Xanthine Oxidoreductase Inhibition Causes Reverse Remodeling in Rats With Dilated Cardiomyopathy
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منابع مشابه
Xanthine oxidoreductase inhibition causes reverse remodeling in rats with dilated cardiomyopathy.
Increased reactive oxygen species (ROS) generation is implicated in cardiac remodeling in heart failure (HF). As xanthine oxidoreductase (XOR) is 1 of the major sources of ROS, we tested whether XOR inhibition could improve cardiac performance and induce reverse remodeling in a model of established HF, the spontaneously hypertensive/HF (SHHF) rat. We randomized Wistar Kyoto (WKY, controls, 18 t...
متن کاملExtreme reverse remodeling in a patient with dilated cardiomyopathy.
R everse remodeling is known to occur in patients with de novo presentations of nonischemic dilated cardiomy-opathy. Predictors include recent onset, female sex, higher left ventricular (LV) ejection fraction by echocardiography at baseline, higher systolic blood pressure, QRS width <120 ms (or absence of left bundle branch block) and normal LV dimensions. Conversely, increased LV size is regar...
متن کاملPrevalence and clinical predictors of reverse remodeling in patients with dilated cardiomyopathy.
BACKGROUND Contemporary therapiesimprove prognosis and may restore left ventricular (LV) sizeand function. OBJECTIVES To examine the prevalence, clinical features and therapies associated with reverse remodeling (RR) in dilated cardiomyopathy (DCM). METHODS The study group comprised 188 DCM patients who had undergone two echo examinations at least 6 months apart. RR was defined as increased...
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BACKGROUND Functional mitral regurgitation (MR) is a common finding in dilated cardiomyopathy. Left ventricular (LV) reverse remodeling with LV size reduction and improvement in LV function is a well recognized phenomenon. We aimed to evaluate the impact of LV remodeling on the mechanism leading to functional MR. METHODS Among 188 patients with non-ischemic dilated cardiomyopathy, 10 patients...
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ژورنال
عنوان ژورنال: Circulation Research
سال: 2006
ISSN: 0009-7330,1524-4571
DOI: 10.1161/01.res.0000200181.59551.71