Myocardial Necrosis in ICU Patients Without Acute Cardiac Disease
Abstract & Commentary
Synopsis: Hypotension may cause cardiac damage in critically ill patients with acute noncardiac diseases, as shown by abnormal serum levels of troponin I.
Source: Arlati S, et al. Intensive Care Med 2000;26: 31-37.
Arlati and colleagues investigated whether "unnoticed" myocardial necrosis could occur after a hypotensive episode in critical care patients with acute noncardiac illness. Thirty-one patients with severe sepsis/septic shock or hypovolemic shock were enrolled in the study. Patients who had had external heart massage, defibrillation, or electrical cardioversion in the previous seven days, symptoms and/or ECG signs typical of acute myocardial infarction at enrollment, complete left bundle branch block on electrocardiogram, or chest trauma in the previous seven days were excluded from the study. Biochemical markers of myocardial necrosis (cardiac troponin I [cTnI], creatine kinase [CK], creatine kinase myocardial band mass [CKMB] and myoglobin were measured in the patients’ blood at 12 hours, 24 hours, and 48 hours after enrollment. The peak values were considered for data analysis. A standard 12-lead electrocardiogram was also recorded upon enrollment and at 24 hours after enrollment.
At enrollment, arterial hypotension (arterial systolic pressure < 90 mm Hg at a heart rate > 100 beats/min) was present in 25 of 31 patients (80.6%). All hypotensive patients needed intravenous infusions of catecholamines. At 48 hours, 12 patients still received catecholamines. Arlati et al considered that hypotensive episodes were nonsignificant if they lasted less than 30 minutes, moderate if 30-60 minutes in duration, and severe if they lasted more than 60 minutes. All biochemical markers increased in relationship to the degree of hypotension with cTnI showing a significant difference (see Table). The longer the hypotensive episode was, the greater the increase. The ECG failed to identify 18 of 23 patients with elevated levels of cTnI. In addition, abnormal levels of cTnI were more frequent in nonsurvivors than in survivors.
| Table | |||
| Plasma Concentrations of cTnI with Respect to Duration of Hypotension | |||
| No Hypotension | Mild Hypotension | Severe Hypotension | |
| (n = 6) | (n = 9) | (n = 16) | |
| CTnI | 0.50 ng/mL | 1.16 ng/mL | 8.50 ng/mL1,2 |
| (0.50-0.50 ng/mL) | (0.55-3.44 ng/mL) | (1.10-20.7 ng/mL) | |
| Values are median and quartiles | |||
| 1. P < 0.05 compared with "mild hypotension" | |||
| 2. P < 0.05 compared with "no hypotension" | |||
COMMENT BY FRANCISCO BAIGORRI, MD, PhD
Serum levels of CK and its MB fraction have been recognized as important indicators of myocardial necrosis. However, levels of CKMB can be increased in patients with skeletal muscle injury or renal failure in the absence of myocardial injury, causing diagnostic confusion. CTnI is a myocardial regulatory protein that modulates the interaction of actin and myosin. Elevated levels in plasma are highly specific for cardiac injury, and are highly correlated with the development of new areas of regional dysfunction determined by echocardiography. The incidence of myocardial injury in critically ill patients has been reported unexpectedly high, using elevated levels of cTnI as a marker (Guest TM, et al. JAMA 1995;273:1945-1949). Fifteen percent of critically ill patients admitted to a medical and respiratory ICU of an academic health center had evidence of myocardial damage based on this biochemical marker. Moreover, these events were associated with increased morbidity and mortality, like the study of Arlati et al indicates.
Arlati et al particularly studied patients with sepsis and patients with hypovolemic shock. It is certainly possible that an integrated inflammatory response during sepsis would result in patchy areas of myocardial damage, but the result of this study underlines the importance of hypotension as a cause of cardiac damage. Incidentally, we must not forget that the majority of hypotensive patients received catecholamines; thus, a concurrent role of the latter in producing myocardial injury cannot be excluded. However, according to Arlati et al, myocardial injury was present within 24 hours from enrollment in 19 of 23 patients with elevated levels of cTnI. Further studies are necessary to confirm these interesting findings.
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