01Approach to the Critical Patient/attcp49

Immediate priorities

›ACS presentation from thrombosed CAA

›STEMI pattern — activate cath lab immediately

›Thrombosed CAA carries high no-reflow and distal embolization risk

›GP IIb/IIIa inhibitor preparation

›NSTEMI/unstable angina pattern

›Antiplatelet loading and urgent cardiology consult

›Risk stratify for early invasive strategy

›Hemodynamic instability

›SBP < 90 mmHg

›MAP < 65 mmHg

›Tamponade from aneurysm rupture

›Muffled heart sounds, JVD, hypotension (Beck triad)

›Immediate echo confirmation

›Pericardiocentesis preparation

›Pulsus paradoxus > 10 mmHg

›High specificity for tamponade physiology

›Escalate to resuscitation bay

›If tamponade confirmed, emergent cardiothoracic surgery consult

Monitoring and stabilization targets

›Hemodynamic monitoring bundle

›Continuous cardiac monitoring

›Ischemia detection (ST changes, T-wave inversions)

›Arrhythmia detection (VT/VF risk with ischemic substrate)

›Continuous pulse oximetry

›SpO2 target > 94%

›Supplemental oxygen for any hypoxemia

›Arterial line consideration

02History/hx69

Presenting symptoms

›Chest pain characterization

›Exertional angina pattern

›Exertional onset, relief with rest

›Slow flow or distal embolization mechanism

›ACS-type symptoms

›Pressure, radiation to arm or jaw, diaphoresis

›Rest pain or new onset severe exertional pain

›Palpitations

›Possible presenting complaint from arrhythmia

›VT/VF from ischemic substrate

›Dyspnea and functional decline

›Exertional limitation

›Silent MI from prior thromboembolism

›Ventricular dysfunction from ischemic cardiomyopathy

›Orthopnea or paroxysmal nocturnal dyspnea

›Heart failure from coronary ischemia

›Assess NYHA functional class

›Syncope or presyncope

›Arrhythmic etiology

›VT from ischemic substrate

›High-risk feature requiring urgent evaluation

›Hemodynamic etiology

›Tamponade prodrome

›Rapidly declining cardiac output

Causal history

›Kawasaki disease history

›Childhood febrile illness with rash, conjunctivitis, lymphadenopathy

03Physical Exam/exam56

Vital signs and hemodynamic assessment

›Hemodynamic stability snapshot

›Blood pressure

›Hypotension: SBP < 90 mmHg (rupture, ACS, tamponade)

›Hypertension: documented risk factor

›Heart rate

›Tachycardia in ACS, tamponade, or HF

›Bradycardia in high-degree AV block from inferior ischemia

›Pulsus paradoxus

›> 10 mmHg suggests tamponade

›Measured with sphygmomanometer over respiratory cycle

›General appearance and stigmata

›Marfanoid habitus

›Tall stature, arachnodactyly, pectus deformity

›High-arched palate

›Diaphoresis and distress

›Sympathetic activation from ACS

›Impending hemodynamic collapse

Cardiac and peripheral exam

›Cardiac auscultation

›Muffled heart sounds

›Pericardial effusion and tamponade

›Correlate with JVD and hypotension

›New murmur

›Coronary artery fistula (continuous machinery murmur)

›Mitral regurgitation from papillary muscle ischemia

›S3 or S4 gallop

›Left ventricular dysfunction from ischemic cardiomyopathy

04Differential Diagnosis/ddx49

Life-threatening diagnoses

›ACS from CAA-related thrombosis

›In-situ thrombosis within aneurysm

›Slow flow and flow stasis mechanism

›ICD-10 I25.41 (CAA of native coronary artery)

›Distal embolization from aneurysm thrombus

›Peripheral coronary occlusion

›May present without obvious culprit lesion on angiography

›Cardiac tamponade from CAA rupture

›True aneurysm (all 3 wall layers) rupture — rare but catastrophic

›More common with giant aneurysms > 20 mm

›ICD-10 I25.41

›Pseudoaneurysm rupture (contained only by adventitia or pericardium)

›Higher rupture risk than true aneurysm

›IVUS helps distinguish pseudoaneurysm from true aneurysm

›Sudden cardiac death

›Giant aneurysms (> 20 mm or > 4x reference diameter)

›VT/VF from ischemic substrate

›ICD consideration in survivors

Close mimics

›Coronary artery ectasia

›Diffuse dilation without focal outpouching

›Distinguished from focal aneurysm by extent of involvement

›Often atherosclerotic in etiology

›ICD-10 I25.41 overlap

›Management principles similar to CAA

›Antithrombotic approach guided by severity

›Coronary pseudoaneurysm

05Laboratory Tests/lt55

Ischemia and cardiac biomarkers

›Troponin (high-sensitivity preferred)

›Serial measurement at 0 and 1–3 hours

›Rule out MI from thrombosis or embolization

›Elevated in any significant myocardial ischemia

›Troponin rise and fall pattern

›Type 1 MI pattern with ACS presentation

›Elevated in tamponade if concurrent ischemia

›BNP or NT-proBNP

›Heart failure from ischemic cardiomyopathy

›NT-proBNP > 125 pg/mL (mmol/l not applicable for this marker)

›Prognosis and severity marker

›Baseline and serial trend if HF suspected

›Guides admission and therapy decisions

›Elevated in right heart strain from tamponade

Inflammatory and etiology-directed labs

›Complete blood count

›Thrombocytosis

›Kawasaki disease association

›Platelet count > 450 × 10^9/L in Kawasaki

›Leukocytosis

›Infectious or vasculitic etiology

›Active Kawasaki disease

›Inflammatory markers

›CRP and ESR

›Elevated in vasculitis, Kawasaki, infectious etiologies

›Kawasaki: CRP > 30 mg/L supports diagnosis

›Autoimmune panel if vasculitis suspected

06Diagnostic Tests/dt90

Scoring Systems

›CAA classification by morphology

›Saccular (focal outpouching)

›Focal dilation involving one vessel wall

›Higher thrombotic risk per unit volume

›Fusiform (diffuse dilation)

›Circumferential dilation of vessel segment

›More common in atherosclerotic CAA

›Giant CAA (> 20 mm or > 4x reference diameter)

›Highest thrombotic and rupture risk

›Indication for anticoagulation plus antiplatelet

›Size-based risk stratification

›Small (< 4 mm or Z-score < 5)

›Lower thrombotic risk

›Aspirin monotherapy generally adequate

›Medium (4–8 mm or Z-score 5–10)

›Dual antiplatelet therapy recommended

›Aspirin plus clopidogrel

›Large/giant (> 8 mm or Z-score > 10)

›Dual antiplatelet plus anticoagulation

›Warfarin (INR 2.0–3.0) or LMWH

›CAAR registry risk data

›1,729 patients, median follow-up 44.8 months

›22% mortality rate at follow-up

›MACE driven primarily by underlying atherosclerotic burden

›Local aneurysm complications (rupture, thrombosis)

›Infrequent at approximately 2% of cases

›Concomitant obstructive CAD drives long-term prognosis

MRI

›Cardiac MRI and MR angiography

›Indications

›Serial follow-up without radiation exposure

›Pediatric and young adult patients requiring lifelong surveillance

›Capabilities

›Aneurysm morphology and dimensions

›Myocardial viability assessment after silent MI

›Limitations

›Spatial resolution lower than CT for small coronary structures

›Respiratory and cardiac gating required

›Motion artifact in patients with arrhythmia

›MRA for noncoronary aneurysm screening

›Aorta and peripheral arterial assessment

›10% of CAA patients have concurrent noncoronary aneurysms

›One-time screening warranted at diagnosis

›ACR Appropriateness Criteria support

›Class I for known or suspected coronary aneurysm evaluation

›Preferred when contrast nephropathy concern exists

CT

›CT coronary angiography (CCTA)

›First-line noninvasive modality for CAA evaluation

›Excellent delineation of aneurysm morphology and dimensions

›Mural thrombus detection

›Spatial relationships and planning

›Relationship to adjacent structures including aortic root

›Surgical planning for left main or giant CAA

›Kawasaki follow-up protocol

›Preferred for serial surveillance in Kawasaki patients

›Avoids invasive angiography for stable patients

›Limitations

›Radiation exposure limiting serial use in young patients

›Contrast nephropathy risk (mitigate with hydration, minimize contrast volume)

›Motion artifact with heart rate > 65 bpm (beta-blocker pretreatment)

›CT of aorta and peripheral arteries

›Co-screening for noncoronary aneurysms

›Aortic aneurysm association (aOR 5.82)

›Peripheral aneurysm prevalence approximately 10%

›CT angiography protocol

›ECG-gated acquisition for coronary evaluation

›Timing bolus or bolus tracking

Ultrasound

›Transthoracic echocardiography (TTE)

›Initial screening modality

›Particularly useful in children and young adults

›Proximal coronary artery visualization

›Ventricular function assessment

›LV systolic and diastolic function

›Wall motion abnormalities from ischemia

›Pericardial effusion detection

›Rule out tamponade in hemodynamically unstable patients

›Semi-quantitative effusion sizing

›Point-of-care ultrasound (POCUS)

›Emergency tamponade exclusion

›Subxiphoid or parasternal view

›Diastolic right heart collapse as tamponade sign

›Perioperative guidance

›Pericardiocentesis guidance

›Access and procedural safety

›Intravascular ultrasound (IVUS)

›Gold standard for vessel wall characterization

›Distinguishes true aneurysm vs. pseudoaneurysm

›Plaque burden and stent sizing

›Used during PCI procedures

›Superior delineation of vessel wall layers

›OCT limited by small scan diameter in large aneurysms

07Disposition/dispo58

Admission criteria

›ICU-level care indications

›STEMI with hemodynamic instability

›Post-PCI care with shock risk

›Mechanical circulatory support consideration

›Tamponade or suspected rupture

›Post-pericardiocentesis monitoring

›Surgical standby

›Giant aneurysm with evidence of new thrombosis

›Anticoagulation initiation and monitoring

›High-risk observation period

›Cardiology ward admission indications

›NSTEMI/unstable angina from CAA thrombosis

›Antiplatelet optimization

›Early invasive strategy planning

›New heart failure from ischemic cardiomyopathy

›Diuresis and HF optimization

›Coronary anatomy clarification

›Rapidly expanding aneurysm on serial imaging

›Surgical consultation prior to discharge

›Antithrombotic therapy optimization

Observation indications

›Extended ED observation or short-stay unit

›Symptomatic patients with stable hemodynamics pending workup

›Troponin rule-out protocol completion

›Imaging results pending

›Post-PCI monitoring for complex aneurysmal intervention

›Higher complication rates than standard PCI

08Treatment/t102

Antiplatelet therapy

›Aspirin (all patients without contraindication)

›Loading dose: aspirin 162–325 mg chewed

›Rapid buccal absorption for ACS

›Class I recommendation for ACS

›Maintenance dose: aspirin 75–100 mg once daily

›Long-term thromboprophylaxis in all CAA

›Continued indefinitely in most patients

›P2Y12 inhibitors for moderate aneurysms

›Clopidogrel 75 mg once daily (maintenance)

›Loading dose: 600 mg for ACS

›Dual antiplatelet for medium-sized aneurysms

›Ticagrelor 90 mg twice daily (ACS context)

›Loading dose: 180 mg

›Superior to clopidogrel in ACS (PLATO trial)

›Avoid in patients requiring chronic anticoagulation where possible

›GP IIb/IIIa inhibitors for PCI with high thrombus burden

›Abciximab or eptifibatide during PCI

›High thrombus burden in CAA-related ACS

›Reduces distal embolization risk

›Short-term use during and immediately post-PCI

›Transition to oral antiplatelet after procedure

›Monitor for bleeding complications

Anticoagulation therapy

›Warfarin for large/giant CAA

›INR target 2.0–3.0

›Indicated for Z-score >= 10 or aneurysm >= 8 mm diameter

›Combination with aspirin in most cases

›Bridging with LMWH during initiation

›Therapeutic anti-Xa 0.5–1.0 IU/mL (twice-daily dosing)

›Until INR therapeutic for 48 hours

›Contraindication: absolute bleeding risk

›Intracranial hemorrhage history

›Active gastrointestinal hemorrhage

›LMWH as alternative or bridging agent

›Enoxaparin 1 mg/kg subcutaneous twice daily

›Dose-adjusted for renal impairment (eGFR < 30: 1 mg/kg once daily)

›Anti-Xa monitoring recommended in renal impairment

›Emerging role of DOACs

›Particularly in pediatric Kawasaki patients

›Not yet standard of care; evidence accumulating

›Caution with thrombolytics

›Extreme caution given rupture risk of aneurysm

›Avoid in large/giant aneurysms

›Consider only if no PCI available for STEMI with small aneurysm

Percutaneous intervention strategies

›ACS with CAA culprit — restoring flow

›Aspiration thrombectomy

›First step in thrombosed aneurysm presenting as ACS

›High thrombus burden common

›Mechanical thrombectomy device

›If aspiration inadequate

›Reserve for refractory cases

›Saccular aneurysm not involving side branch

›Covered stent exclusion (polytetrafluoroethylene-covered stent)

›Excludes aneurysm from flow

›Avoids thrombus persistence in aneurysm sac

›Arteries > 5.5–6 mm may require peripheral stent size

›7F guiding catheter recommended

›Complex procedure with higher complication rate

›Aneurysm involving side branch

›Balloon-assisted or stent-assisted coil embolization

›Preserves side branch flow

›Technique requires significant operator experience

›Adjunct GP IIb/IIIa inhibitor use

›Reduces no-reflow and distal embolization

›Class IIa recommendation in high thrombus burden

Surgical intervention

›First-line surgical indications

›Left main CAA involvement

›CABG with exclusion or ligation of aneurysm

›Highest-priority for surgical referral

›Multiple or giant CAAs

›Surgical patients more likely: giant aneurysm, triple-vessel disease, diabetes

›Percutaneous approach technically unfeasible

›Saphenous vein graft aneurysms

›Post-CABG complication

›Surgical exploration with graft replacement

›Surgical technique principles

›CABG with aneurysm exclusion and ligation

›Distal bypass to preserve myocardium

›Aneurysm sac exclusion prevents future thromboembolism

›Pericardial patch reconstruction in selected cases

›Proximal coronary aneurysms near ostium

›Specialized surgical centers only

Medical risk factor optimization

›Statin therapy

›High-intensity statin for atherosclerotic CAA

›Rosuvastatin 20–40 mg daily or atorvastatin 40–80 mg daily

›LDL-C target < 1.8 mmol/L for established CAD

›Emerging benefit in Kawasaki-related CAA

›Anti-inflammatory and pleiotropic effects

›Consider in giant Kawasaki CAA regardless of LDL

›Antihypertensive therapy

›ACE inhibitor or ARB for established CAD and hypertension

›Ramipril 2.5–10 mg once daily (Class I, established CVD)

›Reduce mechanical wall stress

›Beta-blocker consideration

›Particularly in prior giant aneurysm patients

›Heart rate control reduces dynamic wall stress

›Avoid NSAIDs in patients on aspirin

›Ibuprofen interferes with antiplatelet effect of aspirin

›Competitive inhibition of COX-1

›Substitute acetaminophen for analgesia

›Avoid cocaine and stimulants

›Documented cause of CAA via episodic hypertension

›Endothelial damage and dynamic wall stress

09Special Populations/sp79

Pregnancy

›Cardiovascular physiology in pregnancy

›Increased cardiac output and plasma volume

›30–50% increase in cardiac output by third trimester

›Increased shear stress on aneurysm wall

›Hormonal effects on vascular wall

›Relaxin and progesterone reduce arterial wall integrity

›Elevated rupture risk, particularly in giant aneurysms

›Antithrombotic safety in pregnancy

›Aspirin low-dose (75–100 mg daily)

›Safe in pregnancy throughout gestation

›Avoid high-dose near delivery (platelet inhibition risk)

›LMWH preferred over warfarin

›Warfarin crosses placenta — embryopathy risk weeks 6–12

›LMWH does not cross placenta

›DOACs contraindicated in pregnancy

›Teratogenic and embryotoxic risk

›Switch to LMWH before conception if planned

›Management approach

›Multidisciplinary team: cardiology, maternal-fetal medicine, cardiac surgery

›High-risk obstetric center preferred for delivery

›Delivery planning for giant or symptomatic CAA

›Avoid oral contraceptives containing estrogen

›Increased thrombosis risk with aneurysmal disease

›Progestin-only or non-hormonal contraception preferred

›Imaging: echocardiography and MRI preferred

›Avoid radiation (CT) where possible

›MRI safe after first trimester

Geriatric

›Prevalence and presentation

›Mean age at CAA diagnosis: 65 years in CAAR registry

›Male predominance: 78.5% in registry

›Atherosclerotic etiology predominates in older patients

›Higher prevalence of frailty and comorbidities

›CKD and peripheral artery disease predict worse MACE

›Polypharmacy and drug interaction risk

›Antithrombotic considerations

›Bleeding risk assessment

›HAS-BLED or PRECISE-DAPT scoring for bleeding risk

›Frailty and fall risk elevate bleeding risk

›Anticoagulation in renal impairment

›LMWH dose reduction for eGFR < 30

›Anti-Xa monitoring essential

›Direct thrombin inhibitors (argatroban) for HIT

›Deprescribing and medication reconciliation

›NSAID avoidance in elderly on aspirin

›PPI co-prescription for GI protection on dual antiplatelet

›Revascularization decisions

›Surgical risk assessment

›STS score for mortality prediction

›Heart team decision for surgical vs. percutaneous approach

›Conservative management preference in frail elderly

›Goals of care discussion

›Palliative approach for inoperable giant CAA

Pediatrics

›Kawasaki disease — dominant etiology in children

›Diagnosis criteria

›Fever >= 5 days plus 4 of 5 principal features

›Rash, conjunctivitis, oral changes, extremity changes, cervical lymphadenopathy

›Aneurysm grading in Kawasaki (Z-score based)

›Z-score < 2.5: normal

›Z-score 2.5–5: small aneurysm

›Z-score 5–10: medium aneurysm

›Z-score >= 10: giant aneurysm

›Acute Kawasaki treatment

›IVIG 2 g/kg infused over 10–12 hours

›Within 10 days of fever onset for maximum efficacy

›Reduces aneurysm formation rate from ~25% to ~3–5%

›Aspirin 30–50 mg/kg/day in 4 divided doses (acute phase)

›Reduce to 3–5 mg/kg/day once afebrile for 48 hours

›AHA 2024 Scientific Statement updated guidance

›Long-term CAA management in children

›Antithrombotic by Z-score

›Z-score < 5: aspirin alone

›Z-score 5–10: aspirin plus clopidogrel

›Z-score >= 10: aspirin plus warfarin (or LMWH)

›DOACs as emerging pediatric alternative

›Rivaroxaban studied in Kawasaki giant aneurysm

›Weight-based dosing per pediatric guidelines

›Lifelong follow-up with quantitative coronary dimensions

›Annual echocardiography and periodic CTA

›Activity restriction based on aneurysm grade

10Background/b97

Epidemiology

›Prevalence and demographics

›Found in up to 5% of patients undergoing coronary angiography

›Most are clinically silent and discovered incidentally

›Prevalence higher in specific risk populations

›CAAR registry demographics

›Male sex: 78.5% of cases

›Mean age: 65 years

›Risk factor associations (Taiwan population-based study)

›Coronary atherosclerosis: aOR 7.97

›Aortic dissection: aOR 6.76

›Aortic aneurysm: aOR 5.82

›SLE: aOR 4.09

›Dyslipidemia: aOR 2.48

›Hypertension: aOR 2.09

›Diabetes mellitus: aOR 1.51

›Outcomes data

›CAAR registry (1,729 patients, median follow-up 44.8 months)

›22% all-cause mortality at follow-up

›Local aneurysm complications (rupture, thrombosis): approximately 2%

›Concurrent noncoronary aneurysms

›Present in approximately 10% of CAA patients

›Systemic arterial wall vulnerability

›Kawasaki incidence (US)

›Approximately 9–20 cases per 100,000 children < 5 years

›Leading cause of acquired heart disease in children in developed countries

Pathophysiology

›Mechanisms of coronary artery dilation

›Atherosclerotic mechanism (most common in adults)

›Plaque rupture, intramural inflammation, and medial destruction

›Inflammatory metalloproteinase-mediated extracellular matrix degradation

›Inflammatory mechanism (Kawasaki disease)

›Necrotizing arteritis with medial destruction

›Acute phase: neutrophilic infiltration of all vessel wall layers

›Subacute phase: fibrosis and aneurysm formation

›Connective tissue disorder mechanism

›Deficient elastin or collagen type III (Ehlers-Danlos, Marfan)

›Inadequate support for normal arterial wall tension

›Iatrogenic mechanism

›Balloon and stent overexpansion causing medial injury

›Post-brachytherapy radiation-induced vascular damage

›Thrombotic and embolic complications

›Flow stasis in aneurysm sac

›Turbulent low-velocity flow promotes platelet aggregation

›Virchow's triad: stasis + endothelial injury + hypercoagulability

›In-situ thrombosis

›Mural thrombus formation with sudden occlusion

›Presenting as ACS or sudden cardiac death

›Distal embolization

›Fragmentation of mural thrombus

›Peripheral coronary occlusion producing ischemia

›Classification systems

›Morphological classification

›Saccular: focal outpouching involving < 180 degrees of vessel circumference

›Fusiform: circumferential dilation involving full vessel diameter

›Giant: > 20 mm absolute diameter or > 4x reference vessel diameter

›Pathological classification

›True aneurysm: all 3 vessel wall layers (intima, media, adventitia) involved

›Pseudoaneurysm: contained rupture; only adventitia or surrounding pericardium intact

›Etiological classification

›Atherosclerotic (adult, most common)

›Inflammatory (Kawasaki, vasculitis)

›Noninflammatory (congenital, connective tissue disorder)

›Infectious/mycotic (bacterial, syphilitic, mycobacterial, fungal)

›Iatrogenic (post-PCI)

Therapeutic Considerations

›Antithrombotic strategy framework

›Small aneurysm (< 4 mm): aspirin monotherapy

›Low thrombotic risk; flow reasonably preserved

›Indefinite therapy in absence of contraindication

›Medium aneurysm (4–8 mm): dual antiplatelet

›Aspirin plus clopidogrel

›Reassess after 12 months for monotherapy de-escalation

›Large/giant aneurysm (> 8 mm): triple therapy consideration

›Antiplatelet plus anticoagulation

›Balance thrombotic vs. bleeding risk individually

›Percutaneous vs. surgical decision

›Percutaneous preferred for saccular single aneurysm without left main involvement

›Covered stent for aneurysm not involving side branch

›Coil embolization with adjunct stent if side branch involved

›Surgical preferred for left main, multiple, or giant CAAs

›CABG with aneurysm exclusion

›Higher durability, lower recurrence

›Surveillance imaging principles

›Kawasaki-related CAA requires lifelong quantitative assessment

›Annual echocardiography minimum

›Periodic CTA for precise luminal dimension monitoring

›Atherosclerotic CAA: no established surveillance protocol

›Clinical practice varies by institution

›Serial imaging intervals guided by aneurysm size and symptoms

›Post-intervention surveillance

›Close follow-up for stent thrombosis, restenosis, aneurysm recurrence

›CTA or angiography within 6 months of covered stent placement

›Drug interactions and contraindications

›NSAIDs (especially ibuprofen) contraindicated with aspirin

›Competitive COX-1 inhibition blocks aspirin's antiplatelet effect

›Substitute acetaminophen for analgesia

›Thrombolytics: extreme caution in CAA

›Risk of aneurysm rupture with lytic therapy

›Prefer primary PCI over thrombolysis for STEMI with known CAA

11Patient Discharge Instructions/pdi48

copy discharge instructions

›Diagnosis and medication understanding

›You have been diagnosed with a coronary artery aneurysm (CAA)

›This is a widening or ballooning of one of the arteries supplying your heart

›It can increase your risk of blood clots forming inside the artery

›Take all prescribed blood-thinning medications exactly as directed

›Do not stop aspirin, clopidogrel, or warfarin without calling your cardiologist

›Missing doses can cause a dangerous blood clot to form in the artery

›If taking warfarin, attend all INR blood test appointments

›Your target INR is between 2.0 and 3.0

›Report any unusual bruising, black stools, or blood in urine immediately

›Activity and lifestyle

›Heart-healthy diet

›Mediterranean-style diet low in saturated fat

›Consistent vitamin K intake if on warfarin (avoid large changes in leafy greens)

›Strict avoidance of cocaine and all stimulants

›These drugs directly damage coronary arteries and can cause aneurysm rupture

›Inform your physician of any substance use without fear of judgment

›Activity guidance

›Discuss return to exercise with your cardiologist before resuming vigorous activity

›Avoid contact sports or high-injury activities if on dual antiplatelet or anticoagulation

›Adequate hydration

›Reduces risk of blood clot formation, especially with large aneurysms

›Drink at least 6–8 glasses of water daily

›Follow-up and monitoring

›Cardiology appointment within 1–2 weeks

›Bring a list of all current medications to each visit

›Imaging surveillance plan will be discussed

12References/r58

Guidelines and key sources

›Kawasara A et al. — Management of Coronary Artery Aneurysms

›JACC Cardiovascular Interventions 2018

›Comprehensive management framework for CAA

›PCI techniques including covered stent and coil embolization

›PMID 29976357

›Primary reference for CAA classification and treatment algorithms

›Guides percutaneous intervention planning

›Nunez-Gil IJ et al. — International CAAR Registry

›International Journal of Cardiology 2020

›1,729-patient registry with 44.8-month follow-up

›22% mortality; local complications approximately 2%

›PMID 31378382

›Largest prospective registry for CAA natural history

›MACE driven by atherosclerotic burden, not aneurysm per se

›McCrindle BW et al. — AHA Kawasaki Disease Scientific Statement

›Circulation 2017

›Diagnosis, treatment, and long-term management of Kawasaki disease

›IVIG 2 g/kg and aspirin dosing recommendations

›AHA Scientific Statement — foundational pediatric CAA reference

›Z-score-based aneurysm grading and antithrombotic stratification

›Lifelong surveillance guidelines

›Jone PN et al. — AHA 2024 Kawasaki Disease Update

›Circulation 2024

›Updated guidance on diagnosis and management

›DOACs emerging as alternatives in pediatric giant aneurysm

›AHA 2024 Scientific Statement

›Most current evidence base for Kawasaki-related CAA

Evidence & Review