Cardiac Troponins in Pulmonary Embolism

Abstract & Commentary

Synopsis: In patients with pulmonary embolism, elevated plasma levels of cardiac troponins help to identify a subgroup of patients who are at high risk and who may benefit from more aggressive treatment.

Source: Janata K, et al. Cardiac troponin T in the severity assessment of patients with pulmonary embolism: Cohort study. BMJ. 2003,326:312-313.

Janata and colleagues carried out a study to assess the association between serum concentrations of cardiac troponin T and severity of pulmonary embolism as well as the role of troponin T as a predictor of mortality. They assessed 136 consecutive patients who were admitted to the emergency department of a tertiary care university hospital with pulmonary embolism, confirmed by computed tomography or scintigraphy, between December 1999 and November 2001. Two patients with terminal illness and 7 patients admitted after out-of-hospital cardiac arrest were excluded. In 106 patients troponin concentrations were determined in the first 12 hours after admission. The severity of the event was classified according to the grading system by Grosser1 (see Table). Right ventricular strain in the electrocardiogram was defined as right bundle branch block, T wave inversion in precordial leads, or presence of the S1Q3,T3 pattern.

Six patients had fulminant pulmonary embolism; in 37 it was massive, in 62 it was submassive, and in 1 it was minor. Janata et al reported that troponin concentrations increased with increasing severity of pulmonary embolism (r = 0.56; P < 0.001). Added to that, the median troponin concentration was higher in patients with electrocardiographic signs of right ventricular strain than in patients without these signs (0.03 ng/mL vs < 0.01 ng/mL; P < 0.001). The same happened when signs of right ventricular strain were considered in 93 patients who underwent echocardiography.

As for the prediction of mortality, troponin concentrations were higher in the 5 patients who died than in survivors (0.18 ng/mL vs < 0.01 ng/mL; P < 0.001). A cut-off value for troponin of 0.009 ng/mL was a suitable predictor of death in hospital. The area under the curve was 0.92, and the cut-off value had a sensitivity of 0.80 and a specificity of 0.92. The negative predictive value was 0.99 and the positive predictive value 0.34.

Table

Classification of the Severity of Pulmonary Embolism1

Clinical indicators I (minor) II (submassive) III (massive)  IV (fulminant)
Symptoms and signs Transient symptoms:
dyspnea,
pleuritic pain,
hemoptysis,
fever
Persistent
moderate
symptoms:
sudden dyspnea,
tachypnea,
tachycardia, pain
Persistent severe symptoms: dyspnea, tachypnea, cyanosis, tachycardia, syncope Persistent severe symptoms, plus: shock, cardiac arrest

Systemic blood pressure

 

Normal Normal (slightly depressed) Hypotension Severe hypotension
Pulmonary artery oxygen content (mm Hg) Normal 80 < 70 < 60

Comment by Francisco Baigorri, MD, PhD

A high incidence of clinically unrecognized myocardial injury, according to elevated levels of cardiac troponins, has been reported in critically ill patients, and is associated with increased morbidity and mortality.2 In my hospital almost 30% of ICU patients with acute noncardiac disease have elevated levels of troponin I in the first 24 hours after admission. Tachycardia, arrhythmia, hypotension and treatment with inotropic drugs have all been associated with higher serum troponin concentrations.3

As far as pulmonary thromboembolism is concerned, it has been shown that an elevated cardiac troponin T level is an independent risk factor for a fatal outcome.4 As the study of Janata et al supports, right ventricular dysfunction is more often found in patients with elevated troponins. Experimental and clinical evidence suggest that myocardial ischemia and even right ventricular infarction may result from an acute rise in pulmonary artery pressures and may then cause right ventricular failure which correlates with increased risk of death.

Right ventricular dysfunction also is a well-known complication of chronic obstructive pulmonary disease. In fact, it has been recently reported that elevated troponin I is quite frequent in patients with chronic obstructive pulmonary disease (18%) and it is a strong and independent predictor of in-hospital death in these patients.5 From all this it follows that elevated plasma levels of troponins help to identify a subgroup of patients who are at high risk. However, further studies are needed to determine whether specific and early medical interventions (such as thrombolytics and inotropic vasoactive drugs) in patients with troponin elevation decrease mortality rate.

On the other hand, another lesson to be learned from these results is that we should be aware of conditions such as pulmonary embolism that are associated with elevated cardiac troponin levels in the absence of an acute coronary syndrome. For instance, pulmonary embolism should be considered in the differential diagnosis of patients presenting with undifferentiated chest pain or dyspnea and an elevated cardiac troponin level.6

References

1. Grosser KD. Pulmonary embolism—problems in identifying and treating the condition. Internist. 1980; 21:273-282.

2. Guest TM, et al. Myocardial injury in critically ill patients. A frequently unrecognized complication. JAMA. 1995;273:1945-1949.

3. Noble JS, et al. Troponin I and myocardial injury in the ICU. Br J Anaesth. 1999;82:41-46.

4. Giannitsis E, et al. Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism. Circulation. 2000;102:211-217.

5. Baillard C, et al. Cardiac troponin I in patients with severe exacerbation of chronic obstructive pulmonary disease. Intensive Care Med. 2003;29:584-589.

6. Douketis JD, et al. Elevated cardiac troponin levels in patients with submassive pulmonary embolism. Arch Intern Med. 2002;162:79-81.