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Mitral stenosis acute pulmonary edema and rheumatic fever pneumonitis

2011; Elsevier BV; Volume: 151; Issue: 3 Linguagem: Inglês

10.1016/j.ijcard.2011.06.089

1874-1754

Paulo Roberto Barbosa Évora, Patrícia Martinez Évora, Verena Kise Capellini, Andréa Carla Celotto,

Pericarditis and Cardiac Tamponade

Mitral stenosis, although a heart defect extensively studied over the years, still presents many facts that are controversial, including some physiopathological details. Among these details, a persistent enigma is the occurrence of acute pulmonary edema, even as the first manifestation in patients without accentuated mitral stenosis. We conducted some studies in the eighties, involving 20 patients with isolated rheumatic mitral stenosis, in order to contribute to better understanding the pathophysiology of mitral stenosis. A significant correlation between the mitral valve area and the functional class according to the New York Heart Association (NYHA), the cardiac index, the mitral valve flow rate, the systemic vascular resistance, the total pulmonary resistance, and the resistance at the level of the stenotic valve was observed. No significant correlation was obtained between the mitral area and the pulmonary wedge pressure, the ventricular work the gradient through the mitral valve, and the pulmonary arteriolar resistance [[1]Evora P.R. Manço J.C. Marin Neto J.A. Gallo Jr., L. Carneiro J.J. Gomes U.A. et al.Correlation of intraoperative measurement of the functional valve area with clinical and hemodynamic parameters in patients with mitral stenosis.Arq Bras Cardiol. 1982; 38: 91-98PubMed Google Scholar]. The work capacity measured in the cycloergometer was consistently low in all patients, no significant effect from the use of digitalis and the previous occupational activities was detected, and, there was no significant correlation between these data and the hemodynamic findings and the actual mitral valve area [[2]Evora P.R. Vichi F.L. Mori L.E. Romero L.C. Otaviano A.G. Sader A.A. The mitral valve area and physical capacity determined by cycloergometric test in patients with mitral stenosis.Arq Bras Cardiol. 1982; 38: 193-197PubMed Google Scholar]. Pulmonary function tests were carried out in the preoperative period of cardiac surgery for the correction of mitral stenosis, and the mitral valve area values did not show any statistical correlation with the pulmonary functional parameters [[3]Evora P.R. Manço J.C. Amorim D.S. Carneiro J.J. Sader A.A. Pulmonary function in patients with mitral stenosis.Arq Bras Cardiol. 1981; 37: 451-455PubMed Google Scholar]. Before presenting the hypothesis it is interesting to emphasize three important aspects:1)As already mentioned, it remains an enigma, perhaps one of the greatest and oldest enigmas of Cardiology, the explanation of why some young patients present acute pulmonary edema as the first sign of mitral stenosis, and other patients with major hemodynamic changes are mildly symptomatic or asymptomatic.2)In the course of acute rheumatic fever the occurrence of pulmonary infiltrates is often considered a manifestation of pulmonary congestion, unrelated viral or bacterial pneumonitis, atelectasis, or infarction. These interpretations are undoubtedly correct, but cannot apply to all cases. Inasmuch as the pathologic process in acute rheumatic fever is known to be diffuse, being capable of involving the vascular system and connective tissue in a wide variety of organ systems, the question of rheumatic pneumonitis may be logically advanced in such cases [[4]Lukas D.S. Dotter C.T. Modifications of the pulmonary circulation in mitral stenosis.Am J Med. 1952; 12: 639-649Abstract Full Text PDF PubMed Scopus (9) Google Scholar].3)It is known that structural changes in the alveolar-capillary membrane tend to prevent pulmonary edema, but a final explanation of this fact has not yet been presented [[5]Araujo J. Lukas D.S. Interrelationships among pulmonary capillary pressure, blood flow and valve size in mitral stenosis; the limited regulatory effects of the pulmonary vascular resistance.J Clin Invest. 1952; 31: 1082-1088Crossref PubMed Scopus (8) Google Scholar]. Taken together, these background data suggested the present medical hypothesis. “The occurrence of acute pulmonary edema in mitral stenosis is related to the lowest degree of pneumonitis in acute rheumatic fever manifestation. With less inflammatory reaction affecting the alveolar-capillary membrane, the occurrence of acute pulmonary edema would be facilitated by a smaller increase in pulmonary capillary pressure during physical effort. Moreover, as in most cases of acute rheumatic fever, pneumonia occurs with inflammation, causing thickening of the alveolar-capillary membrane that protects against the occurrence of acute pulmonary edema. On the other hand, the possibility of chronic interstitial pulmonary edema, responsible for mitral stenosis classical symptoms, remains possible (Fig. 1)”. Experimentally, lung edema occurs when the pulmonary venous pressure reaches plasma colloid osmotic levels. The absence of significant pulmonary edema with pulmonary venous pressures in such a range while at rest, or during brief exercise, is a matter of considerable interest. These facts suggest that the alveolar-capillary structures in mitral stenosis are not normally permeable to fluid. The anatomic alterations (i.e. capillary basement membrane thickening and pericapillary fibrosis) that very commonly exist in these structures probably prevent transudation of fluid from the pulmonary capillaries into the alveoli. This is suggested by the frequency with which interstitial pulmonary edema without edema fluid in the alveolar spaces is observed in lung biopsy sections from patients with mitral stenosis [[6]Massumi R.A. Legier J.F. Rheumatic pneumonitis.Circulation. 1966; 33: 417-425Crossref PubMed Scopus (11) Google Scholar]. These pathophysiological data are compatible with the present medical hypothesis, taking into consideration that they would be valid for cases of inflammatory pneumonitis during the outbreak of acute rheumatic fever. Among our 20 studied patients we chose two cases with the following hemodynamic data: a) mitral valve area (0.97 and 1.27 cm2), b) cardiac index (2.80 and 2.87 l/min/m2), c) pulmonary artery pressure (36.7 and 21.0 mmHg); d) pulmonary capillary wedge pressure (23.0 and 19.0 mmHg), e) pulmonary vascular resistance (611 and 365 dyn/s/cm−5), and f) pulmonary arteriolar resistance (278 and 34.7 dyn/s/cm−5). The first patient was a male, 35 years-old, farmer, NYHA Class II and his ergometric stress test was effective (4 min/50 W) without major symptoms. The second patient was a female, 21 years-old, inactive, NYHA Class II and her ergometric stress test was effective (1 min, 10 s/50 W). She had acute pulmonary edema as the first clinical manifestation, soon after the cycloergometric test, and was treated with bed rest, oxygen and diuretics due to signs and symptoms of pre-pulmonary acute edema. Considering our hypothesis, the first patient had been stricken with carditis and pneumonitis during the rheumatic fever attack, with inflammation causing changes and thickening of the alveolar-capillary membrane with consequent “protection” against the occurrence of acute pulmonary edema. On the other hand, the second patient had carditis, no corresponding severity of pneumonitis, without suffering anatomical and functional abnormalities of the alveolar-capillary membrane with consequent susceptibility to the occurrence of acute pulmonary edema. This study was supported in part by Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) and Fundação de Apoio ao Ensino, Pesquisa e Assistência do Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo (FAEPA/HCFMRP/USP), SP, Brazil. None declared. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [[7]Shewan L.G. Coats A.J. Ethics in the authorship and publishing of scientific articles.Int J Cardiol. 2010; 144: 1-2Abstract Full Text Full Text PDF Scopus (699) Google Scholar].