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Query: UMLS:C0034067 (emphysema)
11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In men 40 or more years of age at death, the upper limits of normal (means plus 2 SD) cardiac ventricular weights were 69 g for the right ventricle and 203 g for the left ventricle plus septum. Right ventricular thickness, as usually determined at autopsy, was a relatively poor index of hypertrophy. When one ventricle hypertrophies as a result of stress, the other tends to enlarge simultaneously, even if no stress on it has been evident. Right ventricular weight correlated positively, although not strongly, with severity of emphysema and with the severity of clinical chronic airway obstruction. Correlations between right ventricular weight and pathologic changes in the airways were weak or absent, except that subjects with abnormal large airways, but normal small airways, showed improved correlation between severity of emphysema and right ventricular hypertrophy, compared with the entire series. There was no correlation between left ventricular weight and severity of emphysema. The electrocardiogram was very reliable in the diagnosis of right ventricular hypertrophy (corpulmonale) due to chronic airway obstruction; the chest roentgenogram was somewhat less sensitive in this regard.
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PMID:The right ventricle in chronic airway obstruction: a clinicopathologic study. 13 85

Studies have been carried out to determine the possible physiological effects of contact with carbon black made by the thermal process. Contact was made by ingestion, skin application and/or inhalation. Ingestion and/or skin application do not appear to lead to any changes from the normal. Inhalation exposures do not produce pulmonary function changes (antemortem or postmortem studies) but may lead to moderate to severe "perifocal" emphysema in Rhesus monkeys (not observed in guinea pigs). Inhalation studies also suggest right ventricular septal and to a degree, left ventricular hypertrophy in Rhesus monkeys as an effect. Additional studies are necessary to support these finding and consideration must be given to the variability among exposed subjects as compared to controls.
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PMID:Properties and physiological effects of thermal carbon black. 13 3

A clinicopathological study of 21 patients who died as a result of chronic airways obstruction was carried out. Thirteen patients had been in right ventricular failure for at least one year before death and the other eight patients did not have right ventricular failure. The patients with long-standing right ventricular failure died at a younger age, on average, than those without failure. There were no significant quantitative differences between the two groups in the length of history of chest disease, blood gas estimations, respiratory function tests or degree of polycythaemia. The group with right ventricular failure had significantly larger mean right and left ventricular weights than the group without failure, but there were no significant differences in amounts of emphysema, size of bronchial mucous glands, proportion of small airways lumen in the lung or number of thick-walled peripheral lung vessels between the two groups. The findings did not support the division of this series of patients, with fatal chronic airways obstruction, into two distinct groups broadly defined as 'emphysematous' and 'bronchitic', either clinically or pathologically. A history of right ventricular failure correlated well with the finding of right ventricular hypertrophy at necropsy. Electrocardiographic evidence of right ventricular hypertrophy was found to correspond with the size of the right ventricle at necropsy in 66% of cases. The radiographic diagnosis of emphysema proved an accurate assessment when compared to the necropsy findings, and radiographic estimations of right ventricular enlargement were accurate in 65% of cases. Histological evidence of acute bronchitis was present in 20 of the 21 patients (95%), and five patients showed histological evidence of minor pulmonary thromboembolism. Ten patients in the series showed an increase in the weight of the left ventricular as well as the right ventricle.
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PMID:A clinicopathological study of fatal chronic airways obstruction. 13 10

The accuracy of interobserver variability of roentgenographic analysis for cardiac size in patients dying with chronic bronchitis and pulmonary emphysema were correlated with pathologic data derived from special studies. Three trained observers were able to accurately and consistently diagnose chronic bronchitis and pulmonary emphysema and to detect cardiomegaly on the chest x-ray film. The best criteria for chronic bronchitis and pulmonary emphysema were those of overinflation; however, none of the roentgenographic criteria usually suggested for the specific diagnosis of right ventricular or left ventricular hypertrophy were found to be reliable. The inaccuracy and interobserver variability in the detection of enlargement of specific chambers make it evident that the usual criteria are not valid and that roentgenographic appraisal of cardiac size in these patients in limited to findings of normalcy or cardiomegaly.
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PMID:Evaluation of cardiac size in chronic bronchitis and pulmonary emphysema. 14 Jul 89

Left ventricular function was evaluated prospectively during 1 year in a controlled clinical study of 73 patients with chronic obstructive lung disease. The control group comprised 68 patients matched for age and sex and with no evidence of airways obstruction. Left ventricular hypertrophy was found in 52% and systemic hypertension in 58% of patients in the study group compared with 6% and 15% respectively in the controls. Left ventricular hypertrophy was diagnosed in 70% of patients with chronic bronchitis and in 19% of those with chronic emphysema. Systemic hypertension was observed in 45% of the bronchitic type patients and in 81% of those with emphysema. The incidence of myocardial infarction in the study group was not lower than in the controls. The high frequency of left ventricular hypertrophy in patients with chronic obstructive lung disease can probably be related to a similar high frequency of systemic hypertension. Hypertension per se does not explain left ventricular hypertrophy in all patients with chronic bronchitis, but hypoxemia and acidosis seem to be of pathogenetic importance in these cases.
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PMID:Systemic hypertension, left ventricular hypertrophy and myocardial infarction in patients with chronic obstructive lung disease. 14 14

Reproducibility of the AVA program (version 3.5) was tested (1) by analyzing the same analog tracing 10 times in 150 patients, and (2) by studying the influence of 12 different sets of prior probabilities (PRP), using the digital data from a total of 2718 patients. The same QRS-T diagnosis plus or minus 8 percentage points was found in patients with high posterior probabilities. Variability for the P wave diagnosis was twice as high as for QRS-T results. Failure to select the appropriate set of PrP markedly influenced reproducibility. This was especially true for right ventricular hypertrophy and pulmonary emphysema. 'Mispriorizing' in a subgroup of 199 patients with well-documented myocardial infarction lowered the total number of correct ECG diagnoses on the average between 4.8 and 35%. These results are inherent to Bayes' theorem where PrP are used to achieve minimum assignment error in populations, but where Prp errors may result in wide classification discrepancies. Without errors in PrP reproducibility by the VA program was found to be very high.
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PMID:Reproducibility of diagnostic results by a multivariate computer ECG analysis program (AVA 3.5). 33 6

Left heart diseases, in particular mitral stenosis, are often associated with anatomic and functional alterations of the lung. According to the pulmonary structures involved they could be named chronic secondary intersticial and vascular lung diseases. Congenital heart diseases with pre- or post-tricuspid shunts are also often associated with anatomic and functional alterations of the lung. This condition also constitutes a chronic secondary vascular lung disease (atrial septal defect) or a chronic primary vascular lung disease ( ventricular septal defect, patent ductus arteriosus). Primary lung diseases (interstitial pulmonary fibrosis, pulmonary emphysema, recurrent pulmonary embolism) are often associated with right ventricular hypertrophy with or without dilation, a condition commonly named chronic cor pulmonale. On the whole the interrelationships between heart and lung diseases are as follows: a) anatomic and functional alterations of the lung due to left heart diseases are mediated through pulmonary venous hypertension; b) anatomic and functional alterations of the lung due to congenital heart diseases are mediated through the increased pulmonary blood flow with or without transmission of the systemic blood pressure to the pulmonary vasculature, and c) anatomic and functional alterations of the right ventricle due to primary or secondary lung diseases are mediated through arterial pulmonary hypertension. In summary, the interrelationships between heart and lung diseases are mainly mediated through the pulmonary venous or pulmonary arterial hypertension.
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PMID:Cardiac and pulmonary diseases. A pathophysiologic interelationship. 113 Sep 7

Changes in pulmonary hemodynamics and vascular reactivity in emphysematous hamsters were studied in an isolated lung preparation perfused at constant flow with blood and 3% dextran. Hamsters were treated with intratracheal porcine pancreatic elastase at 70 days of age, and experimental studies were conducted at 1, 3, and 8 mo after treatment. Baseline pulmonary arterial pressure in elastase-treated lungs was increased compared with saline-treated control lungs 1 mo after treatment, but this increase did not progress at 3 and 8 mo. Increases in pulmonary arterial pressure in elastase-treated lungs were temporally correlated with the morphological development of emphysema and right ventricular hypertrophy; both of these were evident at 1 mo after treatment and showed little change thereafter. Pressor responses to hypoxia and angiotensin II were not different between elastase-treated and control lungs at 1 and 3 mo. At 8 mo, however, pressor responses in emphysematous lungs to 0% O2 (but not to angiotensin II) were significantly increased. This was the result of a lack of the normal age-related fall in the hypoxic pressor response. Our results suggest that the right ventricular hypertrophy found in these emphysematous animals results from a chronically increased pulmonary vascular resistance. Furthermore, increases in pulmonary vascular resistance in the early development of emphysema are likely a result of the loss of vascular beds and supporting connective tissue.
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PMID:Pulmonary vascular reactivity and hemodynamic changes in elastase-induced emphysema in hamsters. 144 93

The causes for the development of right ventricular hypertrophy (RVH) in emphysema are not fully understood. In the 1960s, studies of RVH in association with emphysema found no correlation between the extent of tissue damage in the lung and the RV weight. This was thought to disprove the theory that the RVH was due to an increase in pulmonary vascular resistance secondary to capillary destruction. In the present study, the development of RVH was investigated in tight-skin (tsk) mice with genetic emphysema. RVH started to develop in mature to senescent animals between 8 and 16 months of age and progressed thereafter. At 24 months of age, RV weight and the ratios RV/body weight and RV/LV + S weight were, respectively, 52, 96, and 60% greater than in control (pa) mice. At this time blood gas analysis revealed hypoxemia in tsk but not in pa mice. The mean linear intercept of tsk mice was 83% larger and the surface area of the walls of distal air spaces per unit lung volume was 40% smaller than in pa mice. There was a strong correlation between the severity of emphysema, assessed by both techniques, and the RV/LV + S ratio (p less than 0.001 for both). No muscularized arterioles were seen in the tsk mice, and the medial thickness of muscular arteries was almost identical in the two groups. This demonstrates that in emphysema, RVH can develop in the absence of pulmonary vascular changes and is probably due to tissue (and thus capillary) destruction.
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PMID:Tsk mice with genetic emphysema. Right ventricular hypertrophy occurs without hypertrophy of muscular pulmonary arteries or muscularization of arterioles. 214 63

The relationship between the thickness of the walls of small pulmonary arteries (the medial wall thickness as a percentage of external diameter, percentage of medial thickness) in coal miners and control subjects were studied using morphometric techniques and correlated with the degree of right ventricular hypertrophy, severity of coal workers' pneumoconiosis, emphysema, and other chronic lung diseases. Pulmonary arteries less than 100 microns in external diameter were identified and the external diameter, medial thickness, and intimal thickness were quantitatively measured in the lung tissues of 57 coal miners and 15 control subjects with and without other chronic lung diseases. Coal workers' pneumoconiosis, emphysema, and right ventricular hypertrophy were assessed uniformly in all cases. The arterial wall thickness correlated with right ventricular hypertrophy, progressive massive fibrosis, and other chronic lung diseases. Severity of emphysema also showed a weak correlation. Although the functional significance of these findings is not known, we conclude that the muscularization of pulmonary arterioles provides a structural basis for the development of right ventricular hypertrophy in coal miners.
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PMID:Pulmonary arteriolar muscularization in coal workers' pneumoconiosis and its correlation with right ventricular hypertrophy. 214 19


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