Electrophysiological and Electroanatomical Mapping of the Right Atrium in Persistent Atrial Fibrillation: Relation to Collagen Turnover.

BACKGROUND: Atrial fibrillation (AF) is associated with abnormal atrial substrate. We investigated whether patients with persistent lone AF and patients with persistent AF and nonischemic dilated cardiomyopathy (NIDCM) exhibit any differences in electrophysiological and electroanatomical properties of right atrium (RA) and collagen turnover. We also investigated the relationship between mean RA bipolar voltage and collagen turnover. METHODS: Ten patients with a history of persistent lone AF and eight patients with a history of persistent AF and NIDCM were studied. Sinus node recovery times (SNRTs) and effective refractory periods (ERPs) at 600 ms, 500 ms, and 400 ms from the high (HLRA) and low (LLRA) lateral RA, proximal coronary sinus (pCS), and right atrial appendage (RAA) were evaluated, and RA electroanatomic mapping was created. Serum N-terminal propeptide of collagen type I (PINP), cross-linked C-terminal telopeptide of collagen type I (CTx), matrix metalloproteinase-1 (MMP-1), and tissue inhibitor of matrix metalloproteinases (TIMP-1) were measured as markers of collagen synthesis and degradation. RESULTS: No differences were found in SNRTs, ERPs from the HLRA, LLRA at 600 ms, pCS and RAA, mean RA bipolar voltage, serum PINP, CTx, MMP-1, and TIMP-1 between the two groups. In persistent lone AF, serum levels of TIMP-1 were related with mean HLRA and HPRA bipolar voltage. CONCLUSIONS: Persistent AF patients with or without NIDCM, demonstrate similar changes in electrophysiological and electroanatomical properties of the RA, as well as similar structural changes. Moreover, serum markers of collagen synthesis are correlated with bipolar voltage in specific regions of RA in persistent lone AF.

Atorvastatin for diabetic macular edema in patients with diabetes mellitus and elevated serum cholesterol.

BACKGROUND AND OBJECTIVE: To determine the efficacy of atorvastatin in reducing hard exudates and diabetic macular edema. PATIENTS AND METHODS: An uncontrolled clinical case series included 18 eyes with diabetic maculopathy and an elevated baseline lipid profile. All patients were treated with atorvastatin. Ophthalmologic evaluation, including fundus photography and fluorescein angiography, was performed at presentation and repeated at 3, 6, and 12 months. Hard exudates, hemorrhages, and fluorescein leakage at 12 months were evaluated and compared with baseline findings. RESULTS: Eighteen subjects with diabetic maculopathy received atorvastatin, and a significant decrease in total cholesterol and low-density lipoprotein cholesterol was seen (P < .05). Hard exudates and fluorescein leakage were decreased. No evidence of an association between change in hemorrhage status and treatment was found. CONCLUSION: Oral atorvastatin therapy in patients with diabetes mellitus and dyslipidemia seems to reduce the severity of hard exudates and fluorescein leakage in diabetic maculopathy and could be useful as an adjuvant therapy in the management of diabetic macular edema.