coronary perforation diagnosis and Management

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