Introduction

Blunt chest trauma can be a serious yet unrecognized cause of cardiac injury. Non-penetrating chest injuries related to high-speed motor vehicle accidents, falls, crush injuries, or sports can cause structural damage to cardiac chambers and valves, injure coronary arteries, or disrupt the aorta. For example, nearly 20% of traffic-related deaths have evidence of cardiac trauma on autopsy, and up to 15% of all persons who suffer blunt chest trauma are estimated to have cardiac injury.¹ Recognizing the presence of cardiac trauma can be challenging because chest pain or dyspnea may be easily attributed to chest wall contusion or trauma to adjacent organs. Less than 40% of patients with trauma-induced acute myocardial infarction (MI) received rapid reperfusion of the culprit coronary artery.² The severity of cardiac injury ranges from asymptomatic, transient dysrhythmia to fatal cardiac rupture. Unfortunately, there is a paucity of data for incidence, management, and outcomes related to cardiac trauma. Although clinically significant cardiac injuries may occur in only a small minority of patients, delay in prompt diagnosis and treatment can result in worsened outcomes. Using a clinical case to provide context, we will provide a brief clinical overview of trauma-induced coronary artery injury and cardiac contusion.

Clinical Case

A 38-year-old healthy woman presented to the emergency room with chest pain. She was walking to her car in the parking lot of a department store. When she tried to enter her car, a man pushed her out of the way. She continued to hold onto the door as the assailant drove away, leading to a direct collision between a concrete pole and her chest. On arrival, her chest pain resolved spontaneously. Her presenting blood pressure was 113/55 mmHg with a heart rate of 70 bpm. Electrocardiogram (ECG) did not reveal ST or T wave changes. Chest radiograph was normal, and computed tomographic angiogram of the chest ruled out aortic dissection. Initial cardiac troponin I (cTnI) was 0.6 ng/mL. The patient was admitted for further observation. Echocardiogram showed an ejection fraction of 35% with apical and septal wall motion abnormality (Video 1). After 4 hours, a repeat cTnI was 9.7 ng/mL. Due to the increase in cTnI and new cardiomyopathy, she underwent coronary angiogram, which showed dissection of the distal right coronary artery with normal flow (Video 2). The patient was managed conservatively because she was chest pain free and the flow was normal. After 2 days of observation, she was discharged in stable condition on aspirin, metoprolol, and lisinopril. At 2-months follow-up, she remained free of symptoms with complete recovery of ejection fraction to 55-60%.

Video 1

Video 2

Pathophysiology and Clinical Complications

Table 1 summarizes the mechanisms, anatomic location, and clinical complications of cardiac contusion and coronary artery injury. Cardiac contusion is the most common cardiac injury, often in the right ventricle due to its anterior location.³ On histopathology, it causes muscle edema, hemorrhagic infiltrate, and/or necrosis that can serve as the nidus for electrical, structural, and ischemic complications.¹ Electrically, different arrhythmias may occur, including ventricular tachycardia, atrial arrhythmias, or varying degrees of heart block. Ventricular fibrillation may result if precordial impact occurs just before the T wave peak, usually from a projectile with high velocity. Two important structural complications are cardiomyopathy and cardiac rupture. Cardiomyopathy can result from blunt trauma and/or emotional stress but generally improves over time.^1,6 Cardiac rupture, however, is usually fatal. Ischemic complications occur from cardiac contusion or independently from trauma-induced coronary artery injury. Importantly, pre-existing atherosclerosis or collagen vascular disease increases the risk of trauma-induced acute coronary syndrome (ACS).

Table 1

	Cardiac Contusion	Coronary Injury
Mechanism3,4,8	Direct precordial impact Crush injury between sternum and spine Deceleration causing myocardial tear	Arterial twist or shear Strain at the aortic root Direct coronary compression
Common Location3	Right ventricle	Left anterior descending artery (71%) Right coronary artery (19%) Left main coronary artery (6%) Left circumflex artery (3%)
Complications3	Arrhythmia Cardiac rupture Cardiomyopathy Coronary occlusion	Acute MI Arrhythmia Coronary vasospasm Coronary dissection Coronary thrombosis

Evaluation and Diagnosis

Diagnostic evaluation for cardiac injury in a patient with blunt chest trauma begins with assessment and stabilization of vital signs followed by examination of the head, neck, heart, and lungs. Notably, patients with cardiac injury may not present with characteristic or serious symptoms. The presence of hypotension, jugular venous distension, precordial thrill, or new murmur may indicate more serious cardiac injury but is not specific. All patients suspected of cardiac injury should receive 12-lead ECG and chest radiograph. Screening for acute MI with cardiac biomarkers should consist only of cTnI because of its specificity to the myocardium. Creatine phosphokinase and creatine phosphokinase muscle/brain are not as reliable because they may also be elevated from skeletal muscle injury. Patients with progressive chest pain or dyspnea, hemodynamic instability, ischemic ECG changes, or complex arrhythmias warrant an echocardiogram to evaluate for cardiac tamponade, myocardial rupture, or cardiomyopathy. If valvular injury is suspected, an echocardiogram is particularly useful because symptoms can present more subacutely than injuries to the coronary arteries or myocardium.

Management

If initial diagnostic evaluation raises concern for cardiac trauma, patients should be monitored in a setting where therapeutic interventions can be offered with any clinical decompensation. In the setting of ST-segment elevation on ECG, significantly elevated cTnI, or wall motion abnormality on echocardiogram, consideration of trauma-induced ACS should prompt definitive diagnostic testing with a coronary angiogram. Nearly one in five patients with trauma-induced acute MI will have a normal coronary angiogram, likely due to coronary vasospasm.⁷ In patients with an abnormal angiogram, intravascular ultrasound is particularly useful in differentiating dissection from traumatic atherosclerotic plaque rupture. Percutaneous coronary intervention (PCI) is the main treatment of traumatic ACS because thrombolytic therapy is often contraindicated in patients with other traumatic injuries and high risk of bleed. Timing of PCI depends on hemodynamic stability as well as bleeding risk. Because antithrombotic therapy may worsen ongoing hemorrhage, major organ bleeding should be excluded prior to PCI. In patients with no evidence of hemorrhage, emergent PCI is appropriate. Coronary artery bypass grafting is an option for those with surgical coronary disease or structural abnormalities that require surgical treatment. Conservative management or delayed PCI can be a reasonable alternative to patients with active bleeding.⁹ Clinical judgement must be used to balance the risk of ongoing myocardial ischemia/injury versus the impact of ongoing bleeding. Patients without symptoms or ongoing ischemic changes on ECG may be closely monitored. The negative predictive value for cardiac contusion or traumatic ACS with a normal ECG and cTnI 4-6 hours after trauma approaches 100%.¹⁰

Prognosis

Long-term ramifications of blunt cardiac contusion and traumatic ACS are largely unclear due to insufficient follow-up data. In a small cohort of patients with myocardial contusion, there was no significant difference in ejection fraction at rest or during exercise compared with a control group at 1 year, suggesting no significant long-term sequelae after blunt cardiac contusion.¹¹ Prognosis of traumatic ACS depends on the severity of the initial insult and presence of infarct size. Trauma of mild or moderate severity managed conservatively may eventually contribute to delayed coronary stenosis that becomes clinically relevant months or years later.⁷ For this reason, a history of trauma should be sought in patients without traditional risk factors for atherosclerotic coronary disease who present with angina, especially because the majority of traumatic coronary injuries involve the left anterior descending artery.

Conclusion

The clinical case outlines several important points that should be considered when evaluating a patient with blunt chest trauma. Despite a normal ECG with resolution of chest pain, the patient's history prompted evaluation of cTnI and echocardiogram, the findings of which eventually warranted further investigation with a coronary angiogram. Obtaining the diagnosis of new cardiomyopathy and coronary artery dissection was only possible due to high clinical suspicion for cardiac complication from blunt chest trauma. Failing to recognize these complications can lead to inadequate or inappropriate management that may contribute to worsened morbidity and mortality. Correct identification of myocardial or coronary injury allows proper inpatient monitoring and treatment followed by timely outpatient follow-up. This combination helps to ensure the optimal long-term prognosis, a topic needing further research.

References

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5. Bansal MK, Maraj S, Chewaproug D, Amanullah A. Myocardial contusion injury: redefining the diagnostic algorithm. Emerg Med J 2005;22:465-9.
6. Elikowski W, Kudliński B, Małek-Elikowska M, Foremska-Iciek J, Baszko A, Skrzywanek P. [Takotsubo cardiomyopathy in a young woman after a traffic accident with blunt chest trauma]. Pol Merkur Lekarski 2016;40:372-6.
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8. Radojevic N, Radunovic M. Traumatic acute myocardial ischaemia involving two vessels. J Forensic Leg Med 2014;23:9-11.
9. Guo H, Chi J, Yuan M, Qiu Y. Acute myocardial infarction caused by blunt chest trauma: a case report. Int J Cardiol 2011;149:e80-1.
10. Velmahos GC, Karaiskakis M, Salim A, et al. Normal electrocardiography and serum troponin I levels preclude the presence of clinically significant blunt cardiac injury. J Trauma 2003;54:45-50.
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Keywords: Acute Coronary Syndrome, Creatine Kinase, MB Form, Metoprolol, Lisinopril, Thoracic Injuries, Troponin I, Fibrinolytic Agents, Ventricular Fibrillation, Heart Rate, Creatine Kinase, MM Form, Accidental Falls, Plaque, Atherosclerotic, Aspirin, Cardiac Tamponade, Creatine Kinase, BB Form, Risk Factors, Blood Pressure, Heart Ventricles, Thoracic Wall, Follow-Up Studies, Atrial Fibrillation, Stroke Volume, Wounds, Nonpenetrating, Coronary Artery Disease, Electrocardiography, Coronary Angiography, Chest Pain, Myocardial Infarction, Coronary Artery Bypass, Coronary Stenosis, Percutaneous Coronary Intervention, Myocardium, Tachycardia, Ventricular, Heart Block, Cardiomyopathies, Hypotension, Heart Rupture, Muscle, Skeletal, Aorta, Emergency Service, Hospital, Aneurysm, Dissecting, Dyspnea, Thrombolytic Therapy, Atherosclerosis, Biomarkers

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