Avila-Vanzzini N.,Ignacio Chavez National Cardiology Institute |
Leyva C.Z.M.,Ignacio Chavez National Cardiology Institute |
Castellanos L.E.R.,Ignacio Chavez National Cardiology Institute |
Godinez J.A.A.,Ignacio Chavez National Cardiology Institute |
And 2 more authors.
Journal of Cardiovascular Ultrasound | Year: 2015
Background: Excessive weight and obesity (EwO) are independent factors in the development of heart failure; they lead to a state of myocardiopathy via inflammatory and hormonal mechanisms. If excessively accumulated, epicardial fat favors a pro-inflammatory state. Ventricular asynchrony is a marker of heart failure progression and has been poorly studied in EwO. The objective was evaluate the relation between epicardial fat, body mass index (BMI) and mechanical synchrony measured by echocardiography, in healthy individuals with EwO. Methods: We included 55 healthy individuals between the ages of 18 and 35, 17 had a BMI < 25 kg/m2 (30.9%) and 38 had a BMI > 25 kg/m2 (EwO group) (69.09%), anthropometric measurements, transthoracic echocardiogram and synchrony evaluation were obtained. Results: Left atrial volume, telediastolic and telesystolic left ventricular volumes and the baseline volume of the right ventricle were greater in the EwO group (20 mL/m2 vs. 15 mL/m2, p = 0.001; 106 mL vs. 82 mL, p = 0.0149 vs. 32 mL, p = 0.001 and 34 mm vs. 31 mm, p = 0.02, respectively). The Yu index also correlated with epicardial fat, r = 0.53, p < 0.01, whereby the greater the amount of epicardial fat, the greater the dispersion timing of ventricular activation. The systolic synchrony index also correlated with the BMI, p = 0.01. Conclusion: Mechanical intraventricular asynchrony is associated to EwO and the amount of epicardial fat; hence, asynchrony may be one more factor leading to heart failure in EwO individuals. © 2015, J Cardiovasc Ultrasound, All rights Reserved. Source
Osorio H.,CINVESTAV |
Osorio H.,Ignacio Chavez National Cardiology Institute |
Bautista R.,Ignacio Chavez National Cardiology Institute |
Rios A.,CINVESTAV |
And 5 more authors.
Journal of Nephrology | Year: 2010
Background: The purpose of our study was to determine whether increased SGLT2 expression in the kidney of diabetic rats was associated with the development of hypertension and to investigate the effect of phlorizin (P) on blood pressure and SGLT2 expression in diabetic rats. Methods: The animals were divided into two groups: Control (C) and streptozotocin-induced diabetic (D) rats were used to evaluate SGLT2 activity in brush border membrane vesicles (BBMV) using a rapid filtration technique. Others animals were divided into two groups: Normal (NSD) or high salt diet (4%) (HSD), and subdivided in four groups: C, C+P, D, D+P. Systolic blood pressure (SBP) was recorded for 30 days by the use of a telemetric system and at day 30 urine samples (24 h) were collected to evaluate renal function and SGLT2 expression in the renal cortex. Results: At day 30, diabetic animals with NSD or HSD exhibited hyperglycemia, lower body weight, glycosuria, diuresis, decrease natriuresis, increased SBP values and SGLT2 expression. In diabetic rats, phlorizin treatment decreased hyperglycemia and prevented development of hypertension, decreased SGLT2 activity in BBMV but did not modify SGLT2 expression. Conclusions: In conclusion, SGLT2 inhibition prevented the development of hypertension in diabetic rats as well as hyperglycemia, suggesting a hypertensive mechanism associated with SGLT2 activity and the likelihood that increased SGLT2 expression may be associated with progression of diabetic renal complications. © 2010 Società Italiana di Nefrologia. Source