This research study examines the safety and feasibility of aspirin with or without Simvastatin in solid tumor patients at risk for VTE (Venous Thromboembolism - or blood clots - in the arms, lets, lungs, or other part of the body). One-fifth of all thrombotic (clotting) events occur in patients that have cancer. Changes in sP-selectin will be used as a measure of efficacy. We have chosen sP-selectin as the primary marker because of its role in hemostasis, because it is predictive of thrombosis in cancer patients and because of promising preliminary data. We expect that sP-selectin levels will be elevated in patients before therapy with aspirin and/or statin, but that these levels will fall significantly during treatment, rise during the observation phase, and fall during the second study period. Patients who take part in the study have been diagnosed with a solid tumor cancer and are considered to be intermediate to high risk for VTE. The standard of care is to give chemotherapy for solid tumors and treat clots which develop using blood thinners.
Objectives Primary: To determine efficacy of aspirin with and without simvastatin in solid tumor patients at high- or intermediate-risk for VTE, in reducing markers of platelet activation, levels of inflammatory and angiogenic cytokines measured using high-throughput approaches, and clinical and investigational measures of hemostatic activation. Secondary: To determine safety and feasibility of aspirin with or without simvastatin in solid tumor patients at high- or intermediate-risk for VTE
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
SUPPORTIVE_CARE
Masking
NONE
Enrollment
17
81mg/day for 4 weeks
Daily dose of Simvastatin for 4 weeks
participants will be observed for thrombotic evens for 4 weeks
Cleveland Clinic Taussig Cancer institute, Case Comprehensive Cancer Center
Cleveland, Ohio, United States
Change in average sP-selectin levels
Change in sP-selectin levels as indicator of measure efficacy
Time frame: at 16 weeks of treatment
Frequency of major bleeding complications or clinically significant non-bleeding complications per patient
The safety endpoint will be bleeding complications over 17 weeks (16 weeks of study plus an additional week of observation). This will include major bleeding events and clinically significant non-major bleeding events. A bleeding event will be defined as major if it satisfies one or more of the following: decrease in hemoglobin of 2 g/dL or more, leads to transfusion of two or more units of blood or packed cells, occurs in a critical site (intraocular, spinal/epidural, intracranial, retroperitoneal, or pericardial) or leads to death. Clinically significant, non-major bleeding will be defined as bleeding that does not meet the criteria for major bleeding, and has at least one of the following characteristics: multiple-source bleeding; spontaneous hematoma \>25 cm2; epistaxis \>5 min; macroscopic hematuria not related to instrumentation; spontaneous rectal bleeding; gingival bleeding \> 5 min; hemoptysis; hematemesis; or prolonged bleeding (\> 5 min) after venipuncture.
Time frame: at 17 weeks after beginning treatment
Change in average Platelet Factor 4
measure of efficacy using plasma level of platelet activation markers
Time frame: at 16 weeks of treatment
Change in average CD40 ligand
measure of efficacy using plasma level of platelet activation markers
Time frame: at 16 weeks of treatment
Change in average serum thromboxane B2
measure of efficacy using plasma level of platelet activation markers
Time frame: at 16 weeks of treatment
Change in average serum VEGF
measure of efficacy using plasma level of angiogenesis markers
Time frame: at 16 weeks of treatment
Change in average serum angiopoietin-2
measure of efficacy using plasma level of angiogenesis markers
Time frame: at 16 weeks of treatment
Change in average serum hepatocyte growth factor
measure of efficacy using plasma level of angiogenesis markers
Time frame: at 16 weeks of treatment
Change in average serum PECAM
measure of efficacy using plasma level of angiogenesis markers
Time frame: at 16 weeks of treatment
Change in average serum PDGF
measure of efficacy using plasma level of angiogenesis markers
Time frame: at 16 weeks of treatment
Change in average plasma F1.2
measure of efficacy using plasma level of hemostatic activation markers
Time frame: at 16 weeks of treatment
Change in average plasma TAT complexes
measure of efficacy using plasma level of hemostatic activation markers
Time frame: at 16 weeks of treatment
Change in average plasma D-dimer
measure of efficacy using plasma level of hemostatic activation markers
Time frame: at 16 weeks of treatment
Change in the number of thrombotic events
the number of thrombotic events measured by the number of events related to venus thrombosis, pulmonary embolism, visceral vein thrombosis as well as arterial thromboembolic events including stroke, myocardial infarction or arterial embolism
Time frame: 17 weeks after beginning treatment
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