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AimsLeft ventricular remodelling occurs during the chronic course of aortic regurgitation (AR) and aortic stenosis (AS), leading to myocardial hypertrophy and fibrosis. Several studies have shown that extracellular volume fraction (ECV) and indexed extracellular volume (iECV) are important surrogate markers of diffuse myocardial fibrosis (MF). Postoperative data on these cardiovascular magnetic resonance (CMR) extracellular expansion parameters for either AS or AR are scarce. This study aimed to demonstrate the postoperative changes that occur in diffuse MF, and the influence of preoperative MF on the reversal of LV remodelling, in patients with AR or AS.Methods and resultsPatients with severe AR or AS and indications for surgery were prospectively enrolled. Patients underwent pre- and postoperative CMR, and ECV and iECV were quantified. Data from 99 patients were analysed (32 with AR and 67 with AS). After surgery, the left ventricle mass index decreased in both groups (AR: 110 vs. 91 g/m2; AS: 86 vs. 68 g/m2, both P < 0.001). The late gadolinium enhancement fraction (AR: preoperative 1.9% vs. postoperative 1.7%, P = 0.575; AS: preoperative 2.4% vs. postoperative 2.4%, P = 0.615) and late gadolinium enhancement mass (AR: preoperative 3.8 g vs. postoperative 2.5 g, P = 0.635; AS: preoperative 3.4 g vs. postoperative 3.5 g, P = 0.575) remained stable in both groups. Preoperative iECV and ECV were greater in the AR group (iECV: 30 mL/m2 vs. 22 mL/m2, P = 0.001; ECV: 28.4% vs. 27.2%, P = 0.048). Indexed extracellular volume decreased after surgery in both groups (AR: 30–26.5 mL/m2, AS: 22–18.2 mL/m2, both P < 0.001); it was still greater in the AR group (AR: 26.5 mL/m2 vs. AS: 18.2 mL/m2, P < 0.001). Postoperative ECV remained stable in the AR group (preoperative 28.4% vs. postoperative 29.9%; P = 0.617) and increased in the AS group (preoperative 27.2% vs. postoperative 28.6%; P = 0.033).ConclusionPatients with both AR or AS presented reduction in iECV after surgery, unfolding the reversible nature of diffuse MF. In contrast to patients with AS, those with AR developed postoperative iECV regression with stable ECV, suggesting a balanced reduction in both intracellular and extracellular myocardial components.

Introduction: Various questions about methods of diagnosis still remain obscure and there is no effective comparison between them in patients with intermediate risk. Hypothesis: Coronary computed tomography angiopraphy (CCTA) is better than troponins in the detection of coronary artery disease in patients with chest pain and the intermediate probability of acute coronary syndromes (ACS). Methods: Were included prospectively 100 patients with chest pain and TIMI risk score 3 or 4. All patients were submitted to troponin measurements and CCTA. If CCTA showed coronary stenosis ≥ 50%, patient was initiate the ACS treatment and was hospitalized to have coronary cineangiography. If CCTA shows lesions < 50%, the patient was discharged and monitored for 30 days. A second sampling of the troponin was obtained (blinded) from all patients three hours after the first collection. Significant coronary lesion was considered when ≥ 70%. The kit of troponin ADVIA Centaur® TnI-Ultra (Siemens Healthcare Diagnostics, Tarrytown, NY, USA) was used. The CCTA used was the 320-channel Toshiba Aquilium machine. The comparison between methods was performed through the Kappa agreement analysis. Were calculated sensitivity, specificity, and negative and positive predictive values between the sensitivity troponin versus CCTA in the detection of an ACS. Complementary analysis was made by ROC curve calculating the area under the curve (AUC) and the cut-off score of troponin and coronary lesions on angiography/events. Combined events after 30 days were: hospitalization, death and myocardial infarction. Results: The Kappa agreement analysis between troponin and CCTA in the detection of coronary lesions showed low correlation (kappa = 0.022, p = 0.78). Thirty eight (38%) patients were subjected to angiography and significant coronary injury was confirmed at 81.6%. In 62 patients with CCTA lesions < 50%, 2 (3.2%) events were observed in 30 days. Area under the troponin curve related to the presence of significant coronary lesions was 0.401 (IC 95%: 0.156 - 0.646), related to events was 0.808 (IC 95%: 0.695 - 0.922) and related to coronary lesions or events was 0.547 (IC 95%: 0.428 - 0.667). The best percentage variation cutting points of troponin were 20% (sensitivity = 32.3% and specificity = 71%) and 27.5% (sensitivity = 50% and specificity = 75%), respectively related to significant coronary lesions and events. Conclusion: The use of CCTA in patients with intermediate risk for ACS proved to be safe and superior to the sensitive troponin in the detection of coronary heart disease.

Background Coronary artery calcification (CAC) and atherosclerotic inflammation associate with increased risk of myocardial infarction (MI). Vascular calcification is regulated by osteogenic proteins (OPs). It is unknown whether an association exists between CAC and plasma OPs and if they are affected by atherothrombotic inflammation. We tested the association of osteogenic and inflammatory proteins with CAC and assessed these biomarkers after MI. Methods Circulating OPs (osteoprotegerin, RANKL, fetuin-A, Matrix Gla protein [MGP]) and inflammatory proteins (C-reactive protein, oxidized-LDL, tumoral necrosis factor-α, transforming growth factor [TGF]-β1) were compared between stable patients with CAC (CAC ≥ 100 AU, n = 100) and controls (CAC = 0 AU, n = 30). The association between biomarkers and CAC was tested by multivariate analysis. In patients with MI (n = 40), biomarkers were compared between acute phase and 1-2 months post-MI, using controls as a baseline. Results MGP and fetuin-A levels were higher within individuals with CAC. Higher levels of MGP and RANKL were associated with CAC (OR 3.12 [95% CI 1.20-8.11], p = 0.02; and OR 1.75 [95% CI 1.04-2.94] respectively, p = 0.035). After MI, C-reactive protein, OPG and oxidized-LDL levels increased in the acute phase, whereas MGP and TGF-β1 increased 1-2 months post-MI. Conclusions Higher MGP and RANKL levels associate with CAC. These findings highlight the potential role of these proteins as modulators and markers of CAC. In addition, the post-MI increase in OPG and MGP, as well as of inflammatory proteins suggest that the regulation of these OPs is affected by atherothrombotic inflammation.

Cardiac magnetic resonance (CMR) has been shown to predict left ventricular (LV) recovery in patients after acute ST-segment elevation myocardial infarction. The purpose of this investigation was to determine the relative values of infarct transmurality and microvascular obstruction (MVO) using delayed enhancement CMR to predict LV recovery. We studied 17 patients (mean age 60 +/- 10 years, 14 men) presenting with first acute ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention who underwent CMR within 6 days after presentation and again at 6 months. In total 680 myocardial segments were evaluated, of which 267 (39%) demonstrated delayed hyperenhancement (DHE) and 116 (18%) demonstrated MVO. Unadjusted odds ratio (OR) for any improvement in regional LV function with increasing DHE category (50%, 51% to 75%,75% transmurality) was 0.20 (95% confidence interval [CI] 0.13 to 0.30, p0.0001), whereas it was 0.40 (95% CO 0.28 to 0.55, p0.0001) with increasing MVO category (0,50th,50th percentile). However, when coadjusted together, the relation remained robust with regard to degree of transmurality of DHE (OR 0.21, 95% CI 0.13 to 0.36, p0.0001), but the relation was lost for MVO (OR 0.90, 95% CI 0.58 to 1.40, p = 0.64). In conclusion, when using the delayed enhancement technique for assessment of DHE and MVO, degree of infarct transmurality appears to be a more powerful predictor of LV recovery by CMR.

Background: The elevation of troponin (TnI) and creatine kinase-MB (CKMB) after coronary revascularization procedures is frequent, but may not be reliable at identifying a definitive procedure-related myocardial injury. Cardiac magnetic resonance (CMR) is the gold standard in the identification of small areas of myocardial necrosis by late gadolinium enhancement (LGE). The presence of a biomarker early release peak might indicate a nonlethal transient cellular myocardial damage and help to discriminate the patients without procedure-related myocardial lesion. Thus, our objective was to evaluate the amount and pattern of release of biomarkers after coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI) compared with the area of new LGE on CMR. Methods: Patients with indication for coronary revascularization were included. Measurements of high-sensitivity TnI and CK-MB were obtained before and after the procedures, every 6 hours until 48 hours after PCI, and up to 72 hours after CABG. We evaluated the area under the curve (AUC) and peak release of biomarkers and stratified before and 24 hours after the procedure. CMR was performed before and after procedures with quantification of necrosis by LGE. Results: From 150 patients who completed the study, 60 (40%) underwent CABG with cardiopulmonary bypass (CPB), 44 (29.3%) without CPB, and 46 (30.7%) underwent PCI. 130 (86.7%) exhibited release of cardiac biomarkers consistent with myocardial injury, however only 32 (21.3%) had new LGE on CMR. The AUC and peak release of TnI showed a moderate correlation with the mass of new myocardial LGE on CMR (AUC: r = 0.46, P < 0.0001; TnI peak: r = 0.45, P < 0.0001), as well as the AUC and peak release of CKMB (AUC: r = 0.33, P < 0.0001; CK-MB peak: r = 0.35, P Conclusion: The elevation of cardiac biomarkers after coronary revascularization procedures had a low diagnostic power for the detection of new myocardial areas of infarction identified by LGE on CMR. The early release of biomarkers may be useful to rule out the diagnosis of peri-procedural myocardial infarction.