Background. Although lung cancer frequently spreads to the heart, details of cardiac metastases of lung cancer have not been fully discussed. The authors attempted to elucidate the relationship between the mechanisms of cardiac metastasis and a variety of clinical manifestations caused by cardiac metastasis. Methods. Clinical and autopsy records were reviewed in 74 autopsied cases of lung cancer. In cases with cardiac metastasis, the metastatic pathways to the heart were determined by the macroscopic examinations, and the relationship between the metastatic pathways and the clinical manifestations were studied. Results. Metastases to the pericardium or heart were seen in 23 cases (31%). A lymphatic metastatic pathway was detected in 18 cases (hilar lymphatic routing in 12 cases, and mediastinal lymphatic routing in 6 cases), and a hematogenous metastatic pathway was detected in 5 cases. Malignant pericardial effusion was documented in 15 of 23 cases. The metastatic pathway in 14 of 15 cases was lymphatic (hilar lymphatic routing in 10 cases, and mediastinal lymphatic routing in 4 cases). Patients showing lymphatic metastasis had higher incidence of malignant pericardial effusion than those with hematogenous metastasis (P < 0.05). Of 23 cases of cardiac metastasis, myocardial infarction was found in 1 case, resulting from the compression of the coronary arteries by the tumor. Concurrent supraventricular arrhythmias were recorded in eight cases with cardiac metastasis. Patients with cardiac metastasis had higher incidence of arrhythmia than those without cardiac metastasis (P < 0.05). In cases of cardiac metastasis, patients with arrhythmia were older (P < 0.01) than those without arrhythmia. Conclusions. The authors concluded that the hilar lymphatic pathway is essential for early development of malignant pericardial effusion in lung cancer and that aging and cardiac metastasis may be responsible for arrhythmia in patients with lung cancer. Cancer 1992; 70:437–442.

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We previously demonstrated disruptions of the pulmonary capillary endothelium and alveolar epithelium at transmural pressures (Ptm) of 52.5 cmH2O in rabbit by electron microscopy. In the present study, we determined the characteristics of the alveolar edema fluid in this condition by carrying out bronchoalveolar lavage after blood perfusion for 10 min at Ptm of 12.5 (low), 32.5 (intermediate), and 52.5 cmH2O (high). At low Ptm, where our previous studies showed no ultrastructural changes, the volume of alveolar fluid obtained by urea dilution was very small, and the concentrations of proteins, cells, and leukotriene B4 (LTB4) in the bronchoalveolar lavage fluid (BALF) were low. However, at high Ptm the volume of alveolar fluid and the concentrations of total protein and cells in the BALF were greatly increased. The amount of LTB4 in the BALF also increased substantially from 6.0 to 49.5 micrograms (P < 0.001). Intermediate changes were seen at intermediate Ptm. We concluded that exposing pulmonary capillaries to high Ptm results in a high-permeability form of edema. In addition, the presence of LTB4 suggests that chemical mediators are released, possibly as the result of exposure of the reactive capillary endothelial basement membrane, as demonstrated by electron microscopy.

Little attention has been paid to the pathological features of the pulmonary artery in Takayasu arteritis. Autopsy specimens of 6 cases of this disease were studied. Lesions were found in the aortic arch and its brachiocephalic branches in all cases and in both the aortic arch and thoracoabdominal aorta in 5 cases. The pathohistologic characters of the pulmonary artery were very similar to those of the systemic artery. Stenosis-recanalization, so-called blood vessels-in-blood vessels, of the pulmonary elastic arteries were found in four cases. These lesions were not observed in the systemic arteries, and most of the newly formed channels in them seemed to be branches of bronchial arteries. Luminal obstruction of pulmonary muscular arteries was observed in 4 cases, cellular arteritis of muscular arteries in 2 cases, and angiomatoid dilatation of small blood vessels in 2 cases. Thus in this study we found peculiar stenosis-recanalization lesions of the pulmonary elastic arteries, and also showed that the pulmonary elastic and muscular arteries are frequently involved in Takayasu arteritis. These findings suggest that pulmonary hypertension could influence morbidity and long-term mortality in this disease.

On high-resolution computed tomography, the presence of the midzone distribution and nodules within GGOs without traction bronchiectasis suggests CSS rather than CEP.