Biomedical subjects

M Teragaki

Publications and source records attributed to M Teragaki.

At least 55 records · Page 3Linked to original sources

PubMed1992

Clinical significance of reverse redistribution on thallium-201 single-photon emission computed tomography in patients with acute myocardial infarction.

To determine the clinical significance of reverse redistribution (RR), resting thallium-201 myocardial single-photon emission computed tomography was performed once or twice in 80 patients in subacute phase (1 week to 2 months) of myocardial infarction. Thirty eight patients demonstrated RR on at least one study (group RR) and 32 a fixed defect only (group FD). Group RR had significantly smaller defects than group FD. Standardizing the relation of the severity of wall motion abnormality of left ventricle on echocardiogram with that of perfusion defect, in group RR wall motion abnormality in the acute and subacute phase reflected the defect of delayed image, while that in chronic phase, which was thought to reflect the viability of myocardium in the infarct region, reflected the defect of initial image. In serial thallium-201 studies, only the defect of delayed image of group RR improved on the second study, while the defect of initial image of group RR and defect of group FD did not improve. Wall motion of group RR improved with the disappearance of RR, and when RR remained, wall motion did not improve so much. We concluded that RR was thought to be demonstrated in viable myocardium with severe wall motion abnormality.

Adult↗

PubMed1992

Extensive specifically localized myocardial calcium deposition in a hemodialysis patient.

A 51-year-old female who was hospitalized for evaluation of frequent episodes of hypotension, died unexpectedly. At autopsy, there were many fine, white granular deposits in the myocardium, which were more prominent in the subepicardium of the left ventricle than in the subendocardium. Pathologic calcification is sometimes seen in chronic hemodialysis patients and in some organs the sites of calcium deposition are quite specific. There have been few reports concerning the pattern of calcium deposition in the myocardium and, to our knowledge, the reason for this characteristic distribution is unknown. However it may relate to hydrogen ion concentration in the myocardium.

Calcinosis↗

PubMed1991

Plasma levels of platelet-derived growth factor in normal subjects and patients with ischemic heart disease.

Plasma levels of platelet-derived growth factor (PDGF) were measured in 24 normal control subjects, 31 patients with stable angina pectoris, 25 patients with unstable angina pectoris, and 31 patients with acute myocardial infarction (AMI) by a sensitive direct radioimmunoassay. The plasma PDGF level in normal control subjects was 273 +/- 25 pg/ml; there was no significant correlation between the plasma PDGF level and age. Plasma PDGF levels in patients with unstable angina pectoris and acute myocardial infarction were significantly lower than those in normal control subjects and patients with stable angina pectoris (p less than 0.05). In patients with acute myocardial infarction the plasma PDGF level in the chronic phase was significantly higher than that in the acute phase (p less than 0.05). These observations raise the possibility that PDGF is involved in the pathophysiology of ischemic heart disease.

Adult↗

PubMed1991

Circulating immunoreactive endothelin in patients undergoing percutaneous transluminal coronary angioplasty.

Circulating immunoreactive endothelin (ir-ET) in the coronary sinus (CS) and the femoral artery (Ao) was measured in patients who underwent percutaneous transluminal coronary angioplasty (PTCA). Plasma ir-ET level in the CS was significantly increased from 1.6 +/- 0.8 pg/mL to 2.0 +/- 1.0 pg/mL after PTCA (P less than .05). Plasma ir-ET level in the Ao tended to increase after PTCA, but it was not significant. Plasma ir-ET level in the CS was not related to the plasma thromboglobulin level, plasma thrombin-antithrombin complex level, mean blood pressure, or heart rate. These results suggest that the increase of plasma ir-ET level in the CS may be associated with the coronary endothelial injury by PTCA.

Adult↗

PubMed1991

Pheochromocytoma with electrocardiographic change mimicking angina pectoris, and cyclic change in direct arterial pressure--a case report.

A forty-two-year-old man was admitted because of chest pain. Electrocardiograms at admission showed horizontal ST depression in leads, II, III, aVF, V4, V5, and V6. Direct blood pressure monitoring revealed cyclic change between 160/100 mmHg and 70/50 mmHg and heart rate between 80/sec and 120/sec at fifteen minute intervals. The plasma norepinephrine and epinephrine concentrations were elevated during the episodes of hypertension. Pheochromocytoma was found in the right adrenal gland. These cyclic changes in blood pressure and heart rate are an aid for diagnosis.

Adrenal Gland Neoplasms↗

PubMed1991

Two-dimensional and Doppler echocardiographic findings in a case of subaortic "fibrous sac".

We described a 37-year-old man with a subaortic "fibrous sac", admitted for congestive heart failure. On 2-dimensional echocardiography a saccular structure was seen to extend from the left coronary cusp of the aortic valve to the outflow tract of the left ventricle. By color Doppler imaging, a grade 3 aortic regurgitation was recognized. Aortic regurgitant flow was recorded from the left coronary cusp to the saccular lesion. When congestive heart failure became exacerbated, the repeat examination showed the regurgitant flow passing through the perforated bottom of this lesion and reaching the left ventricular cavity. On microscopic examination of the excised valve, capillary proliferation and inflammatory changes were recognized near the annular region of the left coronary cusp. The edge of the valve leaflet and the other 2 cusps were intact. It is likely that our patient had a mycotic aneurysm near the aortic ring. We speculate that aortic regurgitation followed inflammation. It dilated the left ventricular cavity and contributed to congestive heart failure. Inflammation also weakened the tissue near the annulus, causing it to protrude into the subaortic region thus forming a small aneurysm. It may have grown to become a large saccular structure under high aortic pressure. That is, it became a "giant" endocardial pocket with inflammatory process. Finally, the rupture of this sac caused a massive aortic regurgitation, exacerbating congestive heart failure.

Adult↗

PubMed1991

Assessment of superior vena caval blood flow velocity in ischemic heart disease.

In order to evaluate the right atrial function in patients with ischemic heart-disease, we studied the superior vena caval blood flow velocity using pulsed Doppler echocardiography. The subjects included 31 patients with anteroseptal infarction (ANT), 23 with inferior or inferoposterior infarction (INF + POS), 27 with effort angina pectoris (EAP) and 15 with vasospastic angina pectoris (VAP). The systolic peak flow velocity (PFVs) was significantly reduced only in INF + POS compared with those in ANT, EAP and VAP (36.8 +/- 1.8 cm/sec vs 46.9 +/- 2.1 cm/sec, 46.4 +/- 2.1 cm/sec and 42.6 +/- 1.9 cm/sec, p less than 0.05, respectively). No significant difference in diastolic peak flow velocity (PFVd) was found between the 4 groups. PFVs/PFVd was significantly reduced only in INF + POS compared with those in ANT, EAP, and VAP (1.39 +/- 0.05 vs. 1.75 +/- 0.08, 1.76 +/- 0.09, and 1.62 +/- 0.09, p less than 0.05, respectively). These results suggested that INF + POS caused impairment of the right atrial reservoir function.

Analysis of Variance↗

PubMed1990

Circulating immunoreactive endothelin in ischemic heart disease.

Circulating immunoreactive endothelin (ir-ET) was measured in nine patients with acute myocardial infarction (AMI), 10 patients with stable angina pectoris (SAP), and 25 normal control subjects. In patients with AMI, the plasma ir-ET level was elevated in the acute phase and was highest on the day of onset (AMI: 3.8 +/- 1.7 pg/ml, normal control value: 0.5 +/- 0.2 pg/ml). The plasma ir-ET level showed a positive correlation with the wall motion abnormality index (rs = 0.56, p less than 0.01), thrombin-antithrombin III complex (rs = 0.55, p less than 0.01), and beta thromboglobulin (rs = 0.39, p less than 0.05). An especially high plasma ir-ET level was detected in patients in whom the Killip subset was IV. The plasma ir-ET level was not increased in patients with SAP (0.8 +/- 0.3 pg/ml). The plasma ir-ET level is increased in the acute phase of AMI. A pathophysiologic state characterized by cardiac dysfunction, an activated coagulation system, and platelet hyperactivity may be associated with this increase in plasma ir-ET.

Angina Pectoris↗

PubMed1990

The complement system in ischemic heart disease.

The mechanisms by which tissue injury after acute myocardial infarction (AMI) occurs has not been fully elucidated. Recent evidence in experimental models has suggested involvement of the complement system in microvascular and macrovascular injury subsequent to AMI. With respect to angina pectoris, whether or not the complement system is activated is not clear. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation, including C3d, C4d, Bb, and SC5b-9 complexes, in 31 patients with AMI, 17 patients with unstable angina pectoris, 19 patients with stable angina pectoris, and 20 normal volunteers. The plasma C3d levels increased in patients with AMI and in those with unstable angina pectoris (p less than 0.01). The plasma levels of C4d, Bb, and SC5b-9 increased only in patients with AMI (p less than 0.01). The plasma SC5b-9 level was related to peak creatine phosphokinase (r = 0.71) and inversely related to the ejection fraction (r = -0.71). The plasma SC5b-9 level of patients with congestive heart failure was higher than that of patients without congestive heart failure in AMI. These results show that activation of complement system occurs after AMI and show an association of myocardial damage with complement activation. With respect to angina pectoris, the complement system is mildly activated in patients with unstable angina pectoris; however, the cardiac function of patients with unstable angina pectoris is not damaged. The complement system of patients with stable angina pectoris is not activated.

Angina Pectoris↗

PubMed1990

Significance of Q wave disappearance in the chronic phase following transmural acute myocardial infarction.

The mechanism and prognostic implications of Q wave regression following transmural acute myocardial infarction (AMI) were assessed in 54 patients. Of these subjects, 14 lost their Q waves. Exercise myocardial thallium-201 (201Tl) scintigraphy and two-dimensional echocardiography were performed before the patients were discharged from hospital. Two-dimensional echocardiography and electrocardiography were simultaneously repeated about 18 months after AMI. Both the relative 201Tl activity in the infarcted area and the improvement of echocardiographic wall motion index were higher in patients who had lost their Q waves than in those with retained Q waves (70 +/- 14% vs 58 +/- 13%, p less than 0.01; 5.2 +/- 3.0 vs 2.0 +/- 3.4, p less than 0.01, respectively). The prevalence of post-infarction angina pectoris was significantly higher in the former (29% vs 0%, p less than 0.01). We concluded that remnants of viable myocardial muscle might be responsible for Q wave regression following transmural acute myocardial infarction, and the prevalence of post-infarction angina pectoris was high among these patients.

Adult↗

PubMed1989

Assessment of membrane protection by 31P-NMR effects of lidocaine on calcium-paradox in myocardium.

In studying calcium paradox, perfused rat hearts were used to investigate the myocardial protective effects of lidocaine. Intracellular contents of phosphates were measured using the 31P-NMR method. In hearts reexposed to calcium, following 3 minute calcium-free perfusion, a rapid contracture occurred, followed by rapid and complete disappearance of intracellular phosphates with no resumption of cardiac function. In hearts where lidocaine was administered from the onset of the calcium-free perfusion until 2 minutes following the onset of reexposure to calcium, both intracellular phosphates and cardiac contractility were maintained. Therefore, it can be said that cell membranes were protected by lidocaine.

Animals↗

PubMed1989

The complement system in the acute phase of myocardial infarction.

Although some studies suggest that complement activation is involved in the development of acute myocardial infarction, there has been little convincing evidence of a change in the complement system in patients suffering from myocardial infarction. In this study circulating levels of C3a, C3, C4 and the total hemolytic complement titer (CH50) were serially measured in 12 patients with acute myocardial infarction up to 10 days after an attack. The plasma C3a level was greatly elevated throughout the post-attack observation period. The C3, C4 and CH50 levels were significantly increased above those controls on days 8, 9 and 10 after infarction. These findings indicate that there is complement activation in patients with acute myocardial infarction, and suggest a pathogenetic role for complement activation in the development of myocardial damage after infarction.

Acute-Phase Reaction↗

PubMed1989

[Malignant thymoma detected by thallium-201 myocardial scintigraphy].

We present two cases of malignant thymoma which showed a remarkable accumulation of thallium-201 chloride on myocardial scintigraphy. A 69 year-old man underwent stress 201Tl scintigraphy to evaluate myocardial ischemia and abnormal accumulation of thallium activity was observed in the anterior mediastinum by chance. It was more clearly visualized on delayed image. Moreover, abnormal uptake of 67Ga citrate was also observed in the same region. In another 68 year-old woman, there was high uptake on 201Tl scintigraphy, but no abnormal uptake using 67Ga. The diagnosis of malignant thymoma was confirmed by operation in each patient. These two cases had no abnormality in the mediastinum on the chest X-ray film and one of them had no uptake of 67Ga, 201Tl scintigraphy was more useful to detect malignant thymoma.

Aged↗

PubMed1988

The effect of inosine on the post ischemic heart as bio-energy recovering factor in 31P-MRS.

Perfused guinea-pig hearts, which were analyzed by 31P-MRS, were subjected to 30 and 60 minute ischemia and reperfused using two perfusates, one containing 200 microM inosine, and the other without inosine. After 4 hour reperfusion with inosine, ATP levels increased to 95.5% of preischemic value (30 minute ischemia) and 76.2% (60 minute ischemia). However, after 4 hour reperfusion without inosine, ATP levels increased only to 72.2% (30 minute ischemia) and to 48.2% (60 minute ischemia). In 60 minute ischemic hearts reperfused with inosine, left ventricular maximal positive dp/dt (LV dp/dt) was improved significantly to 82.4% after 6 hour reperfusion in contrast to hearts reperfused without inosine (43.1%). Administration of inosine was very useful for increasing myocardial gross energy product and improving cardiac performance.

Adenosine Triphosphate↗

PubMed1988

31P-MRS study of bio-energy recovering phenomenon.

The ATP and creatine phosphate (PCr) contents in isolated guinea-pig hearts were determined by 31P-MRS measurement at 80.75 MHz using the Langendorff technique. Reperfusion of post-ischemic hearts with adenosine for 180 minutes increased ATP to 117.4% and decreased PCr to 59.8% of the preischemic value. Reperfusion without adenosine did not increase ATP and did not decrease PCr. The depressed cardiac function due to ischemia was remarkably improved in post-ischemic hearts by the increase in ATP due to adenosine. We found that the loss of ATP due to ischemia is not necessarily proportional to the extent of myocardial ischemic injury.

Adenosine↗

PubMed1988

Determination of mechanisms of myocardial ischemic injury by 31P-MRS effect of catecholamine on ischemic hearts.

To investigate mechanisms of development in ischemic myocardial injury, intracellular pH and high energy phosphates in perfused guinea-pig hearts were monitored by 31P-MRS. Intracellular ATP content decreased to 1.2% and 26.4% of control during 60 minutes global ischemia, respectively with and without preischemic administration of isoproterenol. Intracellular pH declined to 6.48 and 6.03 respectively. Postischemic cardiac function was severely impaired by isoproterenol. ATP breakdown had little influence on intracellular pH in ischemic hearts. It was verified that inotropic agents can progress ischemic myocardial injury, and that contractile recovery is more correlated with the residual ATP level than intracellular pH.

Adenosine Triphosphate↗

PubMed1988

Influence of exercise on plasma atrial natriuretic factor levels in patients with myocardial infarction.

The influence of dynamic exercise on plasma atrial natriuretic factor (ANF) levels was studied in a group of 10 patients with myocardial infarction (MI) and five patients with atypical chest pain (control group). Exercise protocol consisted of three fixed workloads (25, 50, and 75 watts) every 4 minutes with the use of a supine bicycle ergometer. Plasma ANF levels and hemodynamic indices were measured before, during, and 10 minutes after exercise. In the MI group, plasma ANF levels significantly increased at the 75-watt workload and significantly decreased at 10 minutes after exercise, whereas in the control group, the increase in plasma ANP levels after a 75-watt workload, compared with those at rest, was not significant. Significant correlations of pulmonary artery wedge pressure, right atrial pressure, mean arterial pressure, and heart rate to plasma ANF levels were observed at four points obtained before and during each stage of exercise in the MI group. Furthermore, a significant correlation between maximal creatine kinase levels and plasma ANF levels at a 75-watt workload and a significant inverse correlation between left ventricular ejection fraction and plasma ANF levels at a 75-watt workload were observed. These results suggest that the increase in the circulating ANF level during exercise in MI is associated with elevated atrial pressure resulting from left ventricular dysfunction and that measurement of ANF during exercise may be an indication of the severity of MI and associated left ventricular dysfunction.

Adult↗

PubMed1988

Hereditary hemorrhagic telangiectasia with growing pulmonary arteriovenous fistulas followed for 24 years.

A 47-year-old man was admitted for follow-up of an abnormal chest x-ray. He had a history of epistaxis and a brain abscess and a family history of pulmonary arteriovenous fistulas. Physical examination showed clubbed fingers and telangiectasia of the tongue. Laboratory data revealed evidence of polycythemia and hypoxia. Contrast echocardiography and pulmonary perfusion scintigraphy were suggestive of a right-to-left shunt. From the oxygen tension and content of blood taken at cardiac catheterization, the shunt ratio was calculated to be 57.8%. Multiple bilateral pulmonary arteriovenous fistulas were confirmed by angiography, and the patient was diagnosed as having hereditary hemorrhagic telangiectasia. A review of x-ray films taken over a 24-year period demonstrated that the fistulas in both lungs had been increasing gradually in size at different rates. A right lower lobectomy relieved the hypoxia, but the patient died unexpectedly on the twelfth postoperative day. There was no evidence of fistula rupture on chest film, but no autopsy was performed.

Arteriovenous Fistula↗