Troponins are cardiac regulatory proteins that mediate the interaction between actin and myosin. Cardiac troponin I and T are sensitive and specific biomarkers of myocardial injury. There are various etiologies for elevated troponin values such as renal disease, acute pulmonary embolism, sepsis, heart failure, myocarditis, aortic dissection, cardiac contusion, cardiotoxic chemotherapy and strenuous exercise. Increase in troponin levels does not always equate to myocardial infarction.
There is a high prevalence of elevated troponin levels in patients with sepsis. There are studies, which shows that in patients who were diagnosed to have sepsis and elevated troponin, coronary artery disease was ruled out indicating other possible mechanisms for the rise of the biomarker.
While the mechanism of myocyte damage in sepsis is not fully understood, several pathophysiologic explanations have been hypothesised. Some of the manifestations of sepsis include hypotension, microcirculatory dysfunction, lack of tissue perfusion, and direct hypoxemia, all of which can all result in decreased oxygen delivery. Symptoms that frequently occur in sepsis such as fever and tachycardia can reduce the coronary perfusion and increase the oxygen demand. This can further lead to damage of myocytes and an increase in detectable serum troponin.
It is also known that bacteraemia in sepsis can lead to an increase in inflammatory mediators and release of cytokines, which further causes microvascular dysfunction. This can depress myocardial function and leads to leaky myocardial cells thus rising serum troponin.
When patients with past history of established coronary artery disease, electrocardiographic (ECG) changes, diabetics, episodes of chest pain, and with smoking history, are diagnosed with sepsis and elevated troponin, this warrant further investigation.
The degree of troponin leak is a useful guide in the setting to identify the cause of rise in troponin. The European society of cardiology guidelines suggests that troponin value elevations more than 5 times the upper limit have a high (>90%) positive predictive value (PPV) for myocardial infarction, and up to 3 times the upper limit has a moderate PPV (50-60%) and is likely to be due to another cause. The higher the increase in troponin value from its upper limit, the increased likelihood of an acute myocardial infarction.
We present a 50-year-old male with known case of type 2 diabetes mellitus, who was admitted to the intensive care unit with complaints of high-grade fever with chills for one week and worsening breathing difficulty for two days. On examination he was afebrile, hypotensive, and tachycardic. Necessary initial investigations were done which revealed increased total counts, elevated procalcitonin and troponin I with a normal ECG. His echocardiograph revealed global hypokinesia with moderate left ventricular dysfunction. He continued to be hypotensive requiring vasopressor support. His urine culture growth was positive for gram-negative bacilli (Klebsiella pneumoniae) and was started on appropriate antibiotics. His repeat troponin I was markedly increased (more than 5 times from the baseline).
In view of the persisting hypotension despite antibiotics, and markedly elevated troponin, patient underwent a coronary angiography, which showed triple vessel disease. He was scheduled for a coronary artery bypass graft surgery once the inflammatory markers decreased.
Most of the critically unwell patients have significantly elevated levels of troponin. An individualized approach is mandatory to determine who needs further cardiac investigation. This takes into account ECG changes, degree and fluctuations in serum troponin, risk factors for coronary artery disease, and presence of new regional wall motion abnormalities. It is vital to remember that in patients with sepsis with high cardiac risk factors, an elevated troponin level should rise the possibility of acute myocardial infarction.
Dr. Karishma Puthanpura Department of Critical Care Kauvery Hospital Chennai
