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Inflammation in ST- elevation myocardial infarction: risk factors, patterns of presentation and association with clinical picture and outcome, an observational study conducted at the Institute of Cardiology-National Hospital of Sri Lanka
BACKGROUND: Inflammation in myocardial infarction has a complex immunogenic origin and is suspected to be closely involved in its aetio-pathogenesis as well as outcome. In this study the objective was to further elucidate the clinical correlations of inflammation using clinical parameters and basic...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6518612/ https://www.ncbi.nlm.nih.gov/pubmed/31088357 http://dx.doi.org/10.1186/s12872-019-1104-5 |
Sumario: | BACKGROUND: Inflammation in myocardial infarction has a complex immunogenic origin and is suspected to be closely involved in its aetio-pathogenesis as well as outcome. In this study the objective was to further elucidate the clinical correlations of inflammation using clinical parameters and basic inflammatory markers and how it correlates with patient risk parameters, imaging findings and outcome. METHODS: An observational descriptive cross sectional study was carried out at the Institute of Cardiology, National Hospital of Sri Lanka, where consenting patients presenting for further management of ST- elevation myocardial infarction were recruited. Venous blood samples were collected on admission to assess C-reactive protein levels and on a timed manner to asses Troponin I levels as well as on subsequent days to performs whole blood analysis. Patients underwent 6 hourly axillary temperature assessment. All patients underwent 2D transthoracic echocardiographic analysis via biplane Simpson’s method to ascertain ejection fraction as well. RESULTS: Eighty eight subjects were recruited into the study. Fever was noted in 20.5% (n = 18). Fever was usually intermittent and seen commonly between day 1 and 3 post-acute myocardial infarction. Haematological abnormalities indicative of inflammation were also observed as whole blood analysis demonstrated predominant leukocytosis and elevated C-reactive protein levels. Significant correlation was noted between presence of leukocytosis (P = 0.033) and fever as well as with the presence of diabetes mellitus (P = 0.005). Development of acute heart failure also showed significant correlation with leukocytosis (P = 0.002). Correlation was also observed between LV dysfunction and elevated C-reactive protein and Troponin I levels with P values of P = 0.023 and P = 0.011 (P < 0.05) respectively. CONCLUSIONS: Inflammation is appreciated following acute myocardial infarction. Biochemical evidence of inflammation is commonly seen. Clinical manifestation as fever however is seen less often. Patient factors correlate poorly with inflammation but diabetes mellitus may have a contributory role. Whole blood analysis derangement is a simple test that correlates well with inflammation as well as presence of fever and development of heart failure. Inflammation also correlated with left ventricular dysfunction and may thus have an impact on clinical morbidity and mortality. Delineating associates of inflammation will hopefully help improve therapy of myocardial infarction. |
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