10 research outputs found

    [Indications for MRI in coronary disease]

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    International audienceMagnetic resonance imaging (MRI) has become a useful, even essential, examination in recent years, for the exploration of patients with coronary disease. MRI has several different roles, even though it remains insufficiently requested because insufficiently available. Today it is the reference examination for assessing indicators of ventricular function (volume, ejection fraction, ventricular mass); their prognostic value and importance in determining treatment are well recognized. In the postinfarction period, MRI using late enhancement techniques allows a precise analysis of the extent of necrosis, in terms of segments and transmural involvement. MRI is indicated, especially preoperatively, in cases of ventricular remodeling and its consequences (functional impairment, aneurysms, parietal thrombus). MRI with pharmacological stress may also be used as a tool for detecting myocardial ischemia; in this case, perfusion or first-pass sequences should be used. On the other hand, cardiac MRI for morphologic exploration of the coronary network and measurement of stenosis is not yet routine

    MR evaluation of pulmonary vein diameter reduction after radiofrequency catheter ablation of atrial fibrillation.

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    International audienceFifty consecutive patients aged 52+/-12 years suffering from drug refractory atrial fibrillation (AF) underwent baseline and post-ablation MR angiography (MRA) at a mean follow-up of 4+/-3.5 months. Pulmonary vein (PV) disconnection was performed with a maximum energy delivery of 30 W. MRA allowed a two-plane measurement of each PV ostium. After ablation, no significant stenosis was observed, and only 1/194 (0.5%) and 3/194 (2%) PVs had a diameter reduction of 31-40% in the coronal and axial planes, respectively. There was a significant overall post-procedural PV narrowing of 4.9% in the coronal plane and 6.5% in the axial plane (P=ns between both planes). MRA is an efficient technique that can be used in pre- and postoperative evaluation of AF patients. Using a maximal power delivery limited to 30 W, no significant PV stenosis was observed at mid-term follow-up. Late PV anatomical assessment is needed to confirm these results on long-term follow-up

    MR delayed enhancement imaging findings in suspected acute myocarditis.

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    International audienceThe purpose of the study was to prospectively assess the clinical impact of routinely performed delayed enhancement imaging in suspected acute myocarditis. A two-centre prospective study was performed in patients with suspected acute myocarditis. The protocol included horizontal long axis, vertical long axis and short axis ciné MR and delayed enhancement imaging after Gd-DTPA infusion (0.2 mmol/kg). Sixty consecutive patients were enrolled (aged 49.4 +/- 17.8 years). MRI demonstrated delayed enhancement sparing the subendocardicardial layer in 51.6% of patients, concordant with the diagnosis of acute myocarditis; 16.7% of patients exhibited delayed enhancement involving the subendocardial layer with irregular margins, concordant with the diagnosis of acute myocardial infarction; 31.7% of patients had delayed enhancement imaging that was considered normal. Routine imaging to identify delayed enhancement provided crucial information in suspected acute myocarditis by reinforcing the diagnosis in 51.6% of patients and correcting a misdiagnosed acute myocardial infarction in 16.7% of patients

    Down-regulation of the transcription factor ZAC1 upon pre- and postconditioning protects against I/R injury in the mouse myocardium

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    International audienceAIMS: Myocardial infarction leads to heart failure and death. Ischaemic preconditioning (PreC) and postconditioning (PostC) reduce infarct size in animal models and human. Zac1 was identified as the only gene related to apoptosis and jointly down-regulated upon PreC and PostC. The aim of our study was to investigate the role of Zac1 down-regulation during ischaemia-reperfusion (I/R) in vivo.METHODS AND RESULTS: C57BL/6 mice were submitted to myocardial I/R injury, PreC, or PostC protocols. QPCR and immunochemistry showed that Zac1 expression was down-regulated both at the transcriptional and the protein levels upon PreC and PostC. Zac1(-/-) Knockout mice (n = 7) developed smaller infarcts (54%) than Zac1(+/+) littermates (n = 8) and decreased apoptosis (61.7%) in the ischaemic part of the left ventricle during I/R (Zac1(-/-), n = 6 vs. Zac1(+/+), n = 7; P = 0.0012). Mutants showed under control conditions a decrease of 53.9% in mRNA of Daxx, a pro-apoptotic protein playing a key role in I/R injuries (4.81 ± 0.77, n = 4 Zac1(-/-) mice vs. 10.44 ± 3.5, n = 7 Zac1(+/+) mice; P = 0.0121).CONCLUSION: Our study shows for the first time that Zac1 is down-regulated both at the transcriptional and protein levels upon PreC and PostC in wild-type mice. Moreover, inactivation of Zac1 in vivo is associated with a decreased amount of Daxx transcripts and, upon I/R injury, decreased infarct size and apoptosis. Altogether, our results show that Zac1 down-regulation plays a key role during cardioprotection against I/R injury and support the concept that cardioprotection regulates a network of interacting pro-apoptotic genes including Zac1 and Daxx

    Myocardial expression of a dominant-negative form of Daxx decreases infarct size and attenuates apoptosis in an in vivo mouse model of ischemia/reperfusion injury.

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    BACKGROUND: Apoptosis has been described extensively in acute myocardial infarction and chronic heart failure. Because Daxx (death-associated protein) appears to be essential for stress-induced cell death and acts as an antisurvival molecule, we tested the hypothesis that Daxx is involved in myocardial ischemia/reperfusion-induced cell death in vivo. METHODS AND RESULTS: Transgenic mice overexpressing a dominant-negative form of Daxx (Daxx-DN) under the control of the beta-actin promoter and control wild-type mice underwent an ischemia/reperfusion protocol: 40 minutes of left coronary artery occlusion and 60 minutes of reperfusion. Area at risk and infarct size were measured after dual staining by triphenyltetrazolium chloride and phthalocyanine blue dye. Apoptosis was measured in the ischemic versus the nonischemic part of the left ventricle by terminal deoxynucleotidyl transferase-mediated dUTP biotin nick end labeling staining, enzyme-linked immunosorbent assay, and Western blotting of caspase-3, caspase-8, and poly(ADP-ribose) polymerase. The mitogen-activated protein kinase status was investigated by Western blot analysis. Comparison between groups was assessed by ANOVA or Student t test (statistical significance: P<0.05). Left ventricle tissues from transgenic mice expressed Daxx-DN at the protein level. Area at risk/left ventricle values were comparable among groups. Infarct size/area at risk was 45% reduced in Daxx-DN versus wild-type mice (P<0.001). This cardioprotection was maintained for a 4-hour reperfusion. Ischemia/reperfusion-induced apoptosis was significantly decreased and ERK1/2 prosurvival pathway was activated in ischemic Daxx-DN hearts. CONCLUSIONS: Our study clearly indicates that Daxx participates in myocardial ischemia/reperfusion proapoptotic signaling in vivo
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