Clinical features and risk factors of stroke/thromboembolism and bleeding in the elderly patients with atrial fibrillation / 中华心血管病杂志

<p><b>OBJECTIVE</b>The relationship between stroke/thromboembolic events (TEs) and bleeding as well as age-related risk factors are not fully clear in elderly patients with atrial fibrillation (AF). This study aimed to evaluate the clinical features, incidence and risk factors of stroke and bleeding in elderly AF patients.</p><p><b>METHOD</b>A total of 220 elderly AF patients [mean age (83.1 ± 0.6) years] were followed for (3.2 ± 0.8) years. The CHA(2)DS(2)-VASc score, the HAS-BLED score, annual major bleeding risk and the annual stroke were analyzed.</p><p><b>RESULT</b>The CHA(2)DS(2)-VASc score in patients with 65-79, 80-89 and ≥ 90 years old groups were 2.9 ± 0.2, 5.2 ± 0.2 and 5.6 ± 0.2, respectively (P < 0.001) and the HAS-BLED score were 2.1 ± 0.1, 3.2 ± 0.1 and 3.6 ± 0.1, respectively (P < 0.001), both significantly increased with aging. The annual major bleeding risk increased similarly as the annual stroke risk in the very elderly AF patients (patients 80-89 years old: bleeding risk 3.7 %, stroke risk 6.7 %; patients ≥ 90 years old: 8.7 % and 9.8 %, respectively). The combination of CHA(2)DS(2)-VASc and HAS-BLED could identify those patients with high risk for stroke and bleeding correctly. Twelve (5.5%) patients experienced "bidirectional events" (concomitant TE and haemorrhage), of whom 9 (75.0 %) suffered recurrent TEs.</p><p><b>CONCLUSION</b>The bleeding risk increased similarly as the thromboembotic risk with increasing age in the elderly AF patients, "bidirectional events" is not common but related with worse outcome in elderly AF patients.</p>

Bone marrow mesenchymal cell transplantation reduces left ventricular remodeling in heart failure following acute myocardial infarction / 中华心血管病杂志

<p><b>OBJECTIVE</b>Bone marrow mesenchymal cell (MSC) transplantation has been shown to improve heart failure but the mechanism and the subsequent effects are unclear. We tested the hypothesis that MSC transplantation reduces left ventricular remodeling through the MMP/TIMP system in heart failure following acute myocardial infarction.</p><p><b>METHODS</b>Female SD rats underwent coronary artery ligation to induce myocardial infarction. Four weeks later, the rats were divided into the test group (n = 7) and the control group (n = 7), respectively. The donor MSCs were harvested and expanded from male SD rats (5 x 10(6) in 50 microl PBS) and injected into the ischemic myocardium, while the control group received the same volume of PBS. Left ventricular morphology was then evaluated in both groups through staining with H&E and Masson's trichrome. Immunohistochemical staining was used to examine the expressions of MMP2 and TIMP1, as well as type I and type III collagens, in the scar zones. The protein levels of MMP2 and TIMP1 were determined by Western blotting.</p><p><b>RESULTS</b>MSC differentiated into fibroblast-like cells at 21 days after transplantation in the test group. In addition, many inflammatory cells infiltrated and aggregated in the scar area, but this effect was reduced at day 7 after transplantation. The following changes were noted in the test group compared to the control group: ejection fraction and shortening fraction were higher [(63.43 +/- 3.97)% vs. (36.20 +/- 3.99)%, (31.71 +/- 1.98)% vs. (18.00 +/- 2.07)%, P < 0.05]; dp/dt(min) was reduced [(-4756.24 +/- 270.00) mm Hg/s vs. -2789.53 +/- 624.13) mm Hg/s, P < 0.05]; the left ventricular thinning ratio was significantly higher [(76.34 +/- 2.66)% vs. (64.37 +/- 2.36)%, P < 0.05]; the infarct size was smaller [(36.19 +/- 0.83)% vs. (42.12 +/- 1.88)%, P < 0.05]; type I collagen expression in the scar area was much higher; type III collagen expression was much lower; MMP2 expression was reduced and TIMP1 expression was increased.</p><p><b>CONCLUSION</b>MSC transplantation led to dynamic changes in the collagen network through regulation of MMP2/TIMP1 system and consequently interrupted the progress of adverse LV remodeling in heart failure following acute myocardial infarction.</p>