Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It was established by means of radioimmunoassay that the blood concentration of Digoxin in patients with congestive heart failure depends not only on the dose of the drug given, but also on the stage of cardiac insufficiency. With equal daily doses, higher Digoxin concentrations were observed in patients with more severe cardiac insufficiency. The analysis of the obtained data has demonstrated that in 75% of the patients with signs of digitalis intoxication the concentration of Digoxin in blood exceeded 2.5 ng/ml. In animal experiments it was established that a distinct reduction of the toxic threshold took place in rabbits with acute myocardial infarction, acute pulmonary embolism, congestive cardiac failure, this threshold being determined by the amount of intravenously injected Strophantin that causes persistent ventricular tachycardia.
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PMID:[Digitalis poisoning, risk factors and digitalis intolerance]. 101 87

During the acute phase of myocardial infarction, two groups of patients are observed. Patients in the first group have no significant complications, and approximately 95 per cent of these patients recover fully without any specific therapy. Patients in the second group may have various complications, some of which are benign, whereas others may lead to a fatal outcome. The complications may be divided into four major types: 1. Cardiac arrhythmias and conduction defects. The tachyarrhythmias and bradyarrhythmias are the most frequently encountered complications in patients with acute myocardial infarction. Tachyarrhythmias include ventricular premature beats, ventricular tachycardia, ventricular fibrillation, supraventricular tachycardia, atrial flutter, and atrial fibrillation. Bradyarrhythmias include sinus and junctional bradycardia and various degrees of heart block. Those patients who are unable to reach a hospital and die suddenly presumably succumb to ventricular fibrillation. 2. Left ventricular failure and cardiogenic shock. In more than 33 per cent of patients with acute myocardial infarction, a third heart sound and pulmonary rales may be heard. If they are present for only 24 hours, the physical findings may indicate an alteration of left ventricular failure. However, if they persist for a few days and disappear after medical therapy, mild left ventricular failure may be present. About 12 per cent of patients have acute pulmonary edema, and 10 per cent of patients develop cardiogenic shock. These two complications carry a high mortality rate (40 per cent and nearly 100 per cent respectively). 3. Rupture of the heart. Cardiac rupture may occur in the free wall, ventricular septum, and papillary muscles. These complications, although less frequently encountered, cause a number of deaths in patients with acute myocardial infarction. 4. Thromboembolism. Under this category are included pulmonary embolism, systemic arterial embolism, and systemic venous thrombosis.
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PMID:The acute phase of myocardial infarction. 110 71

In a retrospective study, the P-terminal force in Lead V1 (PTF-V1) was measured in three groups, each of 35 patients, with the respective diagnoses of acute myocardial infarction without pulmonary edema, acute pulmonary embolism, and acute pulmonary edema. In all but one of the patients with acute pulmonary edema, a highly negative PTF-V1 value was obtained, whereas by contrast, all the patients with pulmonary embolism had normal PTF-V1 values. Four of the patients with acute myocardial infarction had abnormal PTF-V1 values, although at the time there was no clinical or radiologic evidence of pulmonary edema. However, one of these patients did develop acute pulmonary edema a few hours later. Measurement of the PTF-V1 is a simple noninvasive test that may, therefore, be useful in separating patients with acute pulmonary embolism from those with acute or impending pulmonary edema.
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PMID:P-wave analysis in myocardial infarction, pulmonary edema, and embolism. 111 59

CK-isoenzymes were measured in 31 patients hospitalised for suspected myocardial infarctions who had an increase in serum creatine kinase (CK) above 50 U/l. Of 26 patients with definite evidence of myocardial infarction, MB-isoenzyme--specific for myocardial necrosis--was demonstrated in 24. MB-isoenzyme was no longer detectable in two patients hospitalised 48 hours after the onset of symptoms. In the remaining five patients only MM-isoenzyme was found, the elevated CK activity in three patients having been due to an intramuscular injection, and in two others due to pulmonary embolism. Measurement of CK isoenzymes proved of great diagnostic value in three patients with sudden circulatory arrest of, at first, unknown cause after successful resuscitation. Acute myocardial infarction was proven by the presence of MB-isoenzyme. In one of these patients an additional BB-isoenzyme was seen, possibly due to concomitant cerebral ischaemia. In all other patients (with angina, after cardioversion, or after major surgical operations) only MM-isoenzyme was detected. MB-CK-isoenzyme was found to be a highly specific, as well as sensitive, indicator of myocardial necrosis. This being a rather difficult method, its use is not justified in the routine diagnosis, but in doubtful instances its value can hardly be overestimated.
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PMID:[The diagnostic value of CK-isoenzymes in suspected acute myocardial infarction (author's transl)]. 124 17

We observed the changes of molecular markers for hemostatic activation in a patient with acute pulmonary embolism treated with 2 x 10(7) unit tissue plasminogen activator (t-PA). Blood samples were obtained before, just after, at 30 min, 1, 2, 6, and 24 hours after the infusion. Molecular markers included thrombin-antithrombin III complex (TAT), plasminogen-alpha 2 plasmin inhibitor complex (PIC), and thrombomodulin (TM). Marked elevation of TAT was observed from immediately after the t-PA infusion to 6 hours after, although it had been observed for only 1 hour in our previous report on the cases of acute myocardial infarction. PIC level was significantly increased during t-PA infusion but returned to almost baseline value 6 hours after the end of t-PA infusion. This finding was almost the same as the one previously reported concerning acute myocardial infarction cases. TM level increased throughout the evaluation, and remained so, even on the 7th day after t-PA infusion. Our present data revealed a clear difference between the reactive TAT increases after t-PA therapy in acute myocardial infarction cases and in acute pulmonary embolism cases. Our present data also revealed a prolonged elevation of TM during the acute period of pulmonary embolism. It is therefore necessary to keep an eye on the changes of molecular markers for hemostatic activation after t-PA therapy in acute pulmonary embolism.
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PMID:[The changes in molecular markers for hemostatic activation after t-PA therapy in case of pulmonary embolism]. 131 73

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

Intraoperative massive pulmonary embolism is extremely rare. We describe such a case in a patient treated for a prolonged period preoperatively with intravenous heparin after an acute myocardial infarction and unsuccessful attempt at angioplasty, emphasizing that the problem should be borne in mind to facilitate expeditious and appropriate management. A clue to the diagnosis is interruption of venous return that is not due to a kink in the cannulae.
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PMID:Massive intraoperative pulmonary embolism. 162 77

Over the past decade there has been an increasing use of thrombolytic agents in the treatment of coronary artery disease, pulmonary embolism, and thromboembolic strokes. The use of thrombolytic agents has been most successful in treating acute myocardial infarction. When treatment with intravenous streptokinase or tissue plasminogen activator (tPA) is initiated within the first 3 to 4 hours from the onset of symptoms, the rate of reperfusion ranges from 60% to 90%, as compared to a rate of 13% to 21% for placebo control. Both streptokinase and tPA have been extensively studied as therapies for acute myocardial infarction, and in general, a higher initial rate of reperfusion is achieved in tPA-treated patients than in streptokinase-treated patients, although the final arterial patency rate may not be different in the two groups due to a higher rate of reocclusion in the tPA-treated population. Furthermore, time dependency for efficacy from the onset of symptoms to the initiation of treatment is less for tPA than for streptokinase. However, the role of thrombolytic agents in the treatment of thromboembolic strokes is more experimental than clinical at the present time. Of all agents, tPA is the most promising and the most extensively studied. This paper will review the experimental data on the use of tPA in acute thromboembolic strokes as well as the existing clinical data on stroke reperfusion.
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PMID:The efficacy and safety of tissue plasminogen activator in acute ischemic strokes. 162 47

Selected secondary diagnoses (e.g. pulmonary embolism) may provide an efficient and inexpensive source of data for quality assurance (QA) monitoring if their absence at admission were known. In June 1990 we modified our hospital abstracting methods to classify each diagnosis into categories: (1) present on admission, (2) acquired during hospitalization, or (3) uncertain. Our experience has confirmed the identification and elimination from QA reports of the majority of pre-existing secondary diagnoses. Examples of secondary diagnosis codes acquired or uncertain were acute myocardial infarction 48%, pneumonias 25%, pulmonary emoboli 54% and cerebral vascular accident/hemorrhage 35%. Abstracting time has increased less than 2 min per discharge. A reabstraction study showed 87% agreement (kappa = 0.733, p less than 0.001) between initial collection and blinded reabstraction. The separation of secondary diagnoses into preexisting or acquired can: (1) be reliably undertaken by discharge abstracters; (2) be efficient in adding minimal time; and (3) enhance the validity and usefulness of data and increase physician acceptance.
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PMID:Acquired conditions: an improvement to hospital discharge abstracts. 179 Mar 24

Massive pulmonary embolism (MPE), as seen in cardiac care units (CCU), is almost invariably characterized by severe obstruction of the pulmonary vasculature and/or a background of poor cardiorespiratory conditions, all contributing their share to a grave overall situation, often compounded by cardiogenic shock and not exceptionally eventuating in cardiocirculatory arrest (CCA). In such circumstances, echocardiography offers both direct and indirect diagnostic elements that may help, among other things, differentiate pulmonary embolism from acute myocardial infarction--the latter not always easily identified, also in view of its possible occurrence in association with MPE. Conversely, some problems are still open concerning the meaning and treatment of right-sided intracavitary thrombus formations revealed by echocardiography. Among less familiar hemodynamic aspects we must consider right-sided pulsus alternans and the so-called ventricularization of pulmonary pressure curves--a phenomenon to be viewed with caution because of possible modifications imputable to the recording system. Bedside pulmonary angiography, now generally feasible with standard CCU equipment, may readily diagnose or rule out MPE in situations where an angiography room is not available or momentarily not accessible. Numerous personal anatomoclinical observations bear witness to the role of electromechanical dissociation (EMD) as a cause of CCA in patients with MPE. Such dissociation may prove at least temporarily reversible, especially in cases not featuring bradycardia and showing narrow QRS complexes; the concurrent administration of fibrinolytic agents along with cardiopulmonary resuscitation may prove successful while it does not seem to invite important hemorrhagic complications.
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PMID:[Pulmonary embolism in the coronary care unit]. 184 68


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