Pulmonary embolism secondary to acute anterior ST-elevation myocardial infarction: a case report

Thrombophilia denotes a condition, whether acquired or hereditary, characterized by increased susceptibility to hypercoagulation.[1] This condition was first described in 1965, coinciding with the discovery of an inherited predisposition to venous thromboembolism (VTE) in patients deficient in antithrombin III.[2]

While arterial and venous thromboses are common in hospitalized patients, acute myocardial infarction (AMI) and pulmonary embolism (PE) stand out as life-threatening conditions. However, the occurrence of AMI complicated by PE is exceedingly rare, especially when considering cases where paradoxical embolism originating from a patent foramen ovale is absent. This report presents a case of AMI complicated with PE. A comprehensive understanding of the pathophysiology of this rare yet critical condition is important for ensuring prompt diagnosis and treatment.

CASE

A 29-year-old male with no prior medical history was admitted to the nearest hospital after experiencing chest pain following alcohol consumption. Electrocardiogram (ECG) revealed ST-elevation in leads V2-V5 (Supplementary Figure 1). In terms of family history, the patient’s father succumbed to PE and his sister experienced VTE during pregnancy. An emergent coronary angiogram (CAG) revealed a significant thrombus burden in the left anterior descending artery (LAD), which, though non-occlusive, was immediately treated with percutaneous thrombus aspiration (Supplementary Figure 2A). As no significant stenotic lesions were noted in the LAD or other coronary branches (Supplementary Figure 2B), angioplasty and stenting of the lesion were deemed unnecessary. Following primary percutaneous coronary intervention (PCI), anti-platelet therapy with tirofiban hydrochloride, aspirin, and ticagrelor was initiated.

The day after the PCI procedure, he was transferred to our hospital presenting with tachypnea, a respiratory rate of 44 breaths/min, blood pressure of 100/58 mmHg (1 mmHg=0.133 kPa), and a diminished SaO₂ level of 83%. Further examination revealed no pulmonary edema. Biomarkers indicative of myocardial infarction were as follows: high-sensitivity cardiac troponin I (hsTnI) at 3,605.9 pg/mL (normal range: 0–0.04 pg/mL) and CK-MB mass at 9.9 ng/mL (normal range: 0–5 ng/mL). Additionally, D-dimer level was elevated at 1,248 ng/mL (normal range: 0–243 ng/mL), and blood gas analysis revealed decreased SO₂ (94.8%, normal range: 95%–100%) and pCO₂ levels (31.8 mmHg, normal range: 35–45 mmHg) but normal PO₂ level (88.7 mmHg, normal range: 80–110 mmHg). ECG revealed sinus tachycardia, SI QIII TIII (Figure 1). In addition, routine echocardiography indicated elevated pulmonary and right heart pressures, with normal cardiac function (ejection fraction, 60%) and signs of PE. Subsequently, computed tomography angiography (CTA) of the pulmonary arteries identified acute PE (Figure 2). Venous thrombolytic therapy (alteplase 100 mg intravenous injection for 2 h) was promptly initiated, resulting in a favorable response.

Figure 1.

Electrocardiogram shows sinus tachycardia, SI QIII TIII (black arrows).

Figure 2.

Pulmonary computed tomography angiography (CTA) scan showing proximal pulmonary embolism (white arrows).

Given the symptoms, CAG findings, and pulmonary CTA findings, the patient received a diagnosis of acute inferior wall ST-elevated myocardial infarction (STEMI) with Killip class I presentation and acute PE (classified as an intermediate-risk group).

Coronary blood flow was restored to Thrombolysis In Myocardial Infarction (TIMI) grade 3 following embolus aspiration, and no residual stenosis or plaque was observed on coronary optical coherence tomography (supplementary Figure 3). Consequently, balloon dilation or stent implantation was not performed. For periprocedural anti-thrombotic therapy, oral aspirin 0.1 g/d + oral ticagrelor 90 mg/12 h+ hypodermic injection enoxaparin sodium 60 mg/12 h was used. A repeated echocardiography indicated a slightly enlarged right heart (internal diameter decreased from 48 mm to 41 mm), left ventricular hypertrophy, mild mitral regurgitation, and mild tricuspid regurgitation. After a 10-day course of treatment and rehabilitation, the patient was discharged home with a treatment plan consisting of oral rivaroxaban 20 mg/d and regular follow-up. This case demonstrated the rare but potentially life-threatening complication of PE following coronary angioplasty. Chromosome fluorescence in situ hybridization analysis revealed that the patient carried a high-risk gene associated with venous thrombosis (mutant heterozygous 5G4G).

DISCUSSION

The patient’s presentation with AMI at initial medical contact and subsequent diagnosis of coronary embolism during CAG highlights the challenges in recognizing complicated or paradoxical PE due to its highly variable clinical manifestations. In this case, the relationship between AMI and PE could not be discerned. Potential causes, such as paradoxical embolism, rheumatic disease-related embolism, and tumor-related emboli were systematically ruled out through lower extremity vascular ultrasound, antiphospholipid antibody test, and tumor marker examination. Chromosome fluorescence analysis indicated a slightly higher genetic predisposition to thrombosis compared to the general population.

A normal and healthy response to bleeding involves the formation of a stable clot to maintain hemostasis, also known as coagulation. However, in pathological states such as hypercoagulability or thrombophilia, there is an increased susceptibility for thrombosis development, which is characterized by exaggerated coagulation or coagulation without the activation of bleeding. Thrombosis is a multifaceted process driven by various factors, resulting in the formation of a blood clot known as a thrombus. Thrombi are heterogeneous and consist of insoluble fibrin, platelet aggregation, accumulated white blood cells, red blood cells and more. Moreover, thrombosis is a pathological condition arising from over-activation of hemostasis, which plays a role in the pathogenesis of various diseases. Notably, thrombosis can occur in the arteries as well as the veins. Arterial thrombosis, such as that seen in myocardial infarction and stroke, is different from venous thrombosis, such as that seen in deep vein thrombosis and PE. The key differences between arterial thrombosis and venous thrombosis are as follows. 1) Risk factors. Arterial thrombosis often relates to atherosclerosis, whereas venous thrombosis frequently results from stagnant blood flow. 2) Pathogenesis. Arterial thrombosis is linked to endothelial cell dysfunction due to blood turbulence, while venous thrombosis is associated with venous stasis and a hypercoagulable blood state. 3) Symptoms. Arterial thrombosis typically presents acutely, while venous thrombosis often exhibits a more chronic onset. 4) Complications. Arterial thrombosis can lead to arterial embolism and infarction, whereas venous thrombosis is associated with PE. 5) Thrombus extension. Arterial thrombi tend to propagate against the direction of blood flow, whereas venous thrombi propagate with the blood flow. 6) Thrombus detachment. Arterial thrombi can detach in whole or in majority to form emboli, while in venous thrombosis, only the tail segment typically detaches to form emboli.

Although the pathophysiology and treatment of arterial and venous thrombosis differ significantly, there may be overlapping risk factors. [3,4] Thromboembolism refers to the migration of a localized thrombus to distant areas, leading to luminal obstruction.

Hypercoagulability disorders are either acquired or inherited.[5] However, actual thrombus formation is attributed to the interaction of genetic and environmental factors,[6-8] resulting in significant inter-individual variability.[9] Genetic mutations are identified in over 30% of patients with VTE.[9] Acquired factors can also affect the clotting cascade, including surgery, pregnancy, hormone replacement therapy, contraceptives, malignancies, inflammation, infection, and heparin-induced thrombocytopenia.[10]

In this case, the most likely etiology appears to be thrombophilia, even though the hereditary thrombophilia test yielded overall normal results. Notably, the patient had a family history of thrombophilia, with his father succumbing to PE and his sister experiencing VTE during pregnancy. Thus, this patient carried an increased risk of hereditary thrombophilia. Given his young age, general good health, absence of relevant risk factors, and negative findings in rheumatic disease and tumor laboratory tests, hereditary thrombophilia emerges as the most plausible etiological factor.

Arterial thrombosis manifests when atherosclerotic plaques rupture, leading to blood clot formation. Venous thrombosis, on the other hand, often occurs post-valvular stasis and results in red thrombosis. For patients presenting with concomitant AMI and acute PE, anti-thrombotic therapies such as thrombolysis, anti-coagulation, and anti-platelet aggregation should be considered as first-line treatment. Fortunately, in this case, the patient did not exhibit high risks of bleeding. The administration of anti-coagulation therapy for acute PE and anti-platelet therapy concurrently serves as secondary prevention for AMI.

This case emphasizes that PE is a multifactorial disease influenced by clinical risk factors and inherited thrombophilia. Moreover, identifying potential risk factors is crucial for arriving at an accurate diagnosis and implementing the appropriate diagnostic workup. Although PE presenting with ST-elevation is extremely rare, only a few cases have been reported.[11,12] In the clinical setting, further differential diagnosis with echocardiography and CTA would be helpful to determine the cause of ST-elevation.

CONCLUSION

Thrombophilia represents a pathological condition characterized by an increased susceptibility to thrombosis and thromboembolism owing to various genetic or acquired factors. This rare case of AMI complicated by PE demonstrated the potential co-existence of these two conditions in patients with thrombophilia or other high-risk profiles. Emergency physicians must remain vigilant while discerning and excluding arterial and venous thrombosis events and should implement appropriate evaluation and treatment strategies to achieve a favorable outcome.