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CardioNerds (Amit Goyal and Daniel Ambinder), join CardioNerds FIT Ambassador, Dr. Natasha Cuk and her co-fellows, Dr. Lily Stern, and Dr. Paul Marano from the Cedars-Sinai Cardiology Fellowship for some late afternoon smoothies on the beach. They discuss the case of a 46-year-old woman who presented with sudden cardiac arrest and was ultimately found to have a mobile intraluminal aortic thrombus adherent to a penetrating ulcer in the ascending aorta. This mobile thrombus was ultimately thought to be the cause of transient ischemia and the patient’s cardiac arrest. We discuss a differential for sudden cardiac arrest, initial management after resuscitated cardiac arrest, a differential for arterial thrombus, and review an illness script for penetrating atherosclerotic ulcers. Dr. Dominick Megna provides the provides the E-CPR for this episode. Audio editing by Dr. Gurleen Kaur (Director of the CardioNerds Internship).

This Case Report has been published in JACC Case Reports!

Claim free CME just for enjoying this episode! 

Disclosures: None
Jump to: Pearls – Notes – References

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Episode Teaching

46W no known PMH BIBA after sudden cardiac arrest. Normal trops, BNP, ECG, TTE. Extubated HD1 w/o any memory of the event.

S/p CCTA w clean cors but aorta with this 😳…

🧵1/ pic.twitter.com/jI89UXNUtq

— Lily K Stern MD (@LilySternMD) November 17, 2021

Pearls – Cardiac Arrest due to Aortic Thrombus

1. After cardiac arrest, the initial ECG obtained after the return of spontaneous circulation can provide important information on the etiology of the arrest. The ECG can narrow our structured differential, for which one approach would be the following breakdown: acute ischemic events, structural heart disease, arrhythmogenic syndromes with no structural abnormality, and then non-cardiac causes such as drugs, toxins, trauma, metabolic arrangements
2. The risk vs benefit of emergent angiography after sudden cardiac arrest depends on balancing the potential benefit from revascularization in an acute ischemic event vs bleeding risks and potential delays in other aspects of care, particularly given that a large percentage of mortality is related to neurologic injury from the arrest, which would not be impacted by immediate angiography. The available randomized controlled trial evidence has not demonstrated a survival or neurologic outcome benefit to immediate angiography, and the decision depends on weighing the risk/benefit for each patient.
3. Due to high flow, a thrombus in the aorta should prompt an investigation for causes focused on the other two ‘points’ of Virchow’s triad (aside from stasis): endothelial injury and hypercoagulability.
4. A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. These lesions are most commonly associated with extensive atherosclerosis, but can also occur related to inflammatory, infectious, or traumatic causes.
5. A PAU is a type of acute aortic syndrome and accounts for up to 8% of total acute aortic syndromes. It may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection. While it is a subtype of aortic syndrome, PAU can also progress to become aortic dissection and rupture.

Notes – Cardiac Arrest due to Aortic Thrombus

1. How might a post-ROSC ECG help determine the etiology of a sudden cardiac arrest?

During our case, we discussed a systematic approach to the differential diagnosis for sudden cardiac arrest. We broke down the causes into the buckets of:

• Acute ischemic events
• Structural heart disease
• Arrhythmogenic syndromes with no structural heart disease
• Non-cardiac causes such as drugs, toxins, trauma, and metabolic arrangements

The post-ROSC ECG can provide immediate information to help narrow our differential. Evidence of acute ischemia (e.g. STEMI) would provide a likely etiology and would direct immediate next steps. We can look at ECG features such as axis and conduction abnormalities to look for evidence of an underlying structural abnormality. We can also see features of arrhythmogenic syndromes without underlying structural defects, such a short or long QT or a Brugada pattern.

2. Should all patients who present with sudden cardiac arrest and for whom ROSC is achieved undergo immediate coronary angiography?

In considering the timing of coronary angiography after sudden cardiac arrest, clinical experience and the available evidence indicate a tension between:

1. The high pre-test probability for acute ischemic events as the etiology for VT/VF arrest, and possible improvement in post-ROSC outcomes from immediate coronary angiography (and revascularization).
2. A large portion of the morbidity and mortality associated with sudden cardiac arrest is driven by neurologic injury. Immediate angiography may expose patients to additional risk (delays in targeted temperature management, bleeding risk), without benefit to a patient’s ultimate outcome due to neurologic injury.

Observational data has suggested a benefit for immediate angiography after resuscitated sudden cardiac arrest, though there was concern for selection bias. Recently, there have been two randomized controlled trials that have investigated the role for immediate angiography after sudden cardiac arrest. These trials are the COACT and PEARL trials, published in 2019 and 2020, respectively. These trials each have their own limitations, though they did not demonstrate a benefit for immediate angiography on outcomes such as mortality or neurologic outcomes. There are multiple ongoing trials to provide further guidance.

The most recent AHA/ACC guideline on the topic recommends immediate coronary angiography for patients with STEMI on the post-ROSC ECG (Class I), and give a Class IIa recommendation that emergency coronary angiography is reasonable for selected patients (e.g. hemodynamically or electrically unstable) with sudden cardiac arrest of suspected cardiac origin without STEMI.

3. What is an illness script for penetrating atherosclerotic ulcers?

Definitions: A penetrating atherosclerotic ulcer (PAU) is a deep atherosclerotic lesion where there is a focal ulceration of the elastic lamina that extends through the medial layer of the aortic wall. PAU is a type of acute aortic syndrome (along with other disease processes such as aortic dissection, intramural hematoma). While a distinct entity, PAU can also progress and lead to intramural hematoma, dissection, and even aortic rupture.

Epidemiology: PAU accounts for 8% of total acute aortic syndromes. It is typically associated with extensive atherosclerosis in older adults (age > 65) and is most commonly found in the descending thoracic aorta. It is less commonly associated with infectious, inflammatory, or traumatic etiologies.

Clinical Presentation: PAU may present with a spectrum of symptoms, including as an incidental finding on cardiothoracic imaging or a severe chest and back pain, like an aortic dissection.

Diagnosis: PAU can be diagnosed by multiple imaging modalities, including computed tomography angiography, magnetic resonance imaging, and transesophageal echocardiography.

4. How are penetrating aortic ulcers treated?

Management of symptomatic penetrating aortic ulcers is similar to management of aortic dissection with indications for surgery including recurrent pain despite medical treatment, hemodynamic instability, aortic diameter enlargement to >55 mm, and significant periaortic hemorrhage. In asymptomatic patients who are hemodynamically stable, management is controversial–some centers support aggressive early surgical intervention while others opt for conservative medical management along with serial surveillance for aortic enlargement.

References

1. Lemkes JS, Janssens GN, van der Hoeven NW, Jewbali LSD, Dubois EA, Meuwissen M, Rijpstra TA, Bosker HA, Blans MJ, Bleeker GB, Baak R, Vlachojannis GJ, Eikemans BJW, van der Harst P, van der Horst ICC, Voskuil M, van der Heijden JJ, Beishuizen A, Stoel M, Camaro C, van der Hoeven H, Henriques JP, Vlaar APJ, Vink MA, van den Bogaard B, Heestermans TACM, de Ruijter W, Delnoij TSR, Crijns HJGM, Jessurun GAJ, Oemrawsingh PV, Gosselink MTM, Plomp K, Magro M, Elbers PWG, van de Ven PM, Oudemans-van Straaten HM and van Royen N. Coronary Angiography after Cardiac Arrest without ST-Segment Elevation. New England Journal of Medicine. 2019;380:1397-1407.
2. Kern KB, Radsel P, Jentzer JC, Seder DB, Lee KS, Lotun K, Janardhanan R, Stub D, Hsu CH and Noc M. Randomized Pilot Clinical Trial of Early Coronary Angiography Versus No Early Coronary Angiography After Cardiac Arrest Without ST-Segment Elevation: The PEARL Study. Circulation. 2020;142:2002-2012.
3. Callaway CW, Donnino MW, Fink EL, Geocadin RG, Golan E, Kern KB, Leary M, Meurer WJ, Peberdy MA, Thompson TM and Zimmerman JL. Part 8: Post–Cardiac Arrest Care. Circulation. 2015;132:S465-S482.
4. Hiratzka LF, Bakris GL, Beckman JA, Bersin RM, Carr VF, Casey DE, Eagle KA, Hermann LK, Isselbacher EM, Kazerooni EA, Kouchoukos NT, Lytle BW, Milewicz DM, Reich DL, Sen S, Shinn JA, Svensson LG and Williams DM. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM Guidelines for the Diagnosis and Management of Patients With Thoracic Aortic Disease. Circulation. 2010;121:e266-e369.

CardioNerds Case Report Production Team