Universidade de São Paulo, São Paulo, SP, Brazil.
Clinics (Sao Paulo). 2012;67(3):213-7. doi: 10.6061/clinics/2012(03)02.
Acute respiratory failure is present in 5% of patients with acute myocardial infarction and is responsible for 20% to 30% of the fatal post-acute myocardial infarction. The role of inflammation associated with pulmonary edema as a cause of acute respiratory failure post-acute myocardial infarction remains to be determined. We aimed to describe the demographics, etiologic data and histological pulmonary findings obtained through autopsies of patients who died during the period from 1990 to 2008 due to acute respiratory failure with no diagnosis of acute myocardial infarction during life.
This study considers 4,223 autopsies of patients who died of acute respiratory failure that was not preceded by any particular diagnosis while they were alive. The diagnosis of acute myocardial infarction was given in 218 (4.63%) patients. The age, sex and major associated diseases were recorded for each patient. Pulmonary histopathology was categorized as follows: diffuse alveolar damage, pulmonary edema, alveolar hemorrhage and lymphoplasmacytic interstitial pneumonia. The odds ratio of acute myocardial infarction associated with specific histopathology was determined by logistic regression.
In total, 147 men were included in the study. The mean age at the time of death was 64 years. Pulmonary histopathology revealed pulmonary edema as well as the presence of diffuse alveolar damage in 72.9% of patients. Bacterial bronchopneumonia was present in 11.9% of patients, systemic arterial hypertension in 10.1% and dilated cardiomyopathy in 6.9%. A multivariate analysis demonstrated a significant positive association between acute myocardial infarction with diffuse alveolar damage and pulmonary edema.
For the first time, we demonstrated that in autopsies of patients with acute respiratory failure as the cause of death, 5% were diagnosed with acute myocardial infarction. Pulmonary histology revealed a significant inflammatory response, which has not previously been reported.
急性呼吸衰竭发生于 5%的急性心肌梗死患者中，占急性心肌梗死后 20%至 30%的致死原因。与肺水肿相关的炎症是否为急性心肌梗死后急性呼吸衰竭的原因仍有待确定。我们旨在描述 1990 年至 2008 年期间因急性呼吸衰竭死亡且生前无急性心肌梗死诊断的患者的人口统计学、病因数据和尸检肺部组织学发现。
本研究共纳入了 4223 例生前无特定诊断的急性呼吸衰竭死亡患者的尸检。218 例（4.63%）患者被诊断为急性心肌梗死。记录每位患者的年龄、性别和主要合并症。肺部组织病理学分类如下：弥漫性肺泡损伤、肺水肿、肺泡出血和淋巴浆细胞性间质性肺炎。通过逻辑回归确定急性心肌梗死与特定组织病理学之间的比值比。
共有 147 名男性纳入本研究。死亡时的平均年龄为 64 岁。肺部组织病理学显示肺水肿和弥漫性肺泡损伤的患者占 72.9%。11.9%的患者存在细菌性支气管肺炎，10.1%的患者存在系统性动脉高血压，6.9%的患者存在扩张型心肌病。多变量分析显示，急性心肌梗死与弥漫性肺泡损伤和肺水肿之间存在显著的正相关。
我们首次证明，在因急性呼吸衰竭导致死亡的患者尸检中，5%被诊断为急性心肌梗死。肺部组织学显示出明显的炎症反应，这是以前未曾报道过的。
