Predictors of Congestive Heart Failure Mortality in Elderly People From the General Population  The CArdiovascular STudy in the ELderly (CASTEL)

Mazza, Alberto; Tikhonoff, Valérie; Casíglia, Edoardo; Pessina, Achille C.

doi:10.1536/ihj.46.419

Cited by 63 publications

(67 citation statements)

References 43 publications

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“…19 -47 Hyperuricemia also predicts stroke in diabetic and nondiabetic subjects 48,49 and predicts the development of hypertension 50 -52 and renal disease in the general population. 53 In these studies, uric acid may be simply "marking" subjects at increased cardiovascular and renal risk.…”

Section: Hyperuricemia Is Increased In Subjects At Cardiovascular Riskmentioning

confidence: 99%

Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?

Kang²,

et al. 2003

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Abstract-Hyperuricemia is associated with hypertension, vascular disease, renal disease, and cardiovascular events. In this report, we review the epidemiologic evidence and potential mechanisms for this association. We also summarize experimental studies that demonstrate that uric acid is not inert but may have both beneficial functions (acting as an antioxidant) as well as detrimental actions (to stimulate vascular smooth muscle cell proliferation and induce endothelial dysfunction). A recently developed experimental model of mild hyperuricemia also provides the first provocative evidence that uric acid may have a pathogenic role in the development of hypertension, vascular disease, and renal disease. Thus, it is time to reevaluate the role of uric acid as a risk factor for cardiovascular disease and hypertension and to design human studies to address this controversy. Key Words: antioxidants Ⅲ hypertension, essential Ⅲ cardiovascular diseases Ⅲ renin-angiotensin system Ⅲ vascular diseases Ⅲ renal disease U ric acid, a product of purine metabolism, is degraded in most mammals by the hepatic enzyme, urate oxidase (uricase), to allantoin, which is freely excreted in the urine. However, during the Miocene epoch (20 to 5 million years ago), 2 parallel but distinct mutations occurred in early hominoids that rendered the uricase gene nonfunctional. 1 As a consequence, humans and the great apes have higher uric acid levels (Ͼ2 mg/dL) compared with most mammals (Ͻ2 mg/dL).Uric acid levels also vary significantly within humans as the result of factors that increase generation (such as high purine or protein diets, alcohol consumption, conditions with high cell turnover, or enzymatic defects in purine metabolism) or decrease excretion. A reduction in glomerular filtration rate (GFR) increases serum uric acid, although a significant compensatory increase in gastrointestinal excretion occurs. 2 Hyperuricemia also may result from increased net tubular absorption. After filtration, uric acid undergoes both reabsorption and secretion in the proximal tubule, and this process is mediated by a urate/anion exchanger and a voltagesensitive urate channel. 3,4 Organic anions such as lactate decrease urate secretion by competing for urate through the organic anion transporter, whereas several substances, including probenacid and benziodarone, have opposite effects. 5 Hyperuricemia is usually defined as Ͼ6.5 or 7.0 mg/dL in men and Ͼ6.0 mg/dL in women.

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Section: Hyperuricemia Is Increased In Subjects At Cardiovascular Riskmentioning

confidence: 99%

Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?

Kang²,

et al. 2003

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“…A combination of ␤1-AR blockers with ACEi (or angiotensin receptor blockers) was subsequently recommended by American Heart Association, and this combination is presently considered a standard therapy for CHF (HFSA, 2006). Nevertheless, despite spectacular success in treatment during the past decade with this treatment regimen, CHF still remains a major cause of morbidity and mortality, particu-larly in the elderly, and a growing problem in most industrialized countries (Mazza et al, 2005). Thus, the search for novel pharmacological approaches to treat CHF continues.…”

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confidence: 99%

Therapeutic Efficacy of a Combination of a β1-Adrenoreceptor (AR) Blocker and β2-AR Agonist in a Rat Model of Postmyocardial Infarction Dilated Heart Failure Exceeds That of a β1-AR Blocker plus Angiotensin-Converting Enzyme Inhibitor

Ahmet¹,

Morrell²,

Lakatta³

et al. 2009

The Journal of Pharmacology and Experimental Therapeutics

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We had proposed previously a novel combination of ␤2-adrenoreceptor (AR) agonist and ␤1-AR blocker that in the rat model of postmyocardial infarction (MI) dilated cardiomyopathy exceeds the therapeutic effectiveness of either monotherapy. In the present study, we compared that treatment with a combination of ␤1-AR blocker and angiotensin-converting enzyme inhibitor (ACEi), a current standard chronic heart failure (CHF) therapy. Two weeks after coronary artery ligation, rats were divided into groups of similar average MI size, measured by echocardiography, and the following 12-month treatments were initiated: fenoterol (250 g/kg/day), a ␤2-AR agonist, plus metoprolol (100 mg/kg/day), a ␤1-AR blocker (␤1-␤2ϩ); metoprolol plus enalapril (20 mg/kg/day), an ACEi (␤1-ACEi); and a combination of all three drugs (␤1-␤2ϩACEi). These treatment groups were compared with each other and with nontreated (nT) and sham groups. The 12-month mortality was significantly reduced in all treatment groups (44% in ␤1-␤2ϩ, 56% in ␤1-␤2ϩACEi, 59% in ␤1-ACEi versus 81% in nT). Bimonthly echocardiography revealed significant attenuation of the left ventricular (LV) chamber remodeling, LV functional deterioration, and MI expansion in all three treatment groups, but effects were significantly more pronounced when treatment included a ␤2-AR agonist. The results indicated that a combination of ␤1-AR blocker and ␤2-AR agonist is equipotent to a combination of ␤1-AR blocker and ACEi in the treatment of CHF in rats, with the respect to mortality, and exceeds the latter with respect to cardiac remodeling and MI expansion. Thus, this novel therapeutic regimen for CHF warrants detailed clinical investigation.

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“…1 Several large studies have provided conflicting results regarding the clinical significance of elevated SUA levels in cardiovascular or cerebrovascular disease. Some concluded that SUA is an independent risk factor for cardiovascular disease (CVD), [2][3][4][5][6] with an apparently stronger association in women than in men, 7,8 in the elderly 9 and in patients with essential hypertension, 10 congestive heart failure 11,12 and type 2 diabetes mellitus. 13,14 In contrast, the Framingham Heart Study concluded that an association with CVD merely reflects the link between SUA and other risk factors, including hypertension, renal disease, elevated lipoprotein levels and the use of diuretics.…”

mentioning

confidence: 99%

Serum Uric Acid as an Independent Predictor of Early Death After Acute Stroke

Karagiannis

Mikhailidis²,

Τζιόμαλος

et al. 2007

Circ J

117

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Predictors of Congestive Heart Failure Mortality in Elderly People From the General Population The CArdiovascular STudy in the ELderly (CASTEL)

Cited by 63 publications

References 43 publications

Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?

Is There a Pathogenetic Role for Uric Acid in Hypertension and Cardiovascular and Renal Disease?

Therapeutic Efficacy of a Combination of a β1-Adrenoreceptor (AR) Blocker and β2-AR Agonist in a Rat Model of Postmyocardial Infarction Dilated Heart Failure Exceeds That of a β1-AR Blocker plus Angiotensin-Converting Enzyme Inhibitor

Serum Uric Acid as an Independent Predictor of Early Death After Acute Stroke

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