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Clinical studies have shown that large doses of prednisone could lower serum uric acid (SUA) in patients with decompensated heart failure (HF); however, the optimal dose of prednisone and underlying mechanisms are unknown. Thirty-eight patients with decompensated HF were randomized to receive standard HF care alone (n = 10) or with low-dose (15 mg/day, n = 8), medium-dose (30 mg/day, n = 10), or high-dose prednisone (60 mg/day, n = 10), for 10 days. At the end of the study, only high-dose prednisone significantly reduced SUA, whereas low- and medium-dose prednisone and standard HF care had no effect on SUA. The reduction in SUA in high-dose prednisone groups was associated with a significant increase in renal uric acid clearance. In conclusion, prednisone can reduce SUA levels by increasing renal uric acid clearance in patients with decompensated HF. Key words: heart failure, uric acid, prednisone, renal uric acid clearance. Des etudes cliniques ont montre qu'une forte dose de prednisone pourrait permettre d'abaisser les taux d'acide urique seriques (AUS) chez les patients atteints d'insuffisance cardiaque (IC) decompensee. Toutefois, la dose optimale de prednisone et les mecanismes sous-jacents demeurent inconnus. Trente-huit patients atteints d'IC decompensee ont ete repartis aleatoirement pour recevoir la norme de soins standard seule (n = 10) ou de la prednisone a dose faible (a 15 mg/jour, n = 8), moderee (a 30 mg/jour, n = 10) ou elevee (a 60 mg/jour, n = 10) pendant 10 jours. A la fin de l'etude, seule la dose elevee de prednisone avait permis d'abaisser les taux d'AUS de facon notable, alors que ni les doses faible et moderee de prednisone ni la norme de soins standard pour l'IC n'ont eu d'effets sur les taux d'AUS. En fait, l'abaissement des taux d'AUS par la prednisone a dose elevee etait associe a une augmentation importante de la clairance renale de l'acide urique. En conclusion, la prednisone pourrait abaisser les taux d'AUS en augmentant la clairance renale de l'acide urique chez les patients atteints d'IC decompensee. [Traduit par la Redaction] Mots-cles: insuffisance cardiaque, acide urique, prednisone, clairance renale de l'acide urique., Uric acid (UA) is the final product of purine degradation with xanthine oxidase. Approximately two thirds of UA is excreted through the kidneys and the remainder through the gastrointestinal tract. [...]

Summary: Pulmonary arterial hypertension (PAH) is a devastating disease that leads to right heart failure and premature death. Historically, we are restricted by limited options for drug treatment. Over the past decade, with advances in our understanding of pathophysiological and molecular mechanisms, many new therapeutic strategies (synthetic prostacyclin and prostacyclin analogues, endothelin receptor antagonists and sildenafil) have been developed for the treatment of PAH, and the clinical efficacy has been tested in many randomized-controlled trials (RCTs). In this overview, we review the evidence for the use of historical and new treatments that arises from the Cochrane Collaboration of Systematic Reviews and from recent RCTs. [Copyright &y& Elsevier]

Objective: The purpose of this study was to screen genetic variations in plakophilin-2 (PKP2) gene in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) and investigate the differences in clinical features between mutation and no-mutation groups., Methods: Thirty unrelated Chinese patients clinically diagnosed with ARVC/D and 50 healthy controls were included. Genomic DNA was isolated from peripheral blood samples. PCR and direct sequencing were used to detect variations in PKP2 gene., Results: Eight PKP2 mutant variants were identified in 10 ARVC/D patients (8 men, 2 women). Among the eight mutation, three (c.2194C>T, c. 1170+ 1G>A and c. 810_813delGGTC) were novel mutation. Clinical features of the PKP2 mutation group were similar to those of the non-mutation group., Conclusions: The rate of PKP2 mutation is 33.3% (10/30) in ARVC/D patients. The penetrance of PKP2 mutation for ARVC/D tends to be higher in man patients. No significant differences could be detected in phenotype characteristics between patients with and without PKP2 mutation.

Objective: To investigate and compare Trp64Arg mutation of beta(3)-adrenergic receptor (beta(3)-AR) gene in simple obesity and metabolic syndrome (MS), and to correlate the mutation difference with sex, total body fat and fat distribution., Methods: Mutation study was carried out with PCR in 295 subjects with simple obesity and 219 subjects with MS. The subjects were stratified by body mass index (BMI) as light obesity group (BMI 25 approximately 29.9 kg/m(2)) and serious obesity group (BMI >/= 30 kg/m(2)) and by mean of waist circumference (WC) as abdominal adipose tissue light depot group (WC < 104 cm in male and WC < 88 cm in female) and serious depot group (WC >/= 104 cm in male and WC >/= 88 cm in female). 175 healthy non-obese subjects were selected as controls., Results: The frequency of Trp64Arg mutation of beta(3)-AR gene was higher in the male subjects with MS than those with simple obesity and non-obese controls (32.25%, 21.01% and 19.91%, respectively, P < 0.05) and also higher than female ones with MS (32.35% vs 23.46%, P < 0.01). It was found by further stratification that the frequency of Trp64Arg mutation of beta(3)-AR gene was higher in the male light obesity group with MS than female light obesity group with MS. The frequency is also higher than that in the male light obesity group of the obese subjects (32.83% vs 17.35%, P < 0.05 and 32.83% vs 20.41%, P < 0.05, respectively). The frequency of mutation was higher in male abdominal adipose tissue serious depot subjects with MS than those with simple obesity (35.71% vs 20.16%, P < 0.05)., Conclusion: Trp64Arg mutation of beta(3)-AR gene may be used as a genetic marker for MS in male.

Objective: It is important to identify patients at risk for atherosclerotic renal artery stenosis because renal artery stenosis is a progressive disease and a potentially correctable problem. This study is to evaluate the prevalence of angiographically-determined renal artery stenosis in a patient population undergoing routine coronary angiography, and to identify the risk factors for renal artery stenosis., Methods: Before the procedure, demographic data, medical history, physical findings and laboratory data were obtained. After coronary angiography, abdominal aortography was performed to screen for the presence of renal artery stenosis over a 8-month period. In 370 patients (237 males, 133 females), mean age was 60.6 (29 to 81) years. And an univariate and multivariate Logistic regression analysis was made to explore the association of the clinical variables with renal stenosis., Results: Renal artery narrowing was identified in 106 (28.6%) patients. Significant renal artery stenosis, defined as a narrowing of the diameter by more than 50%, was found in 63 patients (17.0%) and insignificant (< 50% diameter narrowing) stenosis was found in 43 patients (11.6%). Significant unilateral stenosis was present in 41 (11.1%) patients and bilateral stenosis was present in 22 (5.9%) patients. By univariate and multivariate logistic regression analysis, the association of clinical variables with renal artery stenosis was assessed. Multivariable predictors included age (OR = 1.06, 95% CI: 1.03 approximately 1.10, P < 0.0001), severity of coronary artery disease (OR = 1.65, 95% CI: 1.34 approximately 2.03, P < 0.0001) and peripheral vascular disease (OR = 2.64, 95% CI: 1.27 approximately 5.47, P = 0.0095). The variables such as sex, body mass index, hypertension, smoking history, hyperlipidemia, myocardial infarction, congestive heart failure, renal insufficiency and diabetes mellitus were not associated., Conclusion: Renal artery stenosis is a frequent finding in patients undergoing coronary angiography, especially in older people with generalized atherosclerosis.