Document Detail


Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study.
MedLine Citation:
PMID:  10663277     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: To ascertain if, after an episode of hypotension, unnoticed myocardial necrosis could occur in critical care patients with acute non-cardiac illness and to search for signs of cardiac necrosis. DESIGN: A prospective observational study. SETTING: General intensive care unit (ICU) at a tertiary level hospital. PATIENTS: Thirty-one patients in two groups. Group 1 included 19 patients with severe sepsis/septic shock (ACCP/SCCM Consensus Conference). Group 2 included 12 patients with hypovolemic shock. INTERVENTIONS: Biochemical markers of myocardial necrosis (cardiac troponin I (cTnI), creatine kinase (CK), creatine kinase MB mass (CKMB) and myoglobin) were measured at 12 h (T1), 24 h (T2) and 48 h (T3) after enrollment. A standard 12-lead ECG was recorded upon enrollment (T0) and at T2. Anomalous Q-waves or ST segment depression or elevation was considered diagnostic for acute myocardial infarction (AMI). A hypotensive episode (arterial systolic pressure < 90 mmHg at heart rate > 100 bpm) was considered moderate if it lasted 30-60 min or severe if longer than 60 min. MEASUREMENTS AND RESULTS: At T0 none of the patients had AMI on ECG. At T2 a non-Q AMI developed in five patients. Increased levels of troponin I, myoglobin, CK and CKMB were found in 74.2 %, 96.8 %, 74.2 % and 67.7 % of the patients, respectively. Cardiac troponin I increased in 11 out of 19 septic patients and in all hypovolemic patients. There was a significant difference between the groups (p < 0.05). All biochemical markers increased in relationship to the degree of hypotension with cTnI again showing a significant difference. The longer the hypotensive episode was, the greater was the increase (moderate hypotension: median 1.16; quartiles 0.55-3.44 ng/ml, severe hypotension: median 8.53; quartiles 1.1-20.7 ng/ml; p < 0.05). Abnormal levels of cTnI were more frequent in non-survivors than in survivors (p < 0.05). CONCLUSIONS: Hypotension may cause cardiac damage in critically ill patients with acute non-cardiac diseases as shown by abnormal levels of cTnI. It is likely that a high number of these myocardial necroses may go unnoticed on the ECG.
Authors:
S Arlati; S Brenna; L Prencipe; A Marocchi; G P Casella; M Lanzani; C Gandini
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Publication Detail:
Type:  Comparative Study; Journal Article    
Journal Detail:
Title:  Intensive care medicine     Volume:  26     ISSN:  0342-4642     ISO Abbreviation:  Intensive Care Med     Publication Date:  2000 Jan 
Date Detail:
Created Date:  2000-03-15     Completed Date:  2000-03-15     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  7704851     Medline TA:  Intensive Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  31-7     Citation Subset:  IM    
Affiliation:
Intensive Care Unit "G. Bozza", Niguarda Ca' Granda Hospital, P. za Ospedale Maggiore, I-20123 Milan, Italy.
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MeSH Terms
Descriptor/Qualifier:
Aged
Creatine Kinase / metabolism*
Electrocardiography
Hospital Mortality
Humans
Hypotension / complications*
Intensive Care Units*
Isoenzymes
Middle Aged
Myocardial Infarction / diagnosis
Myocardium / pathology*
Myoglobin / metabolism
Necrosis
Prospective Studies
Sepsis / complications*,  physiopathology
Shock / complications*,  physiopathology
Troponin I / metabolism*
Chemical
Reg. No./Substance:
0/Isoenzymes; 0/Myoglobin; 0/Troponin I; EC 2.7.3.2/Creatine Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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