Background

There are many causes of chest pain. In an elderly man with coronary artery disease risk factors who presents with sudden onset of chest pain and breathlessness, an acute coronary syndrome should be the initial consideration. Pneumothorax is another cause of chest pain and severe dyspnoea; it is well known to cause electrocardiogram (ECG) changes, including ST segment elevation, that can mimic acute myocardial infarction. We present a patient who presented with both a large pneumothorax and a true myocardial infarction.

Case presentation

A 74-year-old man with a history of chronic obstructive pulmonary disease and emphysema developed sudden severe left sided chest pain radiating to his back associated with increasing dyspnoea. This occurred at home at night when he was returning to bed after visiting the toilet. He rapidly became severely distressed and called for an ambulance.

On arrival in the accident and emergency department, the patient was alert, tachypnoeic with a respiratory rate of 26/min, and tachycardic with a heart rate of 124/min. Blood pressure was 152/100 mm Hg and O₂ saturation was 90% on oxygen. On examination his left chest was hyper-resonant with notably decreased air entry. Emergency chest x-ray (fig 1) confirmed a large left sided pneumothorax. The clinical impression was of a spontaneous left sided pneumothorax in a patient with underlying emphysema.

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Figure 1

Chest x-ray demonstrating very large left sided pneumothorax.

A chest drain was inserted with improvement in his dyspnoea although he had ongoing chest discomfort.

At this stage, a 12 lead ECG showed sinus tachycardia with new T wave inversion across the anterior V leads in comparison with the initial tracing (fig 2). Accordingly, the patient was admitted to the coronary care unit where serial ECGs and troponins were performed. The subsequent ECGs showed persistent and deep T wave inversion across the anterior leads and the 12 h troponin was elevated at 0.12 μg/l (reference range 0.0–0.03 μg/l) (figs 3 and 4). This was felt to be consistent with the diagnosis of a non-ST segment elevation myocardial infarction (NSTEMI) and he was managed according to the usual guidelines.

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Figure 2

Initial ECG (note QRS alternans).

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Figure 3

Repeat ECG with new T wave changes and increased QRS voltage.

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Figure 4

Follow-up ECG with deepening T wave inversion.

Investigations

Subsequent coronary angiography demonstrated proximal occlusion of the right coronary artery which refilled from the left coronary artery. There were multiple non-obstructive plaques in the left coronary system but no tight stenosis. The cardiology opinion was that he had a chronic occlusion of his right coronary artery and a recent small plaque rupture probably in the left anterior descending (LAD) branch of the left coronary artery. The presumption was that the stress of a large pneumothorax and subsequent catecholamine surge was the trigger for his coronary syndrome.

Differential diagnosis

The initial diagnosis was of a spontaneous pneumothorax in a patient with known chronic obstructive lung disease. It was considered, initially, that the ECG changes might be secondary to the pneumothorax, but the persistence of the T wave changes and elevated cardiac troponin confirmed the diagnosis of NSTEMI.

Treatment

The patient improved rapidly after insertion of a chest drain, and a repeat chest x-ray showed excellent re-expansion of the left lung. On arrival to the coronary care unit, he had only minor chest discomfort. He was treated with dual antiplatelet therapy in the form of aspirin and clopidogrel as well as low molecular weight heparin for 48 h. β-blockers were avoided because of his underlying lung disease and he was prescribed diltiazem. His chest drain was removed after 48 h and he was discharged home on the fifth day after the coronary angiogram had been performed.

Outcome and follow-up

The patient remains well at follow-up and is free from angina.

Discussion

The association of ECG changes and pneumothorax has now been well described.1^–3 In fact, ECG changes have been listed as the first sign of pneumothorax in patients undergoing anaesthesia.4 There may be differences in the ECG abnormalities which develop with right or left sided pneumothorax. Abnormal axis deviation is more common in patients with the left sided compared with right sided pneumothorax, while changes in the QRS morphology (most commonly right bundle branch block) and T waves (inversion) appear more often in patients with the right sided pneumothorax. Left sided pneumothorax has also been associated with attenuation of the QRS amplitude and sometimes QRS alternans.3

Several case reports cite patients presenting with pneumothorax being initially diagnosed as acute myocardial infarction, and some of these have received thrombolytic therapy5 or undergone invasive coronary angiography before the correct diagnosis of pneumothorax had been made.

One patient has been described as developing a tako-tsubo transient apical left ventricular dilatation in the setting of a pneumothorax.6 A case of acute myocardial infarction in a patient with a spontaneous left sided pneumothorax has been reported previously.7 It is not hard to conceive that the acute stress of a pneumothorax with its associated catecholamine surge, hypoxia and tachycardia could be a potent stimulus that might initiate plaque rupture in a susceptible individual and cause an acute coronary syndrome or myocardial infarction. This corollary could be extended to other stressful events in patients presenting with serious illness who have underlying coronary atheroma.