This document discusses the cardiology perspective on out-of-hospital cardiac arrest (OOHCA). It notes that coronary artery disease is a common underlying cause of OOHCA and that observational studies have found high rates of obstructive coronary anatomy in OOHCA patients. While randomized controlled trials are lacking, registry data suggests early invasive coronary angiography and revascularization may improve outcomes for select OOHCA patients, especially those presenting in ventricular fibrillation or tachycardia. However, patient selection is important as those undergoing early intervention procedures tend to be lower risk. The optimal strategy also remains unclear as not all coronary stenoses may need immediate treatment. Potential harms of early angiography include bleeding complications.

1. OOHCA
The Cardiology
Perspective
Ian Webb
King’s College Hospital

2. • Role of early coronary angiography and
intervention
• Literature review
• Additional considerations
• The King’s Experience

3. • I’m an Interventional Cardiologist
• I don’t particularly like to get up in the middle of the night for
OOHCA arrest patients with so many unknown clinical and
prognostic variables
• I have sympathy with colleagues who question the aetiology, the
diagnostic work-up and early aggressive coronary strategy
• I believe that an artery with 0% stenosis is highly likely to improve
ischaemia and ischaemia-related complications (like VF/VT/LV
dysfunction)
• Can I prove it with Class IA data – No ...
Conflicts of Interest
• ........ And I still believe in therapeutic hypothermia

4. • Incidence of OOHCA in the European population estimated at about 40
per 100,000 per year1
• OOHCA resuscitations by UK Ambulance crews in 2013 ~ 28,000 cases2
(estimated 60,000 call-outs)
• LAS: 80% arrests occur at home, with 20% VF/VT the presenting
rhythm3
• Outcomes in SHR better; mortality increases with every minute delay to
BLS or DCCV4,5
• UK average survival to hospital discharge from decision to resuscitate
8.6% (cf Holland/Seattle/Norway ~20%) 2
• Leading causes of death are CV (acute) and brain injury (late)6,7
1. Atwood C et al. (2005) Incidence of EMS-treated out-of-hospital cardiac arrest in Europe. Resuscitation, 67: 75–80
2. www.england.nhs.uk/statistics/stasistical-work-areas/ambulance-quality-indicators
3. London Ambulance Service Cardiac Arrest Annual Report 2012/2013 [www.londonambulance.nhs.uk].
4. Lindner T et al. Resuscitation 2011; 82:1508-13.
5. 2010 European Resuscitation Council guidelines for resuscitation. Resuscitation 2010;81: 1219-76.
6. Schoenenberger R et al. Survival after failed out-of-hospital resuscitation. Arch Intern Med. 1994;154:2433-7.
7. Laver S et al. Mode of death after admission to an intensive care unit following cardiac arrest. Intensive Care Med 2004;30:2126–2128.

5. • OOHCA is the leading cause of death in IHD patients1
• ‘Obstructive’ coronary anatomy is common in angiographic and post-
mortem series of OOHCA cohorts2-4
> 90% in STEMI / >40% in non-STEMI
• Good data to support early interventional strategy in non-OOHCA
NSTEMI/STEMI5,6
• Little data to guide practice in comotose / I+V patients
- observational / registries / multiple variables
•Observational literature that VT/VF burden reduced in revascularised
ICD patients7,8
1. Zheng Z et al. (2001) Sudden cardiac death in the United States, 1989–1998. Circ.104:2158–2163
2. Spaulding C et al. (1997) Immediate Coronary angiography in survivors of OOHCA. NEJM 1997 336; 1629-1633
3. Davies M (1992) et al. Anatomic features in victims of sudden coronary death: coronary artery pathology. Circ ;85:S I:I-19
4. Dumas F et al.(2010) PROCAT registry. CCI, 3:200-207.
5. 2014 ESC/EACTS Guidelines on Myocardial Revascularisation. Windecker S et al.
6. 2012 ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Steg P et al.
7. Cook J et al. Am Heart J 2002; 143(5): 821-6
8. Gillis A et al. Circulation 2007; 116: II_534

6. •2010 International Consensus on Cardiopulmonary Resuscitation and
Emergency Cardiovascular Care1
- ‘reasonable to perform immediate angiography and PCI in“selected”
patients, despite the absence of STEMI or prior clinical findings such as
chest pain
• 2012 ESC Guidelines support immediate CAG +/- revascularisation2
- STEMI (Class IB)
- Suspected ACS irrespective of ECG (Class IIa B)
•2014 Invasive coronary treatment strategies for out-of-hospital cardiac
arrest: a consensus statement from the European association for
percutaneous cardiovascular interventions (EAPCI)/stent for life
(SFL) groups3
1. 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment
Recommendations. Circulation . Hazinski M et al.
2. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: Task Force Statement for
ESC (2012) Steg P et al.
3. Consensus statement from the European association for percutaneous cardiovascular interventions (EAPCI)/stent for life (SFL) groups.

7. Common practice
OOHCA
STEMI PPCI or Lysis

8. Common practice
OOHCA
STEMI PPCI or Lysis
‘Not sure’
‘Could all be reactive ECG
changes’
‘Nothing to hang your hat
on’
‘Lets see if ‘he does’ and
work him up after’
‘Normal’ ECG
Minor ST-segment
changes
Moderate ST-segment or
T wave changes

9. British Cardiac Society (Intervention Sub-group
meeting) 2014
• 56-year old male
• Unprovoked OOHVF arrest
• Known IHD with prior PCI to his LAD following NSTEMI (several
years ago)
• LBBB
• Prompt resuscitation
• Presents to A+E in stable condition / I+V
 What would you do now?

10. BCS 2014
• ‘Well – the LBBB could well be old. There’s no clear mandate for
CAG’
• ‘It’s unusual for it to be a primary coronary event if he had no
preceding symptoms’
• ‘There’s certainly not enough evidence to rush in there and
potentially de-stabilise the situation.’
• ‘You cannot tell if this is ischaemia or scar-related arrhythmia from
his old MI’

11. BCS 2014
• Cooled
• Recurrent VF on ICU Day 2
• Commenced on amiodorone and taken to the Cath Labs
• Critical in-stent re-stenosis  treated with a single DES in less than a
minute

12. BCS 2014
• Cooled
• Recurrent VF on ICU Day 2
• Taken to the Cath Labs
• Critical in-stent re-stenosis  treated with a single DES in less than a
minute
• No further arrhythmias
• Extubated Day 4
• Discharged to wards Day 6
• Home Day 11

13. 3 fundamental questions
• Is coronary disease a likely aetiological factor?
• What evidence is there for early diagnosis/intervention in
an otherwise stabilised patient?
• What harm can an angiogram do?

14. Spaulding CM. N Engl J Med 1997;336:1629-33.
OOHCA associated with high incidence of IHD
Urgent CAG (84)
Normal 17 (20%)
Non-obstructive CAD 7 (8%)
Obstructive CAD 60 (71%)
Single vessel 22
Multivessel 37
Isolated LM 1
Acute Coronary occlusion 40 (48%)
Survivors to hospital in stable condition
101 non-cardiac causes excluded
80% VT/VF
All ECG’s

15. Positive Negative
Chest discomfort
and ST-elevation 87% 61%
Spaulding CM. N Engl J Med 1997;336:1629-33.
Predictive value
Absence of ST-segment elevation does not
exlude acute coronary obstruction

16. Patients post-ROSC admitted to the intensive care unit.
Florence Dumas et al. Circ Cardiovasc Interv. 2010;3:200-207
2003 – 2008
ROSC survivors to admission
All rhythms
PCI to lesions >50%
STEMI All other

19. • Prevalence of CAD is high – but is it causative?
• How can we prove and treat accordingly?
• Is there a role for early invasive angiography +/-
revascularisation?
Evidence for acute invasive strategy?
• No RCT data
• Registry data (>3,500 patients)
• Multivariate analysis of observational registries

20. EuroIntervention 2014;10:31-37
Non-STEMI
Author n Multivariate predictor of survival
Spaulding 85 Successful PCI (OR 5.2; p=0.004)
Reynolds 241 CAG/PCI strategy (OR 2.16; p=0.02)
Nielsen 986 CAG/PCI strategy (OR 1.56; p=0.008)
Dumas 714 Successful PCI (OR 2.06; p=0.013)

22. Resuscitation 2014 85, 88-95DOI: (10.1016/j.resuscitation.2013.07.027)
Shock
LV support
Antiplatelets etc..
32.7%
39.0%
Registry data
754 consecutive comotose ROSC
6 Tertiary care centres
Unclear timeframe/history
VT/VF only
STEMI excluded
Early <24hrs
Late >24hrs

23. In non-STEMI VF/VT arrests:
- 30% of patients had an acute coronary occlusion
- 60-70% had significant bystander disease
- 30-40% went on to have successful PCI
No angiographic differences between early and late CAG

25. Multivariate logistic regression analysis examining
predictors of in-hospital mortality
Resuscitation 2014 85, 88-95DOI: (10.1016/j.resuscitation.2013.07.027)

26. Unclear if revascularisation itself is of benefit

27. CCI, 2010
2003 – 2008
ROSC survivors to admission n=714
PCI to lesions >50%

28. Patients post-ROSC admitted to the intensive care unit.
Florence Dumas et al. Circ Cardiovasc Interv. 2010;3:200-207
2003 – 2008
ROSC survivors to admission
PCI to lesions >50%

29. Florence Dumas et al. Circ Cardiovasc Interv. 2010;3:200-207
Survival rates according to the performance
and outcome of PCI

30. Features associated with survival to hospital discharge
Younger age
Non-DM status
Arrest in public location
Prompt BLS and ROSC
VF/VT presentation
STEMI ECG pattern
Low admission lactate
Therapeutic hypothermia
Successful PCI OR 2.06 (1.16-3.66; p 0.013)
Only ‘successful’ PCI predictive of mortality
benefit after multivariate analysis
Florence Dumas et al. Circ Cardiovasc Interv. 2010;3:200-207

31. Dortmund
Population >500,000
2007-2008

32. PCI capable HospitalNon-PCI capable Hospital

35. Selection bias?
• Patients undergoing early CAG/revascularisation are
generally:
- younger
- better CPC score post-arrest
- more likely to have STEMI
- more likely to have VF/VT
• Similarly, variability between Centres may not take into
account
- sub-specialty input
- access to Ix / treatment options/pathways
- more formalised MDT approach to patient care

36. Are all coronary stenoses alike?

37. Are all coronary stenoses alike?

38. • STEMI – plaque rupture, heavy thrombus burden, impaired
coronary flow
- clear mandate to restore flow
• Obstructive coronary disease with preserved TIMI flow
- take a view on the complexity of anatomy in conjunction with
the patient and their haemodynamics
- Surgeons rarely taken on emergency CABG in this setting
- Similarly, complex rotablation in heavily calcified vessels or
complex CTO revascularisation NOT an option acutely
No RCT Data
No information about revascularisation strategies from
registry data
Little to guide us on timing (acute vs staged) – except
shock and extent of revascularisation (cf non-comatose
ACS patients)
But worth noting:
PCI revascularisation levels high in STEMI cohorts and
30-50% in non-STEMI groups from registry data

39. What harm can an angiogram do?

40. What harm can an angiogram do?
*Major bleeding approximately 3.5%
*Peripheral ischaemic complications approx 4-11%
*Stroke rates approx 1%
------------------------------------
Radial vs femoral
Use of adjunctive LV support devices
Variable anticoagulation regimens
*IABP – SHOCK II study, NEJM 2012
Early Revascularization in Acute Myocardial Infarction Complicated by Cardiogenic Shock, NEJM 1999
30-40% CPR/VT/VF

41. Dankiewicz et al. ICM 2015

42. What harm can an angiogram do?

43. LV support devices

44. IABP Impella Tandem Heart ECMO
LV support devices
14Fr8Fr 17/15Fr 14-29Fr

45. LV support devices
• Cardiogenic shock is present in 30-40% of OOHCA survivors
• Presents most often within 4-6 hours of the index event
• No device has shown prognostic benefit in comatose or non-comatose
patients1
• Use of IABP/Impella observational series ranges from 10-42%2
• Higher incidence in patients treated emergently by PCI
• Future Role for Impella CP and/or ECMO...
• Principle of haemodynamic support vs vascular access and longer-term
complications (sepsis, blood dyscrasias etc..)
1. ISAR Shock, IABP-SHOCK I and II, PROTECT II
2. Cheng et al. 2009, Sjauw et al. 2009, Hovdenes et al. 2009

46. Pharmacotherapy

47. Acute Stent Thrombosis

48. Acute Stent Thrombosis
• Acute stent thrombosis occurs in 4.6% - 10.9% of ACS patients
complicated by CA1,2
• OR for AST 12.9 following cardiac arrest (95%CI 1.3-124.6; p=0.027)2
• Mortality with AST is high (up to 45%) 3
• Likely factors - non-administration of antiplatelets / heparins2
- malabsorption and altered metabolism4
- highly procoagulant /inflammatory state
- adverse haemodynamic status
1. Shah N et al. JACC 2015;65(10_S)
2. Joffre J et al. Resuscitation 2014; 85(6):769-73
3. Buchanan G et al. Thrombosis 2012
4. Bjelland T et al. Resuscitation 2010;81:1627–31

49. Rosencher J et al. 2015
N=20
OOHCA
PCI

50. Cangrelor
• IV P2Y12 ADP receptor antagonist
• High affinity, reversible
• ½ life 3 minutes
• Normal PLT function after 1hr
• Recent FDA approval

52. London Heart Attack Centre Network 2005
Harefield Royal Free Heart London Chest
Imperial
St. George’s
St. Thomas’s
King’s
8 HAC
Approx 30 Acute admission units
7.5/10million people
>600m2

53. • 9,805 OOHCA calls attended by LAS
• Resuscitation attempted for 4,317 patients
- 92% declared dead on scene / 8% DNR in place
• Of those actively treated by LAS:
• Survival to discharge:
2013/2014
48.6% Witnessed
44.8% Bystander CPR performed
31% Sustained ROSC to Hospital admission
85.7% Primary cardiac aetiology
10.3% Witnessed
32.4% Utstein population (witnessed / Vf or VT / presumed cardiac)
47.6% Treated at HAC
58.8% Use of AED

54. 78% Private
86% cardiac
65% transfer to
hospital
31% sustained ROSC
December Monday
mornings!

55. King’s College Hospital
• PPCI programme 2003
• 1 million catchment
• 4th
busiest London unit
• ~900 STEMI/yr
• 120 OOHCA-I+V/yr

56. OOHCAOOHCA
STEMI
STEMI FAST-TRACK
(Cath Labs)
Rapid evaluation of
comorbidities
+
Cardiac arrest details
STEMI FAST-TRACK
(Cath Labs)
Rapid evaluation of
comorbidities
+
Cardiac arrest details
Coronary angiography
No STEMI
‘ER stop’‘ER stop’
Diagnostic work-up
Additional
history
Additional
history
EchoEcho
Laboratory
values
Laboratory
values
CT
Imaging
CT
Imaging
Obvious non-cardiac
causes excluded

57. Coronary
angiography
STEMI
Non-STEMI ECG
Clear culprit stenosis+
Non-STEMI ECG
Significant stenosis <70%
Good flow (TIMI III)
Non-STEMI ECG
Non-obstructive coronary
disease
PCI of culprit artery
Consider bystander
PCI if:
- unstable
- low risk + prognostic
Consider PCI if:
- clinical correlate
- < intermediate risk
STOP
Review
+ Stenosis >90%, thrombus, <TIMI I/II flow, clinical correlate
* DAPT and statin therapy per NGT
*
*

58. OOHCA
Cath
Lab
Resus
ITU
Home
N = 331
N = 146
(44.1%)
N = 185 (55.9%)
N = 47 (25.4 %)
N = 144 (43.5 %)
2011-2014
OOHCA ROSC
Survivors to Cath-Lab +/or ICU
All I+V cases
Total number to
Cath Lab =193
Data - R.Nerla/F.Jouhra

59. OOHCA presenting rhythms
Data - R.Nerla/F.Jouhra

60. Presumed causes of OOHCA
Data - R.Nerla/F.Jouhra

61. Primary Diagnosis
Data - R.Nerla/F.Jouhra

62. OOHCA
Cath Lab sub-group
Cath
Lab
No angio
PCI
AngioN =181
(93.7%)
N = 12 (6.3%)
N = 117
(65%)
No PCI
N = 59 (32.6%)
N = 331
N = 193 (58.3 %)
Futile N = 6
Other diagnosis more probable N = 6
CABG N = 5
STEMI (92%)
nonSTEMI (38%)
Data - R.Nerla/F.Jouhra

63. Cath Lab sub-group
• Multi-vessel intervention 22%
• 15% cardiogenic shock
- IABP 98% / Impella 1% / ECMO 1%
• Survival to ICU 98%
• Survival to hospital discharge:
PCI
AngioN =181
(93.7%)
N = 117
(65%)
STEMI (92%)
nonSTEMI (38%) P <0.001
Data - R.Nerla/F.Jouhra

64. Survival by diagnosis
P <
0.001
* Including all patients with a definite primitive cardiac cause
for OOHCA
Data - R.Nerla/F.Jouhra
Overall survival to discharge 43.5%
Median ICU stay (d) 3 (0-40)
Mean 6.8 + 8.2
Median Hospital stay 6 (0-87)

65. Work to do...
• Follow-up data
Mortality
Neurological outcomes
ICD implantation
• Improving post-arrest care
LV support (ECMO)
Neurocognitive prognostication
Neuro-rehab
Academic integration

66. Summary
• OOHCA is associated with significant mortality and morbidity
• The major gains in survival are likely to evolve through front-
managed patient care
• The prevalence of coronary disease in OOHCA survivors is
significant
• Whether this is causative or not is uncertain – but aggressive multi-
disciplinary patient management – including early coronary
angiography and revascularisation – appears safe and to confer
better survival and neurological outcomes.