Related Experiment Video
Updated: Oct 16, 2026
Using Extraordinary Optical Transmission to Quantify Cardiac Biomarkers in Human Serum
Published on: December 13, 2017
Cardiac troponins I and T are biological markers of left ventricular dysfunction in septic shock
K M ver Elst1, H D Spapen, D N Nguyen
1Department of Clinical Chemistry, Academic Hospital Vrije Universiteit Brussel (AZ-VUB), B-1090 Brussels, Belgium.
Insights
In septic shock, elevated cardiac troponin I (cTnI) and troponin T (cTnT) indicate myocardial cell injury and are strongly linked to left ventricular (LV) dysfunction. This injury is more common in older, sicker patients with pre-existing heart conditions.
Area of Science:
- Cardiology
- Critical Care Medicine
- Biochemistry
Background:
- Severe sepsis and septic shock often involve left ventricular (LV) failure.
- The role of subclinical myocardial cell injury in this cardiac dysfunction remains unclear.
Purpose of the Study:
- To investigate the relationship between cardiac troponin I (cTnI) and troponin T (cTnT) levels and LV dysfunction in early septic shock.
Main Methods:
- 46 patients with septic shock were enrolled and received fluid resuscitation and catecholamines.
- Cardiac markers (cTnI, cTnT) and LV function (echocardiography) were assessed over 48 hours.
Main Results:
- Elevated cTnI and cTnT were detected in 50% and 36% of patients, respectively.
- cTnI positivity was associated with older age, higher illness severity, and poorer survival.
- LV dysfunction was strongly correlated with cTnI positivity (78% vs 9%) and independently associated with both cTnI and cTnT levels.
Conclusions:
- Clinically unrecognized myocardial cell injury, indicated by elevated troponins, serves as a marker for LV dysfunction in septic shock.
- LV dysfunction is more prevalent in older, critically ill patients with underlying cardiovascular disease.
- Further research is required to elucidate whether myocardial damage causes or results from LV dysfunction in sepsis.
Background:
Cardiac depression in severe sepsis and septic shock is characterized by left ventricular (LV) failure. To date, it is unclear whether clinically unrecognized myocardial cell injury accompanies, causes, or results from this decreased cardiac performance. We therefore studied the relationship between cardiac troponin I (cTnI) and T (cTnT) and LV dysfunction in early septic shock.
Methods:
Forty-six patients were consecutively enrolled, fluid-resuscitated, and treated with catecholamines. Cardiac markers were measured at study entry and after 24 and 48 h. LV function was assessed by two-dimensional transesophageal echocardiography.
Results:
Increased plasma concentrations of cTnI (>/=0.4 microgram/L) and cTnT (>/=0.1 microgram/L) were found in 50% and 36%, respectively, of the patients at one or more time points. cTnI and cTnT were significantly correlated (r = 0.847; P <0.0001). Compared with cTnI-negative patients, cTnI-positive subjects were older, presented higher Acute Physiology and Chronic Health Evaluation II scores at diagnosis, and tended to have a worse survival rate and a more frequent history of arterial hypertension or previous myocardial infarction. In contrast, the two groups did not differ in type of infection or pathogen, or in dose and type of catecholamine administered. Continuous electrocardiographic monitoring in all patients and autopsy in 12 nonsurvivors did not disclose the occurrence of acute ischemia during the first 48 h of observation. LV dysfunction was strongly associated with cTnI positivity (78% vs 9% in cTnI-negative patients; P <0.001). In multiple regression analysis, both cTnI and cTnT were exclusively associated with LV dysfunction (P <0.0001).
Conclusions:
These findings suggest that in septic shock, clinically unrecognized myocardial cell injury is a marker of LV dysfunction. The latter condition tends to occur more often in severely ill older patients with underlying cardiovascular disease. Further studies are needed to determine the extent to which myocardial damage is a cause or a consequence of LV dysfunction.
Related Concept Videos
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
01:19Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
01:30Acute Coronary Syndrome III: Diagnostic Studies
01:30Acute Coronary Syndrome I: Introduction
01:27Myocarditis II: Clinical Features and Diagnostic Tests
01:19Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations