The natural history of chronic aortic insufficiency is a continuum marked by a prolonged initial plateau phase during which the patient is relatively stable, and a later phase of progressive deterioration in left ventricular performance. Once the signs and symptoms of heart failure appear, chronic irreversible changes in left ventricular function may have occurred. Since the likelihood of improvement in left ventricular function after aortic valve replacement is less certain once this point has been reached, current practice is to intervene surgically prior to the onset of substantial deterioration of the left ventricle. However, the stable plateau phase may persist for decades and surgery should not be performed too early since that would subject the patient to premature risk from the operative procedure, as well as from complications of the prosthesis itself.
In the present study, we examined the PF and blood eosinophilia in patients with post-CABG EPEs and non-EPEs, and their possible association with PF and blood levels of IL-5, eotaxin-2, eotaxin-3, and VCAM-1. Our main findings were as follows: (1) the percentage and the number of PF eosinophils correlated significantly with the percentage and the number of blood eosinophils, respectively; (2) PF IL-5 levels were significantly higher than the corresponding serum IL-5 levels in every patient with a post-CABG pleural effusion (there was a significant correlation between the PF and serum IL-5 levels), and PF and serum IL-5 levels correlated significantly with the number and the percentage of PF and blood eosinophils, respectively; (3) PF eotaxin-3 levels were significantly higher than the corresponding serum levels, but there was no significant correlation between PF and serum eotaxin-3 levels, with PF eotaxin-3 levels correlating significantly with the number and the percentage of PF eosinophils; (4) PF eotaxin-2 levels were significantly lower than the corresponding serum levels, and there was a significant correlation between the PF levels and the corresponding serum levels, with PF or serum eotaxin-2 levels not differing significantly between patients with EPEs and those with non-EPEs (no correlation between PF eotaxin-2 levels and PF eosinophil levels); and (5) PF VCAM-1 levels were significantly lower than the corresponding serum levels, and there was no significant correlation between PF and serum levels, with PF VCAM-1 levels being significantly higher in EPEs than in non-EPEs, but there was no correlation between PF VCAM-1 levels and PF eosinophil levels.
A department entitled, “Clinical Investigations,” was inaugurated in the July 1968 issue of this journal. That section contained reports of clinical trials structured to evaluate efficacy of diagnostic and therapeutic modalities. As the new editor of Chest then, I was delighted to receive a gracious letter from the distinguished scientist, Dr. Alvan R. Feinstein, who commented about my choice of title. Dr. Feinstein wrote that he was pleased to see that at least one editorial board believed science could be applied to the study of man and that critical scientific methodology need not be limited to laboratory and animal research.
Typoxemia is a common occurrence in patients with asthma, a fact attributed to ventilation-perfusion (Va/Q) inequality secondary to uneven airway narrowing. Recent studies measuring continuous distributions of Va/Q ratios have detected considerable blood flow perfusing areas in the lung which have low Va/Q ratios. Uneven distribution of ventilation is undoubtedly a major factor causing Va/Q inequality in asthma;2 however, changes in the distribution of pulmonary blood flow are important. In some asthmatic subjects, hypoxemia may be aggravated by the administration of aminophylline2 or isoprenaline,2 perhaps because these drugs act by counteracting compensatory pulmonary vasoconstriction. Compensatory pulmonary vasoconstriction in response to alveolar hypoxia redistributes blood flow to match ventilation, thereby minimizing hypoxemia.
Wagner et al, in a study of five asymptomatic asthmatic patients and one acutely ill asthmatic patient, measured continuous Va/Q distributions using the multiple inert gas elimination technique. They found that five subjects had perfusion to abnormally low Va/Q units, which increased five minutes after isoproterenol was administered by aerosol. After 15 minutes more, all the Va/Q distributions had returned to their control states. These results suggest that the isoproterenol counteracted compensatory pulmonary vasoconstriction, resulting in increased perfusion of low Va/Q units. Va/Q distributions were measured after four subjects with broad control Va/Q distributions breathed 100 percent oxygen for 30 minutes. No change in the Va/Q distributions was observed. The feet that 100 percent oxygen did not have the same effect suggests that compensatory pulmonary vasoconstriction may not be hypoxia induced in asthma, but possibly chemically induced by mediator release.
In response to hypoxia, histamine, a powerful vasoconstrictor is released from mast cells clustered primarily around the pulmonary vasculature. Despite this evidence, much uncertainty exists about the role of histamine as a chemical mediator of compensatory pulmonary vasoconstriction.’
The aims of this study were: a) to examine the Va/Q distributions in moderately severe asthmatic subjects using the multiple inert gas elimination technique, b) to assess the presence of hypoxic compensatory pulmonary vasoconstriction by measuring changes to Va/Q distributions after breathing 100 percent oxygen, and c) to test the hypothesis that histamine is a mediator of compensatory pulmonary vasoconstriction in asthmatic subjects. This was done by administering an intravenous antihistamine (clemastine) and measuring any increase in the dispersion of the Va/Q distribution which may be compatible with the counteraction of compensatory pulmonary vasoconstriction.
Bronchogenic carcinoma was confirmed in each case by bronchial biopsy. There were three cases with squamous cell carcinoma, two of adenocarcinoma, and seven of small cell carcinoma (Table 1). In cach case there was agreement between the biopsy diagnosis and the cytologic evaluation of both the DST slides and the SBW slides. Enumeration of the malignant cells on each slide revealed that in each case there were substantially more cells on the SBW smears (30,477 ±44,569 malignant cells/slide, mean±SD) than on the DST smears (3,708±5,972 malignant cells/slide) (p<0.001, Fig 2). The SBW preparation was judged to be of higher quality in seven cases, the DST in one case and in the remaining four cases the quality of the two slides was felt to be equivalent (Table 1).
When suspected tumors are directly visualized at fiberoptic bronchoscopy, we routinely obtain cytologic specimens with a bronchial brush before performing biopsies. Typically, these brush specimens are smeared onto a microscope slide premoistened with fixative and the brush discarded. For the purposes of this study, before the brush was discarded, it was agitated in an SBW vial containing fixative. This material, which would have otherwise been discarded with the brush, was then analyzed for content of cells and quality of cellular preservation. Results were compared with the results of the matched slides prepared using the direct smear technique (DST).
Portable chest roentgenograms are used regularly to provide useful information about chest pathologic findings in critically ill patients. However, several different types of pathologic conditions are commonly missed on the portable chest roentgenogram. A pneumothorax can be very difficult to identify on supine AP x-ray films because the air may disperse widely throughout the pleural space instead of forming focal collections. Although the use of upright positioning can lessen this problem, complete upright positioning is frequently impossible. As is shown in this and earlier reports, the pneumothorax may be loculated within or behind roentgenographically dense structures, making detection with a portable chest roentgenogram very difficult. Often, the only sign of penumothorax on the supine portable chest roentgenogram is the failure to silhouette a mediastinal structure because of air trapped between the mediastinum and other lung pathologic findings. Pleural effusion also can present a diagnostic dilemma, since it may be difficult to detect the presence of fluid and to differentiate between pleural effusion and posterior-basal atelectasis. It also may be difficult to quantify the amount of fluid present, since it may redistribute in the pleura] cavity and appear merely as a thickened pleural space, a thickened major and/or minor fissure, or simply as a uniform increase in the density of the entire lung field.