Verónica Miksztowicz, Yori Gidron, Alejandro García Escudero, Gerardo Gigena, Ricardo J. Gelpi, Nahuel Fernandez Machulsky, Laura Schreier, Federico Blanco, Bibiana Fabre, Juan Gagliardi, Micaela Lombardo, Gabriela Berg, Basic (bio-) Medical Sciences, and Neuroprotection & Neuromodulation
Psychosocial factors have been linked to cardiovascular diseases independently of traditional risk factors. The impact of psychosocial factors on plaque destabilizing factors, such as matrix metalloproteinases (MMPs) has been proposed although scarcely studied. Objective: To evaluate the relationships between hostility, perceived stress and social support with MMPs activity in patients after an Acute Myocardial Infarction (AMI). Methods: Blood samples were obtained from 76 patients on admission, post-angioplasty, 24. h, 7 days and 3 months after AMI. Hostility, perceived stress and social support were evaluated by validated questionnaires. Results: Social support was positively correlated with patientś ejection fraction (r = 0.453, p = 0.009). Patients with higher infarct size presented increased MMP-2 activity at admission (p = 0.04). Patients with one diseased vessel had more social support than those with three diseased vessels (p = 0.05). The highest values of MMP-2 and MMP-9 activity were observed at the acute event, decreasing, with the lowest activity at 3 months post-AMI (p < 0.001). Only in patients with low social support, hostility correlated with MMP-2 activity, from AMI onset (r = 0.645, p = 0.013), to 7 days post AMI (r = 0.557, p = 0.038). Hostility explained up to 28% of the variance in MMP-2 activity (R2=0.28, p = 0.005). Finally, in patients with high hostility, MMP-9 was positively correlated with IL-1β (r = 0.468, p = 0.02). Conclusions: This study adds weight to the idea that two psychosocial factors, namely hostility and social support, acting jointly, may affect MMP-2 activity. Moreover, in hostile patients, there is a link between IL-1β and MMP-9. These findings support the role of psychosocial factors in plaque destabilization and in the inflammatory process in AMI. Fil: Fernandez Machulsky, Nahuel Hernan. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Gagliardino, Juan Jose. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Ministerio de Defensa. Ejército Argentino. Hospital Militar Central Cirujano Mayor "Dr. Cosme Argerich"; Argentina Fil: Fabre, Bibiana. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Miksztowicz, Verónica Julieta. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Lombardo, Micaela. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: García Escudero, Alejandro. Ministerio de Defensa. Ejército Argentino. Hospital Militar Central Cirujano Mayor "Dr. Cosme Argerich"; Argentina Fil: Gigena, Gerardo. Ministerio de Defensa. Ejército Argentino. Hospital Militar Central Cirujano Mayor "Dr. Cosme Argerich"; Argentina Fil: Blanco, Federico Carlos. Ministerio de Defensa. Ejército Argentino. Hospital Militar Central Cirujano Mayor "Dr. Cosme Argerich"; Argentina Fil: Gelpi, Ricardo Jorge. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiopatología Cardiovascular; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina Fil: Schreier, Laura Ester. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina Fil: Gidron, Yori. Vrije Unviversiteit Brussel; Bélgica Fil: Berg, Gabriela Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Departamento de Bioquímica Clínica; Argentina