Nahuel Fernandez Machulsky1, Juan Gagliardi2, Bibiana Fabre3, Verónica Miksztowicz1, Micaela Lombardo1, Alejandro García Escudero2, Gerardo Gigena2, Federico Blanco2, Ricardo J Gelpi4, Laura Schreier1, Yori Gidron5, Gabriela Berg6. 1. Lipids and Atherosclerosis Laboratory, Clinical Biochemistry Department, INFIBIOC, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Argentina. 2. Hemodynamic Unit, Cardiology Division, General Hospital Dr. Cosme Argerich, Buenos Aires, Argentina. 3. Endocrinology Laboratory, Clinical Biochemistry Department, INFIBIOC, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Argentina. 4. Institute of Cardiovascular Physiopathology and Department of Pathology, Faculty of Medicine, University of Buenos Aires, Argentina. 5. Behavior Medicine, Faculty of Medicine & Pharmacy, Vrije Universiteit Brussel (VUB), Brussels, Belgium. 6. Lipids and Atherosclerosis Laboratory, Clinical Biochemistry Department, INFIBIOC, Faculty of Pharmacy and Biochemistry, University of Buenos Aires, Argentina. Electronic address: gaberg@ffyb.uba.ar.
Abstract
UNLABELLED: 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, 24h, 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 (R(2)=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.
UNLABELLED: 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, 24h, 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 (R(2)=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.