25 research outputs found

    Relationships between NO synthesis inhibitors and renal function.

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    <p>Relationship between asymmetric (ADMA; upper panel) and symmetric (SDMA; lower panel) dimethylarginine plasma levels and estimated glomerular filtration rate (eGFR) in the study population.</p

    Kaplan-Meier survival analyses during follow-up.

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    <p>Composite outcomes of cardiac death and myocardial infarction according to concentrations of plasma arginine (panel A), asymmetric dimethylarginine (ADMA; panel B), and symmetric dimethylarginine (SDMA; panel C), divided by median levels. P values by log-rank test are shown.</p

    Baseline characteristics of the study patients.

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    *<p>By Fisher exact test.</p>§<p>by Wilcoxon Rank Sum Test.</p><p>ACE = angiotensin-converting enzyme; ARB = angiotensin II receptor blocker; CABG = coronary artery bypass graft surgery; CKD = chronic kidney disease; CRP = C-reactive protein; eGFR = estimated glomerular filtration rate; NA = not applicable; PCI = percutaneous coronary intervention.</p

    Cox regression analysis for the primary end point of the study (composite outcome of cardiac death and myocardial infarction).

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    <p>Hazard ratios (HR) in models 1–4 are adjusted for age, hemoglobin and left ventricular ejection fraction; HRs in models 5–7 are also mutually adjusted.</p><p>HRs for CKD are vs. no-CKD; for all other variables, HRs are for values above vs. below median.</p><p>ADMA = asymmetric dimethylarginine; CKD = chronic kidney disease; CI = confidence intervals; SDMA = symmetric dimethylarginine.</p

    Arginine, ADMA and SDMA plasma levels.

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    <p>Arginine (panel A), asymmetric dimethylarginine (ADMA; panel B), and symmetric dimethylarginine (SDMA; panel C) plasma levels (mean±SD values) in healthy subjects (n = 20), in controls with chronic kidney disease (CKD; n = 10), and in NSTEMI patients without (n = 71) and with (n = 33) CKD.</p

    Clinical cases.

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    <p><b>Panel 1</b>. A: ECG at admission. B: ECG at 6<sup>th</sup> day. C, E: T2-weighted images of basal and mid-short axis views, respectively. The increased myocardial signal intensity (arrows) indicates increased water content, hence tissue edema in the anterior, antero-septal and infero-septal walls. D, F: late gadolinium enhancement (LGE) images (basal and mid-short axis views respectively). Necrosis (arrows) and microvascular obstruction (arrowhead) are shown. The edematous myocardial content was 62gr, corresponding to 56% of total left ventricular mass, and LGE was 59gr, corresponding to 54% of total left ventricular mass. The myocardial salvage index (MSI) was 0.05. ΔQTc-AI-MA (max anterior QTc—min inferior QTc) was 200msec. <b>Panel 2</b>. A: ECG at admission. B: ECG at 6<sup>th</sup> day. C, E: T2-weighted images of basal and mid-short axis views, respectively. The increased myocardial signal intensity (arrows) indicates tissue edema in the anterior and antero-septal walls. D, F: LGE images (basal and mid-short axis views, respectively). The edematous myocardial content was 30gr, corresponding to 25% of total left ventricular mass. No LGE was evident. The MSI was 1. No ΔQTc-AI-MA (max anterior QTc—min inferior QTc) was present.</p

    QT-interval evaluation in primary percutaneous coronary intervention of ST-segment elevation myocardial infarction for prediction of myocardial salvage index

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    <div><p>Assessing the efficacy of revascularization therapy in patients with ST-segment elevation myocardial infarction (STEMI) is extremely important in order to guide subsequent management and assess prognosis. We aimed to determine the relationship between corrected QT-interval (QTc) changes on standard sequential ECG and myocardial salvage index in anterior STEMI patients after successful primary percutaneous coronary intervention. Fifty anterior STEMI patients treated by primary percutaneous coronary intervention underwent quantitative ECG analysis and cardiac magnetic resonance. For each patient the difference (ΔQTc) between the QTc of ischemic myocardium (maximum QTc in anterior leads) versus remote myocardium (minimum QTc in inferior leads) during the first six days after STEMI was measured. The QTc in anterior leads was significantly longer than QTc in inferior leads (p<0.0001). At multivariate analysis, ΔQT<sub>C</sub> and peak troponin I were the only independent predictors for late gadolium enhancement while ΔQTc and left ventricular ejection fraction were independent predictors of myocardial salvage index <60%. The receiver operative curve of ΔQTc showed an area under the curve of 0.77 to predict a myocardial salvage index <0.6. In conclusion, in a subset of patients with a first occurrence of early revascularized anterior STEMI, ΔQTc is inversely correlated with CMR-derived myocardial salvage index and may represent a useful parameter for assessing efficacy of reperfusion therapy.</p></div
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