Diagnostic Dilemma: Commotio Cordis, Takotsubo Syndrome or MI with Non-obstructive Coronary Arteries? A Case Report

MI with non-obstructive coronary arteries (MINOCA) encompasses many aetiologies, presenting like MI but with non-obstructive coronary arteries seen on invasive coronary angiogram (ICA).¹ It is increasingly recognised and can account for up to 14% of patients presenting with acute coronary syndrome.²

We discuss the diagnostic and therapeutic dilemmas that can be encountered during the management of an unusual case of MINOCA in a patient with sudden cardiac arrest (SCA) after a car crash.

Case Presentation

A 52-year-old man with well-controlled hypertension developed acute chest pain while driving, resulting in a road traffic accident that caused the airbags in the car to be deployed. Paramedics arrived 6 minutes later and found him to be in VF. Spontaneous circulation returned after 15 minutes of cardiopulmonary resuscitation and five defibrillator shocks. The ECG performed on the way to the hospital revealed antero-lateral ST-segment elevation (Figure 1A).

At the hospital, he was afebrile and his blood pressure was 149/87 mmHg. His oxygen saturation was 94% on a non-rebreather mask. He had dual heart sounds with no murmurs and no obvious external injuries were observed. A repeat ECG 20 minutes later showed rapid AF with resolution of ST-segment elevation (Figure 1B). The high-sensitivity cardiac troponin-I measurement was 1,500 ng/l. Chest X-ray showed pulmonary congestion with no rib fractures and a head CT did not reveal stroke, haemorrhage or other injuries.

ICA was performed immediately, and showed <50% stenoses in the left anterior descending, left circumflex and right coronary arteries. A working diagnosis of MINOCA was made. Subsequently, left ventriculography demonstrated impaired systolic function with mid- and basal-wall ballooning (Supplementary Video 1 ). The left ventricular end-diastolic pressure was 24 mmHg. A diagnosis of takotsubo syndrome (TTS), specifically the basal or ‘reverse’ form of TTS, was made. A transthoracic echocardiogram performed 2 days later revealed normal biventricular function with no wall motion abnormalities (Supplementary Video 2 ).Cardiac MRI (CMR) performed 12 days later demonstrated myocardial oedema in the basal to mid-inferolateral wall with corresponding near transmural late gadolinium enhancement, suggestive of recent MI (Figure 2 ). There were no wall motion abnormalities suggestive of TTS (Supplementary Video 3 ).

As the cause of MI remained unclear, empirical treatment for coronary artery vasospasm with a non-dihydropyridine calcium channel blocker and a dual anti-thrombotic therapy with apixaban and clopidogrel for AF and MI were started. A single-chamber ICD was implanted after the risks and benefits were discussed with the patient. He was discharged after 15 days of hospitalisation. An ICD interrogation 1 week and up to 1 year later did not reveal any arrhythmic events.

Discussion

This case report illustrates the diagnostic and therapeutic dilemmas we faced when managing a patient who was involved in a road traffic accident after having acute chest pain and VF. Given the presence of chest pain, transient ST-segment elevation and troponin rise, an urgent ICA was performed as MI was initially the most likely diagnosis. The diagnosis was then revised to MINOCA when the ICA revealed non-obstructive coronaries. As the underlying cause of MINOCA was not established after ICA, guidelines recommend performing left ventriculography, and this showed a typical basal/’reverse’ TTS morphology.¹ This rare variant of TTS is characterised by basal akinesis/hypokinesis instead of apical ballooning.³ While the exact pathophysiological mechanism of reverse TTS is unknown, there are several theories including catecholamine-induced cardiotoxicity from stress, coronary vasospasm and coronary microvascular dysfunction.³

In addition to left ventriculography, adjunctive tests for microvascular function, coronary reactivity and intravascular imaging can be performed during ICA.¹ In a study by Montone et al. they found that early provocative testing was safe and could identify coronary vasospasm in 46% of MINOCA patients.⁴ The superior resolution of optical coherence tomography is helpful for identifying the culprit lesion in MINOCA, which includes rupture of atherosclerotic plaque, erosion and coronary thrombosis.⁵

CMR is crucial in the work-up of MINOCA as it can ascertain the underlying cause in up to 87% of cases.⁶ The pattern of delayed gadolinium enhancement, together with oedema assessment, help to differentiate between MI, myocarditis and TTS. Data from the Bristol CMR Registry has shown that among patients presenting with suspected MINOCA (n=888), the final diagnosis was MI (n=243; 27%), myocarditis (n=217; 24%), TTS (n=115; 13%) and other cardiomyopathies (n=97; 11%) after CMR.⁷

Although CMR identified the presence of MI in this case, the exact aetiology remained unclear. Plaque rupture or erosion with spontaneous recanalisation is a possibility as intravascular imaging was not performed. Coronary artery vasospasm could not be confidently excluded as provocation testing was not completed in the emergency setting. As the patient had AF when he arrived at the hospital, coronary thromboembolism may also have been a cause.

While the initial impression appears to be consistent with TTS, the CMR features suggest otherwise. Apart from the unusually quick recovery of the wall motion abnormalities (resolved on the transthoracic echocardiogram performed on day 2 of presentation as well as on CMR), the pattern of myocardial oedema seen on CMR was not consistent with TTS. Typical TTS oedema shown on T2-weighted sequences occurs in a distribution that is not restricted to a particular vascular territory.⁸ Furthermore, the areas of oedema should typically match the dysfunctional ventricular contraction areas, which in this case would be all the mid- and basal segments. These areas of T2 hyperintensity should be seen over weeks as time is needed for oedema to resolve.⁸

Instead, what we found in this case was focal basal to mid-inferolateral wall oedema with corresponding near transmural late gadolinium enhancement. This is a typical pattern for MI. Hence, alternative explanations for MI, in the absence of significant coronary stenosis, such as plaque rupture/erosion, vasospasm and thromboembolism were considered.

There are several case reports documenting the close relationship between coronary vasospasm and TTS and there is emerging evidence that TTS and coronary artery spasm may possibly be either two expressions of the same disease or they may share overlapping mechanisms.^9,10

The cause of this patient’s VF arrest was also uncertain. While MI is the most likely cause, TTS presenting with VF has also been reported.¹¹ The car crash and air bag deployment may have caused commotio cordis, a condition characterised by VF caused by blunt chest trauma without musculoskeletal or myocardial damage.¹² A similar case of reverse TTS in a patient with commotio cordis after a car crash has been reported previously, where the initial diagnosis of TTS was made using echocardiography rather than CMR.¹³

The range of possible diagnoses also led to a management dilemma. ICD implantation is well established for survivors of SCA due to ventricular arrhythmias in the absence of reversible causes, but it should also be considered even when there is a possible correctable cause for the ventricular arrhythmia because these patients will have an ongoing higher risk of mortality.¹⁴ In addition, SCA survivors are at high risk of recurrence of VF due to coronary artery vasospasm, and vasodilator therapy alone may not be sufficiently protective.¹⁴ As such, after a risk/benefit discussion, our patient received an ICD with anti-thrombotic and vasodilator therapy.

Conclusion

This case illustrates a stepwise approach to MINOCA evaluation and how the working diagnosis can change with every additional investigation modality. Although CMR played a pivotal role in the work-up, the exact underlying aetiology and pathogenesis of the patient’s MI and VF remained uncertain. Adjunctive investigations during ICA should not be limited to left ventriculography alone. Wider adoption of intravascular imaging and provocation testing in MINOCA patients can enhance diagnostic accuracy and guide therapeutic decisions in this challenging population.