A small study including consecutive patients admitted to the ICU because of an indication for mechanical ventilation, or after thoracic or vascular surgery, found elevated cTnT levels (cutoff, 0.1 Mg/L) in 11 of 34 patients (32%). However, in this study, four cTnT-positive patients had acute myocardial infarction, and thus conclusions about the impact of cTnT in ICU patients are limited.
Studies restricted to patients with sepsis or critically ill patients, of whom most had SIRS or sepsis, are summarized in Table 2. Several authors reported a relationship between elevated cTnI or cTnT levels and left ventricular dysfunction assessed either by echocardiography (LVEF)–. or PAC (LVSWI). In addition, the duration of hypotension and the maximal number of vasopressor doses administered were found to be correlated to cardiac troponin levels. Finally, elevated troponin levels have been shown to be related to the severity of the disease as expressed by global scores such as the acute physiology and chronic health evaluation (APACHE) II score or simplified acute physiology score II as well as short-term prognosis….canadian health and care mall
The studies differ with respect to the incidence of troponin positivity, which may be explained by the heterogeneity of study populations, the type of troponin studied (ie, cTnI, cTnT, or both), and the cutoff level of the troponin test applied. Nevertheless, the results of these studies were very similar in concluding that elevated troponin levels in patients with sepsis indicate a higher severity of disease, the presence of myocardial dysfunction, and a worse prognosis.
Whereas the diagnostic and prognostic impact of elevated cardiac troponin levels in patients with sepsis has been established, the underlying mechanisms still require clarification. Measurements by coronary sinus thermodilution catheters revealed that coronary blood flow did not differ between patients with septic shock and healthy subjects as long as the heart rate was < 100 beats/min, and that coronary blood flow was even higher in patients with septic shock compared to healthy subjects if the heart rate was > 100 beats/min.
Table 2—Prospective Studies on Cardiac Troponin Levels in Critically Ill Adults Mainly Including Patients With Sepsis
|Study||Study Population(Agej yr)||Severity of Disease||Assessment of LV Performance||TroponinPositivity||In-HospitalMortality||Relationships Among Cardiac Troponin Level, LV Performance, and Outcome||Exclusion of Flow-Limiting CAD|
|Fernandeset al||10 pts with sepsis(30 ± 6)||APACHE II score: 25 ± 11||PAC, TTE||cTnI (cutoff, 0.6 Mg/L): 6/10 pts(60%)||4/10 pts (40%); cTnI+, 3 pts||All pts with LVEF < 0.5 were cTnI+; cardiac index and cTnI not related||Not done|
|Spieset al||26 pts with sepsis (approximately 60)||APACHE II: approximately 48||PAC||cTnT (cutoff, 0.2 Mg/L): 18/26 pts (69%)||
);ts T 38
|Higher mortality in cTnT+ pts(p = 0.02)||Not done|
|Turner et al||G1: 15 pts with septic shock (70; age range, 24-77); G2: 6 pts without sepsis, but receiving mechanical ventilation (61; age range, 2477)||APACHE II score: G1, 24 (range, 3-39); G2, 14.5 (range, 8-23)||PAC (except one pt)||cTnI (cutoff, 0.4 Mg/L): G1, 12 of 15 pts (80%); G2, 1/6 pts(17%)||G1, 4/15 pts (27%); G2, 0/6 pts; cTnI +,4/13 pts (31%); cTnI—, 0/8 pts||Correlation minimum LVSWI and maximum cTnI level(r = – 0.72); correlation maximum vasopressor dose and maximum cTnI (r = 0.55)||Not done|
|Arlatiet al||G1: 19 pts with severe sepsis or septic shock (56 ± 4); G2:12 pts with hypovolemic shock (71 ± 4)||Pao2/Fio2 ratio: G1, 198 ± 21 mm Hg; G2, 270 ± 42 mm Hg||Not assessed; hypotension (MAP < 90 mm Hg) graded as moderate (3060 min) or severe (> 60 min)||cTnI (cutoff, 0.5 Mg/L): G1, 11/ 19 pts (58%); G2, 12/12 pts(100%)||G1, 10/19 pts(53%); G2, 5/12 pts (42%)||Correlation abnormal cTnI levels and duration of hypotension (Kendall t, 0.48); weak correlation abnormal cTnI levels and outcome (r = 0.28)||Not done; 2 pts in G1 and 5 pts in G2 had a history of CAD, all of whom were cTnI+; 4 pts from G1 and 1 pt from G2 had ECG evidence of MI|
|Ver Elstet al||46 pts with septicshock (66; IQR, 54-74)||APACHE II score: 24 (IQR, 20-30)||PAC; TEE: LV dysfunction defined as LVEDD > 60 mm, LVEDV > 120 mL, and LVFAC < 0.4||cTnI (cutoff, 0.4 Mg/L): 23/46 pts (50%) cTnT (cutoff, 0.1 Mg/L): 16/ 45 pts (36%)||21/46 pts (46%)||LV dysfunction in 78% of cTnI+ pts, but only in 9% of cTnI— pts(p < 0.0001); correlation ICU admission APACHE II score and peak cTnI (r value, NA) and cTnT (r value, NA); correlation cTnI and LV dysfunction (r value, NA)||Autopsyperformed in 7 cTnI+ and 5 cTnI—pts; LV free wall rupture in 1 cTnI— pt, MI in 1 cTnI+ pt; no MI in 10 pts; contraction band necrosis in 3 cTnI+ pts and in 1 cTnI— pt|
|Ammannetal||G1: 20 pts with SIRS (n = 3), sepsis (n = 9), or septic shock (n = 8)[66 ± 8]; G2: age and sex-matched control subjects||NA||Not systematically cTnI (cutoff, 0.1 assessed Mg/L): G1, 17/ 20 pts (85%); G2, 0||
G1, 6/20 pts(30%); G2, 0 pts; cTnI +, 5/17 pts (29%); cTnI—, 1/9 pts
|Not assessed||In 10/17 cTnI+ pts (59%) relevant CAD ruled out by autopsy, coronary angiography, or stressechocardiography|
|Ammannet al||58 critically ill pts, 27/58 (47%) withSIRS/sepsis, 24/58 (41%) with septic shock (55 ± 21)||SAPS II score: 42 ± 15||TTE||cTnI and cTnT (cutoff, 0.1 Mg/ L): 32/58 of all pts (55%); and 32/51 (63%) of the SIRS/sepsis/ septic shock pts||16/58 (28%)||Lower LVEF in cTnI/T+ pts (48 ± 13%) vs cTnI/T— pts (60 ± 10%; p = 0.0006); correlation cTnI and LVEF (r = -0.44); higher mortality in cTnI/T + pts (p = 0.018)||
In 72% of cTnI/T+ pts, relevant CAD excluded by autopsy, coronary angiography, or stress
37 pts with septic shock(approximately
|TTE||cTnI (cutoff, 1.0 Mg/L): 16/43 pts (43%)||cTnI +: 10/16 (63%) cTnI-: 5/21 (24%)||Correlation cTnI with LVEF (r = -0.7); higher APACHE II score and mortality in cTnI+ pts||Not performed|