Acute pulmonary embolism presenting with electrocardiographic signs and serum biomarkers of ST-segment elevation myocardial infarction: a case report

Abstract

Acute pulmonary embolism (APE) with ST-segment elevation and an upward T-wave is rare, and only a few cases have been reported to date. We herein present a case involving a man in his early 70s with an 8-hour history of dyspnea. Serial electrocardiography (ECG) demonstrated ST-segment elevation in leads V1 to V3 with an upward T-wave, laboratory tests revealed a high serum concentration of high-sensitivity cardiac troponin I, and signs of acute myocardial infarction were present. However, emergency coronary angiography revealed normal coronary arteries. A subsequent computed tomography scan of the pulmonary arteries showed findings consistent with APE. The patient’s chest tightness was relieved after catheter-directed thrombolysis. Postoperative ECG showed that the ST-segment in leads V1 to V3 had fallen back and that the T-wave was inverted. The patient was discharged on rivaroxaban therapy. Clinically, the ECG findings of ST-segment elevation and an upward T-wave in APE can be easily misdiagnosed as acute myocardial infarction. Physicians should maintain clinical suspicion through risk stratification to identify APE.

Introduction

Acute pulmonary embolism (APE) is a significant cause of mortality worldwide. ¹ Following acute myocardial infarction and stroke, APE is the third most common cause of cardiovascular death among patients in developed countries. ² Early diagnosis and intervention are paramount because most deaths from APE occur within the first several hours to days, with more than 70% of deaths occurring within the first hour. ³

Electrocardiography (ECG) is the most crucial test for the evaluation of patients with chest pain or dyspnea. ST-elevation, the most life-threatening acute ECG change, often directs physicians to perform primary percutaneous coronary intervention or thrombolysis. A few conditions other than ST-elevation myocardial infarction (STEMI) can exhibit ST-elevation on ECG examination, such as Prinzmetal angina, Takotsubo cardiomyopathy, Brugada syndrome, left ventricular aneurysm, hypothermia, hyperkalemia, and acute pericarditis. ⁴ However, it is exceedingly rare to find ST-elevation with an upward T wave in a patient with APE, and such findings can easily lead to misdiagnosis of STEMI.

The aim of this case report is to provide clinical support for the differential diagnosis of APE and myocardial infarction in an effort to reduce the potential for misdiagnosis and improve patient care.

Case presentation

A Han man in his early 70 s presented with an 8-hour history of chest tightness and dyspnea after going to the toilet, and his signs were not relieved by taking “Quick-Acting Heart Pills”. The patient had no chest pain, nausea, or vomiting. He denied any history of heart disease, hypertension, or diabetes mellitus. However, the patient had sustained a lumbar compression fracture and had been in bed for more than 20 days.

Medical history

The patient had sustained a lumbar compression fracture more than 2 months previously and had remained in bed for more than 20 days. He had no other chronic medical, surgical, or family history.

Differential diagnoses

The differential diagnoses for acute dyspnea that were considered in this case were acute coronary syndrome, acute exacerbation of asthma or chronic obstructive pulmonary disease, acute pneumonia or bronchitis, APE, pneumothorax, and heart failure.

Investigations

Clinical laboratory test results showed a normal complete blood count and normal electrolyte concentrations. The N-terminal pro–B-type natriuretic peptide concentration was 2597 pg/mL (reference range, <900 pg/mL), and heart failure was suspected. The high-sensitivity cardiac troponin I concentration was high at 99.76 ng/L (reference range, <17.5 ng/L), but the myoglobin and creatine kinase isoenzyme concentrations were normal. ECG showed sinus tachycardia at 113 beats/minute, ST-segment elevation by approximately 0.1 to 0.4 mV with an upward T-wave in leads V1 to V3, and ST-segment depression by approximately 0.1 to 0.3 mV with a flat T-wave in leads I, II, and V4 to V6 (Figure 1).

Figure 1.

Electrocardiogram at admission showing sinus rhythm with ST-elevation and an upward T-wave from precordial leads V1 to V3.

The patient was diagnosed with STEMI, and emergent coronary angiography was performed. However, this imaging examination revealed normal blood flow and no obvious atherosclerotic plaque or stenosis (Figure 2, Videos 1–5).

Figure 2.

Emergent coronary angiography showing normal coronary angiography. (a) Left coronary angiogram. Right anterior oblique caudal: −20° −20° and (b) Right coronary angiogram. Left anterior oblique straight: +45° 0°.

Another laboratory test showed an elevated plasma D-dimer concentration of 16.60 μg/mL (reference range, <0.50 μg/mL); thus, APE could not be excluded. Computed tomography pulmonary angiography showed a filling defect in the left pulmonary trunk and right inferior pulmonary artery, indicating pulmonary embolism in the bilateral pulmonary arteries (see Video 6 and Supplemental Video, which demonstrate the pulmonary embolism in the bilateral pulmonary arteries).

Ultrasound scans of both lower limbs showed right popliteal vein and posterior tibial vein thrombosis (Figure 3). We presumed that because of the lumbar compression fracture and more than 20 days of bed rest, the lower limb venous thrombosis had formed and shed, was transferred to the lungs, and became embedded in the pulmonary arteries, thus causing pulmonary embolism.

Figure 3.

Ultrasound scan showing (a) right popliteal vein and (b) posterior tibial vein thrombosis.

Management

We administered therapy according to the above results and with the patient’s consent. An 8-French catheter was inserted into the pulmonary arteries, which was then used for thrombus aspiration combined with thrombolysis (200,000 units of urokinase) (see Videos 7–9: Video 7 demonstrates left pulmonary trunk embolism, Video 8 demonstrates right pulmonary trunk embolism, and Video 9 shows the results after thrombolysis in the left pulmonary artery). The patient’s chest tightness was relieved after the operation (catheter-directed thrombolysis). Postoperative ECG examination showed that the ST-segment in leads V1 to V3 had fallen back, and the T-wave was inverted (Figure 4).

Figure 4.

Postoperative electrocardiogram showing that the ST-segment in leads V1 to V3 had fallen back, and the T-wave was inverted.

The patient was treated with anticoagulants. Three days later, ECG showed that the inversion amplitude of the T-waves in leads V1 to V3 was reduced (Figure 5).

Figure 5.

Electrocardiogram showing that the inversion amplitude of the T-waves in leads V1 to V3 was reduced 3 days later.

Follow-up

The patient was discharged for subsequent anticoagulation therapy with rivaroxaban to reduce the risk of recurrence of deep vein thrombosis.

Discussion

APE is difficult to diagnose and has high mortality, variable clinical presentations, and diverse ECG findings such as sinus tachycardia, right bundle branch block, P pulmonale, right-axis deviation, an S1Q3T3 pattern (McGinn–White sign), ST-segment depression, and T-wave inversion in leads V1 to V3. The ST-segment is always depressed, usually mildly, and this change can be used as an index of myocardial ischemia and a poor prognosis. In severe cases, the ST-segment elevation is <0.1 mV and usually coexists with the S1Q3T3 pattern.

Kukla et al. ⁵ noted that patients with critical lethality of 1% to 15% could be further risk-stratified by ECG, with an ST-segment ischemia pattern (at least one among III, aVR, or V1–V4 ST-segment elevation or at least two among I, aVL, and V4–V6 ST-segment depression) having higher mortality and complications (odds ratio, 6.35; p = 0.007 and odds ratio, 4.19; p = 0.002). In one case from China, APE was misdiagnosed as STEMI. ⁶ Bilateral large-scale pulmonary embolism was finally diagnosed on the basis of ST-segment elevation in leads aVR, III, V1, and V3R to V5R; ST-segment depression in the leads of the lateral wall; and elevation of myocardial injury markers and cardiogenic shock during hospitalization. ⁶

A study of acute STEMI combined with pulmonary embolism ⁷ showed that pulmonary embolism may occur before myocardial infarction, usually in patients with congenital structural abnormalities of a patent foramen ovale (PFO). In recent years, we have found that PFO is closely correlated with abnormal embolism formation. When patients developed APE, the right heart pressure was higher than the left heart pressure in approximately one of three patients. This allowed the embolus from the venous system to enter the left heart, enter the circulation, and block the coronary arteries. In another setting, when the embolus blocks the pulmonary arteries and branches by 30% to 50%, the increase in pulmonary vascular resistance under the joint action of mechanical obstruction, nerve fluid factors (release of thromboxane A2 and serotonin), and hypoxemia causes increased right heart load, ventricular interval left shift, and limited left heart diastolic early filling; this in turn causes a decrease in cardiac output. Higher right ventricular pressure and depressed cardiac output cause coronary hypoperfusion followed by right ventricular myocardial infarction.^8–14

Our patient was a man in his early 70 s whose ECG showed ST-segment elevation (by approximately 0.1–0.4 mV) in leads V1 to V3 with an upward T-wave, and the postoperative ECG showed that the ST-segment in leads V1-V3 had fallen back with inversion of the T-wave. Three days later, the inversion amplitude of the T-waves in leads V1 to V3 was reduced (Figure 6). This was misdiagnosed as STEMI. However, using coronary angiography and echocardiography (Figure 7), we were able to rule out acute myocardial infarction, which is mostly caused by occlusion of the coronary arteries.

Figure 6.

Multiple electrocardiograms showing that the ST-segments in leads V1 to V3 had changed from elevation to falling back and that the T-waves in leads V1 to V3 had changed from upward to inversion. These findings are similar to the electrocardiographic evolution of ST-segment elevation myocardial infarction.

Figure 7.

Echocardiogram showing no septal deviation, meaning no pressure overload in the right ventricle. (a) Parasternal long-axis view and (b) M-mode.

The patient’s hemodynamics were stable in this case, unlike in previously reported cases. ⁶ Echocardiography revealed no ventricular wall motion abnormalities. In addition, PFO was excluded based on the echocardiographic findings. Because the ECG manifestations of pulmonary embolism are similar to those of STEMI, the mechanism may be related to acute large pulmonary embolism causing a sharp increase in pulmonary artery pressure, increased myocardial oxygen consumption, reduced cardiac beats, and a reduced blood supply to the coronary arteries, eventually leading to myocardial ischemic injury. Another reason for the ST-segment elevation in our case might have been that the embolus almost completely blocked the left lung trunk, which might have affected the ECG performance. Because we used catheter-directed thrombolysis and succeeded in partially opening the left pulmonary artery, postoperative ECG showed that the ST-segment in leads V1 to V3 had fallen back and that the T-wave was inverted. Additionally, subsequent ECG showed that the inversion amplitude of the T-waves in leads V1 to V3 was reduced.

Conclusions

Clinically, the ECG findings of ST-segment elevation and an upward T-wave in APE are very rare and easily misdiagnosed as myocardial infarction. Physicians should thus maintain clinical suspicion through risk stratification to identify APE, although the incidence is extremely low.

Data availability statement

All data in this study are included in the article. Further enquiries can be directed to the corresponding author.

Ethics statement

The reporting of this study conforms to the CARE guidelines. ¹⁵ We have deleted all patient-specific details from this article. Written informed consent was obtained from the patient and his son for publication of this case report, and this case report was approved by the Ethics Committee of Qilu Hospital of Shandong University (approval no. KYLL-2022(ZM)-082).