Dual myocardial imaging with technetium-99m pyrophosphate and thallium-201 for detecting, localizing and sizing acute myocardial infarction.
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Biomedical subjects
Publications and source records attributed to H Henning.
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To assess the usefulness of myocardial imaging with technetium-99m-stannous pyrophosphate for detecting acute myocardial necrosis in patients undergoind cardiac surgery, 66 such patients were stldied. Tc-99m (Sn)-pyrophosphate scans were obtained in all patients 3 to 6 days postoperatively and in 45 preoperatively. Electrocardiograms and serum samples for measuring myocardial isoenzyme of creatine kinase (MB CK) levels were obtained before and serially after cardiac surgery. Seven of the 46 patients undergoing myocardial revascularization had a definite new myocardial infarction as indicated by electrocardiogram and MB CK isoenzyme concentrations, and postoperative pyrophosphate scans were abnormal in all but one. In addition, six of the eight patients with possible myocardial infarction (elevated MB CK levels and persistent ST-T wave depressions) had an abnormal scan postoperatively. Seven of the 20 patients undergoing aortic or mitral valve replacement, or both, had a possible postoperative myocardial infarction by electrocardiogram and MB CK criteria and the myocardial scan was positive in two. All the patients with a normal electrocardiogram and normal MB CK levels had a normal pyrophosphate scan. Preoperative scans were obtained in 22 patients wit; valvular heart disease and were positive in two with a heavy calcified mitral valve on fluoroscopy and in one with a calcified aortic valve. After valve replacement, the pyrophosphate scan became normal in two patients and remained abnormal in the third patient with electrocardiograms and MB CK levels suggesting acute myocardial infarction. We conclude that the Tc-99m (Sn)-pyrophosphate scan is useful for analyzing the occurrence of acute myocardial infarction in patients undergoing cardiac surgery and that, in conjunction with the electrocardiogram, it permits confirmation or exclusion of that diagnosis. Furthermore, false positive pyrophosphate scans may occur in patients with heavy valve calcifications.
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Determination of hepatitis-B-antigen and thrombocytes in 1488 cases of liver diseases, 173 of whom had been treated with immunsuppressive drugs. There was no significant relation between hepatitis-B-antigenemia and thrombocyte-count, nor could an influence of the immunsuppressive therapy be evaluated. The thrombocyte-count was correlated with high significance only to the degree of the liver injury.
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The effects of sublingually administered nitroglycerin on segmental left ventricular wall motion determined by videotracking and radiographic left heart size were evaluated at rest and during submaximal hand grip exercise in 10 patients with previous transmural myocardial infarction. After nitroglycerin, diastolic left heart size decreased in the resting state from an average of 49.5 +/- 5.7 (standard deviation) to 47.9 +/- 5.6 mm/m2 body surface area (P less than 0.01) and during handgrip exercise from a mean of 50.7 +/- 590 to 49.1 +/- 4.7 mm/m2 (P less than 0.05). In the resting state, the average maximal velocity of shortening in segments with normal wall motion increased after nitroglycerin from 18.1 +/- 3.0 to 23.5 +/- 5.5 mm/sec (P less than 0.01), whereas during handgrip exercise alone, the velocity of shortening averaged 25.6 +/- 6.9 mm/sec and increased further after nitroglycerin to 30.1 +/- 10.6 mm/sec (P less than 0.05). The effects of nitroglycerin on the average extent of shortening in normal segments were similar. In all 10 patients, there was a decrease in the number of segments with abnormal wall motion. The number of sites with dyssynergy decreased after nitroglycerin from 24 to 15 in the resting state and from 40 to 22 when nitroglycerin was administered before handgrip exercise. Sublingually administered nitroglycerin appears to decrease left heart size, increase the velocity and extent of shortening in normal left ventricular segments and often reduce the extent of left ventricular wall motion abnormalities at rest and during isometric exercise in patients with previous transmural myocardial infarction.
By radioimmuno-assay we found HBSAg in 4.2% and HBS-Antibodies in 60% in a group of 120 partners of patients with HBSAg-positive chronic liver diseases. The high incidence of HBS-antibodies in the group of partners is supposed to be due to a transmission of very small amounts of HBSAg containing material in a way of occult immunisation. There were no significant relations to the sex of the partners nor the age of the patients or the activity and duration of the disease. Our clinical investigations do not support demands for a strict isolation of patients with positive HBSAg findings nor do they imply that health-care workers should change their professions in case of HBS-antigenemia.
The effects of maintenance oral digoxin therapy on segmental left ventricular wall motion (wall motion videotracking) and left heart size (radiographic left heart dimension) were evaluated in 14 patients with a prior myocardial infarction but without clinical signs or symptoms of congestive heart failure. The left heart dimension decreased in all six patients with cardiomegaly from an average of 55.0 +/- 1.6 (standard deviation) to 52.2 +/- 2.7 mm/m2 body surface area (P less than 0.01) during digoxin therapy. However, there was no significant change in the eight patients with normal heart size. In the resting state, the average extent of shortening in normal segments increased significantly from 3.1 +/- 0.8 to 4.2 +/- 1.2 mm during digoxin therapy. During submaximal handgrip exercise, the extent of shortening averaged 4.0 +/- 1.3 mm and increased further with digoxin therapy to 5.1 +/- 2.1 mm. The effects of digoxin therapy on the maximal velocity of shortening in normal segments at rest and during handgrip exercise were similar. In all 14 patients, there was a decrease in the number of segments with abnormal wall motion at rest or with handgrip exercise during digoxin therapy. With therapy, the number of abnormal sites decreased from 52 to 35 in the resting state and from 84 to 49 during handgrip exercise. Thus, in patients 6 or more months after transmural myocardial infarction, orally administered digoxin decreases cardiomegaly, increases the extent and maximal velocity of shortening in normal left ventricular segments and often reduces the extent of abnormal wall motion at rest or during isometric exercise.
The left ventricular ejection fraction was determined serially with radioisotope angiography in 63 patients with acute myocardial infarction. After the peripheral injection of a bolus of technetium-99m, precordial radioactivity was recorded with a gamma scintillation camera and the ejection fraction calculated from the high frequency left ventricular time-activity curve. Since this technique requires no assumptions with respect to left ventricular geometry, it is particularly useful in patients with segmental left ventricular dysfunction. Serial measurements during the first 5 days after hospital admission were made in 50 patients, 30 of whom were studied during the subsequent 2 to 39 months (mean 19.9 months). Late follow-up serial studies were also performed in an additional 13 patients who had only one measurement of the left ventricular ejection fraction during the early postinfarction period. Early after infarction, the left ventricular ejection fraction was normal (more than 0.52) in only 15 of the 63 patients, and averaged 0.52 +/- 0.05 (standard deviation) in the 27 patients with an uncomplicated infarct. The ejection fraction was reduced in 24 patients with mild to moderate left ventricular failure (0.40 +/- 0.05, P less than 0.0001) and in the 12 patients with overt pulmonary edema (0.33 +/- 0.07, P less than 0.0001). In 35 patients the ejection fraction correlated with the mean pulmonary arterial wedge pressure (r = 0.72). In 15 patients with normal left ventricular wall motion by heart motion videotracking, the ejection fraction was significantly higher (0.53 +/- 0.08) than in the 26 patients with regional left ventricular dysfunction (0.41 +/- 0.10, P less than 0.0001). During the early postinfarction period, the left ventricular ejection fraction improved in 55 percent of patients and remained unchanged or decreased in 45 percent. A further increase in the ejection fraction was noted in 61 percent of patients during the late follow-up period. Patients with an initially low or decreasing ejection fraction had a significantly greater incidence of early mortality and left ventricular dysfunction (P less than 0.02) than those whose ejection fraction was normal or improved to normal early after infarction. These data indicate that the ejection fraction is a sensitive indicator of left ventricular function after acute myocardial infarction and that serial measurements are helpful in predicting early mortality and morbidity.
Ultrastructural investigations of liver biopsies are performed in 20 cases after phenolisatin reexposition and corresponding reactions of the laboratory findings. Alterations of the nucleus (segregation of nucleolus, condensation of chromatin) and of the rough endoplasmatic reticulum ("disarrangement", fragmentation and loss of ribosomes) were evident in all cases. In contrast, changes of the mitochondria (swelling) in various extent could only be observed in some cases. Besides that, frequently lipid includings and occasionally includings like lysosomal residual bodies are to be seen. Thus, as a hypothesis we suggest the nucleus resp. nucleolus to be one site of aggression of phenolisatin containing drugs. Findings already described by light microscopy such as reactions of the v. KUPFER cells and proliferations of the ductuli as well as cell proliferations in the portal fields are documentated by electronmicroscopy, too.
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In 1488 cases of chronic liver disease thrombocyte content of peripheral blood, clinical diagnosis and histologic findings of the liver biopsy were correlated. Ranging from fatty infiltration to fatty cirrhosis or from slightly active chronic hepatitis to active postnecrotic cirrhosis, according to the extent of the liver injury a significant decrease of thrombocyte-count was evaluated. In case of non-active liver disease and posthepatitic status a thrombocytopenia also could be found. Cirrhotic transformation or proliferation of the connective tissue mainly in the periportal fields and inflammatory activity showed a significant correlation to the frequency of a thrombocyte decrease. A pathogenetic relation is ascribed to an increased thrombocyte storage in the spleen depending on the extent of the liver injury and the alteration of the portal blood stream up to a portal hypertension. Our results indicate such correlations of liver injury, portal pressure and platelet-pooling to thrombocyte-count even if the causal dependency cannot be proved.
Sera from 137 patients with mitochondrial antibodies were tested against two different mitochondrial antigens. The mitochondrial antibodies from patients with pseudo-lupus erythematosus (PLE antigen) reacted exclusively with antigen which sedimented on moving-zone centrifugation at a density of 1.10, and contained no antigenic activity when tested against sera from patients with primary biliary cirrhosis (PBC). Purified PBC antigen had no PLE antigen activity at a density of 1.19, and all sera from patients with autoimmune liver disease fixed complement with this fraction. Sera from 54 of 55 patients with PLE reacted with the antigen of the PLE-gradient fraction. But 71 patients with liver disease had no such uniform reaction: sera from 39 patients fixed complement only with the PBC fraction, whereas 32 reacted stimultaneously with both the 1.10 and 1.19 density gradient fraction. The latter pattern was especially found in patients with chronic active hepatitis in whom antibodies to smooth muscle and nuclei were frequently detected.
In the case of 36 female patients who were anamnestically known to have taken laxatives, semiquantitative histological investigations with laparoscopically obtained liver needle biopsies were effected after the exposition with preparations containing phenolisatine. The time gap until exposition was 12 to 24 h (16 cases), 48 h (8 cases), 72 to 96 h (4 cases) and 7 to 14 days (4 cases). The histological result after the exposition is an acute cholangiolitis of the allergic-hyperergic type with edema and a dense eosinophile infiltration of the portal fields with destruction of the epithelium of preformed bile ducts and portally proliferated ductles. In addition, the parenchyma of the liver shows a pleomorphism of the cells in form and colour with a cellular edema and with disseminated acidophilic necroses and necrobioses of the individual cells as well as with little reactive proliferation of the Kupffer's cell. After a period of 8 days the acute process has more or less subsided. Also, in the majority of cases there are histological signs of an aggressive chronic hepatitis of type IIa, partially in the active stage with piece-meal necroses and partially stabilized or in the process of healing. A transition to the picture of hepatitic cirrhosis is possible. In serious cases the picture of a chronic non-purulent destructive cholangitis can be simulated by the hepatocellular and canalicular damage. Thirty-one bioptic pre-examinations from the same results, whereby the acute cholangiolitical exacerbation can be attributed to an exposition of the patients themselves. The clinical picture of the phenolisatine damage in its entirety is induced by medication and is described as a recurrent chronic cholangiohepatitis. Similarities exist between the liver damages caused by chlorpromazine and arsphenamine. When medication is discontinued, the morphologic substrate recedes leaving behind an inactive fibrosis or cirrhosis. The formal and known causal pathogenetic connections are discussed with regard to this clinically important liver disease. Guidelines are then given for histological diagnosis of this damage caused by medication. 14% of the female patients with a histological picture of aggressive chronic hepatitis and hepatitic cirrhosis are affected by this type of liver damage.
In 61 patients (77 studies) who had a transmural myocardial infarction, we compared the left ventricular ejection fraction by echocardiography with the ejection fraction determined by a computerized radioisotope technique that makes no assumptions regarding left ventricular geometry. In 31 studies of 26 patients with normal left ventricular wall motion by videotracking and normal left heart size, ejection fraction averaged 0.57 +/- 0.09 (SD) by ultrasound and 0.62 +/- 0.10 by the isotope method. Measurements of ejection fraction by both techniques correlated well (r = 0.86) and there was complete separation between patients with normal and reduced ejection fraction. In 46 studies of 35 patients in whom left ventricular wall motion abnormalities were recorded by videotracking, ejection fraction by the isotope method averaged 0.46 +/- 0.08, while average echo ejection fraction was 0.62 +/- 0.12. The correlation between the ultrasound and isotope methods in these 46 studies was poor (r = 0.33) and in 28 studies measurement of the ejection fraction by the two techniques was discordant. In 26 of the 27 studies where there was a reduced ejection fraction by the isotope method and a normal ejection fraction by echo, the dyssynergy involved the anterolateral left ventricular wall. These data indicate that echocardiographic measurements frequently overestimate left ventricular performance in patients with previous myocardial infarction associated with anterolateral wall motion disorders.
The authors report on four cases of immediate hepatotoxic reaction following diagnostic re-exposure. In checking 27 patients who had received NPAB treatment for the first time, four were found to have a hepatotoxic reaction that developed within 13--20 days after beginning the treatment. In view of the significance of NPAB for the treatment of cardiac rhythm disorders, further such studies are required in order to define the actual risk involved in this procedure.
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