Linked Life Data

17235264

Source:http://linkedlifedata.com/resource/pubmed/id/17235264

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2007-1-19
pubmed:abstractText
With the introduction of biomarkers like troponin I (cTnI), our ability to identify and quantify myocardial infarction in the postoperative period has been greatly enhanced. Even small elevations of cTnI should be considered as a myocardial infarction. Small increases in cTnI postoperatively have indeed been found to be associated with worse short and long-term outcomes, the higher the cTnI level the worse the outcome. Studies undertaken in the 1980s when postoperative myocardial infarction (PMI) was detected by means of electrocardiogram recordings every 12 hours following operation suggested that this complication occurred on the second or third postoperative day. More recent studies where postoperative myocardial necrosis has been detected by repeated troponin dosages have revealed that, in fact, postoperative myocardial infarction appears much earlier between 12 and 32 hour after the end of surgery. Two types of PMI were identified based on intense troponin surveillance. They stem from two different major pathophysiological mechanisms. One seems to be related to plaque-vulnerability, while the other may be due to the effects of prolonged ischemia. The postoperative period should be regarded as a vulnerable period' that acts synergistically with both plaque and patient vulnerabilities in the development of PMI. Monitoring troponin levels in the postoperative period following surgery enables the identification of patients with myocardial damage and the institution of early aggressive intervention (e.g., intensive beta blockers therapy, adequate analgesia, correction of anemia) in order to prevent the evolution of PMI during this golden period' that lasts about two days. In patients that are prone to develop PMI, and especially in those who are prone to develop PMI related to plaque rupture, prevention can be achieved by better preoperative identification of the vulnerable plaque, and by a better plaque stabilization, either metabolically (e.g., statins) or by actual coronary stenting. Further understanding of the mechanisms underlying PMI, as well as their early identification, may contribute to the reduction of the incidence of PMI and its associated morality in the future.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0375-9393
pubmed:author
pubmed:issnType
Print
pubmed:volume
72
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
965-83
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Postoperative myocardial infarction: pathophysiology, new diagnostic criteria, prevention.
pubmed:affiliation
University Campus Bio-Medico, Rome, Italy.
pubmed:publicationType
Journal Article, Review