Group A) and 12 without (Group B). Thallium and BMIPP abnormalities were quantified as a severity index by a polar map. Regional function was quantified by ventriculography and followed up. RESULTS: Despite no significant difference in coronary risk factors, cardiac function and angiographic findings, the thallium severity index was significantly lower than that of BMIPP (62+/-45 versus 96+/-59) in Group A but not in Group B (104+/-65 versus 115+/-68); the thallium severity index in Group A was significantly lower than that in Group B, but there was no significant difference in BMIPP abnormality between them. The BMIPP severity index correlated significantly with that of thallium in both groups. However, the regression line in Group A shifted downward and was statistically different compared with that in Group B. Regional function at an acute stage was significantly improved from 107+/-31 to 70+/-31 s.d./chord during follow-up in Group A but not in Group B (109+/-62 versus 106+/-52). The ratio of the thallium severity index to that of BMIPP at an acute stage was significantly related to improved regional wall motion during follow-up in the reperfused patients (y=-53x + 65, r=0.667). CONCLUSION: Preinfarction angina preserves myocyte viability relative to fatty acid metabolism, resulting in augmented perfusion-metabolism mismatch and functional improvement in patients undergoing successful reperfusion, indicating cardioprotective effects of preinfarction angina.

Aged↗