Surgical myocardial revascularization of patients with ischemic cardiomyopathy and severe left ventricular disfunction

Objective: To determine long-term survival, identify preoperative factors predictive of a favorable outcome, and assess functional improvement after coronary artery bypass grafting in patients with advanced left ventricular dysfunction. Methods: Between 1995 and 2001, 244 patients who underwent coronary artery bypass grafting and had a preoperative left ventricular ejection fraction less than or equal to 35 percent were included. left ventricular ejection fraction was determined by uniplanar or biplanar ventriculography during left heart catheterization. Indication for surgery was predominance of tissue viability. Functional improvement was evaluated through echocardiography and gated scintigraphy at exercise/ rest. Survival was determined by Kaplan-Meier analysis. Results: Mean left ventricular ejection fraction was 29±4 percent (ranged from 9 percent to 35 percent). An average of 3.01 coronary bypass grafts per patient were performed. In-hospital mortality was 3.7 percent (9 patients). The 4-year survival rate was 89.7 percent. Multivariate correlates of favorable short- and long-term outcome were preoperative New York Heart Association Funcional classification for congestive heart failure class I/II, lower PAsP, higher left ventricular ejection fraction and gated left ventricular ejection fraction Ex/Rest ratio >5 percent. Left ventricular ejection fraction rise from 32±5 percent to 39±5 percent, p <0.001. Gated left ventricular ejection fraction at exercise/ rest increased markedly after surgery: from 27±8 percent/ 23±7 percent to 37±5 percent/ 31±6 percent, p <0.001. Conclusions: In selected patients with severe ischemic left ventricular dysfunction and predominance of tissue viability, coronary artery bypass grafting may be capable of implement preoperative clinical/ functional parameters in predicting outcome as left ventricular ejection fraction and gated left ventricular ejection fraction at exercise/ rest.

Post-mortem histological pulmonary analysis in patients with HIV/AIDS

OBJECTIVES: Certain aspects of pulmonary pathology observed in autopsies of HIV/AIDS patients are still unknown. This study considers 250 autopsies of HIV/AIDS patients who died of acute respiratory failure and describes the demographic data, etiology, and histological pulmonary findings of the various pathologies. METHODS: The following data were obtained: age, sex, and major associated diseases (found at the autopsy). Pulmonary histopathology was categorized as: diffuse alveolar damage; pulmonary edema; alveolar hemorrhage; and acute interstitial pneumonia. Odds ratio of the HIV/AIDS-associated diseases developing a specific histopathological pattern was determined by logistic regression. RESULTS: A total of 197 men and 53 women were studied. The mean age was 36 years. Bacterial bronchopneumonia was present in 36 percent (91 cases) and Pneumocystis jiroveci pneumonia in 27 percent (68) of patients. Pulmonary histopathology showed acute interstitial pneumonia in 40 percent (99), diffuse alveolar damage in 36 percent (89), pulmonary edema in 13 percent (33), and alveolar hemorrhage in 12 percent (29) of patients. Multivariate analysis showed a significant and positive association between Pneumocystis jiroveci pneumonia and acute interstitial pneumonia (Odds ratio, 4.51; 95 percent CI, 2.46 - 8.24; p < 0.001), severe sepsis and/or septic shock and diffuse alveolar damage (Odds ratio, 3.60; 95 percent CI, 1.78 -7.27; p < 0.001), and cytomegalovirus and acute interstitial pneumonia (Odds ratio, 2.22; 95 percent CI, 1.01 - 4.93; p = 0.05). CONCLUSIONS: This report is the first autopsy study to include demographic data, etiologic diagnosis, and respective histopathological findings in patients with HIV/AIDS and acute respiratory failure. Further studies are necessary to elucidate the complete pulmonary physiopathological mechanism involved with each HIV/AIDS-associated disease.

Isquemia miocárdica silenciosa / Silent myocardial ischemia

A isquemia miocárdica é o evento fisiopatológico final da doença arterial coronária (DAC). Quando desprovida de sintomatologia é denominada "isquemia miocárdica silenciosa", sendo a responsável pela maior parte dos eventos isquêmicos totais. Ainda permanecem incertos os porquês da näo percepçäo dolorosa ("angina") de certos episódios isquêmicos, bem como dos mecanismos fisiopatológicos que as desencadeiam. Claro está, no entanto, que os eventos silenciosos e sintomáticos näo se diferem quanto às alteraçöes miocárdicas estruturais e funcionais. O diagnóstico de isquemia silenciosa se estabelece quando da detecçäo de alteraçöes objetivas e características de dano miocárdico isquêmico. Dentre os métodos se configuram, principalmente, a eletrocardiografia de esforço, a monitorizaçäo eletrocardiográfica ambulatorial, o teste de perfusäo com tálio-201 e o ecocardiograma de esforço. Há outros, porém de menor utilizaçäo. Destaca-se a isquemia silenciosa pela sua importante relaçäo com o prognóstico dos portadores de DAC. Muitos estudos relatam participaçäo significativa daquela nos variados desfechos da DAC (angina, infarto agudo do miocárdio e morte súbita). O enfoque terapêutico varia para cada paciente, podendo iniciar-se com a mudança do estilo de vida (alteraçäo dos fatores de risco). A terapêutica medicamentosa se baseia na utilizaçäo de drogas antiisquêmicas (nitratos, beta-bloqueadores e antagonistas dos canais de cálcio) e antiplaquetários. o tratamento mais agressivo inclui a angioplastia coronária, a colocaçäo de stents e a cirurgia de revascularizaçäo do miocárdio.