May 22nd, 2013
Subdural Hematoma and Possible ACS After Syncope
A 54-year-old man with no history of coronary artery disease was walking his dog when he experienced an unwitnessed episode of syncope. He spontaneously regained consciousness within a few minutes. Bystanders took him to the ER, where he underwent noncontrast CT of the head that showed a subdural hematoma with a questionable, small subarachnoid bleed. A 12-lead electrocardiogram showed anterior T-wave inversions, and his troponin T level was positive at 0.4 µg/liter. The patient was admitted to the cardiac intensive care unit.
A 2-dimensional echocardiogram revealed distal anteroseptal and apical wall-motion abnormalities and a left-ventricular ejection fraction of 40%. Because of the intracranial bleed, he was conservatively managed with a beta-blocker, aspirin, and a statin. He remained hemodynamically stable for the next 48 hours without arrhythmias. A repeat CT of the head showed no progression in the subdural hematoma, and no evidence of intracranial bleeding.
1. What would be your next step in managing this patient: cardiac catheterization, coronary CT angiography, evaluation for an implantable cardioverter-defibrillator, or some other alternative?
2. Why would you choose that management approach?
May 29, 2013
This patient’s story begins with syncope that has yet to be explained. Despite the apparent lack of history of CAD, the documented cardiac dysfunction raises the possibility of cardiac syncope. The syncope may have been secondary to ischemia-mediated ventricular tachycardia (VT) or ventricular fibrillation (VF), given the ECG changes, anteroseptal and apical wall-motion abnormalities, and positive troponin. The larger the ischemic territory, the more likely that ischemia may result in VT/VF.
The case author also leads one to consider that the syncope may have been an arrhythmic manifestation of a previously unrecognized cardiomyopathy (e.g., reduced LV ejection fraction). However, syncope is an unusual first manifestation of asymptomatic LV dysfunction, particularly if recent in onset.
Alternatively, the unexplained syncope may have led to a traumatic subdural hematoma and then secondary LV dysfunction, as may occur in the context of an acute stroke syndrome or significant stress (e.g., Takotsubo cardiomyopathy). In this case, the “syncope” may have resulted from a mechanical, unwitnessed fall while the patient was walking his dog. A subdural hematoma rarely manifests as syncope and, therefore, is unlikely to have been the initial clinical event.
I favor coronary angiography (which can be done safely without heparin) to evaluate the patient’s coronary anatomy, as long as his neurologic status is stable. It’s critical to ascertain explanations for the LV dysfunction and the syncope. Coronary CT could be considered as an alternative if there is significant concern about performing coronary angiography in the presence of a subdural hematoma. A cardiac MRI can be useful to look for evidence of scar (e.g., chronic cardiomyopathy) or a Takotsubo-like problem (JAMA 2011; 306:277). Evaluation for an ICD should be deferred until the nature of the heart disease is better delineated.
June 5, 2013
The patient underwent cardiac MRI on day 3, and the report indicated >75% delayed hyperenhancement in the distal anteroseptum and apical septal regions, with evidence of microvascular obstruction suggestive of scar, as well as akinesis of the distal septal walls and apical walls. LV ejection fraction was estimated at 52%. Given the evidence of scar and the recent subdural bleed, coronary angiography was deferred. CT angiography was performed. The report read as follows:
Small, calcified nonobstructive plaque in the proximal portion. There is a significant stenosis of the mid-portion with mixed plaque and thrombus as well. This most likely
represents plaque rupture with a subtotal occlusion, given the poor filling of the LAD distal to this lesion.
The patient remained asymptomatic and hemodynamically stable without arrhythmias during his hospital course. His cardiologist and the electrophysiologist debated about whether to offer an ICD for secondary prevention in the setting of significant scar and presentation with syncope. The patient eventually underwent ICD implantation and was discharged home on standard post-MI therapy.
Three months after discharge, he reported symptoms of shortness of breath and was referred for exercise myocardial perfusion SPECT. He exercised for 11 minutes on the Bruce protocol without chest pain, ECG changes, or arrhythmias. His perfusion images showed a medium-size area of moderate-to-severe reversible ischemia in the apex and distal anterior and anteroseptal regions, with a preserved LV ejection fraction of 57%. The resting perfusion scan suggested viable myocardium in all territories. The patient was continued on medical therapy.
- Was the ICD implantation indicated? If so, why? If not, why not?
- Should an EP study have been done?
- How do you explain the discrepancy between the MRI and the nuclear perfusion results?
- Would you consider coronary angiography and revascularization at this time?
June 13, 2013
- An ICD is not indicated without further investigation. The stress-test results, angina equivalent, and coronary CT findings point to untreated ischemia.
- Once the ischemia (which may be driving the presumed ventricular arrhythmia) is treated, I would consider an EP study to assess inducibility of ventricular tachycardia, given the scar.
- MRI and nuclear findings are complementary and not necessarily at odds, as the two modalities assess different aspects of myocardial structure and function. The transmural extent of hyperenhancement is not described.
- Despite the patient’s good exercise capacity, his original presentation with syncope suggests that ischemia of the anterior wall putatively caused a ventricular arrhythmia. An ICD arguably doesn’t treat the problem but rather the “symptom.” Strong consideration should be given to revascularization, particularly in light of the dramatic initial presentation. However, I would favor medical management of his CAD if the original presentation was not syncope.