Revista medico-chirurgicala a Societatii de Medici si Naturalisti din Iasi · 2016
Inflammatory and Genetic Markers (APO B100 and Angiotensin-Converting Enzyme Gene) in the Coronary Artery Disease.
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Apăvăloaie Maria-Cristina, Bararu Iris, Pleşoianu Carmen Elena, Jitaru Daniela, Dragoş Loredana, Ciocoiu Manuela, Arsenescu-Georgescu Cătălina, Bădescu Magda
Аннотация
AIM: To analyze the correlations between inflammation markers and ApoB100 and angiotensin converting enzyme (ACE) gene polymorphism and the severity of coronary artery disease (CAD).
MATERIAL AND METHODS: We conducted a study in 58 patients with acute coronary syndromes (ACS) who underwent coronarography at the Iasi "Prof. Dr. George I.M. Georgescu' Institute of Cardiovascular Diseases. the patients included in the studies were selected from those who needed a coronarography for unstable angina or acute myocardial infarction. The data were uploaded and processed using the statistical functions in SPPS 18.0 at a 95% materiality threshold.
RESULTS: Elevated inflammation markers were found in all study patients, with small differences in distribution. None of the study patients presented ApoB100 gene mutations. As to ACE polymorphism, a predominance of genotype II in unicoronary patients and ID and DD genotypes in bicoronary and tricoronary patients was found.
CONCLUSIONS: The results of our study confirm the role of genetic and epigenetic factors in the severity and progression of the coronary disease, leaving room for larger and more comprehensive studies and new research perspectives.
MATERIAL AND METHODS: We conducted a study in 58 patients with acute coronary syndromes (ACS) who underwent coronarography at the Iasi "Prof. Dr. George I.M. Georgescu' Institute of Cardiovascular Diseases. the patients included in the studies were selected from those who needed a coronarography for unstable angina or acute myocardial infarction. The data were uploaded and processed using the statistical functions in SPPS 18.0 at a 95% materiality threshold.
RESULTS: Elevated inflammation markers were found in all study patients, with small differences in distribution. None of the study patients presented ApoB100 gene mutations. As to ACE polymorphism, a predominance of genotype II in unicoronary patients and ID and DD genotypes in bicoronary and tricoronary patients was found.
CONCLUSIONS: The results of our study confirm the role of genetic and epigenetic factors in the severity and progression of the coronary disease, leaving room for larger and more comprehensive studies and new research perspectives.