Increased serum troponin in addition to acute coronary syndrome

The article was professionally consulted by Dr. Nguyen Van Duong - Interventional Cardiologist - Cardiovascular Center - Vinmec Central Park International General Hospital.

Elevated serum troponin has been observed in patients admitted to the hospital with chest pain. Often it can be caused by acute myocardial infarction with myocardial necrosis. However, there are also cases of increased troponin not due to myocardial infarction.

Coronary artery disease is one of the main causes of death globally today. In particular, acute coronary syndrome is a condition in which atherosclerotic plaques in the artery lumen are dislodged, forming blood clots, reducing blood flow to the heart or causing arterial blockage, threatening the patient's life. Acute coronary syndrome can occur in two forms as unstable angina and acute myocardial infarction.
When the heart muscle is damaged, the body releases troponin - a substance involved in the regulation of heart muscle contraction into the blood. This substance rises slowly in the blood after 4-6 hours and stays high for several days. Therefore, the troponin test is considered an early diagnostic method of cardiac damage along with other cardiac markers.
However, when chest pain occurs, it is difficult to make a diagnosis based on the results of elevated serum troponin because the typical symptoms of myocardial infarction must be combined with other tests such as electrocardiogram. thing.

The troponin test is usually indicated for patients with suspected acute coronary syndromes, that is, when unstable angina occurs, the patient undergoes an electrocardiogram and a myocardial infarction is detected. ECG with or without ST segment elevation.
Currently, the high-sensitivity 2 troponin hsTnT and hsTnI tests have helped doctors diagnose and detect acute coronary syndromes early and provide prognosis. However, further differential diagnosis of causes of elevated serum troponin beyond acute coronary syndromes and noncardiac syndromes should be continued.

Elevated serum troponin in addition to acute coronary syndrome can be caused by the following:
Heart failure: The patient does not present with typical chest pain, only shortness of breath. Test results showed a moderate increase in troponin levels. Until now, the mechanism of increased troponin due to heart failure is not clear. Some studies have suggested that it may be due to damaged heart muscle cells that degrade the proteins. Besides, there are many factors involved in the process of promoting myocardial cell death such as hormones, nerves, cytokines, ... thereby releasing and increasing serum troponin. Pulmonary embolism due to thrombosis: Patients with pulmonary embolism due to thrombosis who present with hypotension and shock will face a high risk of death. When shortness of breath or acute chest pain occurs, the patient is hospitalized and a troponin test is indicated. The mechanism of elevation of serum troponin in patients with pulmonary embolism is thought to be a sudden increase in pulmonary vascular resistance causing right ventricular distension. Ultrasound showing dysfunction of right ventricular function is the basis for predicting mortality in patients. Aortic dissection: Increased serum troponin (troponin I) occurs in patients with type A acute aortic dissection.

Cardiac Arrhythmias: A tachycardia or bradycardia is one of the most common clinical situations where elevated serum troponin levels are not associated with acute coronary syndromes. Pericarditis: The patient presented with chest pain, after being admitted to the hospital, an electrocardiogram showed a myocardial infarction with increased ST wave on the electrocardiogram. The troponin test revealed a moderate elevation of serum troponin, the mechanism of which is believed to be due to inflammation of the myocardium in the pericardium. Myocarditis: The mechanism by which troponin increases in patients with myocarditis is due to myocardial cell necrosis, especially increased in diffuse myocarditis. The characteristics of elevated serum troponin between myocarditis, minimal myocardial damage, and myocardial infarction are different. Troponin elevation in myocarditis is mild, usually lasting 1 to several weeks, and is of little change. Troponin elevation in minimal myocardial injury also increased slightly but returned to normal rapidly (approximately 2 days later). Meanwhile, the increase in troponin in myocardial infarction is very rapid and then gradually decreases, after 1-2 weeks, it returns to normal. Infective endocarditis: Increased serum troponin in patients with infective endocarditis is the basis for predicting mortality with high risk. Takotsubo cardiomyopathy: This is a common cardiomyopathy in women that is caused by frequent emotional or physiological stress and irritation. Serum troponin levels in patients with Takotsubo cardiomyopathy increased from mild to moderate over about 24 hours. Electrocardiography: In patients undergoing electrocautery to treat arrhythmias and who responded, troponin elevations were higher than in patients who did not respond to this procedure.

Heart infection: Heart infection occurs in patients with blunt chest trauma. Elevated serum troponin was seen in patients with electrocardiographic changes for at least 24 hours. Septic shock: In patients with severe infection with signs of elevated troponin, the cause is thought to be myocardial cell toxicity due to circulating chemicals in the circulatory system, or myocardial ischemia. due to infection causing microcirculatory dysfunction or bacterial toxins.

Increased cardiac troponin not due to myocardial infarction can be caused by the following:
Shock, hypotension: Hypotension reduces perfusion pressure in the myocardium. Renal disease (advanced or end-stage): In patients with advanced or end-stage renal disease may present with diffuse cardiovascular obstruction, left ventricular hypertrophy. Stroke, cerebral hemorrhage: Increased serum troponin has been observed in patients with stroke or cerebral hemorrhage due to an imbalance in the autonomic nervous system. After a stroke, patients may experience complications of myocardial or coronary injury. Exercise: After exercise or strenuous exercise, the body releases troponin into the heart muscle cells. Drug use: Certain sympathomimetic drugs such as acetaminophen, antidepressants, benzodiazepines, opioids, sympathomimetic may increase serum troponin (troponin I).

Sepsis: The mechanism of troponin release in patients with sepsis or systemic disorders has been attributed to myocardial depression, increased demand or decreased cardiac oxygen supply, and myocardial ischemia. Chemotherapy: Some drugs used in chemotherapy at high doses such as anthracycline, chlormethine, mitomycin, trastuzumab can cause cardiotoxicity due to the production of free oxygen radicals, metabolic disturbances, and internal calcium overload. cells, increase lipid peroxidation and lead to elevation of serum troponin. If the patient does not increase troponin after using high-dose chemotherapy drugs, it can be concluded that the patient has no heart damage or only temporary left ventricular dysfunction. Burns: Acute burns over 15% of the body's surface area can increase troponin and increase the risk of cardiac complications and mortality. Differential diagnosis of causes of increased serum troponin due to myocardial infarction, related to coronary artery or not plays an important role, helping to treat myocardial infarction promptly and effectively.
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