Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombo-endarterectomy for chronic thromboembolism of the pulmonary artery can be recommended in patients with NYHA classification III or IV symptoms, mean pulmonary artery pressure greater than 30 mmHg and proximal, greater than 50% obstruction of the pulmonary arterial bed. Pulmonary angiography for localization of thrombi is prerequisite. Surgical techniques encompass lateral thoracotomy with or without extracorporeal circulation and median sternotomy with extracorporeal circulation. As an adjunctive measure, an interruptive procedure for the vena cava is performed. Currently we prefer to operate with the beating heart and normothermia. The most frequent complications are congestive heart failure and hemorrhagic pulmonary edema. In 33 patients total mortality was 20%. On use of a median sternotomy, with normothermia and beating heart there were no deaths. In the presence of distally-localized obstruction, thrombectomy cannot be performed.
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PMID:Surgical treatment for chronic pulmonary thromboembolism. 222 69

We describe our experience with CT of the chest in the diagnosis of pulmonary edema due to congestive heart failure, overhydration, renal failure, or increased capillary permeability. CT is able to detect acinar shadows and air-bronchograms more clearly than conventional radiography. Specific pattern of distribution of edema can be imaged in cross-section due to the elimination of superimposition of structures. In patients with adult respiratory distress syndrome, CT can detect microcystic transformation of the lung, which indicates a worse prognosis. Complications of ARDS, not always clearly visible on bedside chest radiographs, can be identified with CT.
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PMID:CT of pulmonary edema. 266 65

We present a rare case of aortitis syndrome associated with dilatation of aorta and coarctation-like effect due to the intraluminal flap formation originated from dissected wall of the aorta. A 31-year-old woman was admitted to our hospital complaining of shortness of breath, palpitation and cough. On admission, her physical status showed congestive heart failure and hypertension of upper extremities and hypotension of lower extremities. Bruits were audible over the neck, the anterior chest and the back. Serological studies showed active inflammation. Chest X-ray film showed upper mediastinal widening, cardiomegaly and pulmonary edema. Aortitis syndrome was strongly suggested by these clinical findings, so that prednisolone therapy was started on 3rd hospital day. Special examinations were performed several days later when inflammatory changes showed a tendency to improve. Chest CT scan, RI angiography and MRI studies showed an aneurysmal dilatation from the ascending aorta to the mid-thoracic aorta. Aortography demonstrated a flap at the terminal portion of this aneurysmal dilatation and grade II (Sellars) aortic regurgitation. There was a pressure difference of 80 mmHg between the parts abutting cranial and caudal sides of the flap. A surgical operation was, then, performed to correct the pressure difference. The dissected wall was extruded toward the aortic lumen creating a flap (2 cm in length). This flap was resected and an artificial graft was inserted. Histologically, the flap consisted of adventitia, media and intima.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of aortitis syndrome which presented coarctation of aorta due to intraluminal flap formation in the middle of the thoracic aorta]. 272 9

Nisoldipine, a calcium entry blocker, was given to 10 patients with congestive heart failure. During a 2 month follow-up period, 7 of the 10 patients were readmitted with pulmonary edema; daily furosemide doses were increased (128 +/- 87 to 192 +/- 135 mg/day, p less than 0.01), and plasma creatinine increased (1.5 +/- 0.5 to 1.8 +/- 0.6 mg/dl, p less than 0.05) (all values mean +/- SD). Despite this unfavorable clinical course, nisoldipine caused some beneficial chronic (1 month) hemodynamic effects. It decreased systemic vascular resistance (from 1,781 +/- 229 to 1,306 +/- 345 dynes X s X cm-5, p less than 0.01), decreased mean arterial pressure (from 88 +/- 0 to 74 +/- 4 mm Hg, p less than 0.001) and increased stroke volume index (from 27 +/- 6 to 33 +/- 9 ml/min per m2, p less than 0.02). Heart rate, pulmonary capillary wedge pressure and stroke work index did not change. However, nisoldipine's chronic renal and neurohumoral effects were not as favorable. These were assessed during a 5 hour water load (15 ml/kg body weight of 5% dextrose in water) and compared with the effects of a water load before therapy. Nisoldipine did not change creatinine clearance or sodium excretion, but decreased water excretion (from 58 +/- 35 to 46 +/- 40% of water load in 5 hours). Over this 5 hour study, mean plasma vasopressin was also higher with nisoldipine (1.9 +/- 2.3 versus 2.7 +/- 3.2 pg/ml, p less than 0.05), but mean plasma aldosterone was lower (67 +/- 31 to 47 +/- 27 mg/dl, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic renal and neurohumoral effects of the calcium entry blocker nisoldipine in patients with congestive heart failure. 288 Aug 84

The efficacy of oral enoximone, a new positive inotropic and vasodilator agent, was assessed in 12 patients with chronic congestive heart failure (New York Heart Association [NYHA] class II or III) in a double-blind randomized crossover comparison with placebo. Duration of each treatment was 6 weeks and the dose of enoximone was 150 mg tid. Efficacy was assessed by exercise tolerance, symptoms, radionuclide angiography for ejection fraction at rest and during exercise, and Holter monitoring. Two patients were withdrawn before completion of the study, one with pulmonary edema after 1 week on placebo and the other for noncompliance with enoximone therapy. Symptom-limited exercise capacity improved with enoximone by 30% and 43% (p less than .01) compared with baseline after 2 and 6 weeks treatment, respectively. Ejection fraction improved at rest (p less than .02) with enoximone but not with placebo. No change was found during exercise. Heart rate and blood pressure remained unaltered. During treatment with enoximone symptoms of exertional dyspnea and fatigue were improved and NYHA class decreased by at least one class for every patient. Holter monitoring revealed an overall increase (NS) in ectopic activity during enoximone therapy. There were no serious adverse effects and laboratory values did not change significantly. The addition of enoximone to the existing therapy of patients with moderately severe congestive heart failure provided clear and sustained subjective and objective benefit when compared with placebo.
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PMID:Double-blind crossover comparison of enoximone and placebo in patients with congestive heart failure. 296 Apr 73

Chest X-rays were used to evaluate the hemodynamic status of 86 patients with acute myocardial infarction. The chest films, divided into three groups depending on the degree of pulmonary venous hypertension revealed: grade 1, pulmonary-venous congestion; grade 2, interstitial pulmonary edema; grade 3, diffuse alveolar edema. On clinical examination, four grades of congestive heart failure were distinguished in acute myocardial infarction. In 69% of our patients radiological and clinical grading of left ventricular failure led to precisely the same conclusions. Pulmonary capillary wedge pressure was measured in 31 patients with acute infarction. Radiological criteria of the degree of pulmonary vascular congestion, when related to pulmonary capillary wedge measurements, provide a basis for consistent therapy of left ventricular failure secondary to acute myocardial infarction.
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PMID:[X-ray changes in the thoracic organs in acute heart infarct]. 318 76

Between 1980 and 1987, 40 patients with ischemic mitral insufficiency underwent mitral valve replacement (with a mechanical prosthesis) and coronary bypass grafting, 3.5 grafts per patient. The posterior mitral leaflet was preserved in 17 and resected in 23. Five arrived at operation in cardiogenic shock, 15 after recurrent episodes of pulmonary edema, and 20 electively, but in congestive heart failure. Twenty-five had unstable angina, and the remaining had chronic angina. Perioperative and early deaths occurred only in patients with an ejection fraction less than 35%. None of the 21 patients with an ejection fraction greater than 35% died, whereas eight of 19 with an ejection fraction less than 35% died, whereas eight of 19 with an ejection fraction less than 35% died (p less than 0.001). When causes of death in patients with an ejection fraction less than 35% were studied, operative and early mortality was zero of seven with preservation of the posterior mitral leaflet versus eight of 11 with excision of the leaflet (p = 0.035). We concluded that the high mortality in mitral valve replacement for ischemic mitral insufficiency is linked to an ejection fraction less than or equal to 35% and, in this particular group of patients, is due to the surgical destruction of the left ventricular chordae tendineae supportive apparatus. Preservation of this apparatus by preservation of the posterior mitral leaflet drastically reduces operative and early mortality. Preoperative cardiogenic shock, left ventricular aneurysmectomy, and multiple grafting (up to five grafts per patient) did not increase the risk of operation. Extensive revascularization (3.5 grafts per patient) provides improved long-term results.
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PMID:Preservation of the posterior leaflet during mechanical valve replacement for ischemic mitral regurgitation and complete myocardial revascularization. 326 Sep 79

Patients with heart failure should stop smoking, maintain an optimal weight and limit their intake of salt. Alcohol abuse should be avoided. The detection and early treatment of hypertension appears to have had a major impact in preventing heart failure. Diuretics revolutionized the treatment of congestive heart failure and their proper and appropriate use can alleviate peripheral and pulmonary oedema. Diuretics should not be overused and care should be taken to avoid hypokalaemia. Controversy surrounds the use of digoxin in patients in sinus rhythm; the drug should be used in patients in atrial fibrillation. The use of an inotropic drug may be harmful in the presence of coronary artery disease. A reduction in the current use of digoxin might be of benefit to many patients with heart failure. When the drug is prescribed it should be used in a therapeutic and not homeopathic dose. Recent interest has been directed toward the use of vasodilators and the angiotensin-converting enzyme inhibitors in patients with heart failure. In my opinion, these drugs should be used after patients have been treated with thiazide and loop diuretics. Vasodilators are particularly beneficial in acute heart failure or in patients with chronic heart failure when the symptoms are related to fluid overload and volume expansion. The cause of symptoms in patients with chronic heart failure optimally treated with diuretics is controversial. Shortness of breath may not be simply related to the left atrial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changing ideas in the treatment of heart failure--an overview. 330 Sep 78

Total lactate dehydrogenase (LD; EC 1.1.1.27) activity in serum and LD isoenzymes were quantified in 190 patients with acute myocardial infarction (AMI) 24, 48, and 72 h after admission. In 90% of the 570 blood specimens an LD isoenzyme pattern typical of AMI (LD-1/LD-2 greater than 0.76) was found. The other 56 blood specimens showed an LD isoenzyme pattern atypical of AMI (LD-1/LD-2 less than 0.76). They were divided into three groups: 28 specimens with isomorphic pattern (relative increase in all five LD isoenzymes); 18 with relatively increased LD-3 proportion (greater than 35%); and 10 specimens with increased LD-5 proportion (greater than 10%). No difference was found in mean total LD activity in serum between the typical isoenzyme group and the three atypical groups. The LD isomorphic pattern was found in 60% of AMI patients complicated by cardiogenic shock. Fifty percent of AMI patients admitted with pulmonary edema showed increased LD-3 proportion and half of the patients with AMI and congestive heart failure, predominant right, demonstrated increased LD-5 proportion. We conclude that although most patients with AMI present at diagnosis with a typical LD isoenzyme pattern, it is important to recognize that some may present with atypical LD isoenzyme patterns, which may be associated with specific AMI complications.
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PMID:Atypical patterns of lactate dehydrogenase isoenzymes in acute myocardial infarction. 337 25

Twenty patients admitted to hospital with congestive heart failure were evaluated for severe concomitant lumbosacral and leg pain. In each instance the discomfort was worse at night and progressively decreased with a resolution of the pulmonary edema. Neurologic and electromyographic examinations in all but four patients were normal with reflexes, strength and straight leg raising testing normal. An absent Achilles reflex was recognized in two, a diminished knee jerk reflex in one and in a third, weakness in the extensor hallucis longus. Lumbar spinal stenosis was identified in all of the patients with a concomitant degenerative spondylolisthesis present in nine instances and in an additional two a spondylolisthesis with interruption of the neural arch. It is theorized that diminished right heart compliance can induce a sufficient increase in venous volume and pressure within the paravertebral plexus of Batson to acutely exacerbate a chronic lumbar spinal stenosis. In support of this hypothesis, the multiple factors involved in the pathomechanics and physiology of lumbar radiculopathy, spinal stenosis and the role of the paravertebral plexus of veins are examined. Specifically, their response to altered volume and pressure gradients tending to induce venous "creep" as well to alterations in posture and diurnal cycles are reviewed.
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PMID:Night pain associated with diminished cardiopulmonary compliance. A concomitant of lumbar spinal stenosis and degenerative spondylolisthesis. 340 61


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