Early Infarcts Research Articles

Effect of coronary blood flow and site of injection on 99mT c-PYP detection of early canine myocardial infarcts

Effect of coronary blood flow and site of injection on 99mT c-PYP detection of early canine myocardial infarcts

Scintigraphy of induced myocardial infarcts with 99Tcm-gluconate.

A new isotope compound, 99Tcm-gluconate, for detection of myocardial infarction has been tested in dogs. A close correlation was found between the isotope uptake measured in vivo with a gamma camera and the infarct weight of early irreversible myocardial infarcts.

An association between the onset of rigor and loss of vascular competence in early myocardial infarcts

Experimental myocardial ischaemia was induced in 12 anaesthetized mongrel dogs by ligation of the circumflex branch of the left coronary artery. Twenty minutes after ligation 1% sodium fluorescein injected into the artery distal to the ligature evenly perfused the left ventricular wall in the vicinity of the posterior papillary muscle (PPM) but, when injected 90 minutes after ligation, the PPM and adjacent subendocardial myocardium was not perfused by this tracer. Measurements with a linear variable transducer and standard load demonstrated that after 20 minutes ischaemia, the PPM had a similar percentage compressibility to the corresponding unaffected anterior papillary muscle but, after 90 minutes, the compressibility of the PPM was significantly reduced. Scanning electron microscopy of the marginal zone between the perfused and unperfused parts of the myocardium revealed many collapsed vessels which contained small groups of tightly packed erythrocytes indicating that the loss of vascular competence was probably due to the plugging of small vessels by erythrocytes.

Uptake of 99Tcm-gluconate and early histologic findings in induced myocardial infarcts in dogs.

A new isotope, 99Tcm-gluconate, for detection of myocardial infarction has been investigated experimentally. Great differences in isotope uptake between infarcted myocardium and normal myocardium were found in dogs. A close correlation was found between the isotope uptake and the uptake of basic fuchsin (HBFP) at microscopy in early myocardial infarcts.

PATHOLOGY OF ACUTE ISCHEMIC MYOCARDIUM SPECIAL REFERENCES TO (I) EVALUATION OF MORPHOLOGICAL METHODS FOR DETECTION OF EARLY MYOCARDIAL INFARCTS, AND (II) LIPID METABOLISM IN INFARCTED MYOCARDIUM

Morphological changes of early myocardial infarction within 24 hours after the onset of the acute attack were described together with a review of the literatures. For the practical purpose in detecting very early infarcts, enzymatic histochemistry is the most reliable method. Other methods previously reported such as wavy pattern of the muscle fibers and fuchsinophilia are still controvertial. Lipid metabolism in the infarcted myocardium of dogs was studied both morphologically and biochemically. Up to 3 hours, after the coronary ligation, the tissue lipids accumulated in the necrotic areas with a rise of triglyceride, but later than 6 hours the lipids decreased and were lost from the necrotic tissue, while the surrounding living cells were accumulated with neutral lipids. Serum free fatty acids were elevated in the coronary sinus blood in 6 hours after the ligation. Linolic acids were contained in high proportion in both coronary venous blood after 6 hours, and normal myocardial phospholipid. These results may lead to another possible factor in addition to catecholamine activity to elevate serum FFA in acute myocardial infarction that fatty acids may be released partly from tissue phospholipid and once ever accumulated triglyceride.

NEUROPATHOLOGY OF EXPERIMENTAL DECOMPRESSION SICKNESS (DYSBARISM) IN THE GOAT

Neuropathology of experimental decompression sickness (dysbarism) in the goatForty‐four goats were subjected to various decompression procedures and the CNS was examined at various times thereafter. Lesions were found in the spinal cord in 24 animals, but these were minimal in 6; no similar abnormalities were found in the brain. The CNS of 9 control animals was normal. In the affected animals there was focal infarction of the white matter, especially in the cervical and to a lesser degree in the thoracic and lumbar regions. The dorsal columns were particularly affected in the cervical regions. In two cases, soon after decompression, changes were also present in the grey matter of the spinal cord. In the early infarcts, oedema occurred around relevant vessels and their walls later became necrotic. The surrounding white matter showed the changes of Wallerian degeneration although some axons survived. An early macrophage reaction was followed by revascularization and gliosis of the infarcted regions. All affected animals had been treated for signs of CNS bends (Type II), except for 7 which had shown only limb bends (Type I). In view of the nature of the lesions shown here suggestions are made as to their pathogenesis and to their treatment.

Surgical treatment of unstable angina by saphenous vein and internal mammary artery bypass grafting

During a 3 year period, direct myocardial revascularization was performed on an urgent basis in 48 patients with intermittent resting chest pain which persisted more than 24 hours despite in-hospital medical therapy and was accompanied by electrocardiographic changes representative of ischemia. Sixteen patients had saphenous vein (SV) grafts exclusively, and 32 patients each had one or two internal mammary artery (IMA) grafts with or without additional vein grafts. Follow-up ranges from 5 to 41 months (mean, 22 months). Twelve patients had single grafts to the left anterior descending coronary artery (LAD), 18 had double grafts, 16 had triple grafts, and 2 had quadruple grafts. The LAD required grafting in every patient. There was one operative death (2 per cent) and one late death from noncardiac causes. There were two (4 per cent) early postoperative myocardial infarcts and no late infarcts. Actuarial analysis projects a survival rate of 96 per cent 3 years postoperatively. Eighty-one per cent of the survivors are in Functional Class I, 17 per cent are in Class II, and 2 per cent are in Class III. All patients had postoperative angiography 2 weeks after operation. Eighty-six per cent of the SV grafts and all IMA grafts were open. No significant differences were observed between mean preoperative and postoperative left ventricular end-diastolic pressures or ejection fractions, but these parameters were noted to improve after operation in several patients. The remarkably high early and late survival rates, the low incidence of myocardial infarction, and the excellent functional results after rather long follow-up indicate that emergency coronary revascularization provides an effective therapy for unstable angina. The use of IMA grafts, when feasible, is a safe and possibly preferable approach in these patients.

Detection of early myocardial infarcts

Experimental infarcts of 20 min-12 hr duration were produced in the posterior papillary muscle of 35 dog hearts by ligation of the circumflex branch of the left coronary artery, and used to assess histological methods of detecting early infarction. Infarcted, unaffected control, and autolysed control tissue was prepared for light microscopy and stained by the following methods: H & E, PAS, PAS-diatase, PTAH, Masson's trichrome, Connor's crystal violet-acid fuchsin, Puchler's PAS-tannic acid-phosphomolybdic acid-levanol fast cynanine 5RN, Lie's haematoxylin-basic fuchsin-picric acid. Following 40 min-2 h of arterial occlusion or autolysis, affected tissue showed a loss of glycogen which was recognizable in PAS-or Puchtler-stained sections. From 2 h onward the myofibres of infarcted tissue showed structural alterations detectable with H & E but were more clearly shown by PTAH, Connor's, Putchtler's and Masson's stains. After 6 or more h of arterial occlusion the infarcted tissue was clearly defined in all preparations by neutrophil infiltration. Lie's stain, which is said to produce a specific general colour reaction in infarcted tissue, gave inconsistent results and the differentiation time was extremely critical. Thus, although staining by Puchtler's technique appears to be the most valuable method for determining the presence and age of early experimental infarcts, its application to human autopsy material is limited by the glycogen depletion which occurs during autolysis.

'Wavy' myocardial fibers in spontaneous and experimental adrenergic cardiopathies.

Wavy myocardial fibers, especially when associated with focal edema, are a characteristic sign of acute myocardial ischemia. 'Waving' might be induced by the increased hydrostatic pressure of interstitial edema, which squeezes and stretches the neighboring fibers. Beside their regular occurrence in early myocardial infarcts, wavy myocardial fibers are also frequently encountered in cases of acute adrenergic heart injury, especially in fatal cranial trauma and after injection of high doses of catecholamines in experimental animals.

Scanning electron microscopy of the endocardial endothelium overlying early myocardial infarcts

Using scanning electron microscopy, the endothelium of normal left ventricle was compared with that overlying experimentally-induced myocardial infarcts in dogs. Ten minutes after coronary artery ligation there was no apparent difference, but at intervals from 20 to 360 minutes, patches of altered endothelium were evident over the ischaemic muscle. In affected areas there was separation of endothelial cells along intercellular boundaries and the loss of many, but not all, endothelial cells. Up to two hours after coronary ligation the depressions left by the missing cells were smoothly rounded with prominent intercellular lines separating them. However, after six hours, the bases of these depressions were rough and the intercellular lines indistinct due to the loss of a layer of supporting material originally lying between the endothelial cells and underlying connective tissue fibres. Using scanning electron microscopy, the endothelium of normal left ventricle was compared with that overlying experimentally-induced myocardial infarcts in dogs. Ten minutes after coronary artery ligation there was no apparent difference, but at intervals from 20 to 360 minutes, patches of altered endothelium were evident over the ischaemic muscle. In affected areas there was separation of endothelial cells along intercellular boundaries and the loss of many, but not all, endothelial cells. Up to two hours after coronary ligation the depressions left by the missing cells were smoothly rounded with prominent intercellular lines separating them. However, after six hours, the bases of these depressions were rough and the intercellular lines indistinct due to the loss of a layer of supporting material originally lying between the endothelial cells and underlying connective tissue fibres.

Reduction by hyaluronidase of myocardial necrosis following coronary artery occlusion.

Electrocardiographic, enzymatic, and morphologic signs of myocardial ischemic injury following coronary occlusion have previously been shown to be ameliorated by reducing myocardial oxygen requirements, and/or by increasing the availability of oxygen as well as of substrates for anaerobic ATP production. Since hyaluronidase increases diffusion through the extracellular space and may facilitate delivery of substrates to ischemic cells, the influence of its administration on the size of experimentally produced infarcts was studied. In 14 control dogs epicardial electrocardiograms were taken in 10-15 sites on the anterior surface of the left ventricle before and after occlusion of the left anterior descending coronary artery. Twenty-four hours later, transmural specimens were obtained from the same sites from which electrocardiograms had been recorded, and were analyzed for creatine phophokinase (CPK) activity, for histologic changes, and glycogen content. In control dogs, sites exhibiting S-T-segment elevation 15 min after occlusion showed early structural signs of necrosis and glycogen depletion in 97% of specimens taken after 24 hours. The relationship between S-T-segment elevation at 15 min (mv) and CPK activity 24 hours later (IU/mg protein) was log CPK = –0.061 S-T + 1.26. Hyaluronidase (225 u/kg) was given to 15 dogs; no hemodynamic changes occurred but the depression of CPK activity was reduced following occlusion; log CPK = –0.024 S-T + 1.28. Similarly, only 55% of sites that showed S-T-segment elevation prior to hyaluronidase administration exhibited histologic signs of early infarcts and glycogen depletion 24 hours later. It is concluded that hyaluronidase diminished myocardial necrosis following acute coronary occlusion.

A new approach to the histologic diagnosis of early myocardial infarcts.

A new approach to the histologic diagnosis of early myocardial infarcts.

Intracellular plasma protein: a manifestation of cell injury in myocardial ischemia.

THE recognition of early cell injury poses an important problem in the study of disease, namely, the certain diagnosis of early myocardial infarcts. A variety of chemical and histochemical techniques have been tested for use in the identification of early myocardial ischaemia in experimental animals as well as in man1,2. The search has been only partially successful.

Histochemical Changes of Glutamic Oxalacetic Transaminase in Experimental Myocarial Infarction

In an attempt to establish the histochemical changes that occur in early myocardial infarcts, a series of experimental myocardial infarcts of predicable location was produced in 10 rats and the tissues from the normal and injured myocardium at intervals from 6 hours to one week were examined by various histochemical techniques as GOT, SDH and LAP. The earliest changes were recognized in infarcts within the first few hours as to a marked reduction of SDH and GOT of heart muscles. When a healing of necrotic myocardium by the proliferation of fibrous tissues has started, a prominent increase of LAP activity are observed within myocardial infarcts.