Cardiovascular Education

How to overcome Radial loop during coronary angiography

Start with soft J tip wire, advanced blindly. When soft J wire does not advance:

🌸🌸1- Give NTG. Try Wholey soft tip angled wire, under fluoro without angiogram (may just be a small radial, or minor tortuosity, that J cannot cross)– DO NOT USE Glidewire

🌸🌸2- Substraction angiography with sheath or catheter, then smart mask (overlay imaging)
Watch for loop, accessory small radial branches, but also for perforation

🌸🌸3- May try Wholey guided by angio, then 0.018” wire or 0.014 wire (eg, BMW, Whisper) advanced through the loop or sharp angle

🌸🌸4- Advance the softest 4Fr catheter (Glidecath) across the loop

🌸🌸5- Exchange 0.014-0.018 for 0.035” wire, low or medium weight (regular J, or Rosen)

🌸🌸6- Then advance 6 Fr catheters over 0.035”
To be able to advance coronary catheter, loop has to straighten at one point (with 0.014, Glidecath, or 0.035”)

❎If the loop does not straighten at some point with the 0.014” or the Glidecath or the 0.035” wire

❎or if the patient complains of significant pain during the eventual catheter advancement

👉→ the access often needs to be aborted.

🫀 Radial Loop
1️⃣ Stop — don’t push
2️⃣ Contrast shot → confirm loop in
3️⃣ Soft wire — 0.014″ or 0.018″, gently cross
4️⃣ Glide catheter () over wire, keep wet
5️⃣ BAT if needed (small balloon-assisted tracking)
6️⃣ Give vasodilators (NTG/verapamil)
7️⃣ Proceed or switch access if resistance/pain persists

✅✅ Congenital coronary fistulas are often small and benign.

However, a fistula is considered large if it has any of 3 major untoward consequences:

1)) on RHC → (1) significant left-to-right shunting with O2 step-up, pulmonary hypertension, and both right-sided enlargement (fistula to RA) and right- and left-sided enlargement (fistula to RV)

(2) coronary steal, i.e., reduction in blood flow distal to the site of fistulization with myocardial ischemia.

On Angiogram → (3) The proximal segment of the coronary artery attempts to compensate for the steal and undergoes progressive aneurismal dilatation; atherosclerosis, thrombosis, and endarteritis may develop.

🍒🍒Anatomical descriptors:
🦚Some fistulas are
🌸- simple and consist of a single origin and a single track
🌸- complex (multiple origins, distal coronary continuation in a cavity with no separate fistula origin [coronary artery itself fistulizes], or plexiform network).

👉👉A large fistula (any fistula with hemodynamic effect; or fistula track=2× the caliber of the distal vessel in case of single track) should be closed.

🌸Surgical closure consists of ligating its origin or track, or, in case of multiple tracks, patching the distal termination from inside the cavity.

🌸Percutaneous closure is possible when a single large communication is identified (oversized coil embolization).

🫀 Coronary Artery Fistula
Abnormal communication between a coronary artery and:

Cardiac chamber (coronary–cameral)

Great vessel (PA, SVC, etc.)

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⚖️ 2. Hemodynamic Significance

A fistula is clinically significant if ANY of the following:

Volume overload

Chamber dilation (RA/RV ± LV)

Pulmonary hypertension

Qp:Qs ≥ 1.5

Myocardial ischemia (coronary steal)

Arrhythmia, HF, or symptoms

👉 SCAI emphasizes:
“Hemodynamic effect > anatomical size alone”

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🧬 3. Anatomy (Impacts Strategy)

🔹 Simple

Single origin

Single drainage
✔️ Ideal for percutaneous closure

🔹 Complex

Multiple tracts / plexiform

Diffuse termination
❗ Often surgical

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🚨 4. Indications for Closure (SCAI-Aligned)

✅ Class I (Strong)

Close if:

Symptomatic (angina, dyspnea, HF)

Evidence of:

LV/RV volume overload

Ischemia

Pulmonary hypertension

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⚠️ Class IIa (Reasonable)

Large fistula even if asymptomatic

Progressive dilation of feeding artery

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❌ Observation

Small, asymptomatic, no chamber enlargement

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🔧 5. Mode of Closure

🧪 Percutaneous (Preferred when feasible)

Indications:

Single, proximal, well-defined tract

No major side branches

Devices:

Coils (most common)

Vascular plugs

Covered stents (selected cases)

✔️ Goal:

Occlude distal fistula while preserving native coronary flow

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🏥 Surgical

Indications:

Complex anatomy

Multiple fistulas

Giant aneurysm

Associated cardiac surgery

Techniques:

Ligation ± intracardiac patch closure

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⚠️ 6. Complications

Thrombosis of dilated proximal artery

Residual shunt / recanalization

MI (if native flow compromised)

Arrhythmias

Endocarditis

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🧠 7. Practical Cath Lab Pearls

Always define:

Origin → Course → Termination

Assess:

Distal coronary bed (important!)

Avoid:

Proximal coil deployment → risk of native vessel occlusion

Use:

Oversized coils to prevent embolization

Post-closure:

Consider antiplatelet ± anticoagulation (if aneurysmal segment)

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🔍 8. Imaging Approach

Echo → chamber dilation, flow

CT angiography → anatomy

Coronary angiography → gold standard for planning

RHC → quantify shunt (Qp:Qs)

In SCAD do CT angiography at 6 weeks to prove the pt has no residual obstruction 80 to 97% gets recovered

In Spontaneous coronary artery dissection do peripheral angio aortoiliac plus do ct carotid abdominal and vertebral to rule out fibromuscular dysplasia which is almost present in 70% cases...!!

Indications for revascularisation in Spontaneous coronary artery dissection include:

🌼complete vessel occlusion with Thrombolysis In Myocardial Infarction (TIMI) 0 flow which is unlikely to resolve with medical treatment alone,

🌸left main stem involvement,

🍀ongoing ischaemia,

🍁 recurrent chest pain,

🍒haemodynamic instability and

🦚 sustained ventricular arrhythmias.

💠💠💠SPONTANEOUS CORONARY ARTERY DISSECTION

⏯⏯( Conservative management is preferred in stable patients with Spontaenus Coronary Artery Dissection as most dissected segments will heal spontaneously .

⏯⏯Medical therapy is based upon opinion, with no randomised clinical trials in this area.

⏯⏯ Initial treatment is similar to standard ACS patients with the use of dual antiplatelet agents, heparin and beta-blockers to preserve patency of the true lumen and prevent thrombotic occlusion. Glycoprotein IIb/IIIa inhibitors have also been used without complications. However, these agents could potentially delay healing of the intramural haematoma and lead to dissection extension. Thrombolytic agents should not be used due to an increased risk of bleeding and extension of intramural haematoma.

⏯⏯Dual antiplatelet therapy with aspirin and clopidogrel is generally accepted, with no data on the role of more potent antiplatelet agents such as ticagrelor and prasugrel. Although statins are important for ACS treatment in patients with atheroma, the benefit in SCAD is unknown.

⏯⏯Beta-blockers are recommended in all patients, with the potential to reduce arterial shear stress, facilitate healing and reduce long-term recurrence.

⏯⏯Indications for revascularisation include: complete vessel occlusion with Thrombolysis In Myocardial Infarction (TIMI) 0 flow which is unlikely to resolve with medical treatment alone, left main stem involvement, ongoing ischaemia, recurrent chest pain, haemodynamic instability and sustained ventricular arrhythmias.

⏯⏯PCI is the preferred revascularisation strategy but is associated with significant challenges and has reported success rates of

🫀 SCAD in Pregnancy — What Every Cardiologist Must Recognize

Spontaneous coronary artery dissection (SCAD) is a non-atherosclerotic cause of ACS, but in pregnancy it becomes a high-risk, high-stakes diagnosis.

As emphasized by Society for Cardiovascular Angiography and Interventions and European Society of Cardiology guidance:

👉 Pregnancy-associated SCAD (P-SCAD) is more severe, more unstable, and more likely to present with STEMI.

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📌 When to Suspect P-SCAD

✔ Young woman
✔ Late pregnancy or early postpartum (peak: first week postpartum)
✔ ACS without traditional risk factors
✔ Discrepancy: severe angiographic disease but preserved myocardium

⚠ High index of suspicion saves myocardium.

🧠 Pathophysiology (Why Pregnancy?)

Hormonal effects → weakening of arterial media

Hemodynamic stress → ↑ shear stress

Postpartum shifts → trigger dissection

👉 Result: Intramural hematoma ± intimal tear → lumen compression

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🧪 Angiographic Classification (Saw Classification)

(Exam gold – from Jacqueline Saw, Circulation Interventions)

🔹 Type 1 (~30%)

Intimal tear

Double lumen / dye staining
👉 “Classic SCAD appearance”

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🔹 Type 2 (~65%) — Most common

Long diffuse smooth narrowing (>30 mm)

No response to nitrates

2A: normal proximal & distal segments

2B: extends to distal vessel

👉 Think SCAD in long, smooth, mid-distal LAD lesions

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🔹 Type 3 (~5%)

Focal stenosis mimicking atherosclerosis
👉 Requires OCT/IVUS to confirm IMH

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🔹 Type 4 (total occlusion – practical concept)

TIMI 0 flow
👉 Diagnose after wiring or by upstream features

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🎯 Angiographic Clues (Exam Triggers)

✔ Long smooth lesion (>30 mm)
✔ Mid-to-distal LAD most common
✔ Tortuous, non-calcified vessels
✔ Poor branch delineation
✔ No response to GTN

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🩺 Management — Guideline-Based

🟢 Conservative First (Cornerstone)

👉 Preferred in stable patients

✔ Most dissections heal spontaneously
✔ Avoid unnecessary PCI

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🩹 Medical Therapy (Practical Consensus)

Aspirin ± clopidogrel

Beta-blockers (↓ shear stress, ↓ recurrence)

Heparin initially (case-dependent)

⚠ Avoid thrombolysis → risk of IMH extension

⚠ GP IIb/IIIa inhibitors → caution (may delay healing)

⚠ Statins → no proven benefit unless atherosclerosis

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🚑 When to Revascularize

👉 Only if high-risk:

Ongoing ischemia

Hemodynamic instability

Left main involvement

Sustained arrhythmias

TIMI 0 flow unlikely to recover

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⚙️ PCI Challenges (Very High Yield)

Difficulty entering true lumen

Risk of dissection propagation

Side branch loss

Success rate IVUS)

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🔧 PCI Strategy (If Needed)

✔ Minimal stenting
✔ Seal proximal entry tear
✔ Avoid long stents if possible

⚠ Risk:

Late stent malapposition (IMH resorption)

Late thrombosis

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🤰 Pregnancy-Specific Considerations

Use Pregnancy Heart Team

Do not delay necessary angiography

Minimize radiation exposure

👶 Delivery planning is integral to management

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🔁 Future Pregnancy

Increased recurrence risk

Not absolutely contraindicated
👉 Requires individualized counseling

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🧠 Exam/Viva One-Liners

✔ “SCAD is a non-atherosclerotic ACS caused by intramural hematoma compressing the lumen.”

✔ “Type 2 SCAD is the most common—long smooth narrowing in mid-distal LAD.”

✔ “Conservative management is preferred as most SCAD lesions heal spontaneously.”

✔ “PCI in SCAD has high complication rates due to propagation of dissection.”

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💡 Final Takeaways

✔ Think SCAD in young women with ACS
✔ Pregnancy/postpartum = high-risk subset
✔ Do less, not more → conservative wins
✔ Use imaging when in doubt
✔ Recognizing SCAD early changes everything

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🫀 In SCAD, the biggest mistake is treating it like atherosclerosis.

In pericarditis u see diffuse ST elevations in lead II v5 v6 St depression in aVR and v1

To differentiate from acute mi

Proximal LAD occlusion with preserved anterior wall and no visible collaterals suggests supply via the conus branch—Circle of Vieussens.

A classic cath lab teaching scenario:
👉 Angiogram shows proximal LAD occlusion
👉 No visible collaterals from left system
👉 No collaterals from RCA injection
👉 Yet… normal anterior wall on echo, no Q waves
❓ So where is the blood supply coming from?

🔍 The Answer: Circle of Vieussens

👉 Definition
An arterial collateral connection between the conus branch of the RCA and the proximal LAD.
👉 Often overlooked because:

The conus artery may arise from a separate ostium (~30–35% cases)

Standard RCA injection may not opacify it

💡 If you see:

LAD occlusion

No visible collaterals

Preserved LV function

👉 Always suspect conus collateral supply

🎯 How to Demonstrate It

✔️ Perform non-selective RCA injection
✔️ Or disengage catheter and point anteriorly & superiorly
✔️ Specifically try to engage the conus ostium

🫀 Coronary Collaterals — Complete Interventional Cardiology Guide

👉 Collateral circulation = pre-existing or recruitable vascular channels that provide alternative blood flow between coronary territories in the presence of a pressure gradient.

🔑 Core Definitions (Exam + Cath Lab)

Collateral channel (CC): Continuous vascular connection between donor and recipient artery (usable in CTO PCI)

Donor artery: Supplies the collateral

Recipient artery: Receives flow distal to occlusion

🧠 Anatomical Classification

🔹 1. Septal Collaterals (Intramyocardial)

Definition: Channels running within interventricular septum
Example:

LAD septals → RCA/PDA septals

Angio recognition:

Straight, short, non-tortuous

No epicardial silhouette

Cath lab rule:
✔️ First choice for retrograde CTO PCI

🔹 2. Epicardial Collaterals

Definition: Surface-running vessels connecting distal coronaries
Examples:

PLV → LCX

PLV → OM

PDA → distal LAD

Angio recognition:

Tortuous, corkscrew

Clear epicardial course

Cath lab rule:
⚠️ Usable but high perforation risk

🔹 3. Conus → LAD (Circle of Vieussens)

Definition: Arterial ring connecting conus branch (RCA) to LAD
Angio recognition:

Circular/arc loop near RVOT

Retrograde LAD filling

✔️ Classic in proximal LAD occlusion

🔹 4. Atrial / Nodal Collaterals

Definition: Collaterals coursing through atrial tissue
Examples:

Kugel’s artery (RCA ↔ LCX)

AV nodal → LCX

PLV → SA nodal

Angio recognition:

Small, faint, delayed filling

❌ Not suitable for PCI

🔹 5. Bridging Collaterals

Definition: Microvascular channels across occlusion without a continuous lumen
Angio recognition:

Hazy network

No discrete vessel

❌ Not a true CC (CC0)

🔹 6. Homocoronary vs Intercoronary

Homocoronary: RCA → PDA

Intercoronary: LAD ↔ RCA, RCA ↔ LCX

📊 Functional & CTO Classifications

🔹 Rentrop (Perfusion)

Grade 0 → none

Grade 1 → side branches

Grade 2 → partial epicardial

Grade 3 → complete filling

🔹 Werner CC (Morphology)

CC0 → none

CC1 → thread-like

CC2 → side-branch–like (usable)