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Query: UMLS:C0034065 (pulmonary embolism)
 14,979 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum myoglobin was determined by radioimmunoassay in 20 cases of sudden and unexpected death resulting from acute coronary occlusion. There was consistent elevation of myoglobin 2 h after death, with peaking at 3 h. No comparable elevation of serum myoglobin level was noted in patients who had succumbed to pulmonary embolism, ruptured aortic aneurysm, or subarachnoid or intracerebral hemorrhage. Thus, determination of serum myoglobin seems useful in confirming or establishing acute coronary occlusion as the cause of sudden and unexpected death.
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PMID:Determination of serum myoglobin level after death in the diagnosis of sudden coronary artery occlusion. 74 96

Plasma fibrinopeptide A (FPA) concentrations were measured in clinical blood samples incubated in the collecting syringe for different time periods before addition to heparin and Trasylol, and the rate of in vitro generation of FPA was calculated as the mean increment in FPA concentration per minute over the linear portion of the generation curve. 36 normal individuals had a mean plasma FPA level of 0.64 +/- 0.56 pmol/ml and an FPA generation rate of less than 0.5 pmol/ml per min. Clinical samples with elevated plasma FPA levels manifested slow (less than 1 pmol/ml per min) (28 patients) or rapid FPA generation (greater than 1 pmol/ml per min) (33 patients). Slow FPA generation was found in 10/10 patients with venous thrombosis, in 4/4 with aortic aneurysm, and in several patients with acquired hypofibrinogenemia. In one such patient, addition of fibrinogen resulted in rapid FPA generation whereas thrombin addition was without effect. Rapid FPA generation was generally linear, was usually associated with slower fibrinopeptide B generation and was inhibited by parenteral or in vitro heparin. It is thought to reflect increased thrombin activity and was seen in patients with pulmonary embolism, active systemic lupus erythematosus, renal transplant rejection, and after infusion of prothrombin concentrates. The initial rate of FPA cleavage by thrombin at fibrinogen concentrations from 0.05 to 4 mg/ml showed little change between 2 and 4 mg/ml with a Km of 2.99 muM. At a fibrinogen concentration of 2.5 mg/ml the FPA cleavage rate was 49.2 +/- 1.6 nmol/ml per min per U of thrombin. Exogenous thrombin added to normal blood generated 21.7 nmol/ml per U of thrombin FPA in the first minute with a nonlinear pattern reflecting inactivation of thrombin and the presence of alternative substrates. Hence, the thrombin concentration in the blood cannot be calculated from the FPA generation rate. The FPA generation rates in clinical samples with rapid generation (1-28 pmol/ml per min) could be produced by 2 X 10(-5) to 5.6 X 10(-4) thrombin U/ml acting on purified fibrinogen at physiological conditions of pH, ionic strength, and temperature.
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PMID:The generation of fibrinopeptide A in clinical blood samples: evidence for thrombin activity. 99 37

Surgical treatment of cardiovascular complications in patients with Marfan's syndrome is usually recommended with apprehension since the systemic nature of the disease predisposes to early and late complications. To define the incidence of these complications, 30 patients were evaluated after surgical treatment of aortic insufficiency and ascending aortic aneurysm at the Texas Heart Institute. To provide a minimal follow-up period of 5 years, only patients operated upon during of before 1968 were included in this series. There were 9 female and 21 male patients aged 4 to 80 years (mean 44 years). Aortic insufficiency was treated by valvuloplasty in 3 patients and by aortic valve replacement in 27. Graft replacement of the ascending aorta was required in 23 patients, and the aneurysm was excised and the aorta repaired by direct anastomosis in 7. Two patients were lost to follow-up study; 12 of the remaining 28 (42.8 percent) lived 5 years or more. The hospital mortality rate was 20 percent (6 of 30); the causes of death included dissection or rupture of the aorta in three patients, congestive heart failure in two and pulmonary embolism in one. The 24 survivors lived from 5 weeks to 9 years. Follow-up data were available on 22 of these patients. Ten of these (45.4 percent) died of late complications. Seven died suddenly, four of these had redissection, one patient had occlusion of the right coronary artery, and two had ventricular fibrillation of no apparent cause. The remaining three died of noncardiac causes. Although the risk of ascending aortic and aortic valve surgery in patients with Marfan's syndrome is high, 42.8 percent of the patients in our series survived 5 years or more. We believe that surgery should be recommended for patients with Marfan's disease who have dissection of the aorta or severe aortic regurgitation, or both.
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PMID:Surgical experience in patients with Marfan's syndrome, ascending aortic aneurysm and aortic regurgitation. 116 38

A case of inferior vena caval thrombosis secondary to aortic aneurysm is presented with management guidelines. CT scanning, as well as conventional venography and arteriography, is very useful in understanding this process preoperatively. Intraoperative management should prevent pulmonary embolism and should anticipate the possibility of blood loss in excess of that which usually occurs with an uncomplicated aneurysm repair. Detailed review of the literature reveals this is a rare complication of aneurysm disease and a potentially lethal one.
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PMID:Inferior vena cava occlusion secondary to aortic aneurysm. 219 68

We report a case of Behcet's disease complicated by aortic aneurysm and contiguous vena cava thrombosis due to compression. Arterial aneurysms are uncommon in the course of Behcet's disease and are associated with a poor prognosis owing to the risk of rupture. Vena cava thrombosis is found in 10% of cases; pulmonary embolism is infrequent. Venous and arterial lesions usually evolve independently. In most cases they are consecutive to vasculitis. The case reported herein is uncommon because of simultaneous and contiguous venous and arterial lesions. Eighteen months after aorto bi-iliac graft and inferior vena cava ligature, there is no recurrence of thrombosis nor aneurysm with a treatment including heparin, colchicine and azathioprine.
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PMID:[Aortic aneurysm with vena cava thrombosis occurring in Behcet's disease]. 277 98

Between 1982 and 1987, 32 patients with severe aortorenal atherosclerosis had simultaneous aortic and bilateral renal revascularization. All patients were hypertensive. Eighteen patients (56%) had renal insufficiency with a mean serum creatinine (SC) of 2.8 mg/dl. Nine patients had an aortic aneurysm; the remaining 23 patients had aortoiliac occlusive disease of varying severity. Aortic reconstruction was done with either a straight (six patients) or bifurcated (26 patients) Dacron graft. Renal revascularization was accomplished with either bypass (60 arteries) or transaortic endarterectomy (four arteries). One patient died of pulmonary embolism (operative mortality rate 3%). Beneficial blood pressure response was achieved in 28 of 31 survivors, (90%). Among the 18 patients with renal insufficiency, mean SC was 2.80 +/- 1.18 mg/dl preoperatively and 1.65 +/- 0.48 mg/dl postoperatively (p less than 0.001). Among eight patients with severe renal dysfunction before surgery (SC greater than 3 mg/dl), mean SC was 3.90 +/- 0.85 mg/dl before and 1.79 +/- 0.69 mg/dl after operation (p less than 0.001). In follow-up extending to 58 months (mean 27.6 months), five late deaths occurred; cumulative survival was 94% at 2 years and 60% at 4 years. There were no instances of worsening hypertension; one patient had deteriorating renal function. These results indicate that severe aortorenal atherosclerosis can be managed with simultaneous aortic reconstruction and bilateral renal revascularization at low operative risk. In addition, there can be high expectation of significant and persisting benefit in both hypertension and renal dysfunction after operation.
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PMID:Simultaneous aortic reconstruction and bilateral renal revascularization. Is this a safe and effective procedure? 274 98

Pulmonary embolism is a common medical problem whose incidence is likely to increase in our aging population. Although it is life-threatening, effective therapy exists. The treatment is not, however, without significant complications. Thus, accurate diagnosis is important. Unfortunately, the clinical manifestations of pulmonary embolism are nonspecific. Furthermore, in many patients the symptoms of an acute embolism are superimposed on underlying chronic heart or lung disease. Thus, a high index of suspicion is needed to identify pulmonary emboli. Laboratory parameters, including arterial oxygen tensions and electrocardiography, are as nonspecific as the clinical signs. They may be more useful in excluding another process than in diagnosing pulmonary embolism. The first radiologic examination is the chest radiograph, but the clinical symptoms are frequently out of proportion to the findings on the chest films. Classic manifestations of pulmonary embolism on the chest radiograph include a wedge-shaped peripheral opacity and a segmental or lobar diminution in vascularity with prominent central arteries. However, these findings are not commonly seen and, even when present, are not specific. Even less specific findings include cardiomegaly, pulmonary infiltrate, elevation of a hemidiaphragm, and pleural effusion. Many patients with pulmonary embolism may have a normal chest radiograph. The chest radiograph is essential, however, for two purposes. First, it may identify another cause of the patient's symptoms, such as a rib fracture, dissecting aortic aneurysm, or pneumothorax. Second, a chest radiograph is essential to interpretation of the radionuclide V/Q scan. The perfusion scan accurately reflects the perfusion of the lung. However, a perfusion defect may result from a variety of etiologies. Any process such as vascular stenosis or compression by tumor may restrict blood flow. In addition, areas of the lung that are not well ventilated will be poorly perfused. Thus, a ventilation scan and a chest radiograph are essential to optimal interpretation of the perfusion scan. Ventilation/perfusion scans are interpreted as degrees of probability of pulmonary embolism. Emboli are not present in patients with a normal V/Q scan. An embolus is unlikely (10%-15%) among patients with a low-probability V/Q scan. However, small emboli that are nonocclusive may be present, and pulmonary arteriography may be used to further evaluate patients with a high clinical suspicion of pulmonary embolus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pulmonary embolism. 305 85

The diagnostic value of oesophageal echocardiography is most striking in patients in whom precordial studies are of inadequate quality or fail to establish a definitive diagnosis. Oesophageal studies have excellent image quality, can be completed within 10 minutes without complications and, in most instances, enables the clinical question to be answered. In 50 patients referred for suspected thoracic aorta pathology, oesophageal echocardiography correctly excluded or diagnosed the type of aortic dissection, aortic aneurysm or the site of coarctation. Of 35 patients referred with suspected infective endocarditis, oesophageal echocardiography revealed complications in 18 patients, including vegetation, mycotic aneurysm, abscess or chordal rupture. Oesophageal echocardiography is extremely helpful to visualize intracardiac mass lesions. In 27 patients with a history of systemic or pulmonary embolism, the technique confirmed the presence, size and position of a mass lesion in 11 patients. Oesophageal color Doppler flow imaging further expands the diagnostic capabilities, particularly in patients with mitral valve prosthesis. Our experience indicates that oesophageal echocardiography significantly extends the diagnostic potential of echocardiography. Detailed knowledge of cardiothoracic anatomy and its pathologic sequelae is, however, a prerequisite for the efficient and safe application of this method.
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PMID:Oesophageal echocardiography. 332 33

A case of unilateral mismatch on a ventilation/perfusion lung scan due to aortic aneurysm dissection is presented. Pulmonary embolism should not be considered the sole cause of unilateral lung mismatch. Clinical evaluation and pulmonary angiography should be used for a definitive diagnosis.
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PMID:Aortic aneurysm dissection causing V/Q mismatch. 338 23

To better understand declining autopsy rates, data have been gathered prospectively on 1080 consecutive deaths over six years among patients admitted to a medical intensive care/coronary care unit. Overall autopsy rate was 36%. Autopsy rates declined sharply with age from 60% for those aged 16 to 34 years to 23% for those 85 and over (P less than .001). The highest rates by diagnosis were aortic aneurysm (70%), hepatic failure (52%), heart rhythm disturbance (48%), pulmonary embolism (45%), and sepsis (41%). Patients receiving major procedures had a significantly higher autopsy rate (38 versus 29%, P less than .05) but rates bore little relation to prognoses given at admission by house officers, suddenness of death, sex, marital status or year of admission. Even among intensively treated patients, autopsy rates decline strikingly with age, demanding honest re-appraisal to restore the place of autopsy in medical education, clinical research, and quality of care assessment for an increasingly elderly population.
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PMID:Age and the declining rate of autopsy. 378


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