Association between transforming growth factor ß1 and atrial fibrillation in essential hypertensive patients.

BACKGROUND: Transforming growth factor ß1 (TGFß1) was one of the main factors for accelerating atrial fibrosis and has been reported with significantly higher level in plasma of the patients with essential hypertension (EH), especially in those with target organ damage. The contribution of TGFß1 in the pathogenesis of atrial fibrillation (AF) in EH patients remains unknown. METHODS: 75 EH patients with documented AF were divided into the paroxysmal AF group (EH+pAF, n = 44) or the chronic AF group (EH+cAF, n = 31), and 37 EH patients with sinus rhythm (SR) were assigned into the EH+SR group. All data including EH duration, blood pressure, lipids, glucose and left atrial diameter (LAD) measured by ultrasonic cardiogram were recorded. The serum levels of TGFß1 and connective tissue growth factor (CTGF) were detected, and compared with normal controls (NC group, n = 36). RESULTS: The serum levels of TGFß1 and CTGF in all EH groups were significantly higher than those in the NC group (p < 0.001, respectively). Among the EH groups, TGFß1 and CTGF levels were highest in the cAF group, followed by the pAF and the SR groups (p < 0.005). However, no significant difference was observed in TGFß1 and CTGF levels between the cAF group and the pAF group. The serum TGFß1 in AF patients was independently correlated with LAD, the presence of AF, aldosterone, CTGF and age. CONCLUSION: The serum TGFß1 promotes CTGF synthesis and causes left atrial enlargement and remodeling, which is possibly involved in the pathogenesis of AF in EH patients.

Effect of a single high loading dose of rosuvastatin on percutaneous coronary intervention for acute coronary syndromes.

OBJECTIVES: A high loading dose of atorvastatin has been confirmed to reduce postprocedural events in patients undergoing percutaneous coronary intervention (PCI). In this study, we sought to investigate the protective effects of rosuvastatin in patients with acute coronary syndromes (ACS) undergoing PCI and to determine the effect of rosuvastatin pretreatment on the postprocedural levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and monocyte chemotactic protein 1 (MCP-1). METHODS: A total of 125 patients with non-ST-segment elevation ACS were randomized to pretreatment with rosuvastatin (20 mg 2-4 hours before PCI [n = 62]) or placebo (n = 63). All the patients received subsequent long-term rosuvastatin treatment (10 mg/d). The main end point of the trial was the 30-day incidence of major adverse cardiac events (death, myocardial infarction, or unplanned revascularization). Plasma levels of hs-CRP, IL-6, and MCP-1 were detected before PCI and 6 hours, 24 hours, and 3 days after PCI. RESULTS: The primary end point occurred in 8.1% of the patients in the rosuvastatin arm and 22.2% in the placebo arm (P < .01); this difference was entirely attributed to a reduced incidence of myocardial infarction (8.1% vs 22.2%; P < .01). The postprocedural elevation in creatine kinase-MB and troponin I was also significantly lower in the rosuvastatin group at 6 hours, 24 hours, and 3 days. Plasma levels of hs-CRP, IL-6, and MCP-1 increased significantly after PCI in both the rosuvastatin and control groups; however, the postprocedural elevations in hs-CRP and IL-6 levels were significantly lower in the rosuvastatin group than the control group. CONCLUSIONS: A single, high dose (20 mg) of rosuvastatin prior to PCI reduces postprocedural myocardial injury in patients with ACS, with a concomitant attenuation of the postprocedural increase in hs-CRP and IL-6 levels.