May 22nd, 2013
Subdural Hematoma and Possible ACS After Syncope
Indu Poornima, MD and James Fang, MD
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.
Questions:
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?
Response:
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.
Follow-Up:
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.
Further Questions:
- 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?
Response 2:
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.
15 Responses to “Subdural Hematoma and Possible ACS After Syncope”
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This is a syncope study case. The subdural hematoma probably is traumatic, it is important to review the CT scan to establish is acute. The ECG changes could be from the hematoma or cardiac injury you have to review the ECG. The troponin in this case could be from myocardic ischemia, heart failure, arrhythmia, brain injury, etc. I will ask for a complete cardiac enzyme panel and follow it in time and a BNP test. I will perform a functional test looking for ischemia, infarct, myocardial stunning – hibernation and functional capacity. If the patient in not in telemetry I ask for a Holter. Interconsult neurology. With all this information then you evaluate the therapeutic options and then prognosis. Note: In this case you must pay attention to the brain – heart connection and interactions.
How about starting with a good history about the loss of consciousness and past history/exercise endurance/PHM/meds?
This patient probably had a silent MI in the past and now presents with VT/syncope. I don’t think it’s ACS after syncope. I would proceed with cardiac cath now without heparin to evaluate coronary anatomy, since it may impact on further management and help to determine what actually has happenned, and then EP evaluation for AICD.
I would consider first a coronary angiogram.
There is evidence of anterior wall ischemia, and a previous head traumatism (some days before this event) due to ventricular arrhythmias is a strong possibility.
The sub dural hematoma is surely a semi recent pathology due to an unrecognized previous loss of consciousness (or not found by medical history)
Stenosis of LAD or LMC must be considered.
About Troponin very mild positivity: I wonder if it it can be seen in brain process but also let’s consider it is the witness of a few days ago unrecognized SCA.
In conclusion
consider the hypothesis of severe stenosis of Left Main Artery or Left Anterior Coronary artery with unstained ventricular tachycardia.
Due to patient’s condition, the best way to establish CAD, in my opinion, is coronary angiography, in my opinion this’ll help a lot with sincope reason establishment(more or less realistically). the rest could be discussed after CA data.
Coronary angiography would best establish if ECG abnormalities,troponin T elevation, and 2D Echo image abnormality were cause or effect(CT angio may be confounded by age dependent coronary Ca++). In other words, did unrecognized precedent MI create substrate for self terminating arrhythmia resulting in syncope(unwitnessed is an issue here) or are objective findings related to stress cardiomyopathy associated with SDH and small subarachnoid bleed.
Predischarge(at least 4 days post “event”), one could then consider programmed electrical stimulation(EP study)in that if monomorphic VT was demonstrated then ICD implantation may be warranted- particularly, if anatomic substrate is “wild type CAD/IHD.
Syncope during walking is surely not a benign symptom and the probability of a cardiac cause is very high.
ECG and echo are strongly in favor of anterior ischemia making paroxysmal ventricular arrhythmia most likely.
MRI could be an option to look for cardiac ischemia but might not obviate the need for coronary angiography.
The worst possible scenario would be a combination of intracranial bleedind + ACS requiring urgent PCI and Stenting…Let s pray that this is not the case for the patient since dual antiplatelet therapy is (for obvious reasons) contraindicated in this case.
Since the syncope ist strongly suggestive of a cardiac origin, i would perform coronary CT-Angio and MRI to find out about CAD, myocarditis, hibernating myocardium or cardiac scar tissue.
If the cause of the syncope cannot be repaired/treated, i would suggest the following options:
1 perform venricular stimulation, in case of negative result, start optimal heart failure therapy, discharge with Life-Vest + telemetry/Holter-ECG and then re-evaluate the patient later for ICD or even CRTD (if EF remains low and the patient meets the other criteria).
2 perform venricular stimulation, in case of positive results implant ICD now and start optimal heart failure therapy. after discharge re-evaluate the patient later for CRTD (if EF remains low and the patient meets the other criteria).
Would like to know more about the questionable small subarachnoid bleed. If the location and pattern consistent with the trauma it is a nonissue. However if the history or CT appearance suggests the possibility of SAH from anuerysm, this possibility needs to be pursued though far less likely. Do the cath, skip the MRI.
If it is a case of apical ballooning syndrome due to subdural hematoma I believe it should be published as a case report.
The problems here are:
1. Syncope
2. Cause of Syncope; arrhythmia induced secondary to myocardial infarction?
3. Subdural haematoma and risk of worsening with anticoagulant therapy.
Carrying out investigation to identify coronary artery stenosis should only be undertaken if it is going to affect management. In the presence of a recent subdural haematoma coronary revascularisation with PCI which includes patent antithrombim and antiplatelet agents is fraught with great risks and therefore should not be done.
If this is a primary arrhythmia following acute coronary syndrome, Defibrillator yherapy would not be considered indicated by most Device therapists.
Overall, conservative management in the initial 4-6 weeks would be my recommended option for management. After that period when the risk of worsening of the suddural haematoma has lessened, then investigation for reverscularisation and repeat echocardiography to assess the need for Device therapy could be investigated.
One must perform testing for the purpose of a.)establishing causation as to pathogensis and b.)risk stratification. And only thereafter may appropriate and timely treatment be assigned based on patient specific comorbities(such as bleeding risk). Procedures for diagnostic purposes( eg cardiac cath)can, and in this instance, should be separate from same or different procedure for the purpose of intervention to mitigate the natural history of the accurately defined disease state.
Was the ICD implantation indicated?
No. In this case ICD therapy is indicated in patients with syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiological study. So you must have a EP study.
Should an EP study have been done?
Yes but I will wait until we have more information in the heart and brain condition.
How do you explain the discrepancy between the MRI and the nuclear perfusion results?
One possibility is three-vessel coronary artery disease if this patients have balanced ischemia, which yields few or no relative perfusion defects in SPECT but the CT scan exclude this possibility. One theoretic possibility is that MRI has significantly higher spatial resolution, which allows the detection of the subendocardial ischemia better than SPECT maybe the patient have microangipatic disease but the CT report significant stenosis of the mid-portion with mixed plaque and thrombus as well. Other explanation is the localization, the vessels supplying the apex are less than 2 mm in diameter in most cases, the detection of purely apical ischemia would add potential false-positive results to both stress perfusion MRI and SPECT examinations but the clinical information is not compatible with this scenario. Now taking in consideration the 3 months difference between both studies a good explanation is myocardial stunning – hibernation. This could be a spontaneous reperfusion but for the moment I can exclude the possibility of a neurocardiac interaction to explain the discrepancies in this case.
Would you consider coronary angiography and revascularization at this time?
No. I will try optimal medical treatment and cardiac rehabilitation first.
The implantation of the ICD would have been best established as “indicated” (ie appropriate) if no recent infarction classification and EF < 35% or if so classified(type I vs type III MI) if EP study performed after 4 days demonstrated inducible monomorphic VT.
The MRI and MPI(nuclear perfusion) discordance is due to the early phase of MRI imaging not able to distinguish stunned myocardium from scar and the late phase of nuclear perfusion imaging whereby myocardial recovery from stunning has occurred.
Effective medical therapy to this time would not obligate cath/PCI, awaiting clinical ischemia.
Thanks to all for your interest and comments on managing this patient. As discussed earlier he did undergo placement of an ICD based on the thinking that the syncope was related to a primary ventricular arrhythmia in the setting of LV systolic dysfunction. There was much debate about this decision as the arrhythmia could have occured in the context of an acute coronary event. Regardless, he was medically managed for his CAD as he was asymptomatic and had an excellent functional capacity. The patient continues to do well and has not had any ICD events.