BACKGROUND.Patients with cancer who have thrombocytopenia may experience acute coronary syndromes (ACS), and the use of aspirin (ASA) poses an increased risk of bleeding. The purpose of this study was to test the hypothesis that the benefit of ASA therapy in the treatment of ACS would extend to cancer patients with thrombocytopenia and outweigh the risks of severe bleeding.METHODS.The records of all cancer patients diagnosed with an ACS in 2001 and referred for cardiology consultation were reviewed. Patients were divided into 2 groups on the basis of platelet count, >100 cells k/μL and ≤100 cells k/μL. Data were collected on the use of ASA therapy, bleeding complications, and survival rates. The authors assessed group differences by using the Wilcoxon rank sum test or 2‐tailed Fisher exact test, as appropriate. Univariate and multivariate logistic regression models were used to assess factors potentially associated with 7‐day survival.RESULTS.In cancer patients with ACS and thrombocytopenia, those who did not receive ASA had a 7‐day survival rate of 6% compared with 90% in those who did receive ASA (P < .0001). There were no severe bleeding complications. Patients with a platelet count (>100 cells k/μL) who received ASA had a 7‐day survival rate of 88% compared with 45% in those who did not receive ASA (P = .0096).CONCLUSIONS.Therapy with ASA was associated with a significantly improved 7‐day survival after ACS in cancer patients, with or without thrombocytopenia, and not associated with more severe bleeding. Cancer 2007;109:621–627. © 2006 American Cancer Society.

To evaluate interactions between human endothelial cells (ECs) and smooth muscle cells (SMCs) for the development of tissue-engineered vessels, we examined the adhesion and key cell properties of human ECs grown on quiescent human aortic SMCs. ECs attached to SMCs spread more slowly than ECs attached to fibronectin surfaces, and ECs aligned along the direction of the SMCs. ECs attached firmly and less than 5% of the cells were removed by shear stresses as high as 300 dyn cm(-2). Unlike porcine SMCs and co-cultures, human SMCs or co-cultures do not contract under flow, and the human ECs and SMCs in co-culture align toward the direction of flow. A confluent endothelium could be maintained in co-culture for over 30 days, and some of the ECs reoriented perpendicular to the SMCs after 9 days in static culture. Surface tissue factor levels in ECs and SMCs were less in co-culture than in monoculture. Co-culture induced an increase in calponin expression in SMCs. These findings show that human co-cultures can be maintained for long culture periods, where the endothelium remains confluent and responds to long-term exposure to flow, and EC-SMC interactions lead to an increase in SMC differentiation and an EC surface that is less thrombotic.

BACKGROUND. Sunitinib malate is a novel multitargeted receptor tyrosine kinase inhibitor with established efficacy in the treatment of metastatic renal cell carcinoma and imatinib‐resistant gastrointestinal stromal tumor. This report describes the development of heart failure in cancer patients who received this novel agent. METHODS. A retrospective study was conducted at M. D. Anderson Cancer Center during a 1‐year period on patients who received sunitinib and developed heart failure. RESULTS. During 2006, 6 of 224 (2.7%) patients who received sunitinib developed heart failure (HF) that resulted in substantial morbidity and, in some cases, mortality. Symptomatic heart failure occurred soon after initiation of sunitinib (mean onset 22 days after initiation), was associated with decline in cardiac function and elevations in blood pressure, and was not completely reversible in most patients, even after termination of sunitinib therapy. CONCLUSIONS. These observations suggested that sunitinib‐associated heart failure may represent a potentially serious toxicity and underscore the need for careful monitoring of cardiac function and aggressive control of hypertension in these patients. Studies to elucidate potential mechanisms of heart failure and left ventricular dysfunction resulting from treatment with sunitinib are necessary to develop strategies for prevention and treatment of this complication. Cancer 2008. ©2008 American Cancer Society.

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