Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

Abstract. To evaluate the relationship between the adiponectin levels and left ventricular mass index (LVMI) in uncomplicated obese subjects. Fifty-nine subjects were assigned to the obese (BMI≥30 kg/m 2 ) and 58 to the lean (BMI<30 kg/m 2 ) group. Plasma glucose, insulin, serum total cholesterol and high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDL) cholesterol, triglycerides and adiponectin were measured. Insulin resistance was determined by the Homeostasis Assessment Model (HOMA-IR). The left ventricular functions of all subjects were determined by 2D and pulse wave Doppler echocardiography. LVMI was calculated as left ventricular mass (LVM) normalized for height in m 2.7 . The obese group displayed significantly higher LVMI and late mitral inflow velocity. Thirty-three obese subjects met the criteria for left ventricular hypertrophy (LVH) and had lower serum adiponectin levels compared with obese subjects without LVH and lean subjects (p<0.05). Adiponectin was negatively correlated with LVMI (R: -0.277, p: 0.002). Furthermore, during the partial correlation analysis where HOMA-IR was controlled, the negative correlation between adiponectin and LVMI progressed (r: -0.283, p: 0.002). The linear regression analysis showed an independent relationship between LVMI and adiponectin. (β: -0.214, p: 0.01) Obesity is associated with LVH. This study showed direct influence of adiponectin on LVMI. OBESITY leads to serious changes in cardiac structure and functions [1]. These changes are characterized by an increase in left ventricular mass index (LVMI), diastolic dysfunction, and in advanced stages of the condition, systolic dysfunction [2]. It is currently believed that hemodynamic factors alone do not account for obesity-related cardiac structure abnormality. An investigation of possible metabolic inflammatory causes of left ventricular hypertrophy (LVH) in obesity may help the prevention and treatment of these changes [3].Recent studies have shown that adipose tissue acts like an endocrine organ and synthesizes various hormones. One of these hormones is adiponectin, which is believed to possess anti-atherogenic and anti-diabetic qualities [4]. Obesity or other obesity related complications are associated with decreased adiponectin levels [4], and thus is believed to play a role in the etiology of a number of diseases such as obesity, insulin resistance, hypertension, dyslipidemia, and atherosclerotic heart disease. Therefore, hypoadiponectinemia may be a factor in obesity-related LVH [5], which may be an independent effect or result of complications, such as obesity or obesity-related insulin resistance and hypertension [5]. Thus, an improvement in adiponectin levels can be expected to lower obesity-related morbidity and mortality [6]. However, there are few studies in

No abstract

Insulin resistance and fasting insulin is not associated with left ventricular hypertrophy in healthy people, independent of obesity. Obesity appears to be an independent risk factor for left ventricular hypertrophy.

Coronary artery fistulae are very rare congenital anomalies which constitute 0.2-0.4% of all congenital heart diseases. The right chambers of the heart are the most frequent communication site of the coronary fistulae and may cause hemodynamic impairment in the coronary circulation. The fistulae arise frequently from right coronary and left anterior descending arteries. Fistulae from left circumflex artery are very rare. We report a case in which transcatheter embolization was performed with 3-mm Guglielmi detachable coils in a young adult with a rare type of congenital fistula originating from the circumflex artery and draining into the coronary sinus.