Comparison of mid-term outcomes between patients with and without atrial fibrillation undergoing coronary stenting in the second-generation drug-eluting stent era: from the SHINANO registry.

Little is known about the mid-term outcomes of patients with atrial fibrillation (AF) who undergo coronary stenting in the second-generation drug-eluting stent (DES) era. We evaluated the 1-year outcomes of AF patients undergoing percutaneous coronary intervention (PCI) with second-generation DES. This retrospective cohort analysis used integrated data from the SHINANO registry, a prospective observational multicenter cohort study, which enrolled 1923 consecutive patients undergoing PCI for any coronary artery disease. We retrospectively recruited 917 of these patients (mean age, 71.3 ± 10.0 years; male, 77 %) who received PCI with 2nd generation DES. The primary endpoint was net adverse clinical events (NACE: cardiac death, stroke, MI, stent thrombosis, and major bleeding) at 1 year. The secondary endpoints were major adverse cardiovascular events (MACE: cardiac death, stroke, and MI), stroke, MI, and major bleeding at 1 year. One-year follow-up was completed in 871 (94.9 %) patients, of whom 85 had AF. The incidence of NACE (15.4 vs. 7.3 %, P = 0.008), MACE (10.6 vs. 5.4 %, P = 0.047), and major bleeding (6.0 vs. 2.3 %, P = 0.049) were all significantly higher in AF compared to non-AF patients. On multivariate analysis, AF was an independent predictor of NACE (HR 2.32, 95 % CI 1.24-4.34, P = 0.008). In the second-generation DES era, patients with AF undergoing PCI still have a poorer prognosis, with more thrombotic and bleeding events, than those without AF. More attention should be paid to the thrombotic and bleeding risk in AF patients undergoing PCI.

Mitochondrial complex I activity is significantly decreased in a patient with maternally inherited type 2 diabetes mellitus and hypertrophic cardiomyopathy associated with mitochondrial DNA C3310T mutation: a cybrid study.

Mitochondrial respiratory function in a patient with maternally inherited type 2 diabetes mellitus and hypertrophic cardiomyopathy associated with heteroplasmic mitochondrial DNA (mtDNA) C3310T mutation, which replaces the second amino acid of NADH dehydrogenase 1 (ND1) from a hydrophobic Proline to a hydrophilic Serine, was investigated. Mitochondrial respiratory function solely due to mtDNA C3310T mutation was investigated in cybrid system by the fusion of mtDNA-deleted (rho(0)) HeLa cells and exogenous mtDNA either from the proband or from controls. Total oxygen consumption of the proband cybrid cells was significantly decreased compared with those of controls (2.468+/-0.475 versus 2.871+/-0.484 micromol/h/10(7) cells, p=0.0392). Mitochondrial respiratory chain complex I activity of the proband cybrid cells was also significantly decreased compared with those of controls (0.191+/-0.080 versus 0.288+/-0.113 micromol/h/mg protein, p=0.0223). Furthermore, ATP content in the proband cybrid cells was also significantly decreased compared with those in controls (1.119+/-0.344 versus 1.419+/-0.378 pmol/10(5) cells, p=0.044). The present study indicates that mtDNA C3310T mutation may be a pathogenic mutation of maternally inherited type 2 diabetes mellitus and hypertrophic cardiomyopathy in the proband and the family.

Circulating endothelial progenitor cells are reduced in hemodialysis patients.

OBJECTIVE: The risk of cardiovascular disease in hemodialysis patients is far greater than in the general population. Endothelial progenitor cells (EPCs) circulating in the peripheral blood contribute to neovascularization in the ischemic tissue. EPCs are considered to be included in CD34 positive (CD34+) or AC133 positive (AC133+) mononuclear cells (MNCs). This study's aim was to determine the number and functional activity of EPCs in hemodialysis patients and age-matched control subjects. METHODS: The numbers of CD34+ MNCs and AC133+ MNCs in the peripheral blood were quantified by flow cytometry. The peripheral blood EPCs were also examined by an in vitro culture assay. The levels of serum vascular endothelial growth factor (VEGF) were measured by sandwich enzyme immunoassay. RESULTS: The numbers of CD34+ MNCs and AC133+ MNCs were significantly reduced by 56% and 49%, respectively, in hemodialysis patients (n = 50) compared with control subjects (n = 36). The number of EPCs determined by the culture assay was also significantly reduced by 41% in hemodialysis patients compared with control subjects. Multivariate analysis revealed that none of the atherosclerotic risk factors were independent predictors of reduced CD34+ MNC counts. The serum VEGF levels in hemodialysis patients were not different from those in control subjects and did not correlate with CD34+ MNC counts. CONCLUSION: Circulating EPCs are significantly reduced in hemodialysis patients, which might be related to impaired neovascularization and cardiovascular disease in these patients.

Successful treatment of primary cardiac angiosarcoma with docetaxel and radiotherapy.

A 49-year-old man was admitted for primary cardiac angiosarcoma with a cardiac tamponade. Transthoracic echocardiography and contrast-enhanced computed tomography scan demonstrated a large mass in the right atrium and thickening of the right ventricular wall. 18F-labeled deoxyglucose (FDG) positron emission tomography (PET) scan showed increased FDG uptake in the mediastinum and over the heart. The patient responded to combination therapy with docetaxel and radiotherapy and tolerated the treatment well, except for radiation esophagitis, which required a soft diet and resolved 1 month after treatment. This combination therapy resulted in a minimal response with slight regression in the tumor size, but FDG-PET initially showed an increase in FDG uptake by the tumor that was no longer seen after combination therapy. There is no evidence of progression or metastasis even at 12 months after diagnosis.

Circulating endothelial progenitor cells in congestive heart failure.

BACKGROUND: Endothelial progenitor cells (EPCs) circulate in the adult peripheral blood and contribute to neovascularization. EPCs are considered to be included in CD34 positive mononuclear cells (CD34+ MNCs). Kinetics of circulating EPCs in congestive heart failure (CHF) has not been fully investigated. METHODS: We determined the numbers of white blood cells (WBCs), plasma brain natriuretic peptide (BNP), serum erythropoietin, vascular endothelial growth factor (VEGF) and thrombomodulin levels in 16 mild CHF patients (NYHA I, II), 10 severe CHF patients with acute exacerbation (NYHA III, IV), and 22 control subjects. The number of CD34+ MNCs in peripheral blood was quantified by flow cytometry. RESULTS: The ratio of CD34+ MNCs:10(3) WBCs in mild CHF patients was higher than that in control subjects (P<0.05). Interestingly, the ratio of CD34+ MNCs:10(3) WBCs in severe CHF patients at admission was significantly lower than that in control subjects (P<0.005) or in mild CHF patients (P<0.05). Levels of BNP and erythropoietin in severe CHF patients were significantly higher than those in mild CHF patients. However, VEGF and thrombomodulin levels were not different between mild and severe CHF patients. In addition, the ratio of CD34+ MNCs:10(3) WBCs in severe CHF patients increased in proportion to the amelioration of CHF during hospitalization, and this increase correlated with the decrease in BNP level. CONCLUSIONS: The ratio of CD34+ MNCs:10(3) WBCs was decreased in severe CHF. These findings suggest that impaired EPC recruitment might be involved in the pathophysiology of severe CHF.

Increase in circulating endothelial progenitor cells after aortic aneurysm repair.

Rapid endothelialization of prosthetic vessels is essential to avoid fatal complications. We hypothesized that there may be mobilization of endothelial progenitor cells (EPCs) in patients who received aortic aneurysm repair, and measured the number of CD34-expressing EPCs (CD34(+) cells) in these patients. Blood samples were taken preoperatively, 6, 24, and 48 h, and 7 days after surgery in 13 patients with aortic aneurysm. Samples were also obtained from ten age-matched control subjects. The number of CD34(+) cells in the peripheral blood was quantified by flow cytometry. The levels of serum vascular endothelial growth factor (VEGF) were measured using an enzyme-linked immunosorbent assay kit. Baseline CD34(+) cell counts in the peripheral blood showed a tendency to be lower in patients with aortic aneurysm compared with healthy control subjects. The number of CD34(+) cells did not change over 48 h after aortic aneurysm repair; however, it had doubled by the 7th day. On the other hand, the baseline serum VEGF levels did not differ between the patients and control subjects. The VEGF levels increased gradually after vascular repair with a significant elevation after 48 h, which was followed by an increase in CD34(+) cell counts. In conclusion, the circulating CD34(+) cell counts and serum VEGF levels are increased after vascular prosthesis replacement in patients with aortic aneurysm, which might contribute to the rapid endothelialization of prosthetic vessels.