Myocardial necrosis in ICU patients with acute non-cardiac disease: a prospective study.
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.


METHODS
A prospective observational study.


METHODS
General intensive care unit (ICU) at a tertiary level hospital.


METHODS
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.


METHODS
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.


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.
Arlati
S
S
Intensive Care Unit "G. Bozza", Niguarda Ca' Granda Hospital, P. za Ospedale Maggiore, I-20123 Milan, Italy.
Brenna
S
S
Prencipe
L
L
Marocchi
A
A
Casella
G P
GP
Lanzani
M
M
Gandini
C
C
D000368:Aged; D003402:Creatine Kinase / Q000378:metabolism*; D004562:Electrocardiography; D017052:Hospital Mortality; D006801:Humans; D007022:Hypotension / Q000150:complications*; D007362:Intensive Care Units; D007527:Isoenzymes; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis; D009206:Myocardium / Q000473:pathology*; D009211:Myoglobin / Q000378:metabolism; D009336:Necrosis; D011446:Prospective Studies; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology; D012769:Shock / Q000150:complications* / Q000503:physiopathology; D019210:Troponin I / Q000378:metabolism*
D007527:Isoenzymes; D009211:Myoglobin; D019210:Troponin I; D003402:Creatine Kinase