Background There have been a number of recent reports on the use of autologous bone marrow implantation (BMI) in the treatment of peripheral arterial disease, with a clinical response rate of approximately 70%. However, the factors that influence efficacy have not yet been clarified. We have analyzed the relationship between the number of implanted bone marrow cells and the clinical efficacy of BMI. Methods and ResultsEight patients with arteriosclerosis obliterans were treated with BMI. Bone marrow was aspirated from the ilium (500-1,000 ml), the mononuclear cells were separated and then were implanted. The clinical effectiveness of BMI was evaluated by assessing changes in the ankle-brachial pressure index (ABI) and the transcutaneous oxygen pressure (TcO2) between the pre-treatment baseline, with follow-up testing at 4 weeks. These changes were defined as ∆ABI and ∆TcO2. The mean number of CD34-positive cells was 1.04±0.60× 10 6 /kg body weight. There was a strong correlation between the number of CD34-positive cells and ∆ABI (r=0.754, p=0.028). Conclusions It is likely that the number of implanted CD34-positive cells is one of the primary factors that influence the clinical efficacy of BMI. (Circ J 2004; 68: 1189 -1193

trial fibrillation (AF) is associated with serious complications such as arterial thromboembolism, 1 and in patients with nonvalvular AF (NVAF) left atrial appendage (LAA) thrombi are believed to be the source of embolism. 2 In sinus rhythm, the LAA vigorously contracts with a peak emptying flow velocity greater than 50 cm/s, 3 but this is reduced in patients with chronic NVAF. 4,5 Although LAA dysfunction is a significant predictor of thrombus formation, the pathophysiologic mechanisms responsible have not been fully defined. Patients with AF are in a prothrombotic state compared with individuals in sinus rhythm. 6,7 Elevated plasma concentrations of D-dimer and thrombin -antithrombin III complex (TAT), which are markers of the intravascular activation of the coagulation system, have been found in patients with AF, 6,7 but the predictors of a hypercoagulable state in patients with NVAF have not been identified.We hypothesized that LAA dysfunction is associated with the development of a prothrombotic state and that left ventricular dysfunction leads to LAA dysfunction. The present study tested the hypothesis that LAA dysfunction would correlate with elevated levels of natriuretic peptides, which are biochemical markers of left ventricular dysfunction, 8 and with a prothrombotic state. Methods Study PopulationSixty-seven patients with a median age of 70 years (25th and 75th percentile, 65 and 74 years) with chronic NVAF between July 1999 and July 2000 were evaluated and those with a history of AF of more than 6 months duration were enrolled in the study. Patients with NVAF who had been treated with warfarin prior to transesophageal echocardiography (TEE) were excluded. Baseline clinical characteristics included age, sex, details of previous embolic events, the presence or absence of systemic hypertension, the use of aspirin, and the duration of AF. Because there were a substantial number of patients who did not have any symptoms at the onset of AF, the duration of AF was defined as the duration from the first confirmation of AF on electrocardiogram. EchocardiographyAll patients underwent transthoracic and transesophageal echocardiography. The institutional review board approved the research protocol and informed consent was obtained from all patients before undergoing TEE. The left atrial and ventricular dimensions were measured from the M-mode echocardiogram according to the recommendations of the

No abstract

No abstract

In three cases of small coronary artery perforation by guidewires during percutaneous coronary intervention, coronary leakage continued despite prolonged balloon inflation and reversal of heparin. Subcutaneous tissue was selectively delivered to perforated vessels by means of microcatheters in a successful attempt to stop leakage. This method appears to be extremely effective for treating guidewire-induced perforations of distal coronary arteries.