Complications of PCI-Dr. Sushil.pptx

COMPLICATIONS OF
PERCUTANEOUS CORONARY
INTERVENTION
Presented by:
Dr. Sushil Kumar Ray
Resident phase B
Department of cardiology
BSMMU
Chairperson:
Professor AKM Fazlur Rahman
Chairman
Department of cardiology
BSMMU

INTRODUCTION
• In 1980 Gruentzig said, “If I had an enemy I would teach him angioplasty”, which no
doubt refers to the trails and tribulations that a busy interventional cardiologist faces in day-
to-day practice.
• Mortality: 1-20%
• Substantial improvement in coronary devices e.g. DES, adjunctive pharmacotherapy have
greatly reduced early and late complications.
• Major complications of PCI are rare but can be catastrophic if not successfully managed
• It is critical to be vigilant and recognize potential complications at an early stage to try to
reverse the adverse outcome.
Ref-Kini et al., Practical Manual of Interventional cardiology

COMPLICATIONS OF PCI
• According to timing: acute and long
term
• According to location: cardiac
coronary, cardiac non coronary, and
noncardiac
• Types of complications:
Related to vascular access
Related to contrast
Complications specific to PCI:
immediate/ late

Acute complications of PCI
Cardiac Non-cardiac
A. Coronary:
Acute vessel closure
a. Dissection: coronary. Aorto-coronary
b. Thrombosis
c. Embolization: thrombus, plaque, air
d. Side branch occlusion
e. Spasm
f. Pseudo lesion
g. Equipment entrapment
h. Intramural hematoma
Perforation:
Main vessel
Distal vessel
Collateral
Equipment loss or entrapment
B. Non-coronary:
Hypotension , MI
Arrhythmia (VT, VF) , Tamponade
1. Vascular access complications:
Bleeding
Femoral artery dissection
Infection
Femoral AV fistula
Pseudo-aneurysm
2. Thromboembolic complications: e.g.
TIA, stroke
3. Contrast induced complications (AKI,
allergies)
4. Radiation injury

PCI COMPLICATIONS
1. CORONARY ISCHEMIA:
 Dissection
 No-reflow, air or thrombotic embolism
2. DEVICE RELATED FACTORS:
 Coronary perforation
 Stent, wire or catheter misadventures
3. PATIENT-RELATED FACTORS:
 Contrast-induced nephropathy
 Contrast allergy/ anaphylaxis
Complications specific to PCI:
1. No-reflow phenomena (2%)
2. Stent thrombosis (2%)
3. Vessel perforation (0.84%)
4. Stent embolization (0.4-2%)
5. Need for emergent bypass surgery (0.15-
0.3)
6. Wire fracture (0.1%)
7. Stent infection (<1; case report only)

CORONARY DISSECTION
• Definition: Separation of the media by hemorrhage with or without an associated
intimal tear
• Risk factors:
Calcified lesions
Eccentric lesions
Long lesions
Complex lesion morphology (ACC/AHA type B or C); vessel tortuosity
Balloon to artery ratio >1.2 predispose to dissection
Overly vigorous attempt at guide wire passage
Following balloon dilation

DIFFERENTIAL DIAGNOSIS OF DISSECTION
Causes Corrective techniques
1. Streaming of contrast Advanced the guide deeper into the ostium with more
forceful and steady injection of contrast
2. Deep guide intubation Pull the guide a little back
3. Stiff wire straightening the vessel Withdraw the wire with the flexible tip proximal to the new
lesion
4. Overlapping of radio-opaque wire Withdraw the tip proximal to the new lesion
5. A thin branch running parallel to
the index artery
Change the angle projection of the camera
Practical hand book of Advanced interventional cardiology tips
and tricks/ 4th edition/ 356 page

MANAGEMENT OF DISSECTION ACCORDING TO
SITE OF ORIGIN
Site of origin Wire management
Ostium Keep the wire in place
Stent the ostium first
Local (non-
ostial)
Keep the wire in place
Stent the local dissecting area
Local, wire in
false lumen
Keep the wire in place
Insert 2nd wire in true lumen
Remove first wire only after frim evidence that it is in a false lumen
Stent the narrowing area of the true lumen
Practical hand book of Advanced interventional cardiology tips
and tricks/ 4th edition/ 358 page

ACUTE CLOSURE
1. Incidence: very low
2. Causes of acute closure: mechanical obstruction from dissection and
resulting slow flow may cause activation of platelets and formation of a
thrombus.
3. Other causes of acute closure: acute thrombus formation, combination
of dissection with thrombus formation, distal embolization of plaque
and/or thrombus and coronary spasm
4. Angiographic risk factors for acute closure: proximal tortuosity, long
lesions, heavy calcifications, degenerated vein graft, and angulated
lesions
Ref-Practical manual of interventional cardiology-Annapoorna
Kini
Mechanical
obstruction
Stasis of
flow
Platelet activation
and thrombus
formation/ spasm

DIAGNOSIS OF ACUTE CLOSURE
• Slow flow or absence of flow in the distal vessel
• Chest pain,
• Ischemic EKG changes, arrhythmias or hypotension.
Acute closure Vs No-reflow
No reflow is an acute reduction in coronary flow (TIMI grade 0-1) in a
patent vessel with absence of dissection, thrombus spasm, or high-grade
residual stenosis at the original target lesion.

CORONARY NO-FLOW
• No-reflow is defined as stagnant contrast agent in the distal vasculature without
apparent proximal obstruction.
Differential diagnosis of No-reflow:
1. Severe coronary spasm
2. Dissection
3. In situ thrombus
4. Plaque rupture
5. Distal micro embolization

MECHANISM OF CORONARY NO-REFLOW
• Complex and not completely understood
• Proposed mechanism:
Distal embolization of thrombus and/or plaque;
Microvascular spasm (serotonin, thromboxane)
Oxidative stress and reperfusion injury

RISK FACTORS FOR CORONARY NO-REFLOW
• Clinical and lesion characteristics:
LV systolic dysfunction
Hemodynamic instability
Long calcified lesions
Ostial lesions
CTO of RCA
Thrombotic occlusion
Vein graft lesions
• Use of rotational Atherectomy

PREVENTION OF CORONARY RE-FLOW
• Distal embolic protection devices for vein graft intervention
• When performing rotational Atherectomy, routinely use Nitroglycerine, verapamil, and
heparin in combination with the flush solution
• Consider pre-treatment with a GPIIbIIIa inhibitor during PCI in patients with ACS
• Minimize balloon inflation and consider direct stenting in patients with bulky atheroma
or SVG
• Pre-treat with verapamil or adenosine
• Aspiration thrombectomy for thrombus laden lesion
• Prevention of hypotension and bradycardia

MANAGEMENT OF CORONARY RE-FLOW
• Stabilize hemodynamics with medications or IABP
• IC verapamil (100-200mcg)
• IV adenosine (10-20mcg)
• IC nitroprusside (50-200mcg)
• Moderately forceful injection of blood or saline through the manifold
• Additional anticoagulation with Gp IIbIIIa
• In situ thrombus/ plaque rupture: aspiration thrombectomy
• No-reflow due to dissection: additional stenting
• Severe coronary spasm: IC Nitroglycerine
• Distal micro embolization: prophylactic distal filter; proximal protection with proxis device
(reduce embolic burden)
Pharmacologic management of no-
reflow micro embolization syndrome

CORONARY PERFORATION
• Incidence: 0.48-0.57%
• Causes:
Guidewire injury and hydrophilic wires
Rarely: Secondary to vessel rupture from
oversized balloon or stent expansion or
rotational Atherectomy

RISK FACTORS FOR CORONARY PERFORATION
• Clinical factors: advanced age, female gender, CKD
• Angiographic characteristics
Chronic inelastic lesions (previous CABG)
Angulated lesions (>90 degree)
Calcified lesions
CTO
• Procedural characteristics:
Oversizing the devices (balloon angioplasty or stenting)
Use of an athero-ablative device (directional, rotational)
Excimer laser Atherectomy
Cutting balloon, hydrophilic wires

CLASSIFICATION OF CORONARY
PERFORATION
Ellis classification (wire and device perforation) Kini classification (wire
perforation)
Type I: development of an extra-luminal crater without
extravasation (usually benign, rarely may cause delayed cardiac
tamponade)
Type II: pericardial or myocardial blush without contrast jet
extravasation
Type III: extravasation through frank (≥1mm) perforation spilling
into an anatomic cavity chamber
IIIA: directed toward pericardium (High risk of acute cardiac
tamponade)
IIIB: directed toward myocardium (e.g. ventricular cavity): more
benign course (possible fistula formation)
Cavity splitting: perforation into an anatomic cavity, chamber,
coronary sinus etc.
Type I CP: myocardial stain with no
frank dye extravasation
Type II CP: myocardial fan with dye
extravasation into pericardium, coronary
sinus or cardiac chamber.
Textbook of interventional cardiology/ Topol/ 7th edition

Class I and II: conservative
management
Class III: associated with
rapid development of
cardiac tamponade (63%),
need for urgent CABG
(63%), mortality rate (19%)

PERIPROCEDURAL MI
• Universal definition is elevation of cardiac troponin (cTn) or CK-MB greater
than five times the baseline value within 48 hours of the procedure in a patient
with normal baseline cTn level or rise of cardiac troponin value >20% if the
baseline values are elevated, along with evidence of prolonged ischemia as
manifested by chest pain, new ischemic EKG changes, angiographic evidence of
flow limiting complication or side branch closure, or new wall motion
abnormality.

COMMON CAUSES OF PERI-PROCEDURAL MI
1. Acute closure
2. Distal embolization
3. No-reflow
4. Side branch closure
Risk factors for peri-
procedural MI:
1. Patients with ACS
2. Advanced age
3. Multivessel disease
4. SVG lesions

DIAGNOSIS OF PERI-PROCEDURAL MI
• Measurement of cardiac biomarker before and 3-6 hours after procedure
Risk factors for peri-procedural MI
1. Intervention on degenerated venous graft
2. Presence of thrombus
3. CTOs
4. Long lesions
5. Use of rotational or orbital Atherectomy
6. Prolonged balloon inflation
7. Aggressive stent expansion
8. Acute closure, no-reflow and side branch closure

PREVENTION OF PERI-PROCEDURAL MI
• Use of IV GPIIbIIIa inhibitor
• P2Y12 inhibitor
• Statin
• Use of distal embolic protection device (EPD) for SVG intervention

TREATMENT OF PERI-PROCEDURAL MI
• Depends on underlying cause
• Vasospasm or slow flow: IC verapamil, Nitroglycerine, nitroprusside, adenosine
• Most peri-procedural MI are silent
• Conservative management is adequate for modest elevation of biomarkers.
Serial assessment of biomarker is needed.
• Repeat angiography: if persistent ischemic symptoms, EKG changes or Q wave
infarct (to rule out stent thrombosis or dissection)

AIR EMBOLISM
• Incidence: virtually nil if meticulous safety measures are practiced (potentially
lethal but rare)
• Clinical presentation: larger air embolism: pain, hypotension, hemodynamic
collapse, cardiac arrest, ischemic EKG changes and in rare cases death. Small air
embolism may be asymptomatic
• Causes of air embolism: almost always iatrogenic (due to failure to clear air
from manifold system)

CAUSES OF AIR EMBOLISM
• Catheters are not adequately aspirated and flushed
• During introduction or withdrawal of a guidewire, balloon catheter or other
interventional devices
• Rupture of a balloon during high inflation
• During intracoronary medication Injection

DIAGNOSIS OF AIR EMBOLISM
• Detected fluoroscopically
• Intracoronary filling defects during
dye injection
• Abrupt cut-off of a vessel
secondary to occlusion of distal
circulation with air column

PREVENTION OF AIR EMBOLISM
• Do not engage the left main coronary when pulling out the guiding wire unless the patient has
excessive aortic tortuosity or an enlarged aortic root.
• Do not connect the manifold to the catheter with the flush running. This may lead to an air embolism if
the catheter already has a column of air inside it.
• Draw back at least 2cc of blood into the injection syringe and make sure that the interface is free of air
prior to injection.
• Inject some dye into the ascending aorta prior to engaging left main
• Always ensure that all the catheters and tubings are aspirated, flushed and free of air
• Taking adequate care when prepping stents or balloons and ensure that the syringe tip is facing
downwards
• Always inject with the syringe tip facing downwards

MANAGEMENT OF AIR EMBOLISM
• Best immediate therapy: 100% oxygen (minimize ischemic and reabsorption of air bubbles by
diffusion gradient)
• Treat aggressively with IV fluids, atropine or vasopressors for hemodynamic support
• Consider IABP for hemodynamic support
• Dissipate the ‘airlock’with wires and balloon catheters
• Consider catheter aspiration
• Treat no-reflow phenomenon with standard vasodilators (adenosine, verapamil, nitroprusside)
Textbook of Interventional cardiology / Eric J. Topol/ 7th edition/ 476

STENT THROMBOSIS
Academic research consortium definitions of stent thrombosis
Classification
Definitive An acute coronary syndrome with angiographic or autopsy evidence of thrombus or occlusion
within or adjacent to a stent.
Probable Unexplained death within 30d after stent implantation or acute myocardial infarction involving the
target vessel territory without angiographic confirmation
Possible Any unexplained death beyond 30d after the procedure.
Timing
Acute Within 24h (excludes events within the catheterization laboratory)
Subacute 1-30d
Early Within 30d
Late 30d-1y
Very late After 1y
Grossman and Baim’s cardiac catheterization, angiography and intervention 8th
edition/735 page

POTENTIAL MECHANISMS OF STENT THROMBOSIS
A. Patient related factors relating to increased thrombogenecity:
Smoking/ DM/ CKD/ thrombocytosis/ high post treatment platelet reactivity/ premature discontinuation or
cessation of DAPT/ surgical procedures (unrelated to the PCI)
B. Lesion-based factors relating to adverse rheology/ thrombogenecity within stents:
Diffuse coronary artery disease with long-stented segments
Small vessel disease/ bifurcation disease/ thrombus containing lesions/significant inflow or outflow lesions
proximal or distal to the stented segment
C. Stent related factors:
Poor stent expansion/edge dissections limiting inflow or outflow/ delayed or absent endothelialisation of stent
struts/ thicker stent struts/ hyper viscosity or inflammatory and/or thrombotic reactions to specific DES
polymers/ strut fractures/ late malapposition or aneurysm formation/ development of neoatherosclerosis within
stents with new plaque rupture
Grossman and Baim’s cardiac catheterization, angiography and
intervention 8th edition/737 page

HOW TO MINIMIZE OCCURRENCE OF STENT
THROMBOSIS
A. Patient selection: adherence to DAPT, screening for bleeding risk, confirm any
upcoming surgical procedure in recent future (6 weeks for BMS, 6-12 months for
DES)
B. Stent selection and deployment: consider stents with proven lower rates of
thrombosis, appropriate vessel sizing, high pressure stent deployment and post
dilatation, ensure absence of edge dissection, avoiding use of 2 stents in
bifurcation lesion if possible
C. Peri and post-procedure care: potent antiplatelet (ticagrelor, prasugrel), patient
education and clinical follow up for adherence to DAPT, continuation of DAPT
without interruption whenever possible if a dental, endoscopic and surgical
procedures is necessary

TREATMENT OF STENT THROMBOSIS
A. Prompt reperfusion: acute STEMI presentation
B. Fibrinolytic therapy; emergent PCI
C. Emergent thrombectomy: aspiration or mechanical
D. Balloon angioplasty alone
E. IVUS or OCT: to find out the possible causes of stent thrombosis (after thrombectomy)
e.g. stent under expansion or malapposition, residual dissection or significant inflow or outflow
stenosis
F. Mechanical causes of stent thrombosis: stenting
G. In absence of mechanical cause: Hematologic evaluation to exclude hypercoagulable state including
aspirin and clopidogrel resistance

RESTENOSIS/ ISR
• Restenosis is defined as re-narrowing to a diameter stenosis >50%, either within the stent or within
5mm proximal or distal to the stent margin.
• Restenosis is an arterial wall healing response to mechanical injury at the site of a previously treated
coronary stent
• Causes of restenosis:
Multifactorial
Late neointimal hyperplasia
Stent under expansion/ edge dissection/ residual untreated disease/ geographic miss/ strut fracture
Genetic polymorphism
DM, small RVD, long lesion length/ ostial and/or calcified lesions, true bifurcation lesions requiring main vessel and
side branch stents, CTOs and SVGs

ISR
• In-stent restenosis (ISR) is an angiographic diagnosis, defined as recurrent diameter stenosis
>50% within a stent or at its edges (5mm segments proximal and distal to the stent)
• Most common cause of stent failure
• Most common reason for target lesion revascularization (TLR)

MEHRAN SYSTEM FOR ISR CLASSIFICATION
Types of
ISR
Description
Focal
Diffuse (confined within stent)
Proliferative Diffuse within and beyond the stent
Occlusive

FACTORS CONTRIBUTING TO BMS-ISR AND DES-
ISR
Mechanical factors Biological factors (DES ISR only)
1. Stent under expansion (malapposition)
2. Strut fracture
3. Stent gap
4. Geographic miss
5. Edge dissection
6. Uneven or undelivered drug (DES-ISR; stent
damage; non-uniform strut distribution)
1. Drug resistance (often implicated in NIH)
2. Hypersensitivity reaction (often in response
to polymer coating)

ALTERNATIVE THERAPIES FOR ISR
1. Bioresorbable scaffolds
2. Brachytherapy
3. CABG

CONTRAST INDUCED NEPHROPATHY
• Defined as relative increase in serum creatinine of >25% or an absolute
increase >0.5mg/dl
• Mechanism: Toxic ATN

PREVENTIVE STRATEGIES FOR CIN
1. Hydration with normal saline
2. Minimize amount of contrast media
3. Use of non ionic LOCM or IOCM
4. NAC
5. Statins

TAKE HOME MESSAGES
• “An ounce of prevention is worth a pound of cure”

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