Comparison of an implanted abdominal aortic counterpulsation device with the intraaortic balloon pump in a heart failure model

The abdominal aortic counterpulsation device is a round pumping chamber with a valveless opening which is implanted retroperitoneally on the abdominal aorta. The Utah driver is connected to the device through an air conduit and is synchronized on the electrocardiographic signal to provide diastolic aortic augmentation. For comparison an intraaortic balloon was also driven by the Utah driver system. The abdominal aortic counterpulsation device (stroke volume = 30, 40 and 60 ml) and the intraaortic balloon pump (balloon volume = 20 ml) were tested in dogs with acute left ventricular failure. The abdominal aortic counterpulsation device was also tested in normal animals. In acute left ventricular failure the abdominal aortic counterpulsation device at a stroke volume of 30, 40 or 60 ml decreased left ventricular end-diastolic pressure by an average of 28.56 (p less than 0.001), 39.56 (p less than 0.001) and 44.14% (p less than 0.005), respectively; aortic end-diastolic pressure by 24.11 (p less than 0.001), 26.67 (p less than 0.001) and 19.57% (p less than 0.01); and aortic systolic pressure by 18.56 (p less than 0.002), 26.0 (p less than 0.001) and 22.43% (p less than 0.005). It increased cardiac index by 27.58 (p less than 0.02), 35.59 (p less than 0.005) and 43.42% (p less than 0.001) and it provided peak aortic diastolic augmentation of 64.5 (p less than 0.001), 69.78 (p less than 0.001) and 74.43% (p less than 0.001), respectively, above the control aortic end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Autologous and allogeneic bone marrow transplantation for poor prognosis patients with B-cell chronic lymphocytic leukemia

Twenty patients with poor prognosis B-cell chronic lymphocytic leukemia (B-CLL) underwent uniform high-dose chemoradiotherapy followed by rescue with multiple monoclonal antibody-purged autologous bone marrow (BM) (12 patients) or T-cell-depleted allogeneic BM from HLA-identical siblings (8 patients) in a pilot study to assess the feasibility of BM transplantation (BMT) in this disease. All had poor prognosis disease by either staging, BM pattern, tumor doubling time criteria, or cytogenetics. All patients achieved remission criteria (defined as < or = 2 adenopathy, absence of splenomegaly, < or = 20% of the intertrabecular space involved on BM biopsy) before BMT. Despite the use of fludarabine, a median of three treatment regimens were required to achieve BMT eligibility. After BMT, all patients achieved complete hematologic engraftment. Toxicities were not significantly different between autologous versus allogeneic BMT. Two toxic deaths were observed. Of 19 evaluable patients, 17 clinical complete clinical remissions (89%) were observed, with 2 patients (1 allogeneic and 1 autologous) exhibiting persistent BM disease. Complete clinical remissions were documented at the phenotypic and molecular level for the majority of patients in whom dual fluorescence for CD5 and CD20 (15 of 15; 100%) and Ig gene rearrangements (11 of 14; 79%) were performed. Although long-term follow-up is needed to assess any potential impact on the disease-free and overall survival of these patients, this study shows the feasibility of using high-dose chemoradiotherapy and BMT in patients with poor prognosis B-CLL.     

Comparison of the effects of ramipril versus telmisartan in reducing serum levels of high-sensitivity C-reactive protein and oxidized low-density lipoprotein cholesterol in patients with type 2 diabetes mellitus

The effect of ramipril (an angiotensin [AT]-converting enzyme inhibitor), telmisartan (an AT-II type 1 receptor blocker), or their combination on inflammation and lipid peroxidation was assessed in 37 patients with type 2 diabetes who were free of coronary artery disease. All regimens were associated with a significant reduction of C-reactive protein and oxidized low-density lipoprotein cholesterol serum levels (p <0.001). These results further enlighten the mechanisms underlying the cardiovascular beneficial effect of renin-AT system inhibition.