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.
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 hypovolemicpatients. 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 illpatients 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: Esther A P van Bockel; Jaap E Tulleken; Anneke C Muller Kobold; Jack J M Ligtenberg; Tjip S van der Werf; Rob Spanjersberg; Jan G Zijlstra Journal: Intensive Care Med Date: 2003-07-17 Impact factor: 17.440
Authors: Claudio Ronco; Peter McCullough; Stefan D Anker; Inder Anand; Nadia Aspromonte; Sean M Bagshaw; Rinaldo Bellomo; Tomas Berl; Ilona Bobek; Dinna N Cruz; Luciano Daliento; Andrew Davenport; Mikko Haapio; Hans Hillege; Andrew A House; Nevin Katz; Alan Maisel; Sunil Mankad; Pierluigi Zanco; Alexandre Mebazaa; Alberto Palazzuoli; Federico Ronco; Andrew Shaw; Geoff Sheinfeld; Sachin Soni; Giorgio Vescovo; Nereo Zamperetti; Piotr Ponikowski Journal: Eur Heart J Date: 2009-12-25 Impact factor: 29.983