The pathogenesis of an impending infarction and its treatment--an angioscopic analysis.

To clarify the pathogenesis of an impending infarction and to investigate the difference between the pathogenesis of an acute myocardial infarction and an impending infarction, we have performed percutaneous transluminal coronary angioscopy in 13 patients with an impending infarction and in 13 patients with an acute myocardial infarction. As a result, coronary thrombi were observed in 12 of the 13 patients with an impending infarction, and a similar frequency of thrombi was observed in the patients with an acute myocardial infarction. Further, grayish white thrombi were observed in 9 of 12 patients with an impending infarction, but no such thrombi were noted in those with an acute myocardial infarction. Reddish thrombi, however, were observed in all patients with acute myocardial infarction, whereas such thrombi were observed in only 3 of 12 patients with an impending infarction. Informatively, occlusive thrombi occurred more frequently in patients with an acute myocardial infarction than in those with an impending infarction. As a thrombus plays an important role in an impending infarction, we also evaluated the effect of anticoagulant and thrombolytic therapy for an impending infarction in 79 patients. The incidence of recurrent angina and a subsequent acute myocardial infarction were significantly higher in non-heparin-treated patients and in thrombolytic-treated patients than in heparin-treated patients. In conclusion, a thrombus plays an important role in the pathogenesis of an impending infarction and in an acute myocardial infarction, though the characteristics of the thrombus differ in each instance. This difference may account for the differing results of thrombolytic therapy. Heparin was found an effective treatment for myocardial ischemia in an impending infarction.     

Deleterious effects of irradiation and bone marrow transplantation therapy in the genetically anemic an/an mouse

The efficacy and outcome of bone marrow transplantation therapy following lethal irradiation were examined in syngeneic mice that had a hereditary macrocytic anemia (an/an) or were genotypically normal (+/+). Successful RBC and WBC replacement, based on blood cell parameters and donor genetic markers, were observed in all combinations of transplant therapy. Nevertheless, the an/an mice died prematurely several months after treatment, whether they received +/+ or an/an marrow cells. In contrast, the +/+ recipients of either +/+ or an/an marrow cells survived for at least 1 year after transplantation. Premature death of the an/an mice was associated with lymphopenia, anemia, kidney lesions, and severe pathogen-free pneumonitis. On the basis of our results, we hypothesize that the premature deaths of an/an mice are caused by a kind of chronic irradiation damage to which an/an mice are especially susceptible.     

Changes in mitochondrial redox state following an oral glucose load

Summary Changes in cytosol and mitochondrial redox state after an oral glucose load were studied in the liver of rats. The [NAD⁺]/[NADH] ratios increased 4-fold in the cytoplasm and 1.5-fold in the mitochondria 60 min after an oral glucose load, when serum IRI was maximally increased. It is suggested that an increase in mitochondrial redox state following an oral glucose load is due to an enhanced rate of removal of NADH by the respiratory chain, possibly due to an elevated level of insulin available to hepatocytes, and that an increase in cytosol redox state depends on an enhancement in mitochondrial oxidation of cytosol reducing equivalent.     

Myocardial infarction in isolated ventricular non-compaction: contrast echo and MRI

We describe the case of an occasional discovery of isolated ventricular non-compaction in an adult recovered for an acute myocardial infarction, in which only the echocardiogram revealed an isolated ventricular non-compaction, confirmed by MRI: an unusual association between coronary artery disease and isolated ventricular non-compaction.     

Chromosome abnormalities in mice with Hertwig''s anemia

Mice with the recessive hereditary disease, Hertwig's anemia (an/an), exhibit a persistent mild macrocytic anemia and reduced fertility. We examined mitotic figures from bone marrow and kidney cells of adult mice and from liver cells of fetal mice that were genetically normal or had Hertwig's anemia. Uniformly normal mitotic figures were observed in the nonanemic mice (+/+ or +/an). In contrast, 5% to 15% of the mitotic figures were abnormal in mice homozyous for Hertwig's anemia (an/an). These aberrant cells were hyperploid, containing more than the normal complement of c40 chromosomes, but fewer than 80 chromosomes. Cells with abnormal numbers of chromosomes may show decreased viability or proliferative capacity. The occurrence of such abnormal cells in an/an mice could explain (1) the loss of progenitor stem cells during erythroid maturation, resulting in an anemic phenotype; and (2) the depletion of germ cells during ontogeny, resulting in reduced fertility.     

ACE Inhibitors in Heart Failure: Prospects and Limitations

ACE inhibitors have been shown to be effective in reducing the morbidity and mortality of patients with left ventricular systolic dysfunction, but their application to clinical practice in this situation is still limited. In part, the failure to prescribe an ACE inhibitor to a patient with left ventricular systolic dysfunction is due to perceptions regarding their side effects, such as cough and renal dysfunction. Relatively few patients with left ventricular systolic dysfunction and a serum creatinine ≥2 mg/dl receive an ACE inhibitor in clinical practice. In this situation one should consider an agent such as fosinopril, which is metabolized by the liver as well as secreted by the kidney. In patients with moderate renal dysfunction, fosinopril has been well tolerated without an increase in serum creatinine. In patients who develope cough due to an ACE inhibitor, consideration should be given to an angiotensin II type 1 receptor blocking agent, such as losartan. The relative safety and efficacy of an ACE inhibitor compared with an angiotensin II type 1 receptor blocking agent is being explored in a prospective randomized trial (Evaluation of Losartan In The Elderly [ELITE]), as well as the safety and pharmacological effectiveness of adding an angiotensin II receptor antagonist to an ACE inhibitor (Randomized Angiotensin receptor antagonists–ACE-inhibitor Study [RAAS]). There may also be a role for the combination of an aldosterone receptor antagonists and an ACE inhibitor in patients with left ventricular systolic dysfunction. Once an ACE inhibitor is administered to a patient with left ventricular systolic dysfunction it should be continued indefinitely. ACE inhibitors may be of value not only in preventing the progression of heart failure but also in reversing endothelial dysfunction and preventing the development of atherosclerosis and its consequences, such as myocardial infarction.     

Can the Kidney Prevent Cardiovascular Diseases?

The kidneys play an important role in the development of cardiovascular risk factors. It is well known that heavy proteinuria can induce hyperlipidemia, that uric acid is elevated in some renal deficiencies and that hypertension develops in most end stage renal diseases. In prehypertensive states, specially in subjects with a family history of hypertension, some hemodynamic changes take place, characterized by an increase in renal vasoconstriction with a reduction in renal plasma flow and an elevation of sodium reabsorption. The mechanisms for these alterations are not well understood, but an increase in intracytosolic calcium in vascular smooth muscle cells, a reduction in vasodilatory substances such as nitric oxide and an increased sympathetic nervous activity have been proposed. In normotensive subjects with two hypertensive parents a reduction in sodium diet, an increase in protein intake or in arginine diet could prevent established essential hypertension from developing. In borderline hypertension an early therapy with low doses of calcium antagonists, ACE inhibition or diuretics could be indicated.     

Related transplantation with HLA-1 Ag mismatch in the GVH direction and HLA-8/8 allele-matched unrelated transplantation: a nationwide retrospective study

To clarify which is preferable, a related donor with an HLA-1 Ag mismatch at the HLA-A, HLA-B, or HLA-DR loci in the graft-versus-host (GVH) direction (RD/1AG-MM-GVH) or an HLA 8/8-allele (HLA-A, HLA-B, HLA-C, and HLA-DRB1)-matched unrelated donor (8/8-MUD), we evaluated 779 patients with acute leukemia, chronic myelogenous leukemia, or myelodysplastic syndrome who received a T cell-replete graft from an RD/1AG-MM-GVH or 8/8-MUD. The use of an RD/1AG-MM-GVH donor was significantly associated with a higher overall mortality rate than the use of an 8/8-MUD in a multivariate analysis (hazard ratio, 1.49; P < .001), and this impact was statistically significant only in patients with standard-risk diseases (P = .001). Among patients with standard-risk diseases who received transplantation from an RD/1AG-MM-GVH donor, the presence of an HLA-B Ag mismatch was significantly associated with a lower overall survival rate than an HLA-DR Ag mismatch because of an increased risk of treatment-related mortality. The HLA-C Ag mismatch or multiple allelic mismatches were frequently observed in the HLA-B Ag-mismatched group, and were possibly associated with the poor outcome. In conclusion, an 8/8-MUD should be prioritized over an RD/1AG-MM-GVH donor during donor selection. In particular, an HLA-B Ag mismatch in the GVH direction has an adverse effect on overall survival and treatment-related mortality in patients with standard-risk diseases.     

Massive hemothorax caused by intercostal artery bleeding: selective embolization may be an alternative to thoracotomy in selected patients

Massive hemothorax is an indication for thoracotomy. We report a case of an 85-year-old debilitated patient, in whom massive hemorrhage from an actively bleeding intercostal artery was controlled by angiographic embolization. Angiographic embolization proved to be an effective alternative to thoracotomy in this patient, thus avoiding numerous postoperative complications and high mortality. Massive bleeding from an intercostal artery should be considered an indication for angiographic embolization in selected patients.     

A Hemolytic Reaction Implicating Sda Antibody Missed by Immediate Spin Crossmatch

Anti-Sda, an antibody not usually considered to cause of hemolytic transfusion reactions, possibly was related to hemolysis following transfusion of red blood cells expressing strong Sda antigen. Prior to transfusion, the antiglobulin antibody screen performed in LISS and an immediate spin crossmatch were negative. Retrospectively, after hemolysis was detected, an antiglobulin crossmatch with red cells from the transfused unit revealed microscopic incompatibility. The transfused unit proved to have strong expression of Sda antigen-facilitating identification of a weak Sda antibody in our patient. In addition, this case represents an unusual instance in which an antibody screen plus an immediate spin crossmatch failed to detect an incompatibility that would have been apparent had an antiglobulin crossmatch been performed.     

Volume of sella turcica in normal subjects and in patients with primary hypothyroidism and hyperthyroidism.

In an attempt to assess a possible relationship between pituitary size and TSH secretion, the volume of sella turcica was measured in 570 subjects, 26 primary hypothyroid patients, and 34 thyrotoxic patients. The volume of sella turcica, measured by a 3-dimensional approach, increased progressively with age until 20 years of age and was rather constant thereafter in normal subjects. In thyrotoxic patients, the volume of sella turcica was normal in spite of decreased plasma TSH concentration. In contrast, 81% of primary hypothyroid patients had an abnormal enlargement of the sella turcica. The magnitude of an increase of sella turcica inversely related with a decrease in serum T4 and T3 concentrations. On the other hand, the magnitude of an increase of sella turcica correlated well with an increase of circulating TSH. We suggest that an increase of sella turcica indirectly reflects an increase in pituitary size and TSH-secreting capacity, possibly due to hypertrophy and hyperplasia of TSH cells in primary hypothyroid patients.     

The impact of sleep disturbances on adipocyte function and lipid metabolism

Classically, sleep has been considered to serve an essential restorative function for the brain. However, there are an increasing number of studies linking decreased sleep quantity and/or quality in humans to an increased obesity and diabetes risk. Reductions in sleep quantity or quality lead to an increase in hunger and appetite, which chronically could predispose an individual to obesity. Carefully controlled studies have shown that two nights of insufficient sleep is causally linked to a decrease in disposition index, the most commonly used predictor of an individual's diabetes risk, and impairments in glucose tolerance and insulin sensitivity. Thus, sleep appears to play a critical role in modulating energy metabolism in peripheral tissues. Here we will discuss recent work implicating adipose tissue as a potential direct target of disruption of sleep quality, and explore the potential mechanistic links between sleep, adipose tissue and the global control of energy metabolism in humans.     

Left ventricular function with effort in the coronary patient. Study of the correlations with the data on echocardiography, effort ECG, and the teleheart. 2.]

Correlations were established, for 30 coronary patients, between the haemodynamic findings and those adduced from non-invasive techniques - electrocardiography, both at rest and on exercise, telethorax, and echocardiography. Left ventricular function in the coronary patient can be assessed, even before catheterisation, by means of: 1. The clinical findings: angina of effort, an uncomplicated infarct, and an infarct with sequelae each has its own peculiar haemodynamic pattern at rest and on exercise; 2. The ECG finding of an extensive anterior infarct implies a haemodynamic picture vastly different from that with a limited posterior infarction; 3. The appearance of an ischaemic shift in the ST segment on exercise implies an acute malfunctioning of the left ventricle; 4. On the echocardiogram, an end-diastolic volume greater than 150 ml/m2, an ejection fraction less than 0.50 and VCF greater than 0.8 c/s are always accompanied by disturbances in the haemodynamics. By contrast, the cardio-thoracic ratio, except in post-infarct cases complicated by left ventricular failure, gives no predictive indication of cardiac function. These various examinations should therefore be applied to the coronary patient as an index of cardiac function.     

Epidermoid cyst originating from an intrapancreatic accessory spleen

We report a rare case of an epidermoid cyst originating from an intrapancreatic accessory spleen, in a 40-year-old Japanese man with no clinical symptoms. A cystic tumor in the pancreatic tail was detected incidentally by abdominal ultrasonography. The patient was referred to the KKR Tachikawa Hospital for further examination of the tumor. Preoperative imaging findings suggested that the tumor was an epidermoid cyst originating from an intrapancreatic accessory spleen. On both pre-and post-contrast computed tomography and magnetic resonance images, the solid compartment of the tumor had the same X-ray attenuation and intensity as the spleen. Upon surgical excision, the mass consisted of solid and cystic components that were macroscopically evident on the preoperative images. Microscopic analysis revealed that the solid component was an accessory spleen in the pancreatic tail, whereas the cystic component was lined with stratified epithelium representative of an epidermoid cyst. This is the thirteenth report (in English) of an epidermoid cyst originating from an intrapancreatic accessory spleen, and the first case to be diagnosed prior to surgery.     

The postural effects on blood pressure following interruption of the vasomotor nerves of man

Before posterior infradiaphragmatic bilateral resection of the splanchnic nerves and bilateral removal of the first lumbar ganglions, voluntary change to the upright from the horizontal position in six patients who had essential hypertension caused an average decrease of 9 mm. in the systolic blood pressure and an average increase of 8.4 mm in the diastolic blood pressure. The cardiac rate increased an average of 11.8 beats per minute. Following operation, assumption of the upright position produced an average decrease of 9.1 mm. in the systolic blood pressure and an average increase of 3.2 mm. in the diastolic blood pressure. The cardiac rate increased an average of 12.3 beats per minute.     

感染因素与慢性阻塞性肺疾病

慢性阻塞性肺疾病（chronic obstructive pul monary disease,COPD）的发病率、病死率高,社会经济负担重,已成为一个重要的公共卫生问题。除吸烟、化学因素、空气污染等因素外,感染是COPD发展和加重的重要因素。无论在COPD的急性加重期亦或稳定期细菌感染都起着重要作用,有研究表明非典型致病菌和病毒在COPD发生、发展过程中起着重要作用。细菌、非典型致病菌、病毒还可在COPD的发展过程中起协同作用,导致病情反复加重。本文拟对微生物感染和COPD的关系作一综述。     

Cerebellar degeneration and hearing loss in a patient with idiopathic myenteric ganglionitis

A 35-year-old male with an 11-year history of intestinal pseudo-obstruction associated with an idiopathic inflammatory insult of the myenteric plexus and the presence of circulating anti-Hu antibodies developed a neurological syndrome characterized by bilateral hearing loss, deteriorating balance, an unsteady gait and difficulty in estimating distances. A similar neurological syndrome has previously been described in older patients among the paraneoplasic syndromes associated with small-cell lung carcinoma and the presence of circulating anti-Hu antibodies, but never in the rare cancer-free patients with anti-Hu-associated chronic idiopathic intestinal pseudo-obstruction. The patient underwent a steroid treatment. No further episodes of functional intestinal obstruction were observed and, after an initial improvement, the neurological symptoms stabilized, leaving a permanent reduction in hearing function and an unsteady gait. The case shows that an idiopathic inflammatory insult of the myenteric plexus may precede (and perhaps lead to) central nervous system impairment in patients with anti-Hu-associated chronic idiopathic intestinal pseudo-obstruction.     

Development of acute pancreatitis in rats after single ethanol administration and induction of a pancreatic juice edema

The effect of an acute gastral ethanol application and an additional induction of a pancreatic juice edema by an obstruction/hyperstimulation mechanism was studied in rats. Neither ethanol administration nor the combination of ductal obstruction and secretory stimulation resulted in an acute pancreatitis when applied independently. A combination of these factors, however, led to the development of AP in two-thirds of the rats treated in this manner. Its severity was evaluated by the degree of extrapancreatic fat necrosis, the increase in serum amylase and lipase activities, and by histologic investigations. It is assumed that a pancreatic juice edema, provoked by pancreatic secretion at temporary ductal obstruction, could be an important cofactor in formation of ethanol-induced acute pancreatitis.     

Atrial substrate properties and outcome of catheter ablation in patients with paroxysmal atrial fibrillation associated with diabetes mellitus or impaired fasting glucose

Diabetes mellitus has been reported to be an independent risk factor of atrial fibrillation (AF). The present study investigated the atrial substrate properties and clinical outcome of catheter ablation in patients with paroxysmal AF and abnormal glucose metabolism. A total of 228 patients with paroxysmal AF who had undergone catheter ablation for the first time were enrolled. An abnormal glucose metabolism (n = 65) was defined as diabetes mellitus or an impaired fasting glucose. We analyzed the clinical and electrophysiologic characteristics in, and the clinical outcome of, patients with AF with and without an abnormal glucose metabolism. The right atrial (107.2 ± 15.4 vs 96.0 ± 16.5 ms, p < 0.001) and left atrial (108.4 ± 22.3 vs 94.0 ± 17.5 ms, p < 0.001) total activation times were significantly longer in the patients with AF and an abnormal glucose metabolism than in those without an abnormal metabolism. Furthermore, the right atrial (1.46 ± 0.61 vs 2.00 ± 0.70 mV, p < 0.001) and left atrial (1.48 ± 0.74 vs 2.05 ± 0.78 mV, p < 0.001) bipolar voltages were significantly lower in those with AF and an abnormal glucose metabolism than in those without. The AF recurrence rate was also greater in the patients with an abnormal glucose metabolism (18.5% vs 8.0%, p = 0.022) than in those without. The follow-up duration was 18.8 ± 6.4 months. In conclusion, an abnormal glucose metabolism affects the biatrial substrate properties with an intra-atrial conduction delay, decreased voltage, and greater recurrence rate after catheter ablation.