PART III - THE INTERVENTIONAL MANAGEMENT OF OUT-OF-HOSPITAL CARDIAC ARREST
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Updated on April 15, 2022
PART III

The interventional management of out-of-hospital cardiac arrest

Marko Noc1, Peter Radsel1, Emmanouil Poulidakis2, Jan Belohlavek3, Christian Spaulding4
1. Department of Intensive Internal Medicine, University Medical Center Ljubljana; Medical Faculty, University of Ljubljana, Slovenia
2. Department of Cardiology, Hygeia Hospital Athens, Attiki, Greece
3. 2nd Department of Medicine – Department of Cardiovascular Medicine, First Faculty of Medicine, Charles University in Prague and General University Hospital in Prague, Czech Republic
4. Cardiology Department, European Hospital Georges Pompidou, Assistance Publique Hôpitaux de Paris, Paris Cité University, Sudden Cardiac Death Expert Center, INSERM U 970, PARCC, Paris France

Chapter update in progress

Summary

Out-of-hospital cardiac arrest (OHCA) remains the leading cause of death in developed countries and the number of hospital admissions increases every year. If changes indicative of an ST-segment elevation myocardial infarction (STEMI) are present on the post-resuscitation electrocardiogram (ECG), acute culprit lesions may be found in up to 90% of cases. The absence of STEMI does not exclude acute lesions which may still be present in 25- 58% of cases. Interventional cardiologists are therefore increasingly alerted for coronary angiography (CAG) and percutaneous coronary intervention (PCI), and are becoming an important members of the resuscitation team. Selection for immediate CAG/PCI should be individualized to obtain maximal benefit and avoid futility. Index PCI should focus on the culprit lesion. Acetylsalicylic acid, unfractionated heparin and novel P2Y12 inhibitors should be preferred over clopidogrel. In bailout situations, an intravenous P2Y12 inhibitor cangrelor with rapid “onset-offset” in platelet inhibition, might be preferred over GP llb/llla inhibitors because of a high rate of bleeding complications in these patients. Indications for hemodynamic support devices during the postresuscitation phase as well as for veno-arterial extracorporeal membrane oxygenation (VA ECMO) in refractory cardiac arrest (E-CPR) should be individualized.

Introduction

Sudden out-of-hospital cardiac arrest (OHCA) remains the leading cause of death in developed countries with an annual incidence ranging from 36 to 81 events per 100.000 inhabitants [1]. Initial prehospital treatment, known as the “Chain of survival” includes immediate recognition and notification of prehospital emergency service (EMS), bystander cardiopulmonary resuscitation (BLS) eventually directed by a dispatcher, early defibrillation by automated external defibrillator (AED) and advanced cardiac life support (ACLS) [2]. Due to significant improvements in prehospital management, the number of hospital admissions increases every year [3]. Since numerous studies have demonstrated that significant coronary artery disease is present in more than 70% of patients, [4, 5, 6], interventional cardiologists and especially those in “24-7” interventional centers, are increasingly alerted for coronary angiography (CAG), percutaneous coronary intervention (PCI) as well as for implantation of invasive hemodynamic support devices [7].

FOCUS BOX 1

Since the number of patients with out-of-hospital cardiac arrest (OHCA) admitted to hospitals increases and because it is well known that significant coronary artery disease may be present in more than 70%, interventional cardiologists are increasingly alerted for coronary angiography (CAG), percutaneous coronary intervention (PCI) and implantation of invasive hemodynamic support devices.

Characteristics of OHCA patients at hospital admission

Reestablishment of spontaneous circulation (ROSC) on the field may nowadays be achieved in up to 50% of OHCA patients in whom ACLS is initiated [2]. Following ROSC, these patients differ significantly in terms of hemodynamic stability, neurological status and likelihood of ultimate neurological recovery ( Figure 1).

Following ROSC, there is an increased incidence of early post-resuscitation cardiogenic shock which varies from 30% to 40% [8]. The mechanism is multifactorial and includes vasoplegia, left ventricular systolic dysfunction due to global post-resuscitation myocardial stunning and regional ischemia if acute coronary occlusion is present. Up to 40% of initially resuscitated patients may experience recurrent cardiac arrest requiring repeat resuscitation efforts [9].

If OHCA is lay or EMS-witnessed and immediately treated by effective chest compression and rapid defibrillation by AED, ROSC may be rapidly obtained and the patient regains consciousness immediately or upon hospital arrival ( Vignette 1). These patients, who constitute up to 20% of OHCA population, are known as “conscious” survivors or “early awakers”. Because of the short delay from OHCA to ROSC, they do not develop post resuscitation brain injury. If an immediate invasive coronary strategy including CAG and PCI is implemented similarly as in acute coronary syndromes without preceding cardiac arrest, the prognosis of these patients is excellent. Among 119 “conscious” OHCA survivors cumulatively published in PubMed-listed journals, 117 (98%) survived to hospital discharge with normal neurological status [10, 11, 12, 13]. Moreover, in a single center registry, 1-year survival of these patients presenting with ST-elevation myocardial infarction (STEMI) in post resuscitation electrocardiogram (ECG) was >95% which was comparable to matched STEMI patients without OHCA [12].

Unfortunately, suboptimal performance of one or more components of the prehospital “Chain of Survival” is nowadays still a reality in >80% of OHCA patients. Time delay from onset of OHCA to ROSC is therefore typically increased to 15-25 minutes or even more and these patients remain comatose despite ROSC ( Vignette 2) [1]. Coma on hospital admission despite ROSC unequivocally indicates presence of post resuscitation brain injury, the severity of which may ultimately vary from no or mild disability to permanent vegetative state or even brain death. Importantly, the degree of neurological recovery in these, so called “comatose” survivors of OHCA, cannot be predicted on hospital admission when decision for immediate aggressive treatment and especially for CAG and PCI is to be made. While early hospital death (<3 days) in this OHCA subgroup is usually of cardiac origin, later deaths (>70%) are predominately related to the lack of neurological recovery leading to withdrawing/withholding of life support interventions [14]. In contrast to “conscious” survivors of OHCA, overall survival with adequate neurological recovery in “comatose” survivors may therefore at best reach 50-60% [15, 16, 17].

Very experienced cardiac arrest centers nowadays admit also highly selected patients with refractory OHCA without ROSC on the field and ongoing ACLS with chest compression. Upon hospital arrival, these patients may undergo immediate implantation of arterio-venous extracorporeal membrane oxygenation (VA ECMO), a method known as E-CPR which may be performed in the catheterization laboratory ( Vignette 3), emergency room or even in the field by highly specialized prehospital ECMO teams ( Vignette 4) [18]. VA ECMO which is usually followed by immediate CAG and PCI if appropriate, reestablishes organ perfusion and maintains viability until ROSC is regained. Such treatment strategy may nowadays result in a survival with good neurological in 20-30% [19, 20].

FOCUS BOX 2

Clinical presentation of OHCA patients at hospital admission differs significantly in terms of hemodynamic stability, neurological status and likelihood for neurological recovery.

Coronary angiographic features and rationale for immediate PCI

Immediate CAG after hospital admission may reveal very heterogeneous findings which include normal coronary arteries, non-obstructive disease (<50%), intermediate disease (50-70%), obstructive disease (>70%) with stable lesions ( Video 1) and presence of a typical acute culprit lesion defined as an abrupt closure with TIMI 0/1flow ( Video 2) or an angiographic appearance suggesting thrombus or ulcerated plaques with TIMI 2 or 3 flow ( Video 3). In the presence of STEMI in early post resuscitation ECG, an acute culprit lesion may be found in up to 90% of cases [10, 11, 12], [21, 21]. Importantly, the absence of ST segment elevation on the post resuscitation ECG does not exclude acute culprit lesion which may still be present in 25 to 58% of patients [21, 6, 12, 21].

The cause-effect relationship between coronary anatomy and OHCA seems obvious in the presence of an acute culprit lesion. On the other hand, stable obstructive coronary artery disease is more likely an “innocent bystander” although transient ischemia caused by plaque thrombosis followed by spontaneous reperfusion, coronary spasm ( Video 4A and Video 4B) or decrease in perfusion pressure across the tight lesion or collaterals in case of a sudden drop in arterial pressure, is also possible.

The rationale for PCI is to relieve myocardial ischemia and thereby improve electrical stability as well as to decrease the extent of myocardial infarction if acute coronary occlusion is present. This may, in turn, reduce the incidence of recurrent cardiac arrest and acute heart failure which is likely to decrease cardiac mortality in “conscious” OHCA survivors ( Figure 2) and buy time for possible neurological recovery in “comatose” survivors of OHCA.

FOCUS BOX 3

In the presence of ST-elevation myocardial infarction (STEMI) on the early post resuscitation electrocardiogram (ECG), an acute culprit lesion may be found in up to 90% of cases. Absence of STEMI does not exclude acute culprit lesions which may still be present in 25% to 58% of cases.

Scientific evidence supporting CAG/PCI in OHCA

There are many observational cohort trials demonstrating the feasibility and safety of immediate invasive coronary strategy including CAG and PCI. Cumulatively, 161.908 patients undergoing immediate CAG have been reported between 1995 and 2018. ( Table 1) [4, 5, 6] [8, 9, 10] [13] [21, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61, 62, 63, 64, 65, 66, 67, 68, 69, 70, 71, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82, 83, 84, 85, 86, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 97, 98, 99, 100]. Among them, there were 85% “comatose” survivors and 43% presented with STEMI. PCI, performed in 51% of patients, was successful in 85%. Overall hospital survival and survival with good neurological recovery was documented in 76% and 52%, respectively.

Several studies also compared the clinical outcome of patients undergoing immediate CAG/PCI strategy with historical controls undergoing conventional treatment. In a meta-analysis of 10 observational studies including 3103 patients, an immediate CAG/PCI strategy was associated with improved survival (pooled unadjusted OR 2.78; 95% CI 1.89-4.10; p<0.001) [101]. Another study analyzed 3981 patients with OHCA admitted after ROSC; 19% and 17% underwent coronary angiography and PCI within 24 hours, respectively [74]. Survival and favorable neurological outcome were independently associated with early coronary angiography (adjusted OR 1.87; 95% CI 1.15-3.04; p<0.01) and reperfusion (adjusted OR 2.14; 95% CI 1.46-3.14; p<0.01). A propensity-matched analysis from the CARES registry found that early invasive coronary strategy within 24 hours was associated with a 50% increase in survival to hospital discharge (adjusted OR 1.52, 95% CI 1.28-1.80; p<0.01) and favorable neurological outcome (adjusted OR 1.47; 95% CI 1.25-1.71;p<0.01) [82]. Additional analysis demonstrated that PCI was the main predictor of survival. This is in agreement with the largest single-center study from Paris which enrolled 1722 consecutive patients admitted between 2000 and 2013. Propensity–score matching confirmed the association between immediate CAG followed by PCI and both, 30-day (adjusted OR 0.61; 95% CI 0.43-0.81; p<0.01) and 10-year mortality (adjusted OR 0.40; 95% CI 0.23-0.70; p<0.01) [78].

A subgroup of “comatose” survivors without STEMI in postresuscitation ECG has been recently investigated in 4 randomized controlled trials including COACT [102], PEARL [103], TOMAHOWK [104] and EMERGE [105]. Patients were randomized to immediate CAG/PCI performed within 1.5-2.9 hours after the admission and delayed or selective CAG/PCI performed within 47-122 hours after the admission. In all 4 trials there was no difference in a long-term survival with good neurological outcome between the groups. There was also a similar incidence of adverse events including bleeding and need for renal replacement treatment in the TOMAHOWK trial [104]. Delayed/selective strategy also reduced the need for CAG by almost 50% (89-100% in the early group vs 48-65% in the delayed/selective group) with comparable rate of PCI (30-37% in the early group vs 23-43% in the delayed/selective group). Additional ongoing randomized trials including ARREST (NCT02587494), DISCO (NCT02309151) and COUPE (NCT 02641626), which are also enrolling only patients without STEMI in postresuscitation ECG, are expected to confirm these findings [106, 107, 108]. On the other hand, patient based meta-analysis of these randomized trials would be very helpful to investigate if there is a subgroup of comatose survivors of OHCA without STEMI in postresuscitation ECGwho may benefit from an immediate CAG/PCI. Currently we can only hypothesize that these might be patients with hemodynamic instability including cardiogenic shock, malignant ventricular arrhythmias and recurrent cardiac arrest who were excluded from the two largest studies, COACT and TOMAHOWK.

In contrary to “comatose” survivors of OHCA without STEMI, there are no published or ongoing randomized trials addressing immediate CAG/PCI in “comatose” survivors of OHCA with STEMI in postresuscitation ECG. The reason is probably high prevalence of acute coronary lesions and especially acute occlusions in these patients (>90%) which makes randomization rather impossible. Unfortunately, “comatose” survivors of OHCA were systematically excluded also from the numerous randomized trials which unequivocally demonstrated survival benefit of primary PCI in STEMI [26].

FOCUS BOX 4

Many observational cohort trials demonstrated the feasibility, safety and possible survival benefit of immediate CAG in OHCA. Four randomized trials in a subgroup of “comatose” survivors of OHCA without STEMI did not show a survival benefit of an immediate compared to selective/delayed CAG/PCI strategy. There are no published or ongoing randomized trials on immediate CAG/PCI in “comatose” survivors of OHCA with STEMI.

Selection of patients for immediate CAG/PCI

The recommendations for immediate CAG/PCI strategy in OHCA herein presented are based on the previously described randomized trials, numerous observational studies and extrapolation from interventional trials in acute coronary syndromes (ACS) without preceding cardiac arrest. Decision for immediate CAG/PCI should be based also on additional variables such as the cause of OHCA, prearrest comorbidities, time delays during prehospital resuscitation, level of consciousness on admission, post resuscitation 12-lead ECG and hemodynamic status on admission [6, 109]. All these factors should be analyzed per patient basis and the decision-making process individualized to obtain the maximal benefit and avoid futility.

“Conscious” survivors of OHCA with suspected ACS should be treated according to recommendations for STEMI and high-risk NSTE-ACS [110, 7, 110] ( Vignette 1).

The selection of patients becomes more challenging in “comatose” survivors of OHCA, who have uncertain neurological outcome which cannot be accurately predicted when the decision for immediate CAG/PCI has to be made. To facilitate the decision-making process, a practical risk score for early prediction of poor neurological outcome (MIRACLE2) has been recently developed [111]. The score is based on 7 independent early unfavorable variables including unwitnessed cardiac arrest, initial non-shockable rhythm, non-reactive pupils, age, presence of two rhythms, pH less than 7.20 and use of epinephrine during resuscitation. Based on the total MIRACLE2 score, likelihood of poor neurological outcome in “comatose” survivors with OHCA may be estimated already at hospital admission ( Figure 3).

“Comatose” survivors of OHCA with STEMI on the post resuscitation ECG should follow a “STEMI fast track” and go directly to the catheterization laboratory in the absence of significant prearrest comorbidities and unfavorable pre-hospital OHCA settings defined by a low MIRACLE2 score ( Figure 4) ( Vignette 2) [7].

In “comatose” survivors without STEMI in postresuscitation ECG, there are many other possible causes of OHCA. An “Emergency Department Stop” is therefore advised. If a non cardiac cause such as acute respiratory failure, cerebrovascular event, circulatory shock, pulmonary embolism and intoxication is identified, the patient should be admitted to intensive care unit (ICU) and treated accordingly. Patients with OHCA of presumed cardiac cause who are hemodynamically stable, should also be admitted to ICU. CAG/PCI may be performed at later stage if patient regains consciousness and adequate neurological recovery [102, 103, 104, 105]. In hemodynamically unstable patients with favorable pre-hospital course indicated by a low MIRACLE2 score and the absence of significant prearrest comorbidities, it is reasonable to consider immediate CAG/PCI as in high-risk NSTEMI ACS without OHCA [110, 110]. Immediate CAG/PCI is indicated also in patients who develop STEMI or hemodynamic instability during ICU stay if good neurological recovery may be anticipated.

FOCUS BOX 5

Selection of patients for immediate CAG/PCI should be individualized to obtain the maximal benefit and avoid futility. Several factors including the cause of OHCA, pre arrest comorbidities, time delays during prehospital resuscitation, level of consciousness, post resuscitation ECG and hemodynamic status on admission should be analyzed on a per patient basis.

PCI strategy

As expected, there is also a lack of randomized studies addressing PCI strategy and completeness of revascularization in relationship to angiographic characteristics and patient neurological/hemodynamic status on admission [5, 7]. Again, the best evidence may be obtained by extrapolation of randomized ACS interventional studies. These include PRAMI, CvLPRIT, DANAMI 3 PRIMULTI, COMPARE ACUTE and COMPLETE performed in hemodynamically stable STEMI patients [112, 113, 114, 115] and CULPRIT SHOCK in patients with multivessel disease and cardiogenic shock which also included about 50% of patients with resuscitated cardiac arrest [116]

Because there is no post resuscitation brain injury in “conscious” survivors of OHCA, PCI should be performed according to recommendations for STEMI and high-risk NSTE-ACS without cardiac arrest. Accordingly, if an acute culprit lesion is identified, it should be immediately treated [110, 7, 110]. In patients with multivessel disease, PCI of non-culprit lesions may be performed during the index intervention or as a “staged” procedure during the index hospital stay if the patient is hemodynamically stable. In patients presenting with cardiogenic shock, immediate PCI should be limited only to the culprit lesion with “staged” PCI during hospital stay if indicated. Complete revascularization by coronary artery bypass grafting (CABG) should also be considered.

In »comatose« survivors of OHCA immediate revascularization strategy should be, because of uncertain neurological recovery at the time of PCI and increased risks of stent thrombosis (ST), more conservative. ( Figure 5). A single clearly identified culprit lesion should be immediately treated by PCI ( Vignette 2 and 4). Revascularization of additional significant non-culprit lesions should not be performed during the index intervention regardless of hemodynamic status. “Staged” PCI or CABG should be considered if the patient wakes up from post resuscitation coma. This is true also for patients with significant obstructive disease with stable appearance and normal coronary flow ( Vignette 3).

FOCUS BOX 6

While PCI strategy in “conscious” survivors should follow general guidelines for patients with ACS, immediate PCI in “comatose” survivors should be focused only on the acute culprit lesion if present.

It is important to emphasize that also angiographic absence of significant coronary disease is an important finding because it should trigger further search for alternative causes of OHCA ( Vignette 5). If an alternative cause of OHCA is not identified, coronary artery spasm should be considered as a possible trigger [117, 118]. Accordingly, if the patient survives without significant neurological sequelae, coronary artery spasm provocation test may be considered during a staged CAG using either intracoronary acetylcholine or ergonovine [119, 120]. Moreover, optical coherence tomography, which may reveal by CAG invisible ruptured coronary plaques, may also be performed. It is, however, currently unclear how to treat such lesions on top of the optimal medical therapy.

Procedural considerations

Since radial access reduces mortality in the subgroup of patients with STEMI without OHCA [121], it should probably be used as the default strategy also in OHCA if the operator is experienced and if the radial pulse is present. However, femoral access may have an advantage in hemodynamically unstable patients with weak/absent radial pulsations who may require concomitant or post procedural implantation of a percutaneous assist device.

Differentiation between an acute and a chronic total occlusion may sometimes be difficult. In addition to postresuscitation ECG, probing with a soft wire is an easy method to distinguish the duration of the occlusion. In case of fresh thrombus, workhorse soft guidewire usually crosses the occlusion easily in contrast to chronic total occlusion where crossing most often fails.

There is no published data regarding the use of manual thromboaspiration specifically in OHCA which should therefore be used only at the discretion of the operator and not routinely.

Contemporary drug eluting stents should be preferred since they are less likely to be associated with ST.

Anticoagulation and antiplatelet therapy

PCI with stenting is obviously associated with the need for anticoagulation and dual antiplatelet therapy. In “conscious” survivors of OHCA, this treatment should be used according to the current guidelines [7, 110].

In “comatose” survivors, who are at high risk for bleeding due to chest compression and intubation, there is obviously a lack of adequate outcome studies. Intravenous administration of acetylsalicylic acid and unfractionated heparin (UFH) is generally advised if immediate PCI is decided after the assessment of coronary anatomy. Since P2Y12 inhibitors are available only in tablets, administration of crushed tablets via a nasogastric tube remains the only option and should be performed as soon as possible after PCI [7, 110]. Early post-resuscitation state and ongoing targeted temperature management significantly affect clopidogrel absorption and metabolism leading to delayed onset of action with suboptimal or even absent platelet inhibition as long as 48 hours after administration [122, 123]. This clopidogrel shortcoming may be overcome with novel P2Y12 agents and especially ticagrelor, which is not a prodrug and does not require metabolic activation. Despite significantly improved platelet inhibition with ticagrelor [124, 125], there is, however, still a 2-4 hour “gap” of suboptimal platelet inhibition after administration. In cases of high thrombotic burden, complex stenting, or “bail out” situations, a GP llb/llla inhibitors may still be considered. GP llb/llla inhibitor induces an immediate and profound platelet inhibition lasting up to 22 hours [126]. Even a bolus of GP llb/llla without additional infusion might be sufficient to bridge the delayed effect of P2Y12 inhibitors. However, profound inhibition in platelet reactivity should always be weighed against the increased risk of significant post resuscitation bleeding. In this context, a new intravenous agent, cangrelor administered as a bolus followed by 4-hour infusion, with rapid “onset-offset” platelet inhibition may be the preferred drug to bridge the gap between ticagrelor/prasugrel administration and onset of adequate platelet inhibition [127].

FOCUS BOX 7

Anticoagulation/antiplatelet treatment in “conscious” survivors of OHCA should be used according to the current guidelines. In “comatose” survivors intravenous of acetylsalicylic acid and unfractionated heparin are advised. Novel P2Y12 inhibitors and especially ticagrelor, should be administered as crushed tablets via a nasogastric tube. Because of an increased risk of bleeding, GP llb/llla inhibitors should be used only in “bail out” situations.

ST in “comatose” survivors of OHCA

“Comatose” survivors of OHCA are at increased risk for acute and early ST which increases cardiac mortality before potential neurological recovery may be expected. The reported incidence of ST vary widely from 2.5% up to 31% ( Table 2) [35], [128, 129, 130, 131]. The main reason for such variation is probably related to the difficulties in the ST diagnosis since patients are comatose and cannot report chest pain which would prompt repeat 12-lead ECG. In addition, there is a significant heterogeneity in PCI strategy and extent of stenting, selection and timing of dual antiplatelet therapy as well as in use of GP llb/llla inhibitors and cangrelor. Because timely diagnosis of ST is of paramount importance, continuous monitoring of 12- lead ECG if feasible is recommended, or at least routine recording every 4-6 hours until consciousness is regained. New or recurrent ST-elevation, unexplained hemodynamic instability or recurrent malignant arrhythmias including cardiac arrest should prompt immediate redo CAG and PCI if ST is confirmed. Increased incidence of ST, on the other hand, also supports an index PCI strategy focused only on the acute culprit lesion avoiding stable lesions and complex multivessel stenting.

FOCUS BOX 8

“Comatose” survivors of OHCA are at increased risk for ST. New or recurrent ST-elevation, unexplained hemodynamic instability or recurrent malignant arrhythmias including cardiac arrest should prompt immediate redo CAG and PCI if needed.

Invasive hemodynamic support

The role of hemodynamic support in patients with OHCA and cardiogenic shock has not been specifically studied although feasibility, safety and potential benefit of the intraaortic balloon pump (IABP) has been demonstrated survivors of OHCA. [34]. In contrast, the randomized SHOCK IABP trial, which enrolled >40% of patients with resuscitated OHCA and cardiogenic shock, did not demonstrate the benefit of IABP [132]. In the absence of proven benefit, routine implantation of IABP can therefore not be recommended and should be decided on an individual basis. This is true also for active devices including Impella™, TandemHeart™ and VA ECMO. Because of invasiveness, increased complication rates and high cost, these devices may be considered for unstable “conscious” survivors of OHCA and for those “comatose” survivors with a high likelihood of neurological recovery and absence of severe pre-arrest comorbidities.

FOCUS BOX 9

The use of IABP and active devices including Impella™, TandemHeart™ and VA ECMO for severe post resuscitation cardiogenic shock should be decided on an individual basis considering the likelihood of neurological recovery and absence of severe pre-arrest comorbidities.

Refractory cardiac arrest

In patients with refractory OHCA, ongoing ACLS and no ROSC, there are only case reports or small case series of successful PCI during chest compression. Since there is an obvious publication bias to mainly report series with survivors [133], this strategy cannot be recommended in clinical routine. It may be used in selected patients and in situations when cardiac arrest occurs in the catheterization laboratory. Such combined CAG/PCI/ACLS procedure must be performed by experienced interventional cardiologists and ICU physicians with good coordination during the procedure.

A more attractive option in carefully selected patients with refractory OHCA is immediate implantation of an active circulatory assist device such as VA ECMO known as E-CPR [134, 135], or even Impella™[136]. Active support device may promptly restore perfusion, allow for subsequent CAG and PCI and bridge until the recovery of cardiac function. Successful percutaneous implantation of VA ECMO in catheterization laboratory is feasable and safe ( Vignette 3) [95, 137, 138]. ECMO cannulas are implanted using a standard percutaneous Seldinger technique and fluoroscopy guidance ( Video 5) [137]. A much more demanding option is pre-hospital E-CPR which may be achieved only by dedicated and very skilled teams using a surgical cut down technique ( Vignette 4) [139].

A phase two, single centre, open-label randomized ARREST trial performed in 30 patients with refractory OHCA with ventricular fibrillation brought to hospital after 50 minutes of unsuccessful prehospital resuscitation showed improved hospital survival in the E-CPR group (6/14 versus1/15 in standard ACLS group) which persisted also after 6 months [19]. After enrolling 30 patients, the study was terminated by the Data Safety Monitoring Board because the posterior probability of E-CPR superiority exceeded the prespecified monitoring boundary. Much larger Prague OHCA trial randomized 256 patients to either intra-arrest transport, E-CPR and CAG/PCI or regular ACLS continued on site [20]. Although there was no statistically significant difference in the primary endpoint of survival with good neurological outcome at 180 days (31.5% versus 22.0%; p=0.09), E-CPR strategy significantly improved neurological outcome at 30 days (30.6% versus 18.2%; p=0.02). Potential benefits of this strategy are being further addressed by an ongoing randomized controlled trial INCEPTION [140]

We believe that in the absence of unequivocally positive randomized trials, E-CPR strategy should be used only in experienced cardiac arrest centers and in carefully selected patients without major prearrest comorbidities and optimal course of prehospital “Chain of survival” ( Figure 6).The prerequisite for short timed delays between OHCA and VA ECMO reperfusion (≤60 minutes), which is essential for good neurological recovery, is coordination and very close cooperation between prehospital emergency, interventional cardiology and ICU teams.

FOCUS BOX 10

For patients with refractory cardiac arrest, immediate implantation of VA ECMO (E-CPR) followed by CAG/PCI may be life-saving. This strategy may be applied in experienced cardiac arrest centers and in carefully selected patients without major prearrest comorbidities, optimal prehospital “Chain of survival” and expected delay between OHCA and VA ECMO reperfusion of ≤60 minutes.

Interventional cardiologists as “Cardiac Arrest Team” member

The interventional cardiologist should be an essential member of a multidisciplinary team for OHCA treatment which starts with educated lay-bystander on the field and continues through prehospital EMS which transports the patient either to the emergency department or directly to the catheterization laboratory ( Figure 7). The interventional cardiologist is in charge of CAG, PCI, implantation of invasive hemodynamic support as well as for E-CPR in carefully selected patients with refractory cardiac arrest. An ICU specialist, taking care of concomitant intensive care procedures, should join the interventional team already in the catheterization laboratory.

The history and evolution of primary PCI for STEMI shows that there is a need to centralize the care of patients with OHCA to a high volume “24-7” interventional cardiology service and a skilled ICU offering contemporary management. ICU should be closely linked to other hospital services which include electrophysiology, cardiovascular surgery, neurophysiology/imaging and other subspecialties if needed ( Figure 8). Indeed, there is evidence that patients with OHCA admitted to specialized cardiac arrest centers have improved outcomes [141, 142]. Last but not at least, following hospital discharge of an OHCA survivor, there is currently an unmet need in most countries for special rehabilitation programs and facilities which would allow these patients to return to their social environment in optimal conditions.

FOCUS BOX 11

The interventional cardiologist who is charge of CAG, PCI, implantation of invasive hemodynamic support as well as for E-CPR in selected patients, is an essential member of a multidisciplinary team for OHCA treatment.

Conclusion

The interventional management of OHCA is a vital component of post-resuscitation care. Immediate coronary angiography is indicated in case of STEMI but should not be done routinely in no STEMI patients. Further studies are required to better define this more heterogenous group and to prove the effectiveness of mechanical circulatory support in certain patient populations after OHCA.

Personal perspective | Marko Noc

In 1997, a landmark study published in the New England Journal of Medicine identified acute coronary occlusion or unstable coronary lesions as the main cause of OHCA and suggested that PCI could improve survival [6]. Despite this major finding, survivors of OHCA were too long the “forgotten orphans” of interventional cardiology. It required additional independent observational cohort trials and subsequent meta-analyses showing the feasibility, safety and a possible survival benefit of immediate CAG, followed by PCI if necessary, for a gradual adoption of invasive coronary strategy. Because of lack of randomized trials at that time and difficulties in selecting appropriate patients, an EAPCI/SFL consensus document was published in 2014. Using the existing data, this consensus provided initial guidelines for invasive coronary strategies in OHCA. It also defined more precisely the role of interventional cardiologists in the multidisciplinary OHCA team. Following the publication of several randomized trials during the last years including COACT [102], PEARL [103], TOMAHOWK [104] and EMERGE [105], interventional management of OHCA could have been further reshaped as herein presented.

Nowadays, the OHCA treatment pathway is merging with STEMI-primary PCI networks. The history and evolution of primary PCI for STEMI shows that there is a need to centralize the care of patients with OHCA to hospitals of excellence with a high-volume “24-7” interventional cardiology service, an ICU, on-site cardiac and vascular surgery with a cardiac assist program, and an integrated electrophysiology department. Such specialized cardiac arrest centers with skilled interventional cardiologists, performing fluoroscopy-guided percutaneous implantation followed by CAG and PCI, are also essential for treatment of the newly emerging refractory OHCA patients without ROSC on the field who are candidates for E-CPR strategy which may be lifesaving also for in-hospital cardiac arrest, especially if it occurs in the catheterization laboratory [138].

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