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Cardiac Arrhythmias in Acute Coronary Syndromes: Position Paper from the Joint EHRA, ACCA, and EAPCI Task Force

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Cardiac Arrhythmias in Acute Coronary Syndromes: Position Paper from the Joint EHRA, ACCA, and EAPCI Task Force FOCUS ARTICLE Euro Intervention 2014;10-online publish-ahead-of-print August 2014 Cardiac arrhythmias in acute coronary syndromes: position paper from the joint EHRA, ACCA, and EAPCI task force Bulent Gorenek*† (Chairperson, Turkey), Carina Blomström Lundqvist† (Sweden), Josep Brugada Terradellas† (Spain), A. John Camm† (UK), Gerhard Hindricks† (Germany), Kurt Huber‡ (Austria), Paulus Kirchhof† (UK), Karl-Heinz Kuck† (Germany), Gulmira Kudaiberdieva† (Turkey), Tina Lin† (Germany), Antonio Raviele† (Italy), Massimo Santini† (Italy), Roland Richard Tilz† (Germany), Marco Valgimigli¶ (The Netherlands), Marc A. Vos† (The Netherlands), Christian Vrints‡ (Belgium), and Uwe Zeymer‡ (Germany) Document Reviewers: Gregory Y.H. Lip (Review Coordinator) (UK), Tatjania Potpara (Serbia), Laurent Fauchier (France), Christian Sticherling (Switzerland), Marco Roffi (Switzerland), Petr Widimsky (Czech Republic), Julinda Mehilli (Germany), Maddalena Lettino (Italy), Francois Schiele (France), Peter Sinnaeve (Belgium), Giueseppe Boriani (Italy), Deirdre Lane (UK), and Irene Savelieva (on behalf of EP-Europace, UK) Introduction treatment. Atrial fibrillation (AF) may also warrant urgent treat- It is known that myocardial ischaemia and infarction leads to severe ment when a fast ventricular rate is associated with hemodynamic metabolic and electrophysiological changes that induce silent or deterioration. The management of other arrhythmias is also based symptomatic life-threatening arrhythmias. Sudden cardiac death is largely on symptoms rather than to avert progression to more seri- most often attributed to this pathophysiology, but many patients sur- ous arrhythmias. Prophylactic antiarrhythmic management strate- vive the early stage of an acute coronary syndrome (ACS) reaching gies have largely been discouraged. a medical facility where the management of ischaemia and infarc- Although the mainstay of antiarrhythmic therapy used to rely on tion must include continuous electrocardiographic (ECG) and hemo- antiarrhythmic drugs (AADs), particularly sodium channel blockers dynamic monitoring, and a prompt therapeutic response to incident and amiodarone, their use has now declined, since clinical evidence sustained arrhythmias. During the last decade, the hospital locations to support such treatment has never been convincing. Therapy for in which arrhythmias are most relevant have changed to include the acute coronary syndrome and arrhythmia management are now cardiac catheterization laboratory, since the preferred management based increasingly on invasive approaches. The changes in the of early acute ACS is generally interventional in nature. However, clinical approach to arrhythmia management in ACS have been so a large proportion of patients are still managed medically. substantial that the European Heart Rhythm Association, the Acute Both atrial and ventricular arrhythmias may occur in the set- Cardiovascular Care Association and the European Association of ting of ACS and sustained ventricular tachyarrhythmias (VAs) Percutaneous Cardiovascular Interventions established a task force may be associated with circulatory collapse and require immediate to define the current position. DOI: 10.4244/EIJY14M08_19 * Corresponding author: Prof. Bulent Gorenek MD FACC FESC, Eskisehir Osmangazi University Cardiology Department, Eskisehir, Turkey. Tel: +90 222 2292266; Fax: +90 222 2292266. E-mail: [email protected] † EHRA. ‡ ACCA. ¶ EAPCI. Developed in partnership with the European Heart Rhythm Association (EHRA), the Acute Cardio- vascular Care Association (ACCA), and the European Association of Percutaneous Cardiovascular Interventions (EAPCI). The article has been co-published with permission in EP-Europace, European Heart Journal - Acute Cardiovascular Care and EuroIntervention. All rights reserved in respect of European Heart Journal - Acute Cardiovascular Care and EuroIntervention. © The Authors 2014. For EP-Europace, © The Author 2014. 1 Euro Intervention Mechanisms of ischaemia-related ventricular cardioversion (CV)/defibrillation and management of acute volume arrhythmias overload were the principal life-saving measures in the coronary Generation of the ventricular action potential by voltage and sub- care units before the advent of reperfusion therapies, beta-block- 2014;10-online publish-ahead-of-print August 2014 strate dependent ion currents is the basis for the contraction of each ers, antithrombotic therapy, and statins.6 The electrical changes in individual myocardial cell. This ionic balance can be disturbed by acutely ischaemic myocardium, and especially in the border zone insults, such as ischaemia/reperfusion. of an evolving MI, initiate and maintain these arrhythmias (see Arrhythmogenesis early in the course of an ACS, manifested as above). Prompt and adequate revascularization therapy, usually by often polymorphic ventricular tachycardia (VT) or ventricular fibril- interventional reopening of occluded vessels and stabilization of lation (VF) is observed in a minority of patients with acute ischaemia the culprit lesion with a stent, combined with initiation of adequate and is often associated with genetic predisposition.1 Incidence of in- secondary prevention therapies (statin, dual antiplatelet therapy, hospital mortality due to acute heart failure or VT/VF has declined beta-blockers, angiotensin-converting enzyme inhibitors, angioten- markedly with the widespread use of reperfusion strategies. sin receptor blockers) aimed at preventing subsequent acute coro- Acute myocardial ischaemia leads to adenosine tri-phosphate nary events,4 have markedly reduced these life-threatening events deficiency, anaerobic glycolysis causing acidosis, elevation of in modern coronary care units. Patients who present with sustained extracellular potassium (K+), and lysophosphatidylcholine accu- VA in the first few days after a MI can hence be characterized by the mulation. This multifactorial sequence of events results electro- following features, summarized in Figure 1: physiologically in (i) ionic imbalance: (a) shorter duration of the (1) Late presenters (i.e. patients in whom reperfusion therapy was action potential by activation of the substrate related potassium cur- delayed due to an insufficient chain of care from first onset of rent: IKatp and (b) less reduced resting membrane potential through symptoms to transfer to an acute coronary care centre, or long inhibition of the inward rectifying potassium current: IK1; (ii) less patient-related delay, severe acute ischaemia in Figure 1). contractile force by events that culminate in the mishandling of (2) Patients in whom revascularization was not or only partially intracellular calcium (Ca2+); and (iii) a reduced conduction velocity successful due to technical difficulties (severe acute ischaemia because of less functional gap junctions.2 in Figure 1). Myocardial reperfusion may cause profound electrophysiologi- (3) Patients who carry an arrhythmogenic substrate prior to the cal alterations, dependent on the prior duration of ischaemia. A VT acute event, either due to a prior infarction or due to a predispo- occurs more frequently with increasing duration of ischaemia, but sition to electrophysiological instability (‘pre-existing myocar- later in the course of an ACS, and with extensive myocardial dam- dial damage’ in Figure 1). age, the incidence of VT declines. Important contributors involved in arrhythmogenesis are the Na+/Ca2+ exchange pump, the slowly LATE PRESENTERS activating delayed rectifier K+ current and phosphorylation of sar- Even in highly developed healthcare systems, only 70-80% coplasmic reticulum proteins by CAMKII (calcium and calmodulin- of patients who present with ST-elevation myocardial infarc- dependent protein kinase II).3 The intracellular Ca2+ overload (among tion (STEMI) receive reperfusion therapy.7 Some patients never others caused by reactive oxidative stress) will result in spontane- reach out for help to the healthcare system, while the diagnosis is ous Ca2+ oscillations (calcium overload paradox) that trigger early delayed in others. Yet others will present with VF or syncope as the and delayed after depolarizations induced ectopic beats. In addition, initial sign of the acute event, necessitating adequate resuscitation. they will contribute to spatial and temporal dispersion of repolari- High maximal creatine kinase (CK) values, Q waves on the ECG, zation (variation in the action potential duration) and to re-entrant markedly reduced left ventricular (LV) function in the sub-acute arrhythmias based on unidirectional conduction block, fractionation phase after a MI and a long history of symptoms attributable to the of cellular electrograms, and short action potential durations. For infarct prior to first treatment are good markers for these patients arrhythmogenic mechanisms, the currents flowing from the ischae- once they have reached the hospital. Patients at high risk in the mic/reperfused to the non-ischaemic zones are most important. setting of an ACS, easily assessed by clinical risk scores such as The mechanisms responsible for the initiation of these VA may dif- GRACE or TIMI,8-12 are likely to suffer from larger myocardial fer based on the underlying disease (Figure 1)4: (intramural) re-entry damage, especially when the ECG shows prominent ischaemic in ischaemia, whereas triggered activity appears to be the dominant changes, the patient presents with persistent symptoms after initia- mechanism in reperfusion.5 Also when looking at the responsible tion
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