CAMILA ROCON DE LIMA ANDRETA

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Revista / Livro: European Heart Journal-Cardiovascular Imaging ×

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  • article 36 Citação(ões) na Scopus
    Myocardial T1 mapping and extracellular volume quantification in patients with left ventricular non-compaction cardiomyopathy
    (2018) ARAUJO-FILHO, Jose A. B.; ASSUNCAO JR., Antonildes N.; MELO, Marcelo D. Tavares de; BIERE, Loic; LIMA, Camila R.; DANTAS JR., Roberto N.; NOMURA, Cesar H.; SALEMI, Vera M. C.; JEROSCH-HEROLD, Michael; PARGA, Jose R.
    Aims From pathophysiological mechanisms to risk stratification and management, much debate and discussion persist regarding left ventricular non-compaction cardiomyopathy (LVNC). This study aimed to characterize myocardial T1 mapping and extracellular volume (ECV) fraction by cardiovascular magnetic resonance (CMR), and investigate how these biomarkers relate to left ventricular ejection fraction (LVEF) and ventricular arrhythmias (VA) in LVNC. Methods and results Patients with LVNC (n = 36) and healthy controls (n = 18) were enrolled to perform a CMR with T1 mapping. ECV was quantified in LV segments without late gadolinium enhancement (LGE) areas to investigate diffuse myocardial fibrosis. Patients with LVNC had slightly higher native T1 (1024 +/- 43ms vs. 995 +/- 22 ms, P = 0.01) and substantially expanded ECV (28.0 +/- 4.5% vs. 23.5 +/- 2.2%, P < 0.001) compared to controls. The ECV was independently associated with LVEF (beta = -1.3, P = 0.001). Among patients without LGE, VAs were associated with higher ECV (27.7% with VA vs. 25.8% without VA, P = 0.002). Conclusion In LVNC, tissue characterization by T1 mapping suggests an extracellular expansion by diffuse fibrosis in myocardium without LGE, which was associated with myocardial dysfunction and VA, but not with the amount of noncompacted myocardium.
  • article 5 Citação(ões) na Scopus
    Decreased glycolytic metabolism in non-compaction cardiomyopathy by F-18-fluoro-2-deoxyglucose positron emission tomography: new insights into pathophysiological mechanisms and clinical implications
    (2017) MELO, Marcelo Dantas Tavares de; GIORGI, Maria Clementina Pinto; ASSUNCAO JR., Antonildes Nascimento; DANTAS JR., Roberto Nery; ARAUJO FILHO, Jose de Arimateia; PARGA FILHO, Jose Rodrigues; BIERRENBACH, Ana Luiza de Souza; LIMA, Camila Rocon de; SOARES JR., Jose; MENEGUETTI, Jose Claudio; MADY, Charles; HAJJAR, Ludhmila Abrahao; KALIL FILHO, Roberto; BOCCHI, Edimar Alcides; SALEMI, Vera Maria Cury
    Aims The pathophysiological mechanisms of left ventricular non-compaction cardiomyopathy (LVNC) remain controversial. This study performed combined F-18-fluoro-2-deoxyglucose dynamic positron emission tomography (FDG-PET) and 99mTc-sestamibi single-photon emission computed tomography (SPECT) studies to evaluate myocardial glucose metabolism and perfusion in patients with LVNC and their clinical implications. Methods and results Thirty patients (41 +/- 12 years, 53% male) with LVNC, diagnosed by cardiovascular magnetic resonance (CMR) criteria, and eight age-matched healthy controls (42 +/- 12 years, 50% male) were prospectively recruited to undergo FDG-PET with measurement of the myocardial glucose uptake rate (MGU) and SPECT to investigate perfusion-metabolism patterns. Patients with LVNC had lower global MGU compared with that in controls (36.9 +/- 8.8 vs. 44.6 +/- 5.4 mu mol/min/100 g, respectively, P = 0.02). Of 17 LV segments, MGU levels were significantly reduced in 8, and also a reduction was observed when compacted segments from LVNC were compared with the segments from control subjects (P < 0.001). Perfusion defects were also found in 15 (50%) patients (45 LV segments: 64.4% match, and 35.6% mismatch perfusion-metabolism pattern). Univariate and multivariate analyses showed that beta-blocker therapy was associated with increased MGU (beta coefficient = 10.1, P = 0.008). Moreover, a gradual increase occurred in MGU across the beta-blocker dose groups (P for trend = 0.01). Conclusion The reduction of MGU documented by FDG-PET in LVNC supports the hypothesis that a cellular metabolic pathway may play a role in the pathophysiology of LVNC. The beneficial effect of beta-blocker mediating myocardial.