Metabolic effects of the left atrial appendage exclusion (the heart hormone study).

INTRODUCTION: The effect of epicardial left atrial appendage (LAA) occlusion therapy on lipid and glucose metabolism in atrial fibrillation (AF) patients over the long-term follow-up are unclear. METHODS: In a single-center prospective observational study, 60 patients with longstanding persistent AF with cardiovascular risk factors had undergone an epicardial exclusion procedure. Anthropometric parameters and glucose, glycated hemoglobin (HbA1c), insulin, leptin, adiponectin, free fatty acids, beta-hydroxybutyrate, and total cholesterol levels were evaluated on fasting at baseline before the procedure and compared with levels at 24 h, 7 days, 1, 3, 6, and 24 months follow the procedure. RESULTS: The mean age of the patients was 67.5 ± 8.1. Insulin levels significantly increased at 7 days, 1, 3, 6, 12, and 24 months follow-up. The leptin levels showed a significant increase in 6, 12, and 24 months when compared to baseline. Whereas the adiponectin levels showed a significant decrease at 3, 6, 12, and 24 months when compared to baseline levels. In patients with the epicardial procedure, when compared to baseline, glucose, glycated hemoglobin, total cholesterol, and beta-hydroxybutyrate levels did not show any significant changes at baseline and 24 months follow-up. CONCLUSION: The epicardial exclusion ligation in AF patients was associated with significant changes in insulin, leptin, and adiponectin over long follow-up.

Arterial distensibility in patients with ruptured and unruptured intracranial aneurysms: is it a predisposing factor for rupture risk?

BACKGROUND: A risk factor assessment that reliably predicts whether patients are predisposed to intracranial aneurysm (IA) rupture has yet to be formulated. As such, the clinical management of unruptured IA remains unclear. Our aim was to determine whether impaired arterial distensibility and hypertrophic remodeling might be indicators of risk for IA rupture. MATERIAL/METHODS: The study population (n=49) was selected from consecutive admissions for either unruptured IA (n=23) or ruptured IA (n=26) from January to December 2010. Hemodynamic measures were taken from every patient, including systolic and diastolic blood pressure using a sphygmomanometer. Unruptured IA and ruptured IA characteristics, including aneurysmal shape, size, angle, aspect ratio, and bottleneck factor, were measured and calculated from transverse brain CT angiography images. With ultrasound, the right common carotid artery intima-media thickness was measured, as well as the lumen diameter during systole and diastole. Arterial wall strain, distensibility, stiffness index, and elastic modulus were calculated and compared between patients with unruptured IAs and ruptured IAs. A p-value less than 0.05 was considered statistically significant. RESULTS: General demographic data did not differ between patients with unruptured IAs and ruptured IAs. Greater mean intima-media thickness (p=0.013), mean stiffness index (p=0.044), and mean elastic modulus (p=0.026) were observed for patients with ruptured IAs. Moreover, mean strain (p=0.013) and mean distensibility (p=0.024) were decreased in patients with ruptured IAs. CONCLUSIONS: Patients with ruptured IAs demonstrated decreased arterial distensibility and increased intima-media thickness at the level of the carotid arteries. By measuring these parameters via ultrasound, it may be possible to predict whether patients with existing IAs might rupture and hemorrhage into the subarachnoid space.

Mean platelet volume in predicting short- and long-term morbidity and mortality in patients with or without ST-segment elevation myocardial infarction.

Mean platelet volume (MPV) is a marker of platelet activation. An increased MPV is associated with acute myocardial infarction (AMI) and long-term mortality. The aim of this study was to compare MPV in patients with ST-segment elevation myocardial infarction (STEMI) and non-ST-segment elevation myocardial infarction (NSTEMI). Also, we investigated the value of MPV on in-hospital mortality and long-term prognosis of patients with STEMI and NSTEMI. We studied 429 patients with AMI (70.4% male, 61.9 ± 12.4 years; 279 patients with STEMI, 150 patients with NSTEMI). MPV and platelet count were similar in both groups. Elevated MPV increased the risk of death by 3.1-fold (p < 0.001) in STEMI group during the hospitalization. However, increased MPV was not associated with in-hospital mortality in NSTEMI group. The area under the receiver operating characteristic curve of MPV was 0.868 (95% CI, 0.830-0.907) for predicting two-year mortality. A cut-off point of 11.1 fL showed a sensitivity of 81% and a specifity of 77% for prediction of two-year mortality. Kaplan-Meier survival curve showed two-year mortality rate of 12.5% in patients with MPV >11.1 fL versus 9.9% in patients with MPV <11.1 fL (p < 0.001). Cox regression analysis showed MPV to be an independent predictor of two-year mortality (Hazard ratio 1.7; 95% CI 1.5-1.9; p < 0.001). An increased MPV is an independent predictor of in-hospital mortality in patients with STEMI. However, elevated levels of MPV did not predict in hospital mortality in NSTEMI group. The increase in MPV values was independently correlated with two-year mortality in all study patients.