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

One female patient--with slight pure mitral stenosis, mild hypertension and ischemic cardiomyopathy and disabling pulmonary emphysema--developed at 54 years of age permanent atrial fibrillation, had a gratuitous mitral commissurotomy four months later, sustained chronic fibrillation for 13 years, then spontaneously resumed sinus node command at age 67 without any discernible reason. Sinus rhythm was being maintained at follow-up nine months later. Her cardiac status of fair compensation under modest digitoxin and diuretic therapy has neither improved nor worsened with the return of atrial systole. The duration, in this observation, of permanent auricular fibrillation before spontaneous return of sinus rhythm, is one of the longest ever published, exceeded, to the best of my knowledge, only by one case of Lewis and by another one of Reeve and associates. Such an exceptional event points out a fascinating enigma: how can major longstanding atrial dysrhythmias (fibrillation, flutter), whose causes and pathogenesis seem at least partly elucidated, spontaneously disappeer in atria so badly diseased? I think we must humbly confess that no satisfactory explanation is at present available for this disconcerting phenomenon.
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PMID:Spontaneous resumption of sinus rhythm in an elderly patient after 13 years of permanent atrial fibrillation. 47 82

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

Pulmonary capillaries have extremely thin walls to allow rapid exchange of respiratory gases across them. Recently it has been shown that the wall stresses become very large when the capillary pressure is raised, and in anaesthetised rabbits, ultrastructural damage to the walls is seen at pressures of 40 mm Hg and above. The changes include breaks in the capillary endothelial layer, alveolar epithelial layer, and sometimes all layers of the wall. The strength of the thin part of the capillary wall can be attributed to the type IV collagen in the extracellular matrix. Stress failure of pulmonary capillaries results in a high-permeability form of oedema, or even frank haemorrhage, and is apparently the mechanism of neurogenic pulmonary oedema and high-altitude pulmonary oedema. It also explains the exercise-induced pulmonary haemorrhage that occurs in all racehorses. Several features of mitral stenosis are consistent with stress failure. Overinflation of the lung also leads to stress failure, a common cause of increased capillary permeability in the intensive care environment. Stress failure also occurs if the type IV collagen of the capillary wall is weakened by autoantibodies as in Goodpasture's syndrome. Neutrophil elastase degrades type IV collagen and this may be the starting point of the breakdown of alveolar walls that is characteristic of emphysema. Stress failure of pulmonary capillaries is a hitherto overlooked and potentially important factor in lung and heart disease.
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PMID:Stress failure of pulmonary capillaries: role in lung and heart disease. 809 42

The diastolic rumbling murmur of mitral stenosis (MS) may be attenuated in the presence of low cardiac output, right ventricular enlargement, Lutembacher's syndrome, pulmonary emphysema, and obesity. In this report we would like to stress that the presence of tricuspid stenosis (TS) is an additional significant cause of silent MS. The clinical material consisted of 73 patients with rheumatic TS who had undergone cardiac surgery. Five of these cases had clinical findings of TS without auscultatory findings of MS. They were found to have severe MS at the time of operation and to require mitral valve surgery. At cardiac catheterization the mean diastolic gradient (MDG) across the mitral valve (MV) was less than 3 mmHg and pulmonary arterial systolic pressure was 29-42 mmHg. The MDG across the tricuspid valve was 6-17 mmHg. In conclusion, TS can mask clinical and hemodynamic findings of MS. The reason for this is the mechanical barrier imposed by TS proximal to the MV.
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PMID:Severe tricuspid valve stenosis. A cause of silent mitral stenosis. 664 50

Asthma is often triggered by allergic and nonallergic factors in atopic individuals and readily responds to anti-inflammatory and bronchodilator therapy. The differential diagnosis for poorly responsive disease includes severe persistent asthma with associated allergic rhinitis, cardiac disorders such as left ventricular failure or mitral stenosis, vocal cord dysfunction, gastroesophageal reflux disease, recurrent aspiration, chronic obstructive pulmonary disease, emphysema, alpha-1-antitrypsin deficiency, sarcoidosis, hypersensitivity pneumonitis, bronchiectasis, allergic bronchopulmonary aspergillosis, airway neoplasm, and Churg-Strauss vasculitis. A careful history and physical in conjunction with appropriate screening of laboratory information will usually direct the clinician to the correct diagnosis.
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PMID:A 55-year-old man with severe persistent asthma poorly responsive to asthma therapy. 2339 14