SEARCH · PubMed Health

Results for “Pulmonary Infarction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources

PubMed1997

Obesity hypoventilation [corrected] syndrome in the differential diagnosis of a pulmonary mass.

Dyspnea and cyanosis are common presenting manifestations of cardiopulmonary disease. When these findings occur in a cigarette smoker with an apparent pulmonary mass on chest radiograph, the differential diagnosis rapidly narrows to a short list of possibilities that include pulmonary neoplasm, pulmonary infection and pulmonary infarction. Pulmonary hypertension with pulmonary arterial enlargement and hypoxia secondary to alveolar hypoventilation should also, however, be included as a diagnostic possibility in the appropriate setting because the evaluation and treatment of this entity may differ markedly.

Diagnosis, Differential↗

PubMed2004

Echocardiographic parameters discriminating myocardial infarction with pulmonary congestion from myocardial infarction without congestion in the mouse.

Our aim was to establish parameters describing systolic and diastolic function in mice after myocardial infarction (MI) that distinguish MI with pulmonary congestion from MI without congestion. Echocardiography, left ventricular (LV) catheterization, and infarct size measurements were performed on days 3, 5, 7, and 14 after ligation of the left coronary artery in C57BL/6 mice. Sham-operated mice were used as controls (Sham). MI mice with lung weight normalized to tibial length >125% of the average in the corresponding Sham group were considered to have pulmonary congestion (MIchf). MI mice with a smaller increase were called MI nonfailing (MInf). An infarct >40% of total LV circumference measured in two-dimensional long axis distinguished MIchf from MInf on both an average and an individual basis. Mean maximum rate of rise of LV pressure, LV fractional shortening, and posterior wall shortening velocity were significantly lower in MIchf compared with Sham at all time points and to MInf at 7 days. The diastolic parameters mitral flow deceleration velocity, LV end-diastolic pressure, and maximum rate of decline in LV pressure (LVdP/dtmin) discriminated the MIchf groups from Sham at all time points. Mitral flow deceleration velocity and LVdP/dtmin separated MIchf from MInf at 7 days. In addition to distinguishing all the groups on an average basis, left atrial diameter distinguished all MIchf animals from Sham and MInf. In conclusion, significantly increased left atrial diameter and infarct size >40% of total LV circumference may serve as major criteria for heart failure with pulmonary congestion after MI in mice.

Animals↗

PubMed1996

Interruption of pulmonary arterial flow with inadequate ventilation leads to pulmonary infection.

We examined the effect of interruption of pulmonary arterial flow and inadequate ventilation on the development of pulmonary infarction in rats. Pulmonary arterial flow was blocked by the injection of agar into the inferior vena cava and inadequate ventilation was produced by obstructing the left main bronchus with a polypropylene tip. Histological and angiographic examination of the lung demonstrated that: pulmonary artery embolism alone does not induce pulmonary infarction; obstruction of a bronchus does not induce significant changes, but that pulmonary infarction develops when pulmonary artery embolism and obstruction of a bronchus occur simultaneously. It has been thought that pulmonary infarction is caused by acute obstruction of a pulmonary artery, however, the alveolar walls are supplied with oxygen by both the pulmonary circulation and by ventilation. Interruption of pulmonary arterial flow alone is probably not sufficient to induce pulmonary infarction, which is probably caused by deficiency of oxygen supply to the alveolar walls by a synergy between interruption of pulmonary arterial flow and inadequate ventilation.

Animals↗

PubMed1973

Interrelation between alterations in pulmonary mechanics and hemodynamics in acute myocardial infarction.

Pulmonary mechanics were evaluated in 30 patients with acute myocardial infarction by measuring forced expiratory flow rates and total pulmonary resistance (R(T)) with the oscillometric method at the resonant frequency of the chest (6-8) cycle/s). During the first 3 days after infarction, forced expiratory volume (FEV) and forced mid-expiratory flow rate (FEF(25-75%)) were 69% and 60% of predicted values, respectively. 10 or more wk later these values were 95% and 91%. Initially, R(T) was 52% greater than predicted, but was only 4% greater 10 or more wk later. In 11 patients R(T) was measured at both resonant frequency and at 3 cycle/s. Five of these patients had no clinical signs of heart failure, but nine had abnormally high values of pulmonary artery pressure, "wedge" pressure and pulmonary extravascular water volume. All of these patients recovered. Initially, R(T) at resonance was 50% and R(T) at 3 cycle/s was 130% greater than predicted values. 2-3 wk later these figures were -3% and +6% of those predicted, respectively. At 10 wk or more, significant frequency dependence of R(T) had disappeared (R(T) at 3 cycle/s was 7% greater than R(T) at resonance). Isoproterenol inhalation in six patients caused no change in flow rates, R(T) at resonance, or R(T) at 3 cycle/s. R(T) at resonance and at 3 cycle/s, FEV, and FEF(25-75%) correlated significantly with the pulmonary vascular pressures. Patients with more marked arterial hypoxia and larger values for extravascular water volume had greater elevations of R(T) and depression of FEF(25-75%), but linear correlations were not significant. Clinical signs of congestive heart failure significantly correlated with a fall in FEV and FEF(25-75%), the development of frequency dependence of R(T), and elevation of the pulmonary wedge pressure. The initial elevation of R(T) and low flow rates indicate a modest degree of airway obstruction in acute myocardial infarction. Lack of response to isoproterenol suggests that bronchial muscular constriction is not a major factor. Frequency dependence of R(T) accompanied by elevated pulmonary vascular pressures and extravascular water volume indicates that pulmonary congestion causes the development of uneven time constants in the airways. Vascular engorgement and interstitial edema from elevated vascular pressures causing narrowing of the peripheral airways and closure of collateral airways could account for the above findings.

Acute Disease↗

PubMed1975

Pulmonary edema related to changes in colloid osmotic and pulmonary artery wedge pressure in patients after acute myocardial infarction.

Pulmonary artery wedge and plasma colloid osmotic pressures and their relationship to pulmonary edema were investigated in 26 patients with acute myocardial infarction of whom 14 developed pulmonary edema. In the absence of pulmonary edema, both the pulmonary artery wedge pressure and plasma colloid osmotic pressure were in normal range; after onset pulmonary edema, a moderate increase in pulmonary wedge pressure and reduction in plasma colloid osmotic pressure were observed. When the gradient between the plasma colloid osmotic pressure and the pulmonary artery wedge pressure was calculated, highly significant differences were demonstrated (P less than 0.002). In the absence of pulmonary edema, this gradient averaged 9.7 (plus or minus 1.7 SEM) torr; following appearance of pulmonary edema, it was reduced to 1.2 (plus or minus 1.3) torr. During therapy with digoxin and furosemide, reversal of pulmonary edema was closely related to a concomitant change in the colloid osmotic-hydrostatic pressure gradient. These observations indicate that both increases in pulmonary capillary pressure and decreases in colloid osmotic pressure may follow the onset of pulmonary edema. Such decline in colloid osmotic pressure and especially the reduction in colloid osmotic-hydrostatic capillary pressure gradient may favor transudation of fluid into the lungs.

Adult↗

PubMed1996

Mechanisms of sudden death and autopsy findings in patients with Arnold-Chiari malformation and ventriculoatrial catheters.

Neurological and vascular complications of Arnold-Chiari malformation treated with ventriculoatrial shunting may result in sudden or unexpected death. Two patients with Arnold-Chiari malformation and ventriculoatrial shunting had variable clinical manifestations and diagnostic difficulties. A 3-year-old girl with a 1-day history of right-sided heart failure died unexpectedly soon after cardiac catheterization. At autopsy examination an adherent thrombus around the ventriculoatrial catheter tip, pulmonary infarction, and embolic pulmonary arterial hypertensive changes were found. In the second case, a 21-year-old man died suddenly after a brief episode of dyspnea. He had a 1-year history of "asthma" before death. Autopsy examination confirmed pulmonary infarction and embolic pulmonary arterial hypertensive changes. There was no histological evidence of asthma. Deaths in both cases were due to pulmonary infarction stemming from thromboemboli derived from ventriculoatrial catheterization. Both patients had evidence of long-standing clinically unsuspected vascular disease, which may have contributed to death. Cardiac catheterization may also have precipitated death in the first patient. Other possible problems leading or contributing to sudden death in such patients include pulmonary hypertension with chronic cor pulmonale, airway obstruction from recurrent laryngeal nerve paralysis, and shunt blockage with acute hydrocephalus. Lethal brainstem compression may also accompany relatively minor trauma associated with chronic cerebellar tonsillar herniation in these patients.

Adult↗

PubMed2002

[An autopsied case of chronic active Epstein-Barr virus infection complicated in systemic lupus erythematosus and antiphospholipid antibody syndrome].

We have experienced a case of chronic active Epstein-Barr virus infection (CAEBV) complicated in systemic lupus erythematosus (SLE) and antiphospholipid antibody syndrome (APS). A 35-year-old woman was admitted to our hospital with complaints of fever and dyspnea on exertion. She was diagnosed as having SLE on the basis of arthritis, oropharyngeal ulcer, lymphopenia, and positive autoantibodies against DNA, RNP and SSA. The diagnosis of APS was also made because of positive anti-cardiolipin IgG antibodies and the existence of multiple pulmonary infarction with pulmonary hypertension. The administration of 30 mg/day of prednisolone and anti-coagulation significantly improved clinical symptoms. However, she was again admitted to the hospital four months later because of progressive liver damage and pancytopenia. Increment of prednisolone did not improve the clinical situation and she expired because of pulmonary hemorrhage. At autopsy, there were a significant increase of histiocytes with hemophagocytosis and a dense infiltration of atypical lymphocytes in the liver, spleen, lymph nodes and bone marrow. Infiltrated lymphocytes were positive for CD 3 and EBER 1 in immunohistochemical staining and EBVmRNA was detected by in situ hybridization. Final pathological diagnosis was CAEBV with hemophagocytic syndrome in association with lupus nephritis, pulmonary hemorrhage and pulmonary infarction.

Adult↗

PubMed2002

Pulmonary artery involvement in Takayasu's arteritis with lung infarction and pulmonary aspergillosis.

We describe a patient with a chronic case of pulmonary involvement of Takayasu's arteritis in the resected lung. A 49-year-old woman was first diagnosed with Takayasu's arteritis at age 30 years. On her first admission, she presented with Takayasu's arteritis and pneumonia with cavitation in the left lung. After recovering from pneumonia, she was treated initially with prednisolone, 30 mg/day, and remained well until she developed hemoptysis at age 34 years. Findings suggesting aspergilloma were found in the same lobe on chest x-ray film when she was 46 years of age. By age 49 years, the hemoptysis became massive, and she was admitted for surgery. Left upper lobectomy and partial resection of S6 and S8 pulmonary segments were performed. Histologic analysis of the resected lung revealed typical pathologic findings of pulmonary artery involvement in Takayasu's arteritis, such as stenosis recanalization and a vessel-in-vessel feature, but not active vasculitis. Infection probably occurred in the cavity of the infarcted tissue. Pulmonary artery involvement is common in Takayasu's arteritis, but the aspergilloma in this corticosteroid-treated patient is an uncommon complication.

Journal Article↗

PubMed1992

Pulmonary venous infarction secondary to squamous cell carcinoma.

This type of pulmonary venous infarction has not been previously reported, namely: pulmonary vein obstruction from squamous cell carcinoma. Furthermore, this case is unique in that the characteristic pathologic vascular changes observed with pulmonary venous infarction were contrasted with a noninfarcted upper lobe that was removed from the same patient one year later.

Carcinoma, Squamous Cell↗

PubMedDate not supplied

CT of inflation-fixed lungs: wedge-shaped density and vascular sign in the diagnosis of infarction.

To evaluate the role of high resolution CT (HRCT) in the diagnosis of pulmonary infarcts, we selected 83 postmortem lung specimens with subpleural densities from a collection of 180 lungs that had been prepared by a method which allows for a direct radiologic-pathologic correlation. Twelve of the lungs had pulmonary infarcts and 71 lungs had other disorders that had produced a subpleural shadow on HRCT. Lungs were evaluated for the presence of wedge-shaped pleural-based densities and for the presence of an associated vascular sign. There was no significant difference in the incidence of wedge-shaped densities on HRCT between lungs with pulmonary infarcts and lungs with pulmonary hemorrhage, pneumonia, tumor, or edema (p greater than 0.05). A vascular sign associated with a subpleural density was, however, more common (p less than 0.01) in lungs with pulmonary infarcts. We suggest that the vascular sign associated with a wedge-shaped density may be of importance in diagnosing pulmonary infarcts by HRCT.

Humans↗

PubMed2005

A full house: complications from an uncorrected patent ductus arteriosus.

True aneurysms of the pulmonary artery are rare, and are most often due to pulmonary hypertension arising from congenital heart defects. We report the case of a 40-year-old man with an uncorrected patent ductus arteriosus who presented with pulmonary infarction and pneumonia, and subsequently died of cardiac arrest. Autopsy revealed a large pulmonary artery aneurysm, in situ pulmonary artery thrombosis complicated by pulmonary infarction, pulmonary artery dissection, and cardiac tamponade. Although each of these complications is rare in and of itself, this case demonstrates the entire spectrum of complications from a single uncorrected congenital cardiac anomaly.

Adult↗

PubMed1976

Hypoxemia and lung water in acute myocardial infarction.

Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to Class III (frank pulmonary edema) patients. Heart rate and pulmonary wedge pressure (Pw) rose and cardiac index declined with increasing severity of heart failure by clinical classification. There was a significant correlation between PEV and Pw independent of clinical class (r = 0.47, p less than 0.01). PaO2 had a negative correlation with Pw (r = -0.28, p less than 0.01) as well as PEV (r = -0.26, p less than 0.02). We conclude therefore that increased pulmonary hydrostatic pressure secondary to pulmonary venous hypertension in patients with acute myocardial infarction is a major determinant of interstitial edema. At higher values of PEV, PaO2 was lower. The mechanism of hypoxemia in the presence of excessive lung water may be due to multiple factors, including small airway dysfunction and intrapulmonary shunting.

Adult↗

PubMed2001

[Meningococcocemia complicated by disseminated intravascular coagulation, splenic infarction and pulmonary thromboembolism in a young adult: case report].

Mortality of meningococcal septicemia remains high in spite of the improvement of antibiotics treatment and critical care medicine. A 23-year-old male, who had been well until a day earlier, was admitted to the hospital because of a high-grade fever and headache. On the second hospital day, he was still febrile, and it was confirmed that he had disseminated intravascular coagulation. There was no purpuric skin lesion, and a lumbar puncture revealed no abnormality. The condition was complicated by a splenic infarction on the second hospital day, and he suffered a pulmonary infarction on the 8th hospital day. The blood culture was positive for Neisseria meningitidis, making the diagnosis meningococcal septicemia. He was successfully treated with antibiotics and intensive care. Although meningococcocemia in adults is relatively rare in Japan, the disease mortality is still high even in the modern era. Then, once the diagnosis is suspected, it is essential to keep in mind that meningococcal infection requires early recognition of the disease process, prompt initiation of adequate antiinfectious therapy and intensive treatment of multiorgan failure.

Adult↗

PubMed1997

Clinical characteristics of patients with acute pulmonary embolism stratified according to their presenting syndromes.

PURPOSE: The purpose of this investigation is to determine the characteristics of the history, physical examination, chest radiograph, and ECG, and the ventilation/perfusion (V/Q) lung scan probability in patients with pulmonary embolism (PE) stratified according to their presenting syndrome. BACKGROUND: In considering a possible diagnosis of acute PE, it is helpful to consider the patient in terms of the presenting syndrome (pulmonary infarction, isolated dyspnea, or circulatory collapse). In assessing the possibility of acute PE, it would be more useful to know the detailed characteristics of the particular syndrome rather than the clinical characteristics of all patients with PE. METHODS: Patients described in this investigation participated in the national collaborative trial of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED). All had PE diagnosed by pulmonary angiography. None had prior cardiopulmonary disease. All examinations and laboratory tests were obtained within 24 h of the pulmonary angiogram and most were within 12 h of the pulmonary angiogram. RESULTS: Among patients with the pulmonary infarction syndrome, 14 of 119 (12%) had neither dyspnea nor tachypnea. Some patients with circulatory collapse did not have dyspnea, tachypnea, or pleuritic pain. A normal ECG was more prevalent among patients with pulmonary infarction syndrome, 45 of 97 (46%), than among patients with isolated dyspnea syndrome, 2 of 21 (10%) (p<0.01). A PaO2 >80 mm Hg was also more prevalent in patients with the pulmonary infarction syndrome, 27 of 99 (27%), than in patients with the isolated dyspnea syndrome, 2 of 19 (11%). A high-probability V/Q lung scan was less prevalent among the pulmonary infarction group, 38 of 119 (32%), than the isolated dyspnea group, 20 of 31 (65%) (p<0.001). CONCLUSION: Many of the findings in the various syndromes of PE can be understood in terms of the severity of PE as it increases from mild with the pulmonary infarction syndrome to moderate with the isolated dyspnea syndrome to severe with circulatory collapse. The prevalence of various clinical and laboratory characteristics of patients with the syndrome of pulmonary infarction, isolated dyspnea, or circulatory collapse may give clues to the diagnosis or suggest characteristics that may reduce the likelihood of inadvertently discarding the diagnosis of PE.

Acute Disease↗

PubMed1978

[Moderate doses of urokinase (UK) in the treatment of myocardial infarct and pulmonary embolism].

Since 1972, UK in moderate doses have been used in the treatment of severe or massive pulmonary emboli (PE) and of myocardial infarction (MI) present for less than 24 hours. The standard dose is 2,700,000 CTA units per 24 hours administered as a continuous infusion, in association with appropriate heparin therapy and a platelet anti-aggregant agent in order to palliate the hyperagregant effects of thrombolytic drugs. Laboratory surveillance has now been greatly simplified and is limited to that of the associated heparin therapy. In the acute phase of myocardial infarction, a personal randomised study of 120 cases consisting of 60 treated with heparin + UK and 60 with heparin alone showed that UK decreased mortality, cardiac arrhythmias and cardiac failure. Comparative studies at lower doses have failed to show any significant difference between the two groups of patients treated and the authors feel that the use of UK should be reserved for very recent infarctions in young subjects. In PE, the effectiveness of UK was assessed in 180 severe cases. It depended upon the length of time for which the thrombus had been present. Before the 5th day, there was early average revascularisation of 40 p. 100 of the avascular territory. Mortality was reduced to 15 p. 100 and at the 3rd week 32 p. 100 of the survivors had complete revascularisation, and 68 p. 100 partial but adequate revascularisation. Adjuvant therapy such as a combination of Lysil Plasminogen and/or defibrinating agent currently make it possible to reinforce therapeutic thrombolysis.

Clinical Trials as Topic↗

PubMed2001

Displacement of coils into the lung during embolotherapy: clinical importance and follow-up with helical CT.

RATIONALE AND OBJECTIVES: The authors performed this study to evaluate the clinical importance and computed tomographic (CT) appearance of coils displaced into the lung during embolotherapy. MATERIALS AND METHODS: The authors retrospectively studied clinical charts and serial chest images from 25 consecutive patients after coil embolization. Chest radiography was performed in all patients, whereas helical chest CT was performed only in patients in whom dislocated coils were visible on chest radiographs. Coils were applied for the treatment of peripheral arteriovenous (AV) malformations and fistulas (n = 9), renal AV malformations or fistulas (n = 8), and primary or secondary tumors (n = 8). Clinical charts were analyzed for short- and long-term symptoms; chest radiographs and CT scans were reviewed for signs indicative of pulmonary infarction. RESULTS: None of the patients had clinical symptoms suggestive of pulmonary infarction. In two of the 25 patients (8%), displaced coils were seen in the pulmonary vasculature at chest radiography; these patients had been treated for renal AV fistula and peripheral AV fistula, respectively. One patient had two coils in the left hemithorax (upper and lower lobe), and the other patient had two coils in the right hemithorax (middle lobe). Neither of the patients had abnormalities suggestive of pulmonary infarction at helical CT. CONCLUSION: Chest radiography can help confirm the presence of coils displaced to the pulmonary vasculature during embolotherapy. Helical CT can also help rule out the presence of coil-associated pulmonary infarction.

Adolescent↗

PubMed1992

[Surgical treatment of primary cardiac tumors].

Twenty patients with primary cardiac tumors were operated on during the past ten years. The age of 15 female and 5 male patients ranged from 17 to 73 years. Eighteen patients had myxomas, 16 of which located in the left atrium and 2 in the right atrium. Systemic embolism occurred in 8 patients, subsequently caused cerebral infarction in 4, ischemia of extremities in 2, myocardial infarction in 1 and pulmonary infarction in 1. Emergency operation was performed in 5 patients because of severe congestive heart failure. In all cases, removal of myxoma was performed together with the excision of the wall to which the pedicle attached with the use of cardiopulmonary bypass. One patient with pulmonary infarction underwent resection of the infarcted lung simultaneously. Only one patient with severe heart failure died of pulmonary insufficiency one month after the operation. Another patient with cerebral infarction underwent clipping of cerebral aneurysm which appeared later in the infarcted area. The 17 patients including the latter patient showed a good recovery and no local recurrence during the follow-up period of 1 to 120 months. Two patients had malignant tumors, which were malignant fibrous histiocytoma of the left atrium and leiomyosarcoma of the pulmonary artery, respectively. Both of these rare tumors were resected noncuratively and led to the death because of their local recurrence with distant metastasis, though they received adjuvant chemotherapy. The symptoms, complications, diagnoses, surgical treatment and outcome of the primary cardiac tumors are reviewed in this study.

Adolescent↗

PubMed1976

[Effect of furanthril on several hemodynamic indices during the acute stage of myocardial infarction].

Pulmonary arterial pressure, heart rate and peripheral arterial pressure were followed up by the 15th, 45th and 105th minute post intravenous introduction of 40 mg furanthril in patients with myocardial infarction in acute stage (in 42 cases of 12 patients with left cardiac insufficiency and in 14 cases--of 8 patients without cardiac insufficiency). Furanthril induced clearly manifested pressure decrease in the pulmonary artery in patients with left cardiac insufficiency, developing between the 15th and 45th minute and continuing till the end of the second hour and a negligible elevation of peripheral arterial pressure by the 15th minute, followed by a slight decrease of the latter under the initial value by the 45th and 105th minute. Similar tendency, but less manifested, exists and in patients without cardiac insufficiency. Heart rate is kept unchanged. Furanthril does not induce undesirable hypotonic states when applied in those doses in patients who, as a rule, arenot hyptonics.

Acute Disease↗