Coronary artery perforation is a serious complication of percutaneous coronary intervention that can lead to tamponade, shock, and death if not promptly recognized and treated. The summary describes: 1) Coronary artery perforation occurs in 0.2-0.9% of PCIs and presents a challenge in balancing revascularization and risk of bleeding. 2) Initial treatment involves inflating a balloon at the perforation site to seal it off, followed by deployment of a covered stent if needed. 3) For distal perforations, thrombin, coil, or fat embolization may be used to seal the perforation. Close monitoring is needed for at least 24 hours due to the risk of

1. CORONARY ARTERY PERFORATION
AND MANAGEMENT
DR ABHISHEK KUMAR TIWARI
DM RESIDENT,
CARDIOLOGY
COIMBATORE MEDICAL COLLEGE AND
HOSPITAL

2. Coronary artery perforation is defined as evidence of
extravasation of contrast medium or blood from the
coronary artery, during or following percutaneous
intervention.

3. Anatomical CATEGORY –
Proximal or mid vessel
• Usually more profound with greater likelihood of
significant sequelae
Distal vessel
• There the aetiology is often the guide wire (WIRE
EXIT) and the clinical course is frequently benign

4. CLASSIFICATION
• Ellis in 1994

5. OTHER CLASSIFICATIONS-
Fukutomi
• Type I: Epicardial staining without a contrast extravasation
• Type II: Epicardial staining with a visible jet of contrast
extravasation
Kini
• Type I: Myocardial staining without contrast extravasation
• Type II: Contrast extravasation into pericardium, coronary
sinus, or cardiac chambers

7. INITIAL DATA
• Ellis and colleagues reported first large scale series derived
from data obtained from 11 centres, from 1990 and 1991.
• Of 12,900 procedures performed, 62 were complicated by
coronary perforation (0.5%).

8. CURRENT DATA
• The incidence of Coronary Artery Perforation (CAP) has not
changed significantly over two decades.
• It is reported between 0.2% and 0.9%.

10. RISK FACTORS
Patient Factors : Females, Elderly, Frail pts.
Presentation: ACS/MI, CSA.
Lesion Factors: Calcific Lesions, Tortuous lesions, Tapered
vessels, Bifurcation lesions, small calibre,

11. • A study of 38559 patients with 72 perforations reported that
> 40% of perforations were seen in vessels < 2.5mm
diameter.
•Device-lumen mismatch is more important than the
vessel reference diameter.
• Perforation was more likely where the balloon to artery
ratio was 1.3±0.3 compared with a ratio of 1.0±0.3 where no
problem ensued.
1.Javaid A, Buch AN, Satler LF, et al. Management and outcomes of coronary artery perforation during percutaneous coronary intervention. Am J
Cardiol 2006;98:911-4.
2.Ajluni S, Glazier S, Blankenship L, et al: Perforations after percutaneous coronary interventions: clinical, angiographic, and therapeutic
observations. Catheter
Cardiovasc Diagn 32:206– 212, 1994.

12. RISK FACTORS
Material-Balloon selection –1:1 High Pressure but not more
with high pressure. Cutting/Angiosculpt-more bulky.
•Never remove the balloon out totally before you check
with a contrast puff.
Hydrophilic wires-Stiffer wires/CTO
Drugs: GpIIb IIIa inhibitors

13. In a study* of 16,298 patients with 95 perforations, GPI were
used in 33 cases.
When these 33 cases were compared with the other 62 cases
(where GPI were not used), they found no difference in
• Mortality and
• Myocardial Infarction
GPI use was associated with
• Higher incidence of temponade and
• Greater requirement of emergency surgery

14. • Abciximab binds irreversibly to platelet receptors, rendering
platelet activity almost negligible for 24 – 36 hours.
 In case of perforation with Abciximab, unlike the small
molecules Tirofiban and Eptifibatide, simply discontinuing the
infusion of Abciximab will not reverse its effect.
• Platelet transfusion may be required to restore bleeding
time.
 REVASCULARIZATION  BLEEDING BALANCE

15. ATHERECTOMY
• Use of either atherectomy or laser ablative technology =
More perforation than in convention balloo/stent PCI.
• Ellis1 and colleagues reported that incidence of CAP with
balloon angioplasty was 14 OF 908 cases (0.1%), whereas that
of debulking techniques collectively was 48 OF 3820 cases
(1.3%).

16. GUIDE WIRES
• More likely in the terminal sub branches (LESS IN PROX
AND MID).
• They are also less likely to cause frank rupture of the
vessel than a high pressure balloon barotrauma.

17. GUIDE WIRES
• Hence, the appearance more subtle when the wire is the
culprit.
• Fasseas classified 86% of guide wire mediated ruptures as
Ellis type I or II on angiography.
• HYDROPHILIC -80%.
•CREATE LOOP

18. CTO
• CTO= HIGH RISK (STRONGEST INDEPENDENT
PREDICTOR)
• If no balloon inflation where the wire is incorrectly
positioned, there is minimal extravasation of contrast &
blood.
• GPI  withheld until the occlusion is safely crossed &
distal tip of the wire is seated intraluminally.

19. SEQUELE OF CAP
Caused by CAP-
• Blood loss
• Distal ischemia
• Pericardial Temponade
• Cardiogenic shock
• Death

20. SEQUELE OF CAP
Caused by MANAGEMENT STRATEGIES-
• Myocardial Ischemia
• Acute vessel occlusion
• Myocardial infarction
• Operative morbidity and mortality
• Death

21. COMPLICATION RATE

22. DIAGNOSIS
• Not all CAPs are immediately visible.
• Many develop tamponade > 2 to 6 h later.
• The clinical manifestation may be non-specific, and the
patient may simply develop progressive hypotension.
• A high index of suspicion essential for timely diagnosis.

23. MANAGEMENT
Supportive Measures–
• IV FLUIDS
• O2
• Analgesia
• Inotrops
• Atropine
• IABP

25. Inflate balloon at perforation site
•Before inflating a balloon, one should consider
myocardial ischaemia related to balloon inflation time.

26. Inflate balloon at perforation site
Left main:
Direct covered stenting should be considered
Balloon inflation is "sometimes" feasible depending on
haemodynamic status
Consider re-crossing in LCx or LAD after covered stent
implantation with wire in LCx and LAD (CTO guidewires) to
preserve side branch patency
Consider surgery

27. Inflate balloon at perforation site
PROXIMAL MAIN CORONARY ARTERY
Inflation time will depend on haemodynamic status /
ischaemic condition.
DON’T OVERSIZE , 1:1 balloon / artery ratio.
If haemodynamics allow:
Wait 5 minutes then deflate and inject to check
Repeat 4-5 times as required

28. Inflate balloon at perforation site
Balloon inflation for upto 30 min is required.
If the patient can not tolerate ischemia, then perfusion balloon,
if available.
• Fukotomi reported excellent results using perfusion balloon
for Ellis type III rupture

29. IF FAILED-IMPLANT COVERED STENT
6F GUIDING CATHETER
If balloon is inflated at perforation site
Insert a second guiding catheter (second arterial access,
consider femoral ≥ 7Fr) (DOUBLE GUIDE CATHETER
TECHNIQUE)
Parallel guide wire
Deploy covered stent through second guiding catheter

31. IF FAILED-IMPLANT COBVERED STENT
7F/8F GUIDING CATHETER
If balloon is inflated at perforation site
Insert a second guide wire in the same guiding catheter
Implant covered stent

32. IF FAILED-IMPLANT COBVERED STENT
7F/8F GUIDING CATHETER
If balloon is out of the guiding catheter
 Insert a covered stent directly

39. TYPE IV-INTO CAVITY

40. Management of a Type IV similar to a Type III .
Blood leaks into another cardiovascular cavity (often
ventricle or coronary vein).
 Symptoms are usually that of a new shunt rather than
haemodynamic compromise due to a new pericardial
effusion.
Type IV better tolerated by the patient than Type III

42. Type V: Distal segment

43. Type V may be initially missed as the leak into the
pericardium is often small and may requiring panning to the
distal vessel to be appreciated.
Management may require embolisation of the distal vessel
with thrombin, coils or fat.
Beware of collateral flow to the affected territory which can
cause the perforation to persist despite apparently successful
embolisation.

46. Thrombin injection
Thrombin:
Potent platelet activator
Direct and potent promoter of fibrin clot formation

47. Thrombin injection
PREPARATION:
Use the wire lumen of a very small diameter over-
the-wire balloon catheter.
Prepare thrombin, mixed at a concentration of 50–
100 IU per ml in normal saline
Slowly inject 100–300 IU of thrombin via the distal
lumen of the inflated balloon catheter over a period of
3–5 min
Allow balloon to remain inflated for an additional 10–
15 min if possible.

48. Thrombin injection
TRICKS
Very small (approx. 0.5ml) bolus of air can be
injected through the microcatheter to further diminish
retrograde movement of thrombin.
Mix of thrombin with a small amount of contrast to
allow visualisation.

49. COIL EMBOLIZATION
Needs expertise:
Detachable coils, optimal positioning can be
confirmed before releasing
Pushable coils, smaller but no repositioning
 Deliverable through Micro Catheters

50. Autologous subcutaneous fat embolisation:
For distal guidewire perforation
Physical barrier to bleeding
Coagulation activator
Simple, low-cost and universally available treatment
Allow for a subsequent PCI attempt

51. Autologous subcutaneous fat embolisation:
Fat from abdominal or femoral (next to the puncture point) SC
tissue:
Local anaesthesia
Fat globules small enough to be delivered throughout a
thrombo-aspiration catheter ≤1mm if 6Fr, ≤ 1.2mm if 7Fr, a
microcatheter or a OTW balloon:
Pushed by a wire
Or "emulsion" with saline serum injection

52. Autologous subcutaneous fat embolisation:
Catheter positioned just close to the perforation to avoid:
Large peri-procedural infarction by embolisation into
branches
Systemic or cerebral embolisation

53. Post-procedural care
Once the coronary perforation has been treated there is still a
risk of mortality and close surveillance is required during the
first 24 hours.


54. Post-procedural care

55. Heparin reversal should be deferred till balloons and
wires are still in the artery.
ACT---150-200
GPI IMMEDIETLY STOPPED
 WORST PROGNOSIS IF SURGERY WARRANTED

56. THANK YOU