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Biomedical subjects

J T Fallon

Publications and source records attributed to J T Fallon.

At least 181 records · Page 10Linked to original sources
PubMed1984

The results of transvenous endomyocardial biopsy can frequently be used to diagnose myocardial diseases in patients with idiopathic heart failure. Endomyocardial biopsies in 100 consecutive patients revealed a substantial incidence of myocarditis.

Transvenous endomyocardial biopsy is an accepted method to evaluate cardiac transplant rejection, but the clinical diagnostic value of the technique for other forms of cardiac disease has not been established. We performed biopsies in 100 consecutive patients without significant complications. The pathologic diagnostic information obtained was judged to be useful to the clinician in 54 and not useful in 46 patients. In 74 patients with congestive heart failure of unknown etiology and a dilated heart, useful pathologic diagnoses included myocarditis, vasculitis, doxorubicin cardiomyopathy, and congestive cardiomyopathy. In most of the patients with biopsy findings of myocarditis there were no other clinical or laboratory findings indicating the presence of this disease, and the diagnosis of myocarditis would have been overlooked without a biopsy. In 26 patients in whom there was clinical evidence of constrictive or restrictive cardiovascular physiologic characteristics, useful biopsy diagnoses included radiation-induced cardiomyopathy, endomyocardial fibrosis, amyloidosis, or no myocardial disease; in the patients without myocardial disease thoracotomies were performed for constrictive pericarditis. Transvenous endomyocardial biopsy can provide clinically useful information in the evaluation of diseases of the myocardium.

Adult↗
PubMed1984

Coronary thrombolysis with recombinant human tissue-type plasminogen activator.

The thrombolytic potency and myocardial infarct--sparing potential of recombinant tissue-type plasminogen activator (rt-PA) were studied in electrocardiographically monitored, open-chest, anesthetized dogs. Localized coronary thrombosis was produced in the left anterior descending artery by endothelial injury and instillation of thrombin and fresh blood. After 2 hr of stable thrombotic occlusion, rt-PA was infused intravenously. At a dose of 4.3 micrograms/kg/min, time to reperfusion was greater than 40 min (n = 3). However, at higher infusion rates a linear, dose-dependent time to coronary reperfusion was obtained (r = .88): at 10 micrograms/kg/min reperfusion occurred after 31 +/- 2 min (n = 3), at 15 micrograms/kg/min it was at 26 +/- 7 min (n = 4), and at 25 micrograms/kg/min, lysis was accomplished within 13 +/- 3 min (n = 3). Thrombolysis was not associated with alterations in either plasma hemostatic factors (fibrinogen, plasminogen, and alpha 2-antiplasmin) or in systemic blood pressures. Epicardial electrographic measurements revealed a significant reduction in ST elevation in all reperfused hearts. A randomized, blinded study was also carried out with 15 micrograms/kg/min of rt-PA saline in 18 dogs with 30 min of coronary thrombosis. Reperfusion in the treated group occurred after 28 +/- 3 min. No evidence of thrombolysis was noted in the saline-treated group within 240 min. Size of myocardial infarction was determined by triphenyl tetrazolium chloride staining and planimetry. Infarction involved 2.5 +/- 0.5% of the left ventricular wall in the group receiving rt-PA, but 16 +/- 3% of the left ventricle in the saline-treated group (p = .001). It is concluded that intravenous infusion of rt-PA results in rapid, dose-dependent coronary thrombolysis without systemic fibrinolytic activation and that early lysis of coronary thrombi is associated with substantial salvage of myocardial tissue.

Animals↗
PubMed1984

Linear IgA bullous dermatosis v dermatitis herpetiformis. Quantitative measurements of dermoepidermal alterations.

Linear IgA bullous dermatosis (LAD), also known as "atypical dermatitis herpetiformis," is a disorder that is distinct from classic dermatitis herpetiformis (DH). In eight patients with DH and six with LAD, quantitative assessment of a variety of histopathologic variables was made. The number of rete tips with neutrophils in basal vacuoles and the length of the epidermal basement membrane zone (BMZ) associated with these findings were greater in LAD than DH. The number of microabscesses of neutrophils in the dermal papillae and the length of epidermal BMZ associated with them were greater in DH than in LAD. By using the number of microabscesses and the number of rete tips with neutrophils in basal vacuoles in a probability model, we found by retrospective analysis that a correct diagnosis could be made for LAD in 75% of biopsy specimens with a probability of 97% and in all cases of DH with a probability of 92%. Using this model, we made no misdiagnoses. This is the first diagnostic probability model in dermatopathology that expresses a confidence level in diagnosis.

Adult↗
PubMed1983

Relation of immediate and delayed thallium-201 distribution to localization of iodine-125 antimyosin antibody in acute experimental myocardial infarction.

Thallium-201 (TI-201) distribution in acute experimental myocardial infarction (MI) (n = 18) was compared with cardiac-specific antimyosin Fab (AM-Fab) uptake, a specific marker for myocardial necrosis. When antimyosin was injected 4 hours after ligation with TI-201 administered 23 hours 55 minutes later and measurement of myocardial distribution determined 5 minutes after intravenous administration of TI-201, (1) TI-201 distribution closely correlated with microsphere regional blood flow, and (2) an inverse exponential relation to iodine-125 (I-125) AM-Fab uptake was apparent. In another group of 4 animals, TI-201 and AM-Fab were administered intravenously 4 hours after MI, and 36 hours later myocardial distribution was measured. This delayed TI-201 distribution had a close inverse linear correlation with I-125 AM-Fab uptake. This inverse linear relation also was apparent in 28-hour-old MIs in dogs (n = 4) where collateral circulation had been established. TI-201 was administered intravenously at 27 hours after MI, and TI-201 distribution was determined 1 hour later. The present study demonstrated that whereas immediate TI-201 distribution is flow-limited, delayed TI-201 distribution is a marker of cell viability which, due to prolonged circulation time and redistribution, is not flow-limited.

Animals↗
PubMed1983

Evaluation of a QRS scoring system for estimating myocardial infarct size. III. Correlation with quantitative anatomic findings for inferior infarcts.

This study evaluated by quantitative autopsy correlation a previously developed scoring system for estimating the size of myocardial infarcts based on the QRS complex of the electrocardiogram. This system was tested using electrocardiograms from patients with infarcts shown by autopsy to predominate in the inferior third of the left ventricle. The study was limited to patients whose electrocardiogram did not indicate left or right ventricular hypertrophy, left or right bundle branch block, or left anterior or posterior fascicular block. Thirty-one patients from 6 medical centers met these criteria. In the electrocardiogram of 28 of the 31 patients (90%), lead a VF exhibited a Q wave of at least 30 ms. The correlation coefficient between the total QRS score and the percent infarction of the left ventricle was 0.74. In patients without confounding factors in the electrocardiogram and with single infarcts, the electrocardiogram provides a marker for infarcts in the inferior third of the left ventricle and a quantitative QRS scoring system provides an estimate of infarct size.

Aged↗
PubMed1983

Early membrane damage during coronary reperfusion in dogs. Detection by radiolabeled anticardiac myosin (Fab')2.

There is currently great interest in acute coronary reperfusion as a therapeutic modality for severe myocardial ischemia. While some studies have demonstrated a reduction in the overall extent of necrosis by early reperfusion, other studies have identified potentially deleterious effects produced by reflow. Because membrane disruption may be an important mechanism of irreversible cell injury, we measured changes in cell membrane integrity early during reperfusion using radiolabeled anticardiac myosin (Fab')2 antibody fragments in dogs. Our method involved brief periods of exposure to the (Fab')2 so that the levels of (Fab')2 binding indicated the degree of membrane disruption at discrete times during the progression of cell injury. In the first protocol (Fab')2 fragments labeled with either 125I and 131I were injected into the left circumflex coronary artery at the onset of reflow and at 45 min of reflow after a 1-h circumflex artery occlusion. Coronary sinus flow was diverted for 5 min following each injection to prevent recirculation. The (Fab')2 binding ratio (ischemic/control) increased during the first 45 min of reflow in each of eight experiments (mean increase 170%, P less than 0.01). No significant increase in (Fab')2 binding was observed in five additional experiments in which nonspecific (Fab')2 was injected. This indicates that the increase in binding seen with antimyosin-specific (Fab')2 was due to changes in specific binding rather than to alterations in (Fab')2 delivery produced by changes in blood flow distribution. The increase in membrane damage during reflow was confirmed by a second protocol in which each animal received only a single left atrial injection of (Fab')2 followed by rapid excision of the heart. The (Fab')2 binding ratio was 1.7 +/- 0.3 (SEM) in the group that received (Fab')2 at the onset of reflow and 3.7 +/- 0.6 (SEM) (P less than 0.05) in the group that received (Fab')2 after 45 min of reflow. In a third set of experiments in which hyperosmotic mannitol was infused during reflow the mean increase in (Fab')2 binding using the first protocol was only 80 +/- 40 vs. 170 +/- 30% without mannitol (P less than 0.05). Thus, membrane damage develops early during coronary reperfusion following 1 h of circumflex coronary artery occlusion, and part of this membrane damage can be prevented by altering the conditions of reflow. A method involving brief exposure of the myocardium to antimyosin (Fab')2 is promising for detecting changes in membrane integrity during evolving ischemic injury.

Animals↗
PubMed1983

Selective accumulation of low density lipoproteins in damaged arterial wall.

To determine whether damaged arterial wall selectively accumulates lipoproteins, normocholesterolemic rabbits were injected with human radiolabeled low density lipoproteins, high density lipoproteins, and/or albumin 24 hr to 12 weeks after balloon-catheter de-endothelialization of the abdominal aorta. When 125I-labeled low density lipoproteins and 99mTc-labeled albumin were injected simultaneously, the amount of 125I-low density lipoprotein present 24 hr later in abdominal aortas increased steadily, for several weeks, above the amount present at 24 hr in control animals. The increase correlated closely with the degree of re-endothelialization and correlated closely with the degree of re-endothelialization and reached an average maximum for the whole abdominal aorta of three times control when re-endothelialization was between 75 and 85% complete. By contrast, the amounts of 99mTc-albumin or 125I-labeled high density lipoprotein in balloon-damaged abdominal aortas, and the amounts of 125I-low density lipoprotein, 125I-high density lipoprotein, or 99mTc-albumin in undamaged thoracic aortas of injured animals showed no such increase. As early as 2 weeks after de-endothelialization, en face radioautographs made following injection of 125I-labeled low density lipoproteins revealed localized areas of greatest radioactivity around the leading edges of regenerating endothelial islands, broad areas of intermediate radioactivity corresponding to the de-endothelialized areas, and very like radioactivity in the re-endothelialized areas. This pattern occurred rarely with 125I-labeled high density lipoproteins and not at all with 125I-labeled albumin. The results suggest that low density lipoproteins are selectively accumulated by the healing rabbit aorta and that the accumulation is greatest in regions where the endothelium is actively regenerating.

Albumins↗
PubMed1983

Enhanced myocardial protection during ischemic arrest. Oxygenation of a crystalloid cardioplegic solution.

To determine if, during elective cardiac arrest, the myocardial protection afforded by a cold (4 degrees C) crystalloid potassium cardioplegic solution could be improved by oxygenation of the solution, we placed 16 dogs on cardiopulmonary bypass and subjected their hearts to 4 hours of cold cardioplegic arrest. Group 1 hearts (n = 8) received aerated crystalloid solution perfused through the aortic root every 20 minutes. Group 2 hearts (n = 8) were treated identically except that the crystalloid cardioplegic solution was fully oxygenated. Left ventricular function curves (ejecting heart) were generated before arrest (control) and after 45 minutes of reperfusion. A cardiac output of 1,000 ml/min could be attained in only two hearts of Group 1 after reperfusion, whereas all but one heart of Group 2 had excellent functional preservation. Mean postreperfusion adenosine triphosphate (ATP) levels in Group 1 and Group 2 hearts were 62% and 89% of control, respectively (p less than 0.01). Myocardial water content had increased significantly (p less than 0.002) after reperfusion in Group 1, but not in Group 2. During cardioplegic solution infusion, myocardial oxygen consumption (MVO2) was 1.42 +/- 0.15 ml O2/min/100 gm LV for Group 1 and 6.91 +/- 1.27 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Oxygen consumed per minute of arrest was 0.027 +/- 0.003 ml O2/min/100 gm LV for Group 1 and 0.128 +/- 0.015 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Postreperfusion ultrastructural evaluation of two of the Group 1 hearts revealed severe ischemic damage in contrast to the normal ultrastructural appearance of two of the Group 2 hearts. With careful attention given to maintenance of myocardial hypothermia and cardioplegic delivery methods, the myocardial protection afforded by an oxygenated crystalloid cardioplegic solution exceeds that provided by the aerated control and compares favorably with other methods of myocardial protection during ischemic arrest.

Adenine Nucleotides↗
PubMed1982

Myocardial injury: quantitation by cell sorting initiated with antimyosin fluorescent spheres.

Spheres coated with antibodies specific for myosin were used to detect myocardial cell membrane disruption by scanning electron microscopy. Injury in a population of cultured myocytes as then followed and measured by fluorescence-activated cell sorting. This approach provides a unique method for quantitating the evolution of myocardial injury and potentially for assessing the efficacy of interventions aimed at myocardial protection.

Animals↗
PubMed1982

Ischemic heart disease in systemic lupus erythematosus in the young patient: report of six cases.

To clarify the clinical spectrum of coronary arterial abnormalities in systemic lupus erythematosus, the data were reviewed on six patients who had a diagnosis of lupus at ages 15 to 29 years and who had ischemic heart disease before age 35. Two patients had coronary arteritis diagnosed on postmortem examination. In a third patient alterations in coronary arterial anatomy occurred with angiographic improvement temporally related to the initiation of steroid therapy. The other three patients had severe diffuse atherosclerotic coronary disease that was identified in two at postmortem examination. In the third patient the course of the disease strongly suggested coronary atherosclerosis, and eventually coronary bypass grafting was performed for relief of angina. In summary, clinically important extramural coronary arteritis and atherosclerosis both occur, although rarely, in young patients with lupus. Coronary artery disease may occur with or without coexisting active extracardiac lupus manifestations. Short-term steroid therapy and follow-up angiography for those with angina and in whom coronary arteritis is suspected warrant consideration. When stable coronary arterial anatomy is demonstrated on follow-up angiography, management is determined by the patient's symptoms irrespective of the prior history of lupus and, if indicated, cardiac surgery for symptomatic relief can be safely performed.

Adolescent↗
PubMed1982

Renin synthesis by canine aortic smooth muscle cells in culture.

Angiotensin-I generating activity has been detected in homogenates of arterial tissue but it remains unclear whether this enzymatic activity results from the presence of renin itself or from the action of other proteases such as cathepsin D. In an assay system employing anephric dog plasma as substrate and buffered to pH 7.4, we detected angiotensin-I generating activity in homogenates of canine aortic smooth muscle cells. This enzymatic activity was in large part inhibitable by renin-specific antisera raised to pure canine renal renin. Immunofluorescent study of cultured arterial smooth muscle cells was also performed using renin specific antiserum. Granular cytoplasmic immunofluorescence was detected when specific antirenin serum was used but not when preimmune serum was employed. The addition of pure canine renin to the renin antiserum during staining suppressed the granular immunofluorescence confirming the specificity of staining. Finally, biosynthetic radiolabelling studies were performed. Immunoprecipitation of newly synthesized proteins with antirenin serum and staphylococcal protein A followed by gel electrophoresis and autoradiography demonstrated the synthesis of an immunoreactive protein with the molecular weight of renin. Pretreatment of the antirenin serum with pure canine renin resulted in the disappearance of this immunoreactive protein band. Thus these studies provide multiple lines of evidence to indicate the in situ synthesis of renin by vascular smooth muscle cells.

Animals↗
PubMed1982

Evaluation of a QRS scoring system for estimating myocardial infarct size. II. Correlation with quantitative anatomic findings for anterior infarcts.

The ability of an independently developed QRS point score to estimate the size of infarcts predominantly within the anterior third of the left ventricular was evaluated by quantitative pathologic-electrocardiographic correlation. The study was limited to 21 patients with a single infarct documented by postmortem examination, for whom an appropriately timed standard 12 lead electrocardiogram was available that did not exhibit signs of left or right ventricular hypertrophy, left or right bundle branch block or anterior or posterior fascicular block. At necropsy the heart was cut into five to seven slices. The location and size of the infarct was quantitated by computer-assisted planimetry of the slices. The electrocardiogram of 19 (90 percent) of the patients exhibited either a Q wave or an R wave of no more than 20 ms in lead V2. The infarct in the two patients without this electrocardiographic finding was small, occupying 2 and 3 percent of the left ventricle, respectively. The percent infarction of the left ventricle correlated with the QRS point score (r=0.80). Thus in patients without complicating factors in the electrocardiogram and with a single infarct, the electrocardiogram provides a marker for infarction in the anterior third of the left ventricle and permits estimation of infarct size.

Adult↗
PubMed1982

Imaging of acute arterial injury with 111In-labeled platelets: a comparison with scanning electron micrographs.

The relationship between degree of acute arterial injury, extent of platelet deposition, and ability to visualize arterial injury with Indium 111-labeled platelets was studied in 18 rabbits. An aortic lesion was made with a balloon catheter in each animal immediately after injection of autologously labeled platelets. Three nonlesioned rabbits with 111In-labeled platelets served as controls. An additional control study was performed in 12 lesioned rabbits in which nine were injected with 111In-labeled plasma protein and three with 111In-labeled red blood cells. A postmortem scanning electron microscope study of the aortae was made to determine the degree of injury to the intima and the amount of platelet deposition on the damaged arterial wall. The radionuclide scans and scanning electron micrographs were then compared. Lesions were seen in ten of 18 animals with labeled platelets that had extensive regions of denuded endothelium covered by a contiguous layer of platelets. Lesions consisting of patchy deendothelialization and platelet deposition could not be visualized on the scans. Red blood cells and fibrin were not conspicuous on micrographs of the lesions. No lesions were visualized in animals receiving 111In-labeled plasma protein or red blood cells before arterial injury, despite platelet deposition in the lesions.

Animals↗
PubMed1982

Release of atherosclerotic debris after transluminal angioplasty.

To determine if there is release of endothelial cells or plaque contents after percutaneous transluminal angioplasty, effluent from atherosclerotic segments of the aorta and iliac arteries of rabbits were collected before and after angioplasty. No endothelial cells or cholesterol plates were identified in the preangioplasty effluents. Only a few single endothelial cells and cholesterol crystals were found in effluents after angioplasty. We conclude that embolization of endothelial fragments and cholesterol plates occurs during angioplasty, but only to a minor degree, and is probably not clinically important.

Angioplasty, Balloon↗
PubMed1982

Significance of the angiographic morphology of localized coronary stenoses: histopathologic correlations.

Postmortem coronary angiographic morphology was correlated with histologic sections of 73 localized subtotal coronary artery stenoses (50-99% reduction of luminal diameter) to determine whether complicated or uncomplicated atherosclerotic lesions could be detected angiographically. Lesions were divided into two types, according to angiographic morphology: Type I stenoses had smooth borders, an hourglass configurations, and no intraluminal lucencies; type II stenoses had irregular borders or intraluminal lucencies. Histologic sections were also divided into two types: "uncomplicated" stenoses had fatty or fibrous plaques with intact intimal surfaces and no superimposed thrombus; "complicated" stenoses manifested plaque rupture, plaque hemorrhage, superimposed partially occluding thrombus, or recanalized thrombus. Among 35 lesions with type I angiographic morphology, four (11.4%) were complicated lesions histologically. Among the 38 stenoses showing type II angiographic morphology, 30 (78.9%) were complicated lesions. Postmortem angiography thus had a sensitivity of 88% and specificity of 79% for detecting complicated stenoses on the basis of irregular borders or intraluminal lucencies. Pathologic studies have shown that acute occlusive thrombosis of a coronary artery is usually associated with complicated atherosclerotic stenoses. Thus, complicated lesions represent a greater risk factor for acute myocardial infarction or sudden death than do uncomplicated lesions. This study suggests that coronary stenoses characterized angiographically by irregular borders or intraluminal lucencies are probably the clinically more dangerous "complicated" type.

Angiography↗
PubMed1982

Comparison of myocardial preservation with hypothermic potassium and nifedipine arrest.

Preservation of regional myocardial function, high-energy phosphate stores and ultrastructure were assessed in 28 canine hearts subjected to 2 hours of global ischemia at either 12 degrees C or 21 degrees C. The preservation achieved with a potassium arrest solution was simultaneously compared in the same heart with either a nifedipine arrest solution or a potassium plus nifedipine arrest solution. There were no statistically significant differences in regional function recovery between the three arrest solutions at either temperature. At 12 degrees C, slightly better functional preservation was noted for each solution. End-systolic chord length was significantly less elongated after preservation at the lower temperature (p = 0.03). The concentration of ATP and myocardial water content were not significantly better preserved with any solution at either temperature. Myocardial ultrastructure was well preserved regardless of the solution or temperature used. The degree of hypothermia appears to be more important to functional preservation than differences between the three solutions tested. We conclude that with respect to preservation of myocardial function, high-energy phosphate stores, water content and ultrastructure, nifedipine arrest offers no advantages over potassium arrest.

Adenosine Triphosphate↗