ST-elevation myocardial infarction following road traffic accident in a young patient: a case report

Abstract

Background

Acute myocardial infarction is a rare complication in the context of road traffic accidents, with an estimated incidence of approximately 13 per 10 000 trauma cases. Only a few reported cases have undergone coronary angiography and percutaneous coronary intervention.

Case summary

A 30-year-old man was admitted to the trauma unit following blunt chest trauma, limb fractures and pelvic haematoma sustained in a pedestrian road traffic accident. Serial electrocardiogram monitoring revealed new anterolateral ST elevation, with cardiac biomarkers confirming myocardial injury. Following thorough clinical assessment and a multidisciplinary team discussion, the patient was taken for primary percutaneous coronary intervention (PCI). Coronary angiography demonstrated proximal total occlusion of the left anterior descending artery, which was successfully treated with intravascular ultrasound–guided PCI using a drug-eluting stent.

Discussion

Primary PCI was performed without complication in a patient with anterior ST-elevation myocardial infarction (STEMI) secondary to blunt chest trauma, following exclusion of active bleeding. This case highlights the diagnostic challenges and the careful balance required between bleeding risk and timely revascularization in trauma patients presenting with STEMI.

Learning points.

• STEMI in patients with polytrauma is rare yet possible and should not be overlooked; serial ECG monitoring and cardiac biomarker assessment are essential to avoid missing this potentially fatal diagnosis.

• Primary PCI can be performed in polytrauma patients following exclusion of active bleeding, with decisions guided by a multidisciplinary team assessment of bleeding risk vs. the urgency of revascularization.

• Time-sensitive non-cardiac surgical procedures should be deferred for a minimum of 1 month following STEMI treated with DES-PCI, and ideally for at least 3 months, in accordance with both ESC and ACC/AHA guidelines.

Introduction

ST-elevation myocardial infarction (STEMI) is an infrequent complication in trauma patients, with an estimated incidence of approximately 13 per 10 000 cases.¹ Most documented occurrences involve older individuals with established cardiovascular risk factors. We report a case of a young patient without coronary risk factors who developed STEMI following blunt chest trauma sustained during a motor vehicle accident, illustrating the diagnostic challenges and complex decision-making process requiring a multidisciplinary team approach.

Summary figure

Case presentation

A 30-year-old male non-smoker with no significant medical history was brought to the emergency department following a pedestrian road traffic accident. He presented with pain in his left wrist, hip, and chest. He was haemodynamically stable with a patent airway and intact mental status.

Physical examination revealed multiple lacerations with wrist deformity and tenderness over the wrist, chest, and hip. Cardiac examination was unremarkable.

The initial Electrocardiogram (ECG) demonstrated sinus tachycardia with Q waves in the septal leads and minimal ST elevation in high lateral leads (Figure 1). Bedside echocardiography revealed preserved Left ventricular ejection fraction (LVEF), normal wall motion and no pericardial effusion.

Figure 1.

Initial ECG upon presentation to emergency department.

Trauma survey computed tomography scan (CT) demonstrated no thoracic traumatic injury and normal appearance of the heart, pericardium, and great vessels. Multiple pelvic bone fractures were identified, associated with intramuscular haematoma with left extraperitoneal and retroperitoneal extension (Figure 2). CT abdominal angiography confirmed the absence of contrast extravasation, excluding active arterial bleeding.

Figure 2.

Abdominal CT scan shows pelvic bone fracture (red arrow) associated with intramuscular haematoma with extraperitoneal and retroperitoneal extension (yellow arrows).

The patient was managed with intravenous opioids and subsequently underwent non-surgical fixation of the upper limb fractures.

A routine follow-up ECG obtained 16 h later demonstrated new ST elevation in the anterolateral and high lateral leads with reciprocal ST depression in the inferior leads (Figure 3). Cardiac biomarkers were significantly elevated, with troponin I rising from 0.1 ng/mL (reference < 0.01 ng/mL) to >50 ng/mL, confirming myocardial injury.

Figure 3.

Follow-up ECG showing new ST elevation in anterolateral leads with reciprocal changes in inferior leads.

Repeat bedside echocardiography revealed new anteroseptal and apical wall akinesia with moderately reduced LVEF of 35% by the modified Simpson’s method. Right ventricular size and function were normal, with no significant valvular abnormality or pericardial effusion.

A STEMI alert was activated. A multidisciplinary team (MDT) discussion between the cardiology and trauma teams was convened, during which the bleeding risk was carefully assessed. Based on the trauma team’s assessment confirming low bleeding risk in the absence of active haemorrhage, the consensus was to proceed with coronary angiography and intervention if indicated. Following this MDT discussion, the patient was loaded with aspirin, clopidogrel and unfractionated heparin in accordance with the institutional STEMI protocol.

Coronary angiography via right radial access demonstrated total occlusion of the proximal left anterior descending (LAD) artery (Figure 4), with angiographic appearance suggestive of thrombotic occlusion based on thrombus burden and filling defects. Intravascular ultrasound (IVUS) confirmed underlying plaque rupture as the aetiology (Figure 5). The lesion was successfully treated with IVUS-guided PCI using a drug-eluting stent (DES), with restoration of TIMI III flow.

Figure 4.

(A) Coronary angiography shows proximal left anterior descending artery total occlusion. (B) Lesion crossed with wire and prepared. (C) Final result after drug-eluting stent.

Figure 5.

Intravascular ultrasound shows a plaque rupture (arrow).

The patient was transferred to the intensive care unit in stable condition and commenced on guideline-directed medical therapy, including dual antiplatelet therapy (DAPT) and high-intensity statin. Surgical fixation of the pelvic fracture was deferred to allow completion of a minimum 4-week course of DAPT, in the absence of ongoing bleeding or a limb-threatening condition, in accordance with current guidelines for time-sensitive non-cardiac surgery. The hospital course was uneventful with no bleeding complications. The patient was discharged to a rehabilitation centre after 1 week. Follow-up at 1 and 4 months confirmed medication compliance and functional improvement. The patient was subsequently lost to follow-up, and a repeat echocardiogram could not be performed.

Discussion

ST-elevation myocardial infarction is rarely associated with road traffic accidents, with only a small number of cases reported worldwide. Most have involved older patients with polytrauma and have been associated with poor outcomes, including increased in-hospital mortality and prolonged hospital stay.²

Diagnosis is challenging, as chest pain is frequently attributed to traumatic injuries. The absence of coronary risk factors and non-specific initial ECG changes further complicated early recognition in our case. Serial ECG monitoring revealed new anterolateral ST elevation, with cardiac biomarkers confirming myocardial injury while the patient was receiving strong analgesia and reporting only mild chest pain, underscoring the importance of serial clinical and biochemical assessment in uncovering a potentially fatal diagnosis.

The differential diagnosis of ST elevation in trauma patients includes myocardial contusion, stress-induced (Takotsubo) cardiomyopathy, coronary artery dissection, spasm, sub-intimal haematoma, and compression by epicardial haematoma.³ Thorough clinical assessment, trauma survey, echocardiography, and frequent monitoring are essential for accurate diagnosis.

Coronary CT angiography (CCTA) remains the gold-standard diagnostic and therapeutic tool in STEMI; however, its application in trauma patients is complicated by bleeding risk. CCTA may represent a valuable non-invasive alternative, offering lower procedural and bleeding risk with simultaneous assessment of coronary anatomy and traumatic injuries, though it was unavailable as an emergency investigation at our institution. In several previously reported cases, coronary angiography was delayed by up to three weeks due to active bleeding concerns.^3,4

The mechanism of STEMI following blunt chest trauma is most commonly coronary artery dissection, with plaque rupture reported less frequently. The LAD artery is most commonly affected owing to its anterior anatomical position, followed by the right coronary artery and left circumflex artery.^5,6 Intravascular ultrasound confirmed trauma-induced plaque rupture in our case. The pathophysiological mechanism is likely multifactorial, encompassing the direct mechanical impact of blunt chest trauma on the coronary artery wall, the acute surge in circulating catecholamines, and the systemic inflammatory response associated with major trauma, all acting in concert to destabilize vulnerable atherosclerotic plaques and promote coronary thrombosis.

Surgical fixation was deferred for a minimum of four weeks in accordance with ESC and ACC/AHA guidelines for time-sensitive non-cardiac surgery following DES-PCI,^7,8 which consistently recommend deferral for at least 1 month and ideally 3 months, given the risk of stent thrombosis with premature interruption of DAPT.

In conclusion, STEMI in young trauma patients is extremely rare and represents both a diagnostic and therapeutic challenge. Successful management requires a multidisciplinary team approach, carefully balancing the urgency of coronary revascularization against the inherent bleeding risk in the trauma setting.

Lead author biography

Adult Cardiology Fellow at King Fahad Medical City in Saudi Arabia, with a strong interest in academic development and contributing to high-quality clinical practice.

Author contributions

Razan Abdulhakim Bahurmuz (Conceptualization, Writing—original draft [lead], Writing—review & editing [equal]), Razan Issam Alrifaie (Writing—original draft, Writing—review & editing [equal]), and Sami Rashed Alasmari (Supervision [lead])

Consent: The authors confirm that written consent for submission and publication of this case report including images and associated text has been obtained from the patient, in line with COPE guidance.

Funding

None declared.

Data availability

The data underlying this article are available in the main manuscript or the supplemental material.