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María Isabel Coma Canella

Publicaciones científicas más recientes (desde 2010)

Autores: Coma, María Isabel; Artaiz, Miguel; et al.
ISSN 1137-6627  Vol. 40  Nº 1  2017  págs. 35 - 42
Background. Most acute coronary syndromes are caused by the fracture of a vulnerable atherosclerotic plaque. These plaques are thin cap fibroatheromas, which can only be detected with invasive coronary imaging techniques. It is necessary to find a non-invasive biomarker of these vulnerable plaques in order to identify patients at risk without a coronary angiography. Metalloproteinase-1 is an enzyme involved in extracellular matrix metabolism which has been correlated with the rupture of atherosclerotic plaques. Its serum levels in patients with vulnerable plaques remain unknown. Methods. Patients with suspected stable coronary artery disease undergoing coronary angiography in our hospital were included. The coronary arteries were studied with optical coherence tomography to detect vulnerable plaques. Blood samples were taken from a peripheral vein and from the coronary sinus, to assess metalloproteinase-1 levels. Results. Fifty-one patients were included, 13 of whom had at least one vulnerable plaque. There were not significant differences in clinical characteristics, lipid profile or C reactive protein levels, between patients with or without vulnerable plaques. Patients with vulnerable plaques had significant higher metalloproteinase-1 levels both in peripheral (7330 5541 vs 2894 1783 pg/ml, p=0.025) and coronary sinus serum (6012 3854 vs 2707 1252 pg/ml, p=0.047). Conclusions. Patients with vulnerable plaques had significantly higher metalloproteinase-1 serum levels. Further studies with clinical follow up are needed to assess the prognostic value of serum metalloproteinase-1.
Autores: Ravassa, S; Beaumont Javier; Huerta, Ana; et al.
ISSN 0891-5849  Vol. 81  2015  págs. 1 - 12
Oxidative stress (OS) contributes to cardiovascular damage in type 2 diabetes mellitus (T2DM). The peptide glucagon-like peptide-1 (GLP-1) inhibits OS and exerts cardiovascular protective actions. Our aim was to investigate whether cardiac remodeling (CR) and cardiovascular events (CVE) are associated with circulating GLP-1 and biomarkers of OS in T2DM patients. We also studied GLP-1 antioxidant effects in a model of cardiomyocyte lipotoxicity. We examined 72 T2DM patients with no coronary or valve heart disease and 14 nondiabetic subjects. A median of 6 years follow-up information was obtained in 60 patients. Circulating GLP-1, dipeptidyl peptidase-4 activity, and biomarkers of OS were quantified. In T2DM patients, circulating GLP-1 decreased and OS biomarkers increased, compared with nondiabetics. Plasma GLP-1 was inversely correlated with serum 3-nitrotyrosine in T2DM patients. Patients showing high circulating 3-nitrotyrosine and low GLP-1 levels exhibited CR and higher risk for CVE, compared to the remaining patients. In palmitate-stimulated HL-1 cardiomyocytes, GLP-1 reduced cytosolic and mitochondrial oxidative stress, increased mitochondrial ATP synthase expression, partially restored mitochondrial membrane permeability and cytochrome c oxidase activity, blunted leakage of creatine to the extracellular medium, and inhibited oxidative damage in total and mitochondrial DNA. These results suggest that T2DM patients with reduced circulating GLP-1 and exacerbated OS may exhibit CR and be at higher risk for CVE. In addition, GLP-1 exerts antioxidant effects in HL-1 palmitate-overloaded cardiomyocytes. It is proposed that therapies aimed to increase GLP-1 may counteract OS, protect from CR, and prevent CVE in patients with T2DM.
Autores: Ravassa, S; Barba, Joaquín; Coma, María Isabel; et al.
ISSN 1475-2840  Vol. 12  2013  págs. 143
Background: Patients with type 2 diabetes mellitus (T2DM) present subclinical left ventricular systolic and/or diastolic dysfunction (LVD). Dipeptidyl peptidase-4 (DPP4) inactivates peptides that possess cardioprotective actions. Our aim was to analyze whether the activity of circulating DPP4 is associated with echocardiographically defined LVD in asymptomatic patients with T2DM. Methods: In this cross-sectional study, we examined 83 T2DM patients with no coronary or valve heart disease and 59 age and gender-matched non-diabetic subjects. Plasma DPP4 activity (DPP4a) was measured by enzymatic assay and serum amino-terminal pro-brain natriuretic peptide (NT-proBNP) was measured by enzyme-linked immunosorbent assay. LV function was assessed by two-dimensional echocardiographic imaging, targeted M-mode recordings and Doppler ultrasound measurements. Differences in means were assessed by t-tests and one-way ANOVA. Associations were assessed by adjusted multiple linear regression and logistic regression analyses. Results: DPP4a was increased in T2DM patients as compared with non-diabetic subjects (5855 +/- 1632 vs 5208 +/- 957 pmol/min/mL, p < 0.05). Clinical characteristics and echocardiographic parameters assessing LV morphology were similar across DPP4a tertiles in T2DM patients. However, prevalence of LVD progressively increased across incremental DPP4a tertiles (13%, 39% and 71%, all p < 0.001). Multivariate regression analysis confirmed the independent associations of DPP4a with LVD in T2DM patients (p < 0.05). Similarly, multiple logistic regression analysis showed that an increase of 100 pmol/min/min plasma DPP4a was independently associated with an increased frequency of LVD with an adjusted odds ratio of 1.10 (95% CI, 1.04 to 1.15, p = 0.001). Conclusions: An excessive activity of circulating DPP4 is independently associated with subclinical LVD in T2DM patients. Albeit descriptive, these findings suggest that DPP4 may be involved in the mechanisms of LVD in T2DM.
Autores: Coma, María Isabel; Artaiz, Miguel; et al.
ISSN 1826-1868  Vol. 5  Nº 2  2010  págs. 58 - 63
Autores: Garcia-Fernandez, N; Echeverría, A.; Sánchez, Alfonso; et al.
ISSN 1320-5358  Vol. 15  Nº 2  2010  págs. 178 - 183
Autores: Garcia-Velloso, Maria Jose; Coma, María Isabel; Peñuelas, Iván; et al.
Libro:  Medicina Nuclear en la práctica clínica
2012  págs. 295-305