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Reactive pulmonary artery vasoconstriction in pulmonary consolidation evaluated by color Doppler ultrasonography.

A total of 122 patients with pulmonary consolidation on chest radiographs underwent color Doppler ultrasonography to evaluate hemodynamic change in regional pulmonary artery in pulmonary consolidation due to various causes. The diseases underlying pulmonary consolidation included 66 simple pneumonia, 37 obstructive pneumonia, 13 tumor consolidation and 6 pulmonary infarctions. Blood flow signals in consolidation were detected by color-flow mapping. The degree of reactive vasoconstriction was evaluated from analysis of the spectral waveform of the blood flow in the segmental pulmonary artery by several vessel resistance-indicating Doppler ultrasound (US) indices, including pulsativity index (PI), resistive index (RI), and acceleration time (AT). The results showed that reactive vasoconstriction was most marked in obstructive pneumonia, followed by simple pneumonia, and least in tumor consolidation (p < 0.001, Kruskal-Wallis test and p < 0.001, Dunn's test for comparison of PI, RI and AT values between different groups of pulmonary consolidation). No flow was detected in pulmonary infarction. We conclude that color Doppler US is a useful tool for evaluating reactive vasoconstriction in pulmonary consolidation. The different degrees of reactive vasoconstriction may be helpful in exploring the possible etiology of pulmonary consolidation.

Blood Flow Velocity↗

Effect of nasal continuous positive airway pressure on pulmonary edema complicating acute myocardial infarction.

Cardiogenic pulmonary edema is a frequent cause of reparatory failure. We investigated the effects of nasal continuous positive airway pressure (CPAP) in patients with severe pulmonary edema associated with acute myocardial infarction. Twenty-nine consecutive patients were divided into 3 groups: firstly, 7 intubated patients who received mechanical ventilation at study entry comprised the intubation group. The rest of the patients were randomly assigned to either of the following 2 groups: 11 patients who received oxygen plus CPAP delivered by a nasal mask (CPAP group), and 11 patients who received oxygen only via face mask (oxygen group). All patients in the intubation group had cardiogenic shock. Two patients (18%) in the CPAP group and 8 patients (73%) in the oxygen group required mechanical ventilation with endotracheal intubation (p=0.03). The hospital mortality rate in the CPAP group (9%) was significantly lower than the oxygen group (64%, p=0.02). The pulmonary artery wedge pressure and heart rate were significantly lower in the CPAP group than in the oxygen group 24 h after study entry (p<0.05 and p<0.01). The mean pulmonary artery pressure 48 h after study entry was 18+/-5 mmHg in the CPAP group and 25+/-8 mmHg in the oxygen group (p<0.05). The PaO2/FiO2 ratio increased in the intubation group (168+/-69 to 240+/-57, p<0.05) and the CPAP group (137+/-17 to 253+/-67, p<0.01) 24 h after study entry. Arterial plasma endothelin-1 concentrations decreased significantly earlier in the CPAP group than in the oxygen group (p<0.05). In patients without cardiogenic shock, nasal CPAP lead to an early improvement in oxygenation and hemodynamics, and decreased the mortality rate. Early and active respiratory management is recommended in patients with pulmonary edema associated with acute myocardial infarction.

Aged↗

Ongoing role of pulmonary embolectomy.

Pulmonary embolism remains a frequent and often fatal disorder. For the majority of patients, anticoagulation with heparin followed by warfarin represents the primary mode of treatment. Thrombolytic therapy is recommended for the patient with massive pulmonary embolism that has produced hypotension. Embolectomy is reserved for the patient with post embolic systemic hypotension who has an absolute contraindication to thrombolysis or who deteriorates despite thrombolytic therapy. Following successful embolectomy the surgeon must treat the complications of the surgery and prevent recurrence. Complications include cerebral infarction, pulmonary infarction and endobronchial hemorrhage, right ventricular failure, local or systemic bleeding and venous stasis. A case of successful pulmonary embolectomy with a complicated postoperative course is presented and the pathophysiology and treatment of the complications are discussed.

Adrenal Gland Diseases↗

The spectrum of pulmonary embolism. Clinicopathologic correlations.

Pulmonary embolism (PE) is still underdiagnosed even in hospitalized patients. In our recent experience, out of 92 postmortem cases of massive or submassive PE, only 28% were diagnosed before death, whereas the false-positives accounted only for 3% of cases. Similar conclusions have been drawn from large-scale autopsy studies performed in Norway and in the United States. The most important causes of an incorrect diagnosis are failure to suspect PE, and the protean nature of the disease. Remarkable differences actually exist concerning the point of origin and the final localization, as well as the size and age of thromboemboli, the presence or absence of pulmonary infarction, and the underlying pathology. Often a fatal embolus is relatively small but hardly tolerated because of the underlying cardiopulmonary situation. Attention should be called to the frequent autopsy finding of multiple PEs and pulmonary infarctions of apparently different age. This finding is important since it indicates that these patients suffered successive embolizations and the eventual death might have been prevented if an early diagnosis had been made.

Humans↗

Radiographic features of pleural effusions in pulmonary embolism.

A prospective analysis of 155 patients with pulmonary embolism was undertaken to describe the radiographic characteristics of associated pleural effusions and related abnormalities. Approximately one half of these patients had pleural effusions. Patients with other potential causes of effusion, such as heart failure, pneumonia, or cancer, were eliminated from further analysis. In the remaining 62 patients, radiographic evidence of pulmonary infarction accompanied pleural effusions in one half of the cases. One third of patients with parenchymal consolidation had no evidence of effusion. Atelectasis and other nonspecific radiographic abnormalities occurred in less than one fifth of the cases. Typically, pleural effusions were small and unilateral, appeared soon after symptoms of thromboembolism began, and tended to reach their maximal size very early in the course of the disorder. Pulmonary infarction was associated with larger effusions that cleared more slowly and were more often bloody in appearance on thoracentesis. Chest pain occurred in all but one patient and was a valuable diagnostic clue. Pain and pleural effusions were always ipsilateral and almost always unilateral, but neither correlated well with the presence or time course of infarction. Effusions that were delayed in onset or that enlarged late in the course were associated with recurrent pulmonary embolism or superinfection. These radiographic features may be helpful in the diagnosis and management of pulmonary embolism.

Adult↗

[Surgical resection of cardiac metastasis of thyroid cancer--a case report].

A case of metastasis of thyroid cancer into the cardiac cavity is described. A 73-year-old female suffered from sudden chest pain, dyspnea and dizziness and admitted to a local clinic on emergency. A diagnosis of bilateral multiple pulmonary infarction was made by lung perfusion scintigraphy. However, a mass migrating between the right atrium and the right ventricle across the tricuspid valve was demonstrated by echocardiography, and the patient was referred to us under a diagnosis of myxoma complicated with pulmonary infarction. Incision of the right atrium disclosed a gelatinous mass resembling frog eggs, attached to the right ventricle side of the anterior cusp of the tricuspid valve and swinging across the orifice of the valve. The gross lesion was removed completely. Since the histological diagnosis was clear cell carcinoma, no surgery was performed on the pulmonary artery. Postoperative re-examination by ultrasonography and CT revealed thyroid cancer as the primary lesion.

Adenocarcinoma↗

Comparative effects of tissue plasminogen activator, streptokinase, and staphylokinase on cerebral ischemic infarction and pulmonary clot lysis in hamster models.

BACKGROUND: The effects of alteplase (rtPA), streptokinase, and staphylokinase (rSak) on focal cerebral ischemia (FCI) and on pulmonary clot lysis (PCL) were studied in hamsters. METHODS AND RESULTS: ++FCI was produced by ligation of the left middle cerebral artery (MCA) and common carotid artery (CCA) and a 10-minute occlusion of the right CCA. FCI was measured after 24 hours by 2,3, 5-triphenyltetrazolium chloride staining. (125)I-fibrin-labeled plasma clots were injected via the jugular vein, and clot lysis was determined from residual radioactivity at 90 minutes. Study drugs were given intravenously over 60 minutes. FCI increased from 1.2 (0. 27 to 2.3) mm(3) (median and 17th to 83rd percentile range, n=24) in controls to 19 to 27 mm(3) with thrombolytic agent, with maximal rates at 0.13+/-0.05 mg/kg rtPA, 0.23+/-0.09 mg/kg streptokinase, and 0.037+/-0.025 mg/kg rSak. PCL increased from 18+/-2% (mean+/-SEM, n=27) in controls to approximately 85% with thrombolytics, with maximal rates at 0.12+/-0.03 mg/kg rtPA, 0.17+/-0.05 mg/kg streptokinase, and 0.018+/-0.002 mg/kg rSak. All agents caused maximal FCI and PCL rates at similar doses without alpha(2)-antiplasmin and fibrinogen depletion. Injection of 6 mg/kg human plasminogen combined with streptokinase caused a "systemic fibrinolytic state" with fibrinogen depletion. Maximal rates of FCI were obtained with 0.097+/-0.077 mg/kg streptokinase (P=0.26 versus streptokinase alone) and of PCL with 0.010+/-0.002 mg/kg (P=0.006 versus streptokinase alone). CONCLUSIONS: Thrombolytic agents cause similar dose-related extension of FCI after MCA ligation and PCL, irrespective of the agent or systemic plasmin generation.

Animals↗

Studies on the occurrence of circulating immune complexes in vascular diseases.

The presence of circulating immune complexes was studied in 347 samples of serum from 212 patients with various vascular diseases. Two quantitative methods (complement-consumption assay and C1q-solubility test) were used for the measurement of the concentration of the complexes. Immune complexes were detected in each group of patients tested (coronary arteriosclerosis, myocardial infarction, cerebral artery sclerosis, arteriosclerosis obliterans, phlebothrombosis, pulmonary infarction). A high proportion of positivity was recorded in myocardial infarction (in 43 patients out of the 94 tested) and in arteriosclerosis obliterans (7 out of 11 cases). The possible pathogenic role of the circulating immune complexes is discussed.

Aged↗

A way to select on clinical grounds patients with high risk for pulmonary embolism: a retrospective analysis in a nested case-control study.

We studied 196 patients with suspicion of pulmonary embolism (PE), subsequently confirmed in 98 by positive pulmonary angiography and excluded in 98 by normal or near-normal perfusion lung scan. Patients had a clinical questionnaire for history, and, soon after. a radiograph, blood gas analysis, and an ECG. Clinical and instrumental signs were matched in patients with confirmed and unconfirmed PE to find those more frequent in embolic patients and, thus, more characteristic of PE. The following were: previous PE, immobilization and thrombophlebitis (p < 0.05); dyspnea and cough (p < 0.05); enlarged descending pulmonary artery (DPA), enlarged right heart, pulmonary infarction, Westermark sign (p < 0.001), and elevated diaphragm (p < 0.05); hypoxemia. No ECG sign was more frequent in PE. Thereafter, all variables were processed separately with a logistic multiple regression analysis and those significantly associated to PE were tested in a final logistic model that was able to predict the actual result of angiography or scintigraphy; accordingly, previous PE, immobilization, thrombophlebitis, enlarged DPA, pulmonary infarction, Westermark sign, hypoxemia were significantly associated with a high risk of PE (from 2.8 to 15 times greater than in patients without these signs). Therefore, we may conclude that clinical assessment and noninvasive tests may help to detect patients at higher risk for PE where heparin coverage should be started while waiting for conclusive diagnostic procedures.

Adult↗

Surgical treatment of cardiac myxoma and its complications.

A total of 20 patients (15 women, five men) were operated on for cardiac myxoma. Their ages ranged from 17 to 74 (mean 56) years. Myxoma was located in the left atrium in 18 patients and in the right in two. Systemic embolism occurred in eight patients, causing cerebral infarction in three, ischaemia of the extremities in two, occlusion of the external carotid artery with cerebral infarction in one, myocardial infarction in one and pulmonary infarction in one. Five patients with severe congestive heart failure required emergency surgery. All myxomas were removed using cardiopulmonary bypass with excision of the attachment walls. Details are given of additional surgery performed on some of the patients. Two patients died, one from pulmonary insufficiency after emergency surgery and the other from an unrelated problem. The remaining 18 patients showed a good recovery and are doing well with no intracardiac recurrence, although one with cerebral infarction underwent clipping of an aneurysm, which was detected later in the infarcted area.

Adolescent↗

Association of clinical manifestations with HLA-B alleles in Takayasu arteritis.

HLA-DNA typing using PCR-SSOP and PCR-DCP methods was performed in 85 patients with Takayasu arteritis and 492 healthy controls who had been typed for HLA by serological method. Frequencies of HLA-B52 (B*5201) and B39 (B*3901 and B*3902) were significantly increased in the patients. Frequency of HLA-DRB1*1502 was also increased but it was suggested to be a reflection of its linkage disequilibrium with B52. Association of HLA-B52 and B39 with seven clinical manifestations--pulmonary infarction, ischemic heart disease, aortic regurgitation, systemic hypertension, renal artery stenosis, cerebrovascular disease, and visual disturbance--in 132 HLA-typed patients with Takayasu arteritis was studied. In HLA-B52 positive TA patients, aortic regurgitation (vs B52(-)-B39(+), OR=3.8, P<0.05, vs B52(-)-B39(-), OR=5.49, P<0.001), ischemic heart disease (vs B52(-)-B39(+), OR=12.05, P<0.05, vs B52(-)-B39(-), OR=2.85, P<0.05), and pulmonary infarction (vs B52(-)-B39(+), OR=5.74, P<0.03) were found to be significantly prevalent. On the other hand, in HLA-B39 positive TA patients, frequency of renal artery stenosis was significantly increased (vs B52(+)-B39(-), OR=12.14, P<0.001, vs B52(-)-B39(-), OR=5.21, P<0.03). These observations have suggested that HLA-B52 molecule and B39 molecule would contribute to different clinical manifestations by binding different antigenic peptides to cause inflammations. Thus HLA-B molecule may play an important role in pathogenesis or determining clinical manifestations of Takayasu arteritis.

Alleles↗

"False negatives" and "false positives" in acute pulmonary embolism: a clinical-postmortem comparison.

Although recent advances have been made in understanding its epidemiology, diagnosis and treatment, pulmonary embolism (PE) is still largely undetected and untreated, and the mortality rate has not appreciably changed in the last decades. The aim of this study was to: compare the postmortem frequency of massive and sub-massive PE during two different time periods in the same general hospital; ascertain whether the percentage of correct clinical diagnosis of PE has changed; identify factors which might contribute to the inaccuracy of the clinical diagnosis of PE. Altogether, 288 patients with autopsy-proven PE and adequate clinical data were collected in the first period; 182 subjects with the same characteristics were found in the second period. Cases observed from 1989 through 1994 were evaluated in terms of frequency of false negatives and false positives, predictive value of the clinical diagnosis of PE, and correlations between clinical and post-mortem diagnosis of PE on one side and several independent variables such as age, gender, associated diseases, recent surgery on the other. In our hospital the frequency of massive and submassive PE at autopsy was 8.6% from 1966 through 1974, 12.6% from 1989 through 1994 (p < 0.01). The percentage of correct clinical diagnosis of PE was 19.6% in the former period, 21.6% in the latter (NS) with 78.57% of false negatives and only 1.73% of false positives. Altogether the true positives were 21.42%, most of them being patients with massive PE. Clinical findings showed the coexistence of heart disease in 51.6% of the cases, congestive heart failure in 20.15%, metabolic disease in 7%, stroke in 12.5%, recent surgery in 12.5%. Autopsy revealed the presence of pulmonary infarction in 22% of cases, malignancy in 24.0%, pneumonia in 17.05%, acute myocardial infarction in 14.8%. Seventy percent of the cases in whom the point of origin of thromboemboli could be demonstrated had one or more thrombus in the district of inferior vena cava, more frequently at the level of the femoral and iliac veins. The positive predictive value of the clinical diagnosis of PE was 0.60, the negative predictive value 0.84. Multivariate logistic regression analysis showed that the clinical diagnosis of PE was hindered by the presence of pneumonia, facilitated by admission to the Cardiological Department. Age, duration of hospitalization, presence of pulmonary infarction, cancer, obesity, stroke, heart failure and recent surgery did not influence the clinical diagnosis of PE in this series. A positive correlation (p < 0.05) was found between autopsy rate and the percentage of correct clinical diagnosis of PE in the various hospital departments. This relationship needs further investigation, all the more so as in most countries the autopsy rate has been dramatically declining in recent times, especially in late life. In conclusion, at least in some institutions, the autopsy frequency of PE has increased during the last decades, and this increase has not been paralleled by a significant improvement in clinical diagnosis.

Acute Disease↗