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Biomedical subjects

Carlo Giuntini

Publications and source records attributed to Carlo Giuntini.

7 recordsLinked to original sources

Survival and restoration of pulmonary perfusion in a long-term follow-up of patients after acute pulmonary embolism.

We followed prospectively 834 consecutive patients (70% inpatients), evaluated for suspected pulmonary embolism, for a median time of 2.1 years (range, 0-4.8 yr), and compared the survival rates in patients with proven pulmonary embolism (n=320) with those without (n=514). In multivariate analysis, we modeled the probability of surviving in patients with pulmonary embolism as a function of the extent of pulmonary vascular obstruction at baseline. Among patients with pulmonary embolism, a scintigraphic follow-up was pursued to assess the restoration of pulmonary perfusion over a 1-year period. We found that massive pulmonary embolism (vascular obstruction>or=50%) is a risk factor for mortality within the first few days after onset but, subsequently, has no significant effect on survival. The adjusted risk of death in patients with massive pulmonary embolism was 8-fold higher than in patients without embolism within the first day after the incident event. By contrast, the adjusted risk of death for patients with minor or moderate pulmonary embolism (vascular obstruction<50%) was no higher than in patients without embolism at any time after onset. Most of the patients who survived a year after pulmonary embolism showed a nearly complete restoration of pulmonary perfusion with a considerable improvement in arterial oxygenation. Four (1%) of the 320 patients with pulmonary embolism at presentation developed chronic thromboembolic pulmonary hypertension. These patients featured persistent large perfusion defects in sequential lung scans. Pulmonary embolism with vascular obstruction>or=50% is a strong, independent predictor of reduced short-term survival. This underscores the need for a prompt diagnosis of the disease. Monitoring the resolution of pulmonary embolism by lung scanning may prove useful in identifying patients with persistent perfusion abnormalities who may be at risk of chronic thromboembolic pulmonary hypertension.

Adolescent↗

Spirometrically gated high-resolution CT findings in COPD: lung attenuation vs lung function and dyspnea severity.

STUDY OBJECTIVES: The aim of this study was to investigate the relationship between high-resolution CT (HRCT) lung attenuation measurements, acquired under spirometric control of inspiratory and expiratory lung volume, and pulmonary dysfunction as well as dyspnea severity in patients with COPD. PATIENTS AND DESIGN: In 51 patients with COPD, we compared by linear regression, univariate and multivariate logistic regression airflow limitation (FEV(1)/vital capacity [VC]), hyperinflation (percentage of predicted residual volume [RV%]), parenchymal loss (percentage of predicted diffusing capacity of the lung for carbon monoxide [Dlco%]), and Medical Research Council (MRC) dyspnea scale with relative area with attenuation values < - 950 HU at 90% of VC [RAI(950)] and < - 910 HU at 10% of VC, respectively, and with mean lung attenuation measured at the same levels of VC (mean CT lung density at 10% of VC, and mean CT lung density at 90% of VC [MeanCTEXP]). RESULTS: All HRCT attenuation measurements were significantly related with functional abnormalities and dyspnea severity. In multivariate logistic models, with 1 indicating worse changes in dichotomous outcome variables, MeanCTEXP independently predicted FEV(1)/VC (odds ratio [OR], 0.24; 95% confidence interval [CI], 0.11 to 0.56), RV% (OR, 0.57; 95% CI, 0.42 to 0.77), and MRC dyspnea scale (OR, 0.63; 95% CI, 0.48 to 0.82), while RAI(950) independently predicted Dlco% (OR, 1.90; 95% CI, 1.37 to 2.65). CONCLUSIONS: Spirometrically gated measurements of HRCT lung attenuation reflect differently functional changes and dyspnea perception in COPD. Inspiratory measurements assess the extent of emphysematous tissue loss, and expiratory measurements may reflect airflow limitation and lung hyperinflation with attendant dyspnea perception. Pulmonary dysfunction in COPD cannot be assessed by a single modality of lung attenuation measurement.

Adult↗

Elective surgery for giant bullous emphysema: a 5-year clinical and functional follow-up.

BACKGROUND: So far, very few studies in the literature have reported data on the long-term follow-up of patients who have undergone surgery for giant bullous emphysema (GBE), and much still needs to be known on the late fate of these patients. AIMS: To evaluate patients who have undergone elective surgery due to GBE, early and late mortality following surgery, the early and late reappearance of bullae, and the early and late modifications of clinical and functional data. SUBJECTS AND METHODS: Forty-one consecutive patients (36 men; mean [+/- SD] age, 48.4 +/- 14.8 years) who underwent elective surgery for GBE were enrolled in a prospective study, and were studied both before and after undergoing bullectomy for a 5-year-follow-up period. Analyses were performed on the whole population and on two subgroups of patients who were divided on the basis of the absence of underlying diffuse emphysema (group A; n = 23) or the presence of underlying diffuse emphysema (group B; n = 18). RESULTS: The early mortality rate was 7.3% (within the first year), and the late mortality rate was 4.9% (overall mortality rate at 5 years, 12.2%; mortality rate in group B, 27.8%). Bullae did not reappear and residual bullae did not become enlarged in any patients at the site of the bullectomy. During the follow-up, the dyspnea score was reduced significantly soon after bullectomy and up to the fourth year of follow-up; intrathoracic gas volume also was reduced significantly (average, 0.7 L). The same was true for the FEV1 percent predicted and the FEV1/vital capacity ratio, which kept increasing until the second year; then, from the third year of follow-up these values were reduced, yet remained above the prebullectomy values until the fifth year of follow-up. When considered separately, the patients in group B appeared to be the most impaired, clinically and functionally (eg, FEV1 showed a similar significant increase up to the second year in both groups after surgery, while a different mean annual decrease was appreciable from the second to the fifth year of follow-up: group A, 25 mL/year; group B, 83 mL/year. Furthermore, patients in group B were the only ones who contributed to the mortality rate, on the whole showing a behavior similar to that of patients who had undergone lung volume reduction surgery. CONCLUSIONS: In patients with GBE who were enrolled in the study prospectively and were investigated yearly during a 5-year-follow-up period, elective surgery appears to have been fairly safe, and allowed clinical and functional improvement for at least 5 years. Better results may be expected in patients without underlying diffuse emphysema.

Adult↗

Pulmonary embolism: lung scan and computed tomography.

The diagnosis of pulmonary embolism may be confounded by a clinical presentation that is often subtle or atypical. Therefore pulmonary angiography, although invasive, has been widely used to prove pulmonary embolism. The aim of this review is to discuss the value of non-invasive techniques, such as lung scan and chest computed tomography scan, in the diagnosis of pulmonary embolism. Ventilation-perfusion scan has demonstrated a very high specificity (97%) but a quite low sensitivity (41%) in the diagnosis of pulmonary embolism, while perfusion lung scan not associated with ventilation scan has shown a specificity of 92% and a considerably high sensitivity (87%). The chest computed tomography scan has not yet shown a definite degree of specificity and sensitivity in the diagnosis of pulmonary embolism, although we suppose that this technique will become widely used. However, we emphasize that the diagnosis of pulmonary embolism is not a mere technical problem.

Humans↗

Cigarette smoke extract induces oxidative stress and apoptosis in human lung fibroblasts.

Cigarette smoke is a mixture of chemicals having direct and/or indirect toxic effects on different lung cells. We investigated the effect of cigarette smoke on human lung fibroblasts (HFL-1) oxidation and apoptosis. Cells were exposed to various concentrations (1, 5, and 10%) of cigarette smoke extract (CSE) for 3 h, and oxidative stress and apoptosis were assessed by fluorescence-activated cell sorting and confocal laser fluorescence microscopy. Both oxidative stress and apoptosis exhibited a dose-response relationship with CSE concentrations. Lung fibroblasts also showed marked DNA fragmentation at the Comet assay after exposure to 10% CSE. Coincubation of HLF-1 cells with N-acetylcysteine (1 mM) during CSE exposure significantly reduced oxidative stress, apoptosis, and DNA fragmentation, whereas preincubation (3 h) with the glutathione-depleting agent buthionine sulfoximine (125 microM) produced a significant increase of oxidative stress. Cigarette smoke is a potent source of oxidative stress, DNA damage, and apoptosis for HFL-1 cells, and we speculate that this could contribute to the development of pulmonary emphysema in the lungs of smokers.

Acetylcysteine↗