This presentation is related to interventional cardiology, especially coronary intervention. this gives information regarding to various complications faced during coronary intervention. it includes puncture complication, coronary complication, radiation hazards and complication due to contrast injection. this presentation also give information on management of complications faced during coronary angiography and percutaneous coronary interventions. along with this few evidence review of management are also added. this will help the residents in cardiology and also practicing cardiologist in minimizing complications and better management of patient.

1. Complications of CAG and
PCI

2. Introducti
on
Radiographic visualization of coronary arteries
after injection of radio opaque contrast media.
As with any invasive procedure complications
are also associated with CAG
These complication can range from minor
complications such as contrast allergy to
devastating complications like MI, CVA and
even death

3. 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

5. Radial
Artery
Spasm
(RAS)
• RAS, defined as the temporary, sudden
narrowing of the radial artery.
• Incidence: 4% to 20%.
• Predictors of RAS :
• radial artery anomaly (eg, high
takeoff),
• small radial diameter,
• female sex,
• number of puncture attempts,
• moderate-to-severe pain during
radial artery cannulation.
• S/S:
• forearm discomfort
• resistance to wire, sheath, or
catheter advancement
• may worsen with further
manipulation.

6. Consequence of RAS
• need to cross over to another access
site.(most frequent)
• catheter/sheath entrapment (<1%)
• radial eversion endarterectomy.

8. Radial Artery Perforation
• Rare complication (<1%)
• occur due to inadvertent wire advancement into small side branches causing
perforation or avulsion due to catheter advancement.
• Radial artery perforation can cause serious bleeding, which if severe, or not
managed appropriately, can lead to compartment syndrome.
• Prevention: If any resistance or difficulty is felt upon wire advancement or
patient reports any discomfort, advancement of the wire and catheter
should be stopped immediately.
• Angiography should be performed to delineate the anatomy, assess for
possible anatomic anomalies, and exclude complications

11. Radial
Artery
Dissection
• Can occur due to vessel injury following
instrumentation.
• management is analogous to that of radial
perforation
• sealing of the dissection using a guide or
sheath often sufficient.

12. Hematom
a
• Hematomas can be categorized using the Early
Discharge After Transradial Stenting of Coronary
Arteries grading:
• Grade I: 5 cm (local hematoma,
≤
superficial);
• Grade II: 10 cm (hematoma with
≤
moderate muscular infiltration);
• Grade III, >10 cm below the elbow—
forearm hematoma and muscular
infiltration;
• Grade IV, above the elbow; and
• Grade V, anywhere with ischemic threat
(compartment syndrome).
• Management:
• Manual compression.
• Sphygmomanometer inflated immediately
proximal to hematoma
• Surgical intervention

13. Radial
Artery
Occlusion
(RAO)
• Preserving radial artery patency is important as the
presence of RAO limits the use of the radial artery
for potential
• future cardiac catheterizations
• use as a conduit in patients undergoing
CABG
• for creation of AV fistulae in patients with
ESRD
• Often unnoticed because most patients are
asymptomatic.
• Radial artery patency should be assessed before
discharge and at the first postprocedural visit
• Prevention: Adequate anticoagulation
• Treatment should be considered for patients with
RAO who are symptomatic
• Anticoagulation
• Percutaneous revascularization.

14. • Arterial Pseudoaneurysm
• It is a rare vascular complication (0.03%– 0.09%)
• suspected in the presence of a pulsatile swelling at the access site
• Mx: Compression with a radial hemostasis device,
• ultrasound-guided compression,
• thrombin injection
• surgical repair.
• AV Fistulas
• prolonged compression using a hemostatic band,
• percutaneous treatment using covered stents, and surgery.

15. Femoral
Access
Complication
s
• Hematoma
• Pseudoaneurysm
• Arterial-Venous Fistula
• Retroperitoneal Hemorrhage
• Dissection
• Distal Embolization
• Nerve Injury

16. Femoral
Hematom
a
• Multiple punctures
• Back wall/through and through puncture
• Poor hemostasis with closure device or
manual hold
• Laceration of femoral artery
• Laceration/puncture of adjacent vessels
• Kinked sheath at arteriotomy
• Access site not over bony structures  cant
adequately control bleeding with
compression
• Any of the above with anticoagulation

17. Manageme
nt
• Small hematomas good manual pressure
• Large hematomas are difficult to manage with
external compression
• Pressure is distributed too widely and can lead
to injury of adjacent femoral nerve or
compression of vessel distal to bleeding site 
accentuates bleeding
• These are best managed by rapid internal
tamponade technique, +/- surgery or covered
stent placement along with supportive
measures

18. Pseudoaneurysm
• Site of access below pubis
 cant compress
adequately
• Poor manual hold
technique/weak hands
• Multiple punctures in
close proximity
• Late/delayed failure of
closure device

19. Manageme
nt
• less than 2cm in size and assymptomatic,
may not require intervention
• If 2cm or greater in size and with narrow
neck, ultrasound guided compression or
thrombin injection is effective
• Wide neck pseudoaneurysms are not ideal
for thrombin injection, and may require
surgical intervention

20. AV Fistula
Causes
• Low access site
• Improper technique
• Multiple punctures: more likely to hit vein
and artery simultaneously
• Needle inserted medial to artery and at
lateral angle
Mx: Typically not treated unless large shunt
leads to symptoms or CHF

21. Dissection
• Most often due to poor access technique- “partial needle insertion”
or simply forcing J wire to go if resistance felt
• Use of hydrophillic and/or stiff wires
• Advancing wire without fluoro imaging

22. Manageme
nt
• Most dissections are retrograde, and simply
removing wires/equipment will allow them
to heal over time
• Antegrade dissections can occur upon
withdrawl of shaped catheters or bulky
devices (ie: valvuloplasty balloons, large
diameter sheaths, etc.) and should be
treated.
• Antegrade dissections typically can be
managed with a combination of balloon
angioplasty and stent placement

23. Retroperiton
eal
Hematoma
(RPH)
• High access site/non-compressible access site
• Use of Femostop or poor manual hold in obese
patientslarge pannus leads to pressure being
applied DISTAL to arteriotomyblood then tracks
upwards through femoral canal into abdomen
instead of into thigh because Femostop or
manual pressure is creating a physical barrier
• Laceration of adjacent vessels
• Wire perforation of small branches in pelvis
• use of non J-tipped wires

25. Suspect RPH if:
• Abdominal or flank pain
• Hypotension
• Decreasing Hematocrit level
Management:
• Reversal of Anticoagulant
• Volume expansion with IV
fluid and Blood transfusion
• Compression of Access site
• Balloon inflation proximal to
site of Bleed
• Covered stent
• Surgical Intervention

26. Distal
Embolizati
on
• Can occur due to disruption of plaque by
catheters/wires, or thrombus formation
around sheath, catheters.
• Important to assess distal pulses before and
after procedure.
• Complains:
• Painful leg
• Impaired sensation and motor
function in the distal extremity.
• O/E:
• Loss of peripheral pulses
• appearance of a white painful foot.

27. Livedo
Reticular
is

28. Preventio
n

29. Manageme
nt
• use of anticoagulation during
prolonged procedures and
intraaortic balloon pump use.
• thrombolytic therapy
• percutaneous thrombectomy
• vascular surgery consultation

30. Complications
related to
contrast
media
• Local and allergic reaction to
contrast
• Anaphylactoid reaction
• Contrast induced nephropathy
• Hyper and Hypothroidsm

31. Contrast
Related
Complication
s
• Allergic Reaction to Contrast
• Allergy to contrast medium is a common but
rarely serious
• Risk is estimated to be 4% to 12% and 1% to
3% for ionic and nonionic contrast agents,
respectively.
These reactions can be:
• Mild: nausea, vomiting, and localized uticaria
with pruritus.
• Moderate: laryngeal or facial edema and
bronchospasm.
• Severe: respiratory or cardiac arrest and
shock

32. Prevention of
Contrast
allergy
Prophylactic measures can decrease the
incidence and severity but do not entirely
eliminate the risk.

33. Manageme
nt

34. Contrast
Induced
Nephropathy
CI-AKI is defined as
• An absolute sCr increase of ≥0.5 mg/dl OR
• A ≥25% relative increase in sCr from
baseline within 48-72 of Contrast exposure

35. Risk factors for CIN
Patient Related Presenting Factors Procedural Factors
CKD ACS Contrast Volume
Diabetes Hypotension Type of Contrast
Advanced Age HF Previous Exposure within
72 hrs
Anemia Volume Depleted IABP Use
EF < 40% Medications
PVD

36. Mechanis
m of CIN

37. Risk
Assessment
• Mehran Score

38. A limitation of this scoring system is
that, calculation is possible only after
Contrast administration
But it is Clinically desirable to predict
the risk of CIN pre exposure
Such a pre-procedural CIN is proposed
by Maioli et al, which is now widely
used

40. Preventio
n
• Adequate Hydration prior to procedure
• POSEIDON trial : IV fluid given 12 hrs prior to
procedure as LVEDP significantly reduces CI-
AKI.
• IVF = 1 ml/kg/hr (max 100 ml/hr), 12 hrs pre
and upto 24 hrs post procedure
• CHF (NYHA > 2) or LVEF <35% = 0.5 ml/kg/hr
(max 50 ml/hr)
• In Cases of Emergrnt procedure: fluid bolus of 3
ml/kg prior to procedure, Hydration during
procedure and 12 hrs after, if possible
• SBC and NAC
• No benefits was seen with NAC, but few
studies report benefits with SBC

41. • As per ESC guidelines NAC is not to be used
alone, although it may be used in addition
to standard IV hydration regimens.
• Routine use of NAC for CI-AKI prevention is
class III in ACC/AHA guidelines
• KIDGO guidelines recommend using oral
NAC together with IV hydration regimen, in
patients with increased risk of CI-AKI

42. STATINS
• High dose statins (Rosuvastatin 40 mg,
Atorvastatin 80 mg, Simvastatin 80 mg) has
shown efficacy in preventing CIN in few
studies.
• PRACTO-ACS: High dose rosuvastatin
significantly reduced 30 days CV and renal
events (Death, Dialysis, MI, Stroke or persistent
renal damage) in patients undergoing PCI
• TRACK-D: largest trial showing significant
reduction in CI-AKI for statin group (p= 0.01)
• PROMISS (Simvastatin): No Benefit

43. Algorithm for
risk
assessment
and
prevention of
CI-AKI

44. Renal guard System : REMEDIAL Trials

45. Manageme
nt
• Decline in Renal Function
• MC finding in CIN is asymptomatic
transient decline in Renal function, which
normalizes in 10-14 days.
• Serum Creatinine
• In High risk patients serial monitoring of
sCr should be done
• Electrolytes and fluid balance
• If oliguric renal failure occurs,
management should done as ARF with
Acid-Base, Electrolytes and Fluid balance
• Dialysis
• May be required in some patients, with a
minority requiring permanent dialysis

46. Radiation
Hazards
Various Imaging modes are used during
CAG and PCI
• Fluoroscopy:
• For real time visualization of moving structures
and interventional devices.
• Typical exposure is 20-35 mGy/min at 7.5 to 15
fps. Maximum recommended is 88 mGy/min.
• Cine Mode:
• used to acquire quality images.
• Exposure is 10-20 times more than fluoroscopy.
Usual exposure is 150-250 mGy/min.
• DSA:
• used for imaging noncardiac stationary vessels.
• Has highest exposure rates of 300-500
mGy/min at 1-4 fps.

47. Types of radiation Hazards
• It includes cancer and genetic mutations.
• Independent of amount of exposure and
no lower threshold limit.
Stochastic Effect:
• Includes tissue reactions from radiation
exposure.
• The severity of tissue reactions increases
with dose, and a minimum dose exists
below which no observable effect occurs
Deterministic effects:

48. Skin hazards due to radiation and its
time duration

50. Annual
Dose
Limit

51. Intra op Strategies to Minimize
Exposure
• Proper use of lead aprons and shields.
• Default to low dose rate fluoroscopy
• Maintaining a long x-ray source–patient distance and a short patient–
image receptor distance.
• Activate x-ray only when clinically indicated
• Never use acquisition imaging to overcome poor fluoroscopic image
quality.

53. Preventive
Measures to
Reduce
exposure

54. Complicatio
ns specific
to PCI
• 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.
1. No-reflow phenomena (2%)
2. Stent thrombosis (2%)
3. Air embolism (0.1-0.3%)
4. Coronary dissection (1%-4%)
5. Vessel perforation (0.84%)
6. Stent embolization (0.4-2%)
7. Need for emergent bypass surgery (0.15-0.3)
8. Wire fracture (0.1%)

55. Coronary
dissectio
n
• 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

56. Coronary
dissection

59. 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

60. 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

62. 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

63. 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

64. Classification of coronary perforation
Ellis classification (wire and device perforation)
Type I: 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.

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

71. Coronary No-flow
• No-reflow is defined as stagnant contrast agent in the distal vasculature without
apparent proximal obstruction.
• inability to perfuse myocardium after opening of a previously occluded or
stenosed epicardial coronary artery
Differential diagnosis of No-reflow:
1. Severe coronary spasm
2. Dissection
3. In situ thrombus
4. Plaque rupture
5. Distal micro embolization

73. Mechanis
m 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

74. 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

75. Prevention of coronary no-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

76. Management
of coronary
re-flow
• Stabilize hemodynamics
with medications or
IABP

77. Management of coronary re-flow
• 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)

79. 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)

80. 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

81. 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

83. Prevention of air embolism
• 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

84. 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)

86. 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
Mechanical
obstruction
Stasis of flow
Platelet activation and
thrombus formation/
spasm

87. 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.

89. Periprocedural MI

90. Risk factors for peri-procedural MI
1.Patients with ACS
2.Advanced age
3.Multivessel disease
4.Intervention on degenerated venous graft
5.Presence of thrombus
6.CTOs
7.Long lesions
8.Use of rotational or orbital Atherectomy
9.Prolonged balloon inflation
10.Aggressive stent expansion
11.Acute closure, no-reflow and side branch closure

91. Mechanis
m and
causes

92. Diagnosis of peri-
procedural MI
Measurement of cardiac biomarker before and 3-6 hours
after procedure

93. Prevention
of peri-
procedural
MI
• Use of IV GPIIbIIIa inhibitor
• P2Y12 inhibitor
• Statin
• Use of distal embolic protection device (EPD) for
SVG intervention

94. 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)

95. Stent thrombosis
Grossman and Baim’s cardiac catheterization,
angiography and intervention 8th
edition/735 page
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

96. 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

97. 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

98. 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

99. EMBOLIZATION OF PERCUTANEOUS CORONARY
INTERVENTION EQUIPMENT
• potentially catastrophic complication of PCI
• Can lead to MI, stent thrombosis, perforation with tamponade, and
occasionally death
• Incidence
• Old generation stents: 3%
• Newer stents: 0.3%
• angioplasty equipment fragments: 0.2% - 0.38%

100. Management
• Retaining the wire in position is crucial
• Various methods can be used for the retrival
• Snares
• advance a small diameter balloon through the unexpanded stent, inflate the
balloon, and attempt to drag the stent back into the guide catheter
• pass a second wire alongside the embolized stent, attempting to enter one
of the struts and then attach a single torquing device to both wires used to
twist the wires together followed by withdrawal of the wire
• deploy the embolized stent in its unintended location

105. Acute
Hemodynami
c Collapse

106. 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
Grossman and Baim’s cardiac catheterization,
angiography and intervention 8th
edition/737
page

107. 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)

108. Mehran system for ISR classification
Types of ISR Description
Focal
Diffuse (confined within stent)
Proliferative Diffuse within and beyond the stent
Occlusive

109. 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)

111. Alternative therapies for ISR
1. Bioresorbable scaffolds
2. Brachytherapy
3. CABG

112. Cardiac
Complicatio
ns
• Arrhythmias
• Electrolyte abnormality: Hypokalemia,
hypomagnesaemia
• Catheter and wire manipulation
• Conus artery block.
• Ischemia: due to Coronary dissection
and Spasm
• Prevention and management
• Correction of Electrolyte abnormality
• Minimal and careful manipulation of
catheter and wires
• Antiarrhythmic rugs (amiodarone)
• Electrical Cardioversion

113. Coronary Artery
Dissection

114. Coronary
Artery
Dissectio
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