ECG-changes in pulmonary embolism vs. coronary occlusion - clinical case

A 62-year-old man with a history of deep vein thrombosis and known factor V Leiden mutation was admitted with exertional, squeezing chest pain. The chest pain subsided, but the dyspnea persisted. On admission he was hemodynamically stable with a heart rate of 90/min and a blood pressure of 130/90 mmHg. He was asymptomatic at rest but became clearly dyspneic when walking to the bathroom.

Sinusrythme. T-inversions in leads V1-V3. T-inversion i lead III. S-wave in lead 1.

The ECG showed T wave inversion in lead III, subtle changes in aVF, and T wave inversions in the precordial leads V1–V3. Cardiac troponin T was 175–190 ng/L with a significant rise over two hours. Based on chest pain, T wave changes and troponin elevation he was diagnosed with NSTEMI. D dimer was 8.4 mg/L.

Bedside echocardiography showed limited acoustic windows without definite hypokinesia of the left ventricle. The patient was referred for urgent coronary angiography, which demonstrated patent coronary arteries. During the procedure he developed atrial fibrillation.

The ECG is now even more suggestive og pulmonary embolism, which shows in addition to changes in the previous ECG, a taller R-wave in V2 og and V3 suggesting right-ventricular strain. T-wave inversion in inferior leads.

CT of the thorax revealed the actual diagnosis. There was a central pulmonary embolism with thrombus material in both pulmonary arteries extending to segmental branches in all lobes. The patient was treated with anticoagulation.

The decisive ECG pattern

Kosuge et al. (Am J Cardiol 2007) showed that the simultaneous presence of negative T waves in both lead III and lead V1 had a sensitivity of 88 percent and a specificity of 99 percent for pulmonary embolism when differentiating from acute coronary syndrome. The positive predictive value was 97 percent and the negative predictive value was 95 percent.

In this patient we see exactly this classical pattern. There were precordial T wave inversions in V1–V3 combined with T wave inversions in the inferior leads (II, III, aVF). In addition there was an S wave in lead I, representing right axis deviation. The classical S1Q3T3 pattern has a sensitivity of only 15–25 percent, although it is quite specific when present.

Other ECG findings such as P pulmonale, S1Q3T3 and low voltage were described as specific for pulmonary embolism, but they occurred infrequently and were therefore of low sensitivity. This is why the combination of T wave inversion in III and V1 is so useful. It is seen much more often than the classical but rare signs.

Clinical clues

Dyspnea is not a typical symptom of acute coronary syndrome in isolation. When dyspnea occurs in ACS it is often due to pulmonary congestion secondary to an acute myocardial infarction, and in such cases symptoms are also present at rest. Our patient had no symptoms at rest but became markedly dyspneic on exertion.

Taken together

• known factor V Leiden mutation and previous DVT

• a D dimer of 8.4 mg/L

• the characteristic ECG pattern

• dyspnea only on exertion

this clinical picture should have raised suspicion of pulmonary embolism already on admission.

It is important to note that factor V Leiden mainly increases the risk of venous thrombosis. The risk of arterial thrombosis and coronary artery disease is only slightly increased and is not regarded as an independent risk factor for coronary disease.

Troponin is not synonymous with myocardial infarction

In acute settings elevated troponin is often given great weight, and a coronary event quickly becomes the working diagnosis. It must be kept in mind, however, that several serious conditions can produce troponin elevation:

• pulmonary embolism, as in this patient

• myocarditis

• takotsubo cardiomyopathy

• aortic dissection

• sepsis with myocardial injury

  
  

All of these conditions can have an adverse prognosis and require treatment strategies that are completely different from coronary angiography. Troponin elevation in pulmonary embolism reflects right ventricular strain and myocardial injury and is in fact a prognostic marker in pulmonary embolism.

Clinical learning points

• It is important to recognise ECG changes associated with pulmonary embolism. Simultaneous negative T waves in III and V1 offer a simple and accurate way to distinguish pulmonary embolism from acute coronary syndrome in patients who have negative T waves in the precordial leads.

• The patient must always be assessed as a whole. Chest pain with ECG changes is not always ACS. History, risk factors and the clinical presentation must be interpreted together.

• Elevated troponin should be evaluated critically. It warrants coronary assessment when ACS is suspected, but other serious diagnoses have to be considered, especially when the clinical picture is not typical for myocardial infarction.

• D dimer is important. In patients with moderate to high pretest probability of pulmonary embolism, as in this case, a markedly elevated D dimer is a signal that should not be ignored.

  
  

The knowledge from Kosuge et al. should be part of the clinical toolkit. When you encounter a patient with T wave inversions in both the inferior and the right precordial leads, pause and consider pulmonary embolism as a differential diagnosis before you conclude that it is ACS.