Development of a nuclear magnetic resonance system for in situ analysis of hydrogen storage materials under high pressures and temperatures.

A NMR system for in situ analysis of hydrogen storage materials under high pressure and temperature conditions was developed. The system consists of a gas pressure and flow rate controlling unit, a temperature controller, a high temperature NMR probe tunable for both (1)H and other nuclei, and a sample tube holder. Sample temperature can be controlled up to 623 K by heated N(2) gas flow. Sample tube atmosphere can be substituted by either H(2) or Ar and can be pressurized up to 1 MPa under constant flow rate up to 100 ml/min. During the NMR measurement, the pressure can be adjusted easily by just handle a back pressure valve. On the blank NMR measurement, (1)H background noise was confirmed to be very low. (1)H and (11)B NMR spectrum of LiBH(4) were successfully observed at high temperature for the demonstration of the system. The intensity of the (1)H NMR spectra of H(2) gas was also confirmed to be proportional to the applied pressure.

[A case of malignant pericardial effusion due to breast cancer successfully controlled by intrapericardial chemotherapy using pirarubicin].

We report a case of malignant pericardial effusion due to breast cancer that was successfully controlled by intrapericardial chemotherapy using pirarubicin. A 53-year-old woman underwent breast conserving therapy for left breast cancer in 1996. She was given CAF therapy and UFT as adjuvant therapy. Three years and 10 months after operation, she had malignant pericardial and pleural effusion. Pericardiocentesis and pleurocentesis were performed immediately. Pericardial effusion relapsed after some time and she was treated with intrapericardial chemotherapy using pirarubicin. After this treatment she has not suffered from pericardial effusion for 1 year and 4 months to date. This case suggests that intrapericardial chemotherapy is effective for malignant pericardial effusion.

Serial MRI and (1)H-MRS of Wernicke's encephalopathy: report of a case with remarkable cerebellar lesions on MRI.

Before and after the administration of thiamine (vitamin B(1)), MRI and proton magnetic resonance spectroscopy ((1)H-MRS) were serially performed in a patient with Wernicke's encephalopathy demonstrating remarkable cerebellar lesions on MRI. Before thiamine administration, high signal intensities were observed in the thalamus around the third ventricle and in the superior portion of the cerebellar vermis and hemisphere on fluid-attenuated inversion recovery (FLAIR) and T2-weighted MR images. After thiamine administration, the high signal intensity in the former region disappeared immediately, while that in the latter regions persisted. The low level of N-acetylaspartate (NAA)/creatine (Cr) in the thalamus before thiamine administration improved to some degree on the (1)[H]-MRS images taken after thiamine administration. In the cerebellum, a lactate peak was observed before thiamine administration, and the NAA/Cr level did not improve after thiamine administration, suggesting that irreversible necrosis occurred. It is suggested that serial MRI/(1)H-MRS observation may be helpful in determining the neuronal viability of Wernicke's encephalopathy and the prognostic implications of sequelae such as Korsakoff's syndrome and cerebellar ataxia.

Idiopathic adrenal hemorrhage.

A case of idiopathic adrenal hemorrhage is reported. A 76-year-old woman exhibited a left adrenal tumor, 3 cm in diameter, on abdominal computed tomography. The patient was receiving aspirin medication for atrial fibrillation. There was no evidence of increased adrenal hormones. The mass enlarged to 6 cm in diameter within 18 months, and malignancy was suspected. The mass was diagnosed as adrenal hematoma by operative findings.

Direct discrimination and full-day disclosure of ventricular parasystole on new heart rate tachograms.

INTRODUCTION: To discriminate ventricular parasystole from fixed coupling interval ventricular premature complexes (VPCs), we developed a new diagnostic method using a dot distribution pattern corresponding to VPCs recorded on a heart rate tachogram using ambulatory ECG monitoring data. We tested our hypothesis that widely scattered VPC dots on instantaneous heart rate tachograms indicate a constant VPC-VPC interval compatible with parasystole. METHODS AND RESULTS: Patients with frequent VPCs > 5,000/day) were divided into two groups depending on the tachogram dot distribution patterns: group S (n = 10, aged 61 +/- 16 years) showed widely scattered VPC dot distribution, whereas group F (n = 10, 60 +/- 17 years) showed fixed VPC dot distribution limited to a narrow zone. Using digitized R-R interval data, full-day heart rate tachograms and VPC-VPC intervals were depicted simultaneously. Group S demonstrated constant basic VPC-VPC intervals (1,285 to 2,052 msec, mean 1,738 +/- 219), with a coefficient of variation (CV) of 0.061 +/- 0.018. Their VPC coupling intervals were markedly variable (651 +/- 113 msec; CV = 0.193 +/- 0.034). Each patient's basic VPC-VPC intervals showed small diurnal alterations (minimum -13% +/- 3% to maximum +15% +/- 6%). VPC-VPC intervals in group F were not constant and showed marked variation. Group F VPC coupling intervals were shorter and constant (480 +/- 30 msec, P = 0.0002; with CV = 0.076 +/- 0.013, P < 0.0001). CONCLUSION: Ventricular parasystole with constant VPC-VPC intervals consistently became evident based on VPC dot patterns recorded on heart rate tachograms.

Cyclic bursts of ventricular premature contractions of more than one minute intervals.

Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs.

[Evaluation of restenosis after percutaneous transluminal coronary angioplasty using a Doppler index, the Tei index].

Cardiac function and restenosis were evaluated after percutaneous transluminal coronary angioplasty (PTCA) using a Doppler index (the Tei index). Thirty-eight patients, 31 men and 7 women (mean age 57 years) with ischemic heart disease were studied. The underlying heart diseases were angina pectoris without left ventricular asynergy in 16 patients and old myocardial infarction (OMI) with left ventricular asynergy in 22 . Ejection fraction was measured by M-mode echocardiography and deceleration time, and the interval between cessation and onset of the mitral inflow velocity (a), ejection time at aortic valve (b), and the Tei index [(a-b)/b] were measured by M-mode echocardiography performed before and 6 months after PTCA. The ejection fraction, deceleration time and Tei index showed no changes after PTCA in patients with angina pectoris with or without restenosis. In patients with OMI with restenosis, the Tei index increased slightly after PTCA, from 0.56 +/- 0.15 to 0.61 +/- 0.13. The deceleration time changed from 0.23 +/- 0.03 to 0.24 +/- 0.02 msec, and the ejection fraction from 0.46 +/- 0.11 to 0.51 +/- 0.17, neither significantly. However, in patients with OMI without restenosis (15 out of 22 patients), the Tei index significantly improved after PTCA, from 0.55 +/- 0.13 to 0.48 +/- 0.12 (p < 0.05). In patients with left ventricular asynergy due to old myocardial infarction, without restenosis, the Tei index significantly improved after PTCA. The Tei index is useful for evaluating restenosis after PTCA in patients with OMI.

Carbamazepine-induced sinus node dysfunction and atrioventricular block in elderly women.

We report on four elderly women in whom carbamazepine was suspected of inducing sinus node dysfunction (3 patients) and atrioventricular block (1 patient). Patients were treated with carbamazepine, 200 to 600 mg a day, for trigeminal neuralgia (n = 3) or epilepsy (n = 1). After 1 to 16 months of carbamazepine therapy, these patients were admitted to our emergency room because of bradyarrhythmia. Their conduction disturbances on electrocardiographic monitoring disappeared immediately after the cessation of carbamazepine intake. Provocation tests were performed on three patients. Because of renal insufficiency, one patient could not undergo the provocation test. Her carbamazepine clearance was markedly decreased. Carbamazepine induced sinus arrest in two patients within 48 hours after intake, but did not induce atrioventricular block in the remaining patient. In two patients, computer simulation of carbamazepine pharmacokinetics was performed and disclosed a clear-cut relationship between the plasma concentration of carbamazepine and the frequency of sinus arrest. During the test, the maximum plasma carbamazepine concentration in these two patients did not exceed the therapeutic range. However, it did exceed the range in the one with a negative test. Our results suggest that careful monitoring of ECG and plasma drug concentration is required with carbamazepine therapy, especially in elderly women.

Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty.

BACKGROUND: The Cutting Balloon is a novel dilatation catheter for coronary angioplasty (InterVentional Technologies Inc). It produces longitudinal, microsurgical incisions in the vessel wall before the actual dilatation. It is assumed that these controlled surgical incisions relieve hoop stress and reduce vessel wall injury and eventually restenosis. However, no clinical indicator to support the theory of reduced injury has been described. Certain clusters of differentiation (eg, CD11, CD18 on the leukocytes) are implicated in leukocyte adhesion, increased permeability, and opsonization. Therefore, they might serve as clinical indicators of the injury level of the vessels after angioplasty. METHODS AND RESULTS: We randomly selected 64 patients with isolated left anterior descending coronary artery disease for either Cutting Balloon angioplasty or conventional balloon angioplasty. The expression of CD18 and CD11b on the surface of neutrophils was determined by flow cytometric analysis. Serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) were also measured. The expression of both the CD18 and CD11b in the coronary sinus blood gradually increased and reached its maximum at 48 hours after angioplasty. The sICAM-1 levels in the coronary sinus serum also increased after angioplasty. Percentage increases of CD18 and CD11b expression and the increase of the sICAM-1 levels at 48 hours after angioplasty (as ratios to baseline values before angioplasty) were less in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group (CD18, 1.10+/-0.05 versus 1.31+/-0.05, P<0.05; CD11b, 1.23+/-0.06 versus 1.72+/-0.10, P<0.001; sICAM-1, 1.12+/-0.05 versus 1.25+/-0.02, P<0.05). In all patients, the late lumen loss at follow-up angiogram positively correlated with the increased levels of CD11b (R=0.59, P<0.001) and sICAM-1 (R=0.38, P<0.05) at 48 hours after angioplasty. CONCLUSIONS: Balloon angioplasty upregulated Mac-1 (CD11b/CD18) on the surface of the neutrophils and increased sICAM-1 levels in association with late loss increase. These changes were significantly smaller in the Cutting Balloon angioplasty group than in the conventional balloon angioplasty group. This suggests that Cutting Balloon angioplasty may produce less vessel wall injury and, consequently, less neutrophil activation, which may account for the lower rate of restenosis.

Detection of platelets activated during acetylcholine-induced coronary vasospasm.

Although platelet activation may play a role in coronary artery spasm, platelets activated following coronary vasospasm have not been clinically detected. We performed flow cytometric analysis of activation-dependent granular proteins, CD62P (P-selectin), CD63, PAC-1 (activated glycoprotein [GP] IIb/IIIa) and thrombospondin on the platelet plasma membrane in patients who exhibited acetylcholine-induced coronary vasospasm and compared findings with those in control patients without vasospasm. We simultaneously investigated the plasma levels of thrombin anti-thrombin III complex (TAT), plasmin alpha2-plasmin inhibitor complex (PIC), and thrombomodulin. In patients with vasospasm, the expression of CD62P, CD63 and PAC-1 on the platelet membrane surface increased in coronary sinus blood samples following coronary vasospasm, although the expression in aortic samples did not change. The TAT level also increased in the coronary sinus after vasospasm. Platelets might be activated by coronary vasospasm within the coronary circulation. The platelet activation process may be modulated by thrombin generation.

An IDDM patient who complained of chest oppression with ischemic changes on ECG in insulin-induced hypoglycemia.

A 34-year-old female IDDM patient complained of chest oppression in hypoglycemic episodes and electrocardiograms revealed reversible ischemic changes occurring concomitantly with hypoglycemia. The ECG changes improved and the chest oppression disappeared following increasing blood glucose level by glucose intake. Master's double load test and treadmill load test were positive for ischemic changes. Radioisotopic myocardial scintigraphy by thallium and BMIPP did not show any filling defects and coronary angiography revealed no remarked stenosis in the coronary arteries. She had no mitochondrial tRNA(Leu) (A-->G) gene mutation at nucleotide position 3243, but both the patient and her mother had a G-to-A transition within the replication origin of the light strand at nucleotide position 5744 of the mitochondrial gene. As the patient's maternal family had no history of ischemic heart disease, it is not clear whether mitochondrial gene mutation at nucleotide position 5744 reflects the occurrence of cardiac ischemia. Some disorders of microcirculation in capillary vessels in cardiac muscles may occur in such patients.

Ischemic change on electrocardiogram induced by hypoglycemia in a diabetic patient.

A 34-year-old female patient who presented to our hospital had been treated with insulin for diabetes since she was 25 year old. For the previous year she had experienced chest pain on exertion and during hypoglycemia. During both chest pain and exercise tests, ST depression and flattening of the T wave were recognized in leads II, III, aVF, and V2-V6 on the electrocardiogram, and thus ischemic heart disease was suspected. Cardiac catheterization was performed, but no organic stenosis or spasms were found. Hypoglycemia (41 mg/dl) was induced by intravenous injection of rapid insulin (total 18 U, 0.4 U/kg). However, no coronary change was seen, although she felt chest pain and the same ischemic electrocardiographic changes occurred. We hypothesized the causes of the ischemic change to be both the effects of insulin on the cardiovascular system and the physiologic stress induced by the existence of microvascular abnormality. Special care should therefore be taken with diabetic patients being treated with insulin or hypoglycemic agents.

Clinical significance of neutrophil adhesion molecules expression after coronary angioplasty on the development of restenosis.

To investigate the neutrophil activation process following percutaneous transluminal coronary angioplasty (PTCA), we examined the expressions of Mac-1 (CD11b/CD18), L-selectin (CD62L), and sialyl-LewisX (SLX) on the surface of neutrophils after the PTCA procedure, by flow cytometric analysis. Twenty-nine patients with single vessel coronary artery disease of the left anterior descending artery who underwent elective PTCA were enrolled. In the 17 patients without restenosis at the follow-up angiography, the mean channel fluorescence intensity (MFI) for CD18, CD62L and SLX did not change after PTCA. Only the CD11b level was increased at 48 h after the PTCA. In the remaining 12 patients who developed restenosis, the MFI values for CD18 and CD11b were increased at 24 h and 48 h after the PTCA. The MFI value for CD62L was decreased and that for SLX was increased at 48 h after the PTCA. These changes were more prominent in the coronary sinus blood samples than in those of the peripheral blood samples. Our data indicate the down-regulation of L-selectin, probably by shedding, as well as the up-regulations of Mac-1 and sialyl-LewisX, especially in patients with restenosis. It is suggested that neutrophil activation by an interaction between the selectin family and carbohydrate ligands after PTCA may play a role in the development of restenosis, as does the integrin family.

Effect of enalapril maleate on cerebral blood flow in patients with chronic heart failure.

The effect of enalapril on cerebral blood flow (CBF) was studied in 11 patients with chronic heart failure (NYHA II or III, dilated cardiomyopathy in 6 and old myocardial infarction in 5). CBF was evaluated by analyzing the Patlak-Plot curve obtained from radionuclide angiography with technetium-99m hexamethylpropylene amine oxime (99mTC-HM-PAO). Cardiac index (CI) and stroke volume (SV) were simultaneously measured by impedance cardiography. These measurements were performed before and at four weeks after daily administration of 5 mg enalapril. The stroke volume, cardiac index, and heart rate were not significantly changed after four weeks of enalapril administration. However, CBF was increased by 6.5% from 36.72 +/- 4.66 to 39.13 +/- 5.65 mL/100g/min (P < 0.05). These results suggest that enalapril increased cerebral blood flow, which was not related to increased cardiac output in congestive heart failure. Patlak-Plot analysis of radionuclide angiography using 99mTC-HM-PAO may be available for quantitative assessment of brain perfusion.

Impaired left ventricular diastolic filling occurs in diabetic patients without atherosclerotic coronary artery disease.

Using left ventriculography, left ventricular diastolic function was studied in 24 diabetic patients who had angina pectoris without atherosclerotic large-vessel coronary artery diseases (group A, 14 patients with exercise-induced ischemic ST-T changes as seen during electrocardiogram; group B, 10 patients without such changes). In groups A and B, the global peak filling rate was significantly less than that in control patients without diabetes or cardiac diseases. The ratio of the global time to the peak filling rate to the diastolic time was higher in both groups A and B than in the control groups. However, the total of time differences, defined as the sum of the time differences between global time to the peak filling rate and each of the three regional time to the peak filling rate, was greater in group A than in either group B or the control patients. Total time difference was similar in group B and the controls. Left ventricular diastolic filling was impaired in diabetic patients without large-vessel coronary artery disease. Impaired diastolic filling was present regionally in patients with ischemic ST-T change but globally in those without such change.

Tricuspid valve infectious endocarditis associated with dental treatment.

A 52-year-old man with neither congenital heart disease nor history of drug abuse had a spiking fever after dental treatment and was diagnosed with pneumonia at a local clinic. He was treated with antibiotics and his fever went down. Ten months later, he had again pyrexia and suffered from congestive heart failure. He admitted to our hospital and tricuspid valve endocarditis was proved by echocardiography. He was treated with penicillin. However, during the treatment, he developed a pulmonary embolism. So he underwent surgical treatment. We should take dental treatment into account one of predisposing causes of tricuspid endocarditis.

[Successful surgical treatment of aortic regurgitation due to annuloaortic ectasia and mitral regurgitation caused by tendon rupture in a case of osteogenesis imperfecta].

A 54-year-old man presented with osteogenesis imperfecta complicated with both aortic regurgitation due to annuloaortic ectasia and mitral regurgitation secondary to tendon rupture. He had spinal and carpal deformities in his childhood, and heart murmurs were identified at the age of 25. He was admitted complaining of dyspnea on effort. His height was 142 cm and his weight was 46 kg. He had kyphosis, scoliosis and carpal deformity. Blue sclera was not observed. Chest radiography showed cardiomegaly and lung congestion. Echocardiography showed annuloaortic ectasia, mild aortic regurgitation, and serious mitral regurgitation due to postero-apical tendon rupture. Bone deformity and his statues were indicative of osteogenesis imperfecta. He received modified Bentall and mitral valve replacements.

Acute myocardial infarction during pregnancy.

We report a 30-year-old woman who developed an acute myocardial infarction at 24 weeks of gestation. She did not undergo any kind of acute intervention. On the 8th hospital day, premature delivery was performed safely following premature rupture of membrane. Coronary angiogram was normal and no spasm was induced by provocative test with ergometrine maleate. The patient had abnormal values of fibrinogen, thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex. Thus, thrombus formation might have been associated with the onset of acute myocardial infarction. This is the first case of acute myocardial infarction during pregnancy, showing normal coronary angiogram and negative pharmacological provocation of coronary spasm.

Early detection of platelet activation after coronary angioplasty.

BACKGROUND: Although platelet activation has been considered an important reaction after percutaneous transluminal coronary angioplasty (PTCA), it is still difficult to detect the activated platelets in vivo directly. METHODS: To detect platelets activated at an early stage after PTCA, blood samples were take from the coronary sinus and the aorta in 22 patients with coronary artery disease, who underwent PTCA for a lesion of the left anterior descending artery. Ten patients with coronary artery disease, who underwent diagnostic coronary angiography only, were compared with them. The expression of activation-dependent granular protein, CD62P (P-selectin) and CD63, on the platelet membrane surface was analysed using flow cytometry. The plasma thrombomodulin level was also measured. RESULTS: The percentage of platelets positive for CD62P (0.53 +/- 0.04 to 0.80 +/- 0.11%, P < 0.01) and CD63 (16.0 +/- 1.4 to 19.8 +/- 2.0%, P < 0.05) increased after PTCA in the coronary sinus, although it did not change in the aorta. The plasma thrombomodulin level also increased after PTCA in the coronary sinus (16.7 +/- 1.0 to 20.4 +/- 2.0 mu/ml, P < 0.05). However, these parameters did not change after coronary angiography only. After PTCA, the plasma thrombomodulin level was correlated with the percentage of platelets positive for CD62P (r = 0.88, P < 0.001) and with that for CD63 (r = 0.69, P < 0.001) in the coronary sinus. CONCLUSIONS: PTCA produced activation of circulatory platelets, which might have been caused by balloon-induced vascular endothelial injury. One should take care to avoid needless vascular injury during the PTCA procedure to inhibit the platelet activation.

A mechanism of ischemic preconditioning during percutaneous transluminal coronary angioplasty.

Manifestation of ischemic preconditioning and its mechanisms during percutaneous transluminal coronary angioplasty (PTCA) was evaluated. Twenty-two patients with angina pectoris, who had one-vessel coronary artery disease of the proximal left anterior descending artery but without visual collateral circulation, underwent elective PTCA performed by balloon inflations of 90 s, repeated three times or more. Changes in standard 12-lead electrocardiogram, hemodynamics and oxygen saturation of the great cardiac vein by a fiber-optic catheter were analyzed. Anginal chest pain occurred in 21 patients (95%) during the first balloon inflation, and in only 9 patients (41%) during the third inflation. In comparison with the first inflation, the third produced less shifts in ST junction (p < 0.01) and peak T (p < 0.01), which were measured and averaged by 4 chest leads from V2 to V5. The heart rate-blood pressure product during the third inflation was equivalent to that during the first. The great cardiac vein oxygen saturation decreased equally during the first and third inflations. However, the ratio of the saturation at reactive hyperemia after balloon deflation to baseline was higher (p < 0.01) in the third than in the first inflation. The adenosine content of the great cardiac vein measured in 11 patients just prior to balloon deflation was also higher (p < 0.05) in the third inflation than the value in the first. Repeated coronary artery occlusion during PTCA could cause ischemic preconditioning, which may be derived from mechanisms common to accelerated reactive hyperemia, for example an increase in intrinsic adenosine levels.