Peripheral Vascular Disease Archives - Cardionerds

CardioNerds join Dr. Tony Li Yi Wei, Dr. Rodney Soh Yu Hang, and Dr. Zan Ng Zhe Yan from the National University Heart Centre Singapore for a cocktail drink on the top of marina bay sands. They discuss the following case featuring a young woman with recurrent ACS ultimately found to have Takayasu Arteritis. The ECPR for this episode is provided by Dr. Teng Gim Gee and Professor Tan Huay Cheem. Episode audio was edited by student Dr. Shivani Reddy.

A 37-year-old woman presents with chest pain. She has a background history of Hashimoto thyroiditis, gestational diabetes, and anemia of chronic disease and possible iron deficiency. Her significant medical history includes ischemic heart disease with prior coronary angiogram showing triple vessel coronary artery disease for which she underwent coronary artery bypass graft surgery (CABG) with LIMA-LAD, SVG-OM, SVG-RCA. After CABG, she had recurrent admissions in the subsequent year with acute coronary syndromes where she underwent percutaneous coronary intervention (PCI) to SVG-OM, RI, proximal LAD, and distal LAD. She was a non-smoker and had been compliant with her medications. For her current presentation, she underwent myocardial perfusion imaging which showed a large sized area of inducible ischemia in the LCx territory.  Repeat coronary evaluation showed occluded SVG-OM, occluded LIMA-LAD where she underwent PCI. Clinically, she was noted to have weak brachial and radial pulses on the left side with systolic blood pressure difference between both arms. CT Thoracic Angiogram demonstrated concern for underlying large vessel vasculitis such as Takayasu arteritis. ESR was elevated at 34. Rheumatology was consulted and she was diagnosed with Takayasu arteritis and started on prednisolone and azathioprine. Given her young age, absence of traditional atherosclerotic risk factors, and progressive coronary disease, Takayasu arteritis was deemed the underlying etiology of her coronary disease.

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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Focusing on young patients presenting with myocardial infarction (MI), the definition is often arbitrary, with most studies using an age cut off of around 40-45 years. As we know, the risk factor profile of the younger population is different with lower prevalence of traditional cardiovascular risk factors, and women of this age group are generally premenopausal.

Causes of MI among such patients can be divided into four groups, although a considerable overlap exists between all groups.

The first etiology is that of atheromatous CAD, which is linked to conventional risk factors in older patients that we are familiar with. This includes smoking, lipid abnormalities including familial hyperlipidemia, insulin resistance, hypertension, and obesity. Other more novel risk factors include hyperhomocysteinemia and elevated lipoprotein (a).

Secondly, there are non-atheromatous coronary pathologies. These include conditions such as spontaneous coronary artery dissection especially prevalent in peripartum females. Other considerations include vasculitides with coronary artery involvement such as Kawasaki disease with coronary artery aneurysms as well as Takayasu disease, coronary vasospasm, and microvascular dysfunction

The third etiology is that of hypercoagulable states leading to recurrent arterial and venous thrombosis. Examples include antiphospholipid syndrome and Factor V Leiden mutations. Acquired hypercoagulable states like nephrotic syndrome, thrombotic thrombocytopenic purpura, solid organ malignancy, and myeloproliferative disorders have possible associations with arterial disease in the form of MI (REF). Embolic phenomenon may also cause coronary obstruction (from thrombi, infective vegetations, cardiac masses, etc).

Finally, recreational drug use must be considered, although it is the least common etiology in Singapore because of strict laws prohibiting it. Cocaine use is associated with MI by inducing coronary vasospasm as well as hypercoagulability, and long term cocaine use also leads to accelerated atherosclerosis as well as nonischemic cardiomyopathy.

Takayasu’s arteritis is classified as a large-vessel vasculitis because it primarily affects the aorta and its primary branches. It has a worldwide distribution; however the greatest prevalence is seen in Asia. Women are affected in 80-90% of cases, with an age of onset that is usually between 10 and 40 years.

The onset of symptoms in Takayasu arteritis (TAK) tends to be subacute and diagnosis is often only made at the point where there is significant vascular disease leading to symptoms due to resultant ischemia in the affected vascular territory.

Physical examination is what led to the clinical suspicion of a large vessel vasculitis in our patient.

Measurement of BP should be done in all four extremities to evaluate for arterial stenoses. Many patients with TAK will have partial or complete occlusion of one or both subclavian, axillary, or brachial arteries, or the brachiocephalic artery, leading to low-pressure readings in the ipsilateral arm. Similarly, femoral or more distal arterial stenoses will lower leg blood pressures and stenosis of the aorta may lead to bilateral low blood pressure readings.

Bruits may be heard over the bilateral carotid, subclavian, axillary, renal, and femoral arteries, as well as the abdominal aorta. Cardiac auscultation may reveal signs of aortic valvular disease, pulmonary hypertension, or heart failure. Pulses should be felt for and evaluated at bilateral temporal, carotid, brachial, femoral, and dorsal pedal arteries, and any arterial tenderness should also be noted. Signs of limb ischemia should be sought.

In most cases, a clinical diagnosis of Takayasu arteritis can be made in a patient with both suggestive clinical findings (eg, constitutional symptoms, hypertension, diminished or absent pulses, and/or arterial bruits) and imaging showing narrowing of the aorta and/or its primary branches.

There are no specific diagnostic laboratory tests for TAK. As a disease with systemic inflammatory process, the erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may be elevated but normal values do not exclude Takayasu arteritis.

Patients with suspected TAK should undergo imaging of the arterial tree by MR or CT angiogram to evaluate the arterial lumen, looking out for smoothly tapered luminal narrowing or occlusion that is sometimes accompanied by thickening of the wall of the vessel. 18 F-FDG – Positron emission tomography (PET), often in combination with CT (PET-CT) or MR (PET-MR) is an increasingly utilized test to evaluate for possible large-vessel vasculitis. The finding of “hot” segments (ie, those with increased standardized uptake values of fludeoxyglucose-F18) in the right clinical setting may be suggestive of large-vessel vasculitis. There is increasing use of PET to aid in the diagnosis of TAK.

Although definitive, getting a histological diagnosis via biopsy of the large arteries is impractical and rarely done. However, occasionally arterial tissue may become available after a revascularization procedure or aneurysm repair

American College of Rheumatology classification criteria were developed to help distinguish one form of vasculitis from another, however they are limited in terms of their use in clinical practice. The criteria are

Patients are said to have TAK if at least three of the six criteria are present. Although these criteria have been widely used by clinical researchers and clinicians to help diagnose patients, accurate diagnostic criteria have yet to be developed.

Management is targeted at tackling the inflammation in the various vascular territories and also endovascular or surgical procedures for critical areas of stenosis that have contributed to irreversible ischemia or aneurysm.

For example, as in this case, significant coronary artery disease leading to myocardial infarctions were addressed with surgical and/or percutaneous revascularization as per usual care for atherosclerotic CAD. Significant peripheral arterial disease can be treated in a similar fashion.

As for systemic anti-inflammatory therapy, the mainstay of treatment would be systemic glucocorticoids guided by the care of a rheumatologist.

In terms of long-term follow-up, monitoring disease activity and response to therapy may be challenging for clinicians, given the absence of specific laboratory tests or validated assessment criteria for disease activity.

CardioNerds co-founder Dr. Dan Ambinder joins CardioNerds join Dr. Pooja Prasad, Dr. Khoa Nguyen and expert Dr. Abigail Khan (Assistant Professor of Medicine, Division of Cardiovascular Medicine, School of Medicine) from Oregon Health & Science University and discuss a case of mechanical valve thrombosis. Audio editing by CardioNerds Academy Intern, student doctor Adriana Mares.

 A 23-year-old pregnant woman with a mechanical aortic valve presented to the maternal cardiac clinic for a follow-up visit. On physical exam, a loud grade three crescendo-decrescendo murmur was audible and transthoracic echocardiography revealed severely elevated gradients across the aortic valve.  Fluoroscopy confirmed an immobile leaflet disk. Thrombolysis was successfully performed using a low dose ultra-slow infusion of thrombolytic therapy, leading to normal valve function eight days later.

Treatment options for mechanical aortic valve thrombosis include slow-infusion, low-dose thrombolytic therapy or emergency surgery. In addition to discussing diagnosis and management of mechanical valve thrombosis, we highlight the importance of preventing valve thrombosis during the hypercoagulable state of pregnancy with careful pre-conception counseling and a detailed anticoagulation plan.

See this case published in European Heart Journal – Case Reports.

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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How can we counsel and inform women with heart disease who are contemplating pregnancy?

Adapted from the 2018 ESC Guidelines for the management of cardiovascular diseases during pregnancy

What is the differential diagnosis for a new murmur in a pregnant person who has undergone heart valve replacement?

What are diagnostic modalities for the evaluation of suspected prosthetic valve thrombosis?

What are the treatment options for prosthetic valve thrombosis in pregnant patients?

What are the anticoagulation and antiplatelet strategies for pregnant patients with mechanical heart valves?

CardioNerds co-founder Dr. Dan Ambinder joins Dr. Abdelrhman Abumoawad, Dr. Leili Behrooz from the Boston University Vascular Medicine over hot chocolate in Boston. They discuss two interesting cases of lower extremity edema caused by May-Thurner syndrome. Dr. Naomi Hamburg (Professor of Vascular Medicine and Cards at BU/BMC) provides the ECPR for this episode. Audio editing by CardioNerds Academy Intern, Dr. Akiva Rosenzveig.

“To study the phenomena of disease without books is to sail an uncharted sea, while to study books without patients is not to go to sea at all.” – Sir William Osler. CardioNerds thank the patients and their loved ones whose stories teach us the Art of Medicine and support our Mission to Democratize Cardiovascular Medicine.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

US Cardiology Review is now the official journal of CardioNerds! Submit your manuscript here.

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Case 1: A 34-year-old woman with HIV on HAART presenting with left leg swelling and non-healing new foot ulcer for 3 months. She works as a cashier. On exam, her BMI is 35 kg/m2 and there are intact pulses bilaterally. Her left leg has varicose veins in the territory of the great saphenous vein, hyperpigmentation, edema, and a foot ulcer. Her right leg appears normal. Venous Duplex ultrasonography showed chronic partially occlusive thrombus in the left common femoral and profunda femoral veins and decreased doppler respiratory variation on the left side. She was treated with debridement and compression therapy for ulcer healing. She was referred to vascular surgery and underwent contrast venography that demonstrated collateral circulation from the left lower extremity (LE) to the right lower extremity, and stenotic lesion at the left common iliac vein (LCIV). She was diagnosed with May-Thurner syndrome, and a venous stent was placed, and the patient was started on aspirin 81 mg daily for 6 months.

Case 2: A 71-year-old man presented with left lower extremity pain and edema. He underwent a left lower extremity venous Duplex ultrasound that showed chronic thrombus in the left proximal to distal femoral vein and acute thrombus in the left popliteal vein and was started on anticoagulation (AC). The patient was also having palpitations and was found to have paroxysmal atrial fibrillation. He underwent pulmonary vein isolation during which it was noted that his LCIV was subtotally occluded. He underwent CT venogram which showed lumbosacral osteophytic compression of the LCIV known as bony May-Thurner syndrome. Given minimal symptoms, the decision was made not to pursue interventional options and to manage conservatively with AC which the patient needs regardless.

Classic May-Thurner syndrome is venous outflow obstruction due to external compression of the left common iliac vein by the right common iliac artery causing venous stasis which can lead to DVT. It is more common in women of reproductive age. Osteophytic/bony variant of May-Thurner Syndrome is when a prominent vertebral osteophyte compresses the iliac vein which is more common in older patients.

For another fascinating case of May-Thurner Syndrome, presenting with CTEPH, enjoy CardioNerds episode 53. Case Report: CTEPH & May Thurner Syndrome – Temple University.

May-Thurner syndrome is often asymptomatic but may present with pain and swelling of the left leg with or without the presence of DVT. Some patients will develop signs of venous insufficiency such as varicose veins, pigmentations, and venous ulcers. Risk factors include scoliosis, female sex, use of oral contraceptives, and pregnancy. As demonstrated in CardioNerds episode #53, chronic thrombo-embolic pulmonary hypertension may be a long-term sequela.

Features suggestive of proximal obstruction in the venous Duplex for the initial assessment of DVT or venous insufficiency raise suspicion for May-Thurner syndrome. These features include loss of respiratory variation of the venous blood flow. IVUS is the gold standard to diagnose May-Thurner Syndrome and can also provide information regarding the chronicity of the thrombus, which could help decide management (for example, whether to perform thrombolysis of acute clot burden). CT/MR venography may have high sensitivity and specificity to detect iliac vein compression nearing 95%. It is also useful in ruling out other causes of iliac vein compression such as osteophyte compression of the iliac vein.

Management mainly focuses on addressing the patient’s symptoms. For patients with moderate to severe symptoms and significant venous stenosis, endovenous stenting is used rather than conservative management.

There are a paucity of data to clarify the optimal antithrombotic regimen following venous stent placement. Practrice patterns varry significantly in terms of antiplatelet/anticoagulant choice and the duration of treatment.

The presenct of complications such as DVT, venous stasis ulcer, etc should be managed as usual.

CardioNerds (Daniel Ambinder and Amit Goyal) join Dr. Arielle Schwartz (Emory University cardiology fellow), Dr. Joshua Zuniga (former Emory vascular medicine fellow and now USC cardiology fellow), and Dr. Patrick Zakka (UCLA cardiology fellow) from the Emory University School of Medicine. They discuss a case of a young woman with new onset hypertension refractory to 3 antihypertensive agents who is ultimately diagnosed renovascular hypertension due to fibromuscular dysplasia complicated by saccular aneurysm. Dr. Bryan Wells (Director of Vascular Medicine at Emory University) provides the ECPR for this episode. Audio editing by CardioNerds Academy intern, Dr. Christian Faaborg-Andersen.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

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Gornik HL, Persu A, Adlam D, Aparicio LS, Azizi M, Boulanger M, Bruno RM, de Leeuw P, Fendrikova-Mahlay N, Froehlich J, Ganesh SK, Gray BH, Jamison C, Januszewicz A, Jeunemaitre X, Kadian-Dodov D, Kim ES, Kovacic JC, Mace P, Morganti A, Sharma A, Southerland AM, Touzé E, van der Niepen P, Wang J, Weinberg I, Wilson S, Olin JW, Plouin PF. First International Consensus on the diagnosis and management of fibromuscular dysplasia. Vasc Med. 2019 Apr;24(2):164-189. doi: 10.1177/1358863X18821816. Epub 2019 Jan 16. Erratum in: Vasc Med. 2019 Oct;24(5):475. Erratum in: Vasc Med. 2021 Aug;26(4):NP1. PMID: 30648921.

Olin, Circulation. 2014;129:1048-1078. Fibromuscular Dysplasia: State of the Science and Critical Unanswered Questions A Scientific Statement From the American Heart Association

S.H.KimMD, MPH†Jeffrey W.OlinDO‡James B.FroehlichMD, MPH§XiaokuiGuMA§J. MichaelBacharachMD‖Bruce H.GrayDO¶Michael R.JaffDO#Barry T.KatzenMD∗∗EvaKline-RogersMS, RN, NP§Pamela D.MaceRN††Alan H.MatsumotoMD‡‡Robert D.McBaneMD§§Christopher J.WhiteMD‖‖Heather L.GornikMD, MHS†. Clinical Manifestations of Fibromuscular Dysplasia Vary by Patient Sex: A Report of the United States Registry for Fibromuscular Dysplasia. JACC. Volume 62, Issue 21, 19–26 November 2013, Pages 2026-2028

CardioNerds (Amit and Dan) join join Dr. Andrew Dicks (Vascular medicine physician at Prisma Health, former fellow at Mass General Vascular) and Dr. Prateek Sharma (Vascular interventional & medicine fellow at MGH) for an ice-cold drinks at the Esplanade in Boston, MA to discuss a case about a patient who developed a pulmonary embolism and masterfully discuss the diagnosis and management of of pulmonary emboli. Dr. Ido Weinberg (Director, Vascular Medicine Fellowship at MGH) provides the ECPR for this episode.

Case Abstract: A 59-year-old Spanish-speaking man with no significant past medical history presents after falling 15-20 feet from a ladder and landing on his back. He was found to have an L1 fracture and left radial fracture and underwent T12-L2 fusion with neurosurgery on hospital day 1 and ORIF of left radial fracture with orthopedic surgery on hospital day 2. On hospital day 5, he develops acute onset tachycardia with HR in the 130s bpm with new O2 requirement associated with mild shortness of breath at rest without any chest discomfort. His labs were notable for an elevated troponin and proBNP. He underwent CTPA which demonstrated acute bilateral occlusive pulmonary emboli (PE) extending in the right and left main pulmonary arteries. TTE demonstrated right ventricle dilation. The patient was started on a heparin infusion and a PE response team (PERT) meeting was held to discuss treatment options. Given recent surgery, use of thrombolytic therapy was felt to be too risky and thus he was taken for percutaneous thrombectomy in the cath lab. PA pressure prior to intervention was 51/21 mmHg. The patient underwent suction thromboembelectomy with the Flow Triever device with extraction of thrombus and improvement in PA pressure to 19/11 mmHg. He was treated with anticoagulation thereafter and discharged home two days after the procedure.

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1. While there are markers to suggest PE, such as ECG findings or evidence of RV dilatation, a PE cannot be confirmed without imaging.
2. Elevation of cardiac biomarkers and evidence of RV dysfunction are used to risk stratify PE, not the degree of thrombus burden or locale of thrombus.
3. Enoxaparin is the preferred anticoagulant to initiate at time of PE diagnosis if comorbidities allow.
4. Optimal treatment of intermediate risk PE remains uncertain as there is little data about long-term outcomes. Aggressive treatment should be used judiciously and chosen on a case-by-case basis.
5. PE response teams (PERT) allow for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy.

1. What is a PERT team and why is it helpful?

• We have several tools and approaches for the management of PE. There are also many subspecialities involved in the care of patients with PE, including vascular medicine, intervention cardiology, hematology, pulmonology, cardiac surgery, radiology, emergency department, intensive care, and more. As such, the best treatment plan for a given patient with PE can be challenging, especially if the services involved in treatment of the PE function in silos.
• PERT, or PE Response Team, was built to address this concern. It is a multidisciplinary team that originated at MGH whose goal is to coordinate care for high-risk PE patients and advance PE-related care in the institution.
• PERT allows for multidisciplinary expert opinion in the face of scarce evidence to determine what is felt to be the best management strategy.

2. How do we risk stratify patients with PE?

• Risk stratification is largely dependent on the hemodynamic significance caused by the PE. In addition to vital sign derangement, patients with PE should also be evaluated for evidence of cardiac strain due to PE by checking for evidence of RV dilatation on CT or TTE and for elevation of cardiac biomarkers. The combination of this information is used to risk stratify patients. Additionally, risk stratification tools, such as the PESI and sPESI scores, are used to guide risk stratification.
• Based on the ESC 2019 guidelines, PEs are stratified into high risk, intermediate-high risk, intermediate-low risk, or low risk.
  • High risk: evidence of hemodynamic instability as defined by hypotension or shock.
  • Intermediate-high risk: evidence of both RV dysfunction on imaging AND elevated cardiac biomarkers in the absence of HD instability
  • Intermediate-low risk: evidence of either RV dysfunction on imaging OR elevated cardiac biomarkers in the absence of HD instability
  • Low risk: no evidence of cardiac dysfunction on imaging or labs and no evidence of HD instability.
• Risk stratification is important as it helps guide medical management of patients. Important factors that have not been associated with PE severity include degree of thrombus burden and location of clot.

3. What do we know about optimal management of patients with intermediate risk PE?

• Unfortunately, data is fairly limited with regards to the optimal management strategy for patients with intermediate risk PE, namely whether anticoagulation alone is sufficient versus if a patient would benefit from more advanced therapies. All patients should be started on anticoagulation, preferably SQ enoxaparin if comorbidities allow, as soon as possible (if there are no contraindications to anticoagulation). However, choosing which patients would benefit from more advanced therapies remains limited.
• Thrombolysis has been associated with lower all-cause mortality in patients with intermediate-risk PE when compared to anticoagulation alone. However, not surprisingly, thrombolysis was also associated with more major bleeding, including intracranial hemorrhage. In the ULTIMA trial, catheter directed thrombolysis was shown to improve RV dysfunction more quickly compared to anticoagulation at 24 hours. However, at 90 days, there was no difference in degree of RV dysfunction between the two groups.
• Percutaneous thrombectomy devices have been shown to be safe and effective at reducing RV size. However, there are no head-to-head comparisons of these modalities versus anticoagulation or thrombolysis and data is limited regarding the long-term efficacy.
• Choosing the correct patient to proceed with advanced therapies remains challenging and the decision is often made on a case-by-case basis. There are ongoing randomized control trials that will hopefully assist in guiding this decision making.

4. What about management for those with high-risk PE?

• High risk PEs mandate aggressive and rapid treatment.
• Thrombolysis has been shown to have a mortality benefit compared to anticoagulation. 
• Catheter directed thrombolysis can be considered in high-risk PE; however, rapid implementation needs to be available.
• VA-ECMO has also been demonstrated to reduce mortality in these patients.

5. What additional treatment options are available for patients with PE who are not improving on anticoagulation and have a contraindication to thrombolytic therapy?

• There are several contraindications to thrombolytic therapy, including recent surgery, CVA, or bleeding. Percutaneous and surgical thrombectomy should be considered in these patients.
• Surgical thrombectomy is effective but does require significant anticoagulation during the surgery while the patient is on cardiac bypass. For this reason, patients that have a contraindication to thrombolysis might not be able to tolerate the high levels of anticoagulation required for the surgery and thus a surgical thrombectomy might not be a feasible option.
• There are several percutaneous thrombectomy devices on the market currently which have been shown to be safe and effective at reducing the RV size in the acute period. Because these devices do not require thrombolytic agents, the risk of bleeding is lower and there is less ICU utilization. However, there have not been head-to-head comparisons between these devices and other treatment modalities.

1. Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J. 2020;41(4):543-603. doi:10.1093/eurheartj/ehz405
2. Robertson L, Jones LE. Fixed dose subcutaneous low molecular weight heparins versus adjusted dose unfractionated heparin for the initial treatment of venous thromboembolism. Cochrane Database Syst Rev. 2017;2:CD001100. doi:10.1002/14651858.CD001100.pub4
3. Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med. 2014;370(15):1402-1411. doi:10.1056/NEJMoa1302097
4. Chatterjee S, Chakraborty A, Weinberg I, et al. Thrombolysis for pulmonary embolism and risk of all-cause mortality, major bleeding, and intracranial hemorrhage: a meta-analysis. JAMA. 2014;311(23):2414-2421. doi:10.1001/jama.2014.5990
5. Kucher N, Boekstegers P, Müller OJ, et al. Randomized, controlled trial of ultrasound-assisted catheter-directed thrombolysis for acute intermediate-risk pulmonary embolism. Circulation. 2014;129(4):479-486. doi:10.1161/CIRCULATIONAHA.113.005544
6. Subramaniam RM, Mandrekar J, Chang C, et al. Pulmonary embolism outcome: a prospective evaluation of CT pulmonary angiographic clot burden score and ECG score. AJR Am J Roentgenol. 2008;190(6):1599-1604. doi:10.2214/AJR.07.2858
7. Jain CC, Chang Y, Kabrhel C, et al. Impact of Pulmonary Arterial Clot Location on Pulmonary Embolism Treatment and Outcomes (90 Days). Am J Cardiol. 2017;119(5):802-807. doi:10.1016/j.amjcard.2016.11.018
8. Tu T, Toma C, Tapson VF, et al. A Prospective, Single-Arm, Multicenter Trial of Catheter-Directed Mechanical Thrombectomy for Intermediate-Risk Acute Pulmonary Embolism: The FLARE Study. JACC Cardiovasc Interv. 2019;12(9):859-869. doi:10.1016/j.jcin.2018.12.022

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!

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Disclosures: None
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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

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.

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.

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.

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CardioNerds (Amit Goyal & Daniel Ambinder) join University of Florida cardiology fellows (Ashley Mohadjer, Hussain Khalid, and Morgan Randall) for an authentic Gainesville-style tailgate! They discuss a fascinating case of severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome. Dr. Khanjan Shah provides the E-CPR and  a message for applicants. Episode notes were developed by Johns Hopkins internal medicine resident Richard Ferraro with mentorship from University of Maryland cardiology fellow Karan Desai.  

Jump to: Patient summary – Case media – Case teaching – References

The CardioNerds Cardiology Case Reports series shines light on the hidden curriculum of medical storytelling. We learn together while discussing fascinating cases in this fun, engaging, and educational format. Each episode ends with an “Expert CardioNerd Perspectives & Review” (E-CPR) for a nuanced teaching from a content expert. We truly believe that hearing about a patient is the singular theme that unifies everyone at every level, from the student to the professor emeritus.

We are teaming up with the ACC FIT Section to use the #CNCR episodes to showcase CV education across the country in the era of virtual recruitment. As part of the recruitment series, each episode features fellows from a given program discussing and teaching about an interesting case as well as sharing what makes their hearts flutter about their fellowship training. The case discussion is followed by both an E-CPR segment and a message from the program director.

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A woman in her 60s with a past medical history of type 2 diabetes, hypertension, and hypothyroidism presented to the University of Florida with a chief complaint of “Someone told me my neck artery was blocked.”  Someone call 227-346-6373.  What does that spell? CardioNerd!   

She noted exertional pain in both legs with limited exertion. Has a family history of CAD and MI in her father in his 20s. Her only medications were baby aspirin, atorvastatin 80mg, and thyroid replacement. Her blood pressures were noted to be dropping and so her regimen was being titrated off as a result. Physical exam was notable only for poorly palpable pulses in all extremities. To further work this up, a myocardial perfusion scan, CTA head/neck/abdomen, and ABIs were ordered. ABI on the right was 0.86 and on the left was 0.76 with monophasic doppler waveforms throughout. CT abdomen exhibited an occlusion of the abdominal aorta from just below the renal arteries extending to the common iliac arteries with distal reconstitution. CT head/neck showed occlusion of the right carotid artery, complete occlusion of the right innominate artery, near complete occlusion of the right vertebral artery, and delayed flow in the right posterior cerebral artery. On the left side, she had high-grade subclavian stenosis. Myocardial perfusion imaging exhibited no defects.  

On subsequent visits her exercise tolerance improved with an exercise regimen, but blood pressures were more and more difficult to obtain. As a result, revascularization was pursued with stenting of the left subclavian artery. She was discharged, but returned a few hours later with severe left sided pulsatile headache and nausea/vomiting. She was admitted for monitoring, but fortunately improved and discharged with close outpatient follow-up.  She continued to improve in the outpatient setting. After MRI brain and extensive work-up, she was deemed to have cerebral hyperperfusion syndrome following revascularization.  She had no further complications and was monitored thereafter.  Final diagnosis: severe peripheral artery disease (PAD) and cerebral hyperperfusion syndrome.

• A
• B
• C
• D
• E
• F

A: ECG
B: ABIs
C: CT Angiogram
D: CT Angiogram – head and neck
E: Pre and post subclavian stentinng
F: CT head and neck – follow up

1. What are the risk factors and prevalence of PAD? 
   • PAD refers to atherosclerotic peripheral artery disease, and is the accumulation of plaque in various peripheral arterial beds akin to CAD involving coronary arteries.  6% of adults over the age of 40 have PAD, and 30% of American adults over the age of 70. This all leads to an annual healthcare expenditure in the US of ~$4 billion! PAD is associated with a 3-4x increased risk of cardiovascular events.  Furthermore, mortality overall is 15-20% at 5 years in patients with PAD.  
   • Risk factors for PAD include all the risk factors for ASCVD we consider for CAD, including diabetes, hypertension, and hyperlipidemia.  

1. What Should We Look for on Physical Exam with PAD?  
   • Get a brachial blood pressure (Class Ib AHA/ACC Recommendation), listen for bruits (areas of turbulent flow), and look at the extremities for: skin color changes, temperatures changes, loss of hair, or ulcerations (typically at the tips of digits). In patients with claudication and/or risk factors for PAD, these can all be signs of PAD.  In particular, palpate the dorsalis pedis and tibialis pulses.  
   • In office maneuvers can also include Buerger’s test where the affected limb is elevated from a supine position till pallor is observed. In a normal limb, even elevating to 90 degrees should not elicit pallor; however, in an ischemic limb, especially severe ischemia, elevation to even 20 degrees for 30 to 60 seconds can lead to pallor. Then when returning the limb to resting position, the pink color will return slowly (I.e., >20 seconds) and may demonstrate rubor as there is reactive hyperemia (dilation of the arterioles) in attempt to remove metabolic waste and restore circulation.  
   • At the bedside, we should also test for diseases commonly associated with PAD, particularly diabetes. Testing for diabetic neuropathy is critical in patients with PAD, as it is a modifiable risk factor and can make patients prone to developing diabetic foot ulcers.  
   • Remember, that there are classic locations for arterial ulcers but often patients have a mixed picture given concomitant venous insufficiency and/or diabetes. These arterial ulcers tend to occur where arteries terminate, including between the digits and tips of the toes. Furthermore, they can occur at areas of increased pressure, including the lateral malleolus. 

1. How do we obtain and interpret ABIs in chronic limb ischemia? 
   • ABI stands for Ankle-Branchial Index. This means taking the ankle blood pressure and indexing it against the brachial blood pressure. 
   • The ABI is an easily done test. To ensure we have an accurate ABI, we typically ask the patient to rest for at least 5-10 minutes prior to measuring ankle pressure. We also want to make sure we have the appropriate cuff size, and thus in the limbs the cuff width should be at least 40% of the limb circumference. 
   • We can start by taking the brachial pressure in one arm. After obtaining our initial brachial SBP, we then proceed with taking a blood pressure from either the dorsalis pedis or posterior tibial artery on the same side, with the cuff just above the ankle. We utilize a continuous wave doppler signal to identify the pulse and insufflate the cuff to just above where the Doppler signal disappears. 
   • We then slowly release the pressure in the cuff and record where the systolic pressure returns and repeat the process for the artery (e.g., DP or PT) that was not tested and then move onto to the contralateral limb. We then finally obtain the SBP in the brachial on the side opposite from where we started. The ABI for a specific extremity is then the highest pressure in a lower extremity limb (DP or PT) divided by the highest systolic brachial pressure in either limb.  
   • As discussed above, we usually calculate the ABI at bedside using a continuous-wave doppler probe, but when blood pressures are low or if there is significant venous congestion leading to pulsatile flow (e.g., congestive heart failure), the venous signal can be difficult to distinguish from the arterial signal.  
   • Briefly, a normal ABI is considered 1.0 to 1.4; 0.91 to 0.99 is considered borderline; and <0.9 and >1.4 are considered abnormal. In patients with symptoms of PAD (e.g., claudication), ABI has a sensitivity of ~ 95% and specificity of 100% of diagnosing lesions with >50% stenosis in one or major lower extremity vessels. An ABI > 1.4 suggests the presence of calcified vessels and we need additional vascular studies, such as measurement of the toe brachial index (TBI) or pulse volume recordings (PVR) to assess for significant PAD. The vessels in the toe have been shown to be less prone to medial calcification. 
   • Finally, segmental brachial index measurements are also considered abnormal if there is a decrease in 20 mmHg or more between adjacent levels in the lower extremity, a decrease in segmental brachial index of 0.15 or more over time, or a difference in systolic pressure more than 30 mmHg between contralateral limbs.  

1. How Do We Treat Symptomatic PAD? 
   • Exercise! First and foremost, supervised treadmill exercise training is a Class Ia recommendation from the AHA/ACC guidelines. Multiple studies have shown exercise to be beneficial in improving time and distance to developing claudication symptoms and increasing pain-free walking distance up to 180%. Notably, an exercise trial is recommended prior to any attempted revascularization.   
   • As with CAD, lifestyle measures to mitigate ASCVD risk factors are vital, including diet, weight loss, and smoking cessation. Statins are a key to medical management (Class Ia recommendation).  In symptomatic PAD or asymptomatic PAD but with positive ABIs, the general recommendation is to start low dose aspirin (versus P2Y12 monotherapy). There is increasing data exploring the role of DOAC + Aspirin, and generally the addition of low dose DOAC improves morbidity in PAD but at the expense of increased bleeding events. 
   • If there is no or minimal improvement with conservative management, including exercise, a trial of  cilostazol, a phosphodiesterase 3 inhibitor, should be considered as it has been shown to increase walking distance and claudication symptoms (Class Ia). However, note that cilostazol is contraindicated in patients with congestive heart failure per the FDA, though in practice we especially avoid the medication in patients with NYHA Class III-IV heart failure.  

1. When Should We Revascularize?  
   • Revascularization is generally recommended if the patient with chronic limb ischemia remains symptomatic despite guideline-directed medical therapy and conservative lifestyle management (Class IIa). There are separate recommendations for patients with acute or chronic limb-threatening ischemia. Endovascular revascularization is further recommended for patients with symptomatic claudication and hemodynamically significant aortoiliac disease (Class Ia) and can be considered with hemodynamically significant femoropopliteal disease (Class IIa). In patients with non-healing wounds or gangrene, surgical revascularization is recommended to re-establish blood flow (Class Ic-LD).  

References

1. Beckman, J. A., Ansel, G. M., Lyden, S. P., & Das, T. S. (2020). Carotid Artery Stenting in Asymptomatic Carotid Artery Stenosis: JACC Review Topic of the Week. Journal of the American College of Cardiology, 75(6), 648-656. 
2. Huibers, A. E., Westerink, J., de Vries, E. E. et. al. (2018). Editor’s choice–cerebral hyperperfusion syndrome after carotid artery stenting: a systematic review and meta-analysis. European Journal of Vascular and Endovascular Surgery, 56(3), 322-333. 
3. Gerhard-Herman, M. D., Gornik, H. L., Barrett, C. et. al. (2017). 2016 AHA/ACC guideline on the management of patients with lower extremity peripheral artery disease: executive summary. Vascular Medicine, 22(3), NP1-NP43. 
4. Aboyans, V., Ricco, J. B., Bartelink, M. L. E., Björck, M. et. al. (2018). 2017 ESC Guidelines on the Diagnosis and Treatment of Peripheral Arterial Diseases, in collaboration with the European Society for Vascular Surgery (ESVS) Document covering atherosclerotic disease of extracranial carotid and vertebral, mesenteric, renal, upper and lower extremity arteries Endorsed by: the European Stroke Organization (ESO) The Task Force for the Diagnosis and Treatment of Peripheral Arterial Diseases of the European Society of Cardiology (ESC) and of the European Society for Vascular …. European heart journal, 39(9), 763-816. 

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