Collateral presence and extent do not predict myocardial viability and ischemia in chronic total occlusions: A stress-CMR study.

BACKGROUND: Well-developed collaterals are assumed as a marker of viability and ischemia in chronic total occlusions (CTO). We aim to correlate viability and ischemia with collateral presence and extent in CTO patients by cardiac magnetic resonance (CMR). METHODS: Multicentre study of 150 CTO patients undergoing stress-CMR, including adenosine if normal systolic function, high-dose-dobutamine for patients with akinetic/>2 hypokinetic segments and EF ≥35%, otherwise low-dose-dobutamine (LDD); all patients underwent late gadolinium enhancement (LGE) imaging. Viability was defined as mean LGE transmurality ≤50% for adenosine, as functional improvement for dobutamine-stress-test, ischemia as ≥1.5 segments with perfusion defects outside the scar zone. RESULTS: Rentrop 3/CC 2 defined well-developed (WD, n = 74) vs poorly-developed collaterals (PD, n = 76). Viability was equally prevalent in WD vs PD: normo-functional myocardium with ≤50% LGE in 52% vs 58% segments, p = 0.76, functional improvement by LDD in 48% vs 52%, p = 0.12. Segments with none, 1-25%,26-50%,51-75% LGE showed viability by LDD in 90%,84%,81%,61% of cases, whilst in 12% if 76-100% LGE (p < 0.01). There was no difference in WD vs PD for ischemia presence (74% vs 75%, p = 0.99) and extent (2.7 vs 2.8 segments, p = 0.77). CONCLUSIONS: In a large cohort of CTO patients, presence and extent of collaterals did not predict viability and ischemia by stress-CMR. Scar extent up to 75% LGE was still associated with viability, whereas ischemia was undetectable in 25% of patients, suggesting that the assessment of CTO patients with CMR would lead to a more comprehensive evaluation of viability and ischemia to guide revascularization.

[Contrast-induced nephropathy: An update]. / Néphropathie induite par les produits de contraste : une mise à jour.

Contrast-induced nephropathy (CIN) is common in hospitalized patients. Its occurrence is associated with an increased hospitalization stay and cost, morbidity and mortality. Thus, preventives strategies remain a major issue. Patients that are referred for cardiac catheterization are among the most vulnerable to develop CIN due to their comorbidities. Moreover, in some cases, such preventives measures cannot be introduced due to emergent clinical settings. After a summary regarding the properties of iodinated contrast medium, the aim of this work was to review the definition, pathophysiology, diagnosis and preventive strategies related to CIN.

Antioxidant supplements for non-alcoholic fatty liver disease and/or steatohepatitis.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is characterised by fatty deposition in the hepatocytes of patients with minimal or no alcohol intake and without other known cause. NAFLD includes a wide spectrum of histologic abnormalities ranging from hepatic steatosis to non-alcoholic steatohepatitis (NASH), or even cirrhosis. Antioxidant supplements, therefore, could potentially protect cellular structures against oxidative stress and the resulting lipid peroxidation. OBJECTIVES: To systematically evaluate the beneficial and harmful effects of antioxidant supplements versus no intervention, placebo, or other interventions for patients with NAFLD or NASH. SEARCH STRATEGY: We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (June 2006), the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 2, 2006), MEDLINE (1966 to June 2006), EMBASE (1980 to June 2006), and the Chinese Biomedical Database (1978 to June 2006). No language restrictions were applied. SELECTION CRITERIA: Randomised clinical trials evaluating any antioxidant supplements versus no intervention, placebo, or other interventions in patients with NAFLD or NASH. Our inclusion criteria for NAFLD or NASH were based on history of minimal or no alcohol intake, imaging techniques showing hepatic steatosis, and/or histological evidence of hepatic damage (including simple steatosis, fatty infiltration plus nonspecific inflammation, steatohepatitis, fibrosis, and cirrhosis), and by exclusion of other causes of hepatic steatosis. DATA COLLECTION AND ANALYSIS: We extracted data from the identified trials and contacted authors. We used a random-effects model and fixed-effect model with the significant level set at P = 0.05. We evaluated the methodological quality of the randomised trials by looking at how the generation of allocation sequence, allocation concealment, blinding, and follow-up were performed. We made our analyses following the intention-to-treat method by imputing missing data. MAIN RESULTS: We identified six trials: two were regarded of high methodological quality and four of low methodological quality. None of the trials reported any deaths. Treatment with antioxidant supplements showed a significant, though not clinically relevant, amelioration of aspartate aminotransferase levels, but not of alanine aminotransferase levels, as compared to placebo or other interventions. Gamma-glutamyl-transpeptidase was decreased, albeit not significantly, in the treatment arm. Radiological and histological data were too limited to draw any definite conclusions on the effectiveness of these agents. Adverse events were non-specific and of no major clinical relevance. AUTHORS' CONCLUSIONS: There is insufficient data to either support or refute the use of antioxidant supplements for patients with NAFLD. It may be advisable to carry out large prospective randomised clinical trials on this topic.

Bile acids for non-alcoholic fatty liver disease and/or steatohepatitis.

BACKGROUND: Non-alcoholic fatty liver disease is a condition characterised by fatty deposition in the hepatocytes of patients in patients with minimal or no alcohol intake. Some patients develop non-alcoholic steatohepatitis. Bile acids may potentially protect cellular structures and may be of benefit in patients with non-alcoholic fatty liver or steatohepatitis. OBJECTIVES: To systematically evaluate the beneficial and harmful effects of bile acids versus no intervention, placebo, or other interventions for patients with non-alcoholic fatty liver or steatohepatitis. SEARCH STRATEGY: We searched The Cochrane Hepato-Biliary Group Controlled Trials Register (July 2005), the Cochrane Central Register of Controlled Trials (CENTRAL) in The Cochrane Library (Issue 2, 2005), MEDLINE (1966 to July 2005), EMBASE (1980 to July 2005), and The Chinese Biomedical Database (1978 to July 2005). No language restrictions were applied. SELECTION CRITERIA: Randomised clinical trials evaluating any bile acids versus no intervention, placebo, or other interventions in patients with NAFLD. DATA COLLECTION AND ANALYSIS: We extracted data from the identified trials as well as contacted authors. We evaluated the methodological quality of the randomised trials by assessing the generation of allocation sequence, allocation concealment, blinding, and follow-up. We made our analyses following the intention-to-treat method by imputing missing data. MAIN RESULTS: We identified four randomised clinical trials randomising 279 patients. Only one of the trials was considered a low-bias risk trial. One of the trials reported a non-liver-related death in the bile acid group. No significant differences were found regarding mortality or improvement in liver function tests observed after treatment with ursodeoxycholic acid. Data on the radiological and histological responses were too scant to draw any definite conclusions. Adverse events were non-specific and considered of no major clinical relevance. AUTHORS' CONCLUSIONS: Presently, there are insufficient data to support or refute the use of ursodeoxycholic acid for patients with non-alcoholic fatty liver or steatohepatitis. It may be advisable to carry out large randomised clinical trials on this topic.