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Editorial Out-of-Hospital Cardiac Arrest Getting Beyond the Tip of the Iceberg Leonard Ilkhanoff, MD, MS; Jeffrey J. Goldberger, MD, MBA Sudden Cardiac Death: The Scope Article see p 815 Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017 Sudden cardiac death (SCD), which is responsible for approximately 300 000 deaths in the United States, refers to an unexpected death from a cardiovascular cause in a person with or without preexisting heart disease. Most studies include cases that are associated with death occurring within 1 hour of an acute change in clinical status or an unexpected death that occurred within the previous 24 hours,1 but this definition is not specific for sudden arrhythmic death. The most common sequence of events leading to arrhythmic SCD is the degeneration of ventricular tachycardia (VT) into ventricular fibrillation (VF), often followed by asystole or pulseless electric activity. The transition of shockable rhythms (VT/VF) to more ominous rhythms such as asystole or pulseless electric activity depends on various factors, but is highly dependent on time; the longer the time interval, the more likely the VT/VF degenerates to pulseless electric activity or asystole. Although VF and VT together represent the initial rhythm in half of all outpatient cardiac arrests, data suggest that with each passing minute of untreated VF, the likelihood of survival is reduced by 7% to 10%.2 Preexisting coronary artery disease and its sequelae (eg, acute myocardial ischemia, scarring from previous myocardial infarction, heart failure) are manifest in 80% of SCDs.3 Dilated nonischemic and hypertrophic cardiomyopathies account for the second largest number of SCDs, whereas other cardiac disorders such as congenital heart disease and underlying genetically determined ion channel anomalies account for 5% to 10% of SCDs.3 Although the cascade of events triggering SCD are complex and are currently active areas of investigation, the general goals of reducing SCD are focused on (1) identifying and preventing sudden death in high-risk individuals by using efficacious therapies such as medications and implantable cardioverter defibrillators (ICDs), (2) organizing resuscitation services to improve response to and efficiency and effectiveness of treatments directed to individuals who experience cardiac arrest, and (3) improving survival rates for individuals who experience SCD by implementing and organizing specialized services at hospitals that deliver postresuscitation care. Multifaceted approaches have been implemented to reduce the number of SCDs. In this issue of Circulation, Hulleman et al4 assess the role of ICDs in reducing the incidence of resuscitation for out-of-hospital cardiac arrest (OHCA) caused by lethal ventricular arrhythmias, the specific target for ICD therapy. They found that the incidence of VF-OHCA decreased during a 10-year period in north Holland from 21.1/100 000 inhabitants per year to 17.4/100 000 inhabitants per year, and that ICD therapy likely explained approximately one third of this decrease (1.2/100 000 inhabitants per year). Interestingly, the incidence of non-VF-OHCA increased during the same time period from 12.2/100 000 inhabitants per year to 19.4/100 000 inhabitants per year, leading to an overall increased rate of OHCA. Although many assumptions are made in this report, any one of which could affect the results, the sensitivity analyses as well as concordance with other data5– 8 suggest that these estimates have substantial validity. This validity enables us to use these important data to provide a global perspective on the tremendous efforts that have been put forth during the past several decades on prevention of SCD. SCD Prevention Response to OHCA Hulleman et al4 note that the decline in VF-OHCA is modest overall, ⬇ 17.5%, which highlights the continued need for efforts to improve our response to OHCA. Many countries have identified areas to improve OHCA treatment. Efforts focus on best practices in resuscitation medicine and emphasize the need for continuous quality improvement in processes of care that may translate to improved outcomes for patients with OHCA. This chain of survival includes dissemination of knowledge to improve delivery of bystander cardiopulmonary resuscitation, increasing the distribution and early use of automated external defibrillators in highly trafficked areas such as malls and airports, and rapid emergency medical services activation and time to initiation of resuscitation efforts.9 Despite these advances in out-of-hospital cardiopulmonary resuscitation, survival to hospital discharge after cardiac arrest in most major metropolitan centers in the United States remains poor. Survival to hospital discharge was recently estimated to be 5% to 10% among OHCAs that were treated by emergency medical services personnel.9,10 In addition, the majority of SCDs occur at home, often where the event is unwitnessed. As a result, automated external defibrillators, which improve resuscitation rates for witnessed arrests,11 may The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association. From the Northwestern University Feinberg School of Medicine & Bluhm Cardiovascular Institute, Chicago, IL. Correspondence to Jeffrey J. Goldberger, MD, Northwestern University Feinberg School of Medicine, Division of Cardiology, 251 East Huron, Feinberg Pavilion 8-503, Chicago, IL 60611. E-mail [email protected] (Circulation. 2012;126:793-796.) © 2012 American Heart Association, Inc. Circulation is available at http://circ.ahajournals.org DOI: 10.1161/CIRCULATIONAHA.112.123588 793 794 Circulation August 14, 2012 Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017 have limited effectiveness in reducing overall mortality from SCD. Delays in emergency medical services (personnel reaching a witnessed SCD individual, not having an automated external defibrillators readily available, and not initiating immediate cardiopulmonary resuscitation) may contribute to rapid deterioration of a life-threatening ventricular tachyarrhythmia to asystole. More important, unwitnessed SCD carries a grave prognosis, largely because the time to resuscitative efforts is delayed and resuscitative efforts may not even be initiated in one third of cases.10 –12 It is important to note that improvement in postarrest therapies and approaches are not likely to influence the number of OHCAs, only the outcome. Although there are significant limitations in delivering optimal services to individuals with OHCA, some metropolitan areas that have adopted organized approaches to resuscitative medicine have shown that overall rates of survival from OHCA—in particular, witnessed VF— can improve over time.9,10 Time to first shock has averaged 6 minutes in Rochester, MN, and between 2006 and 2008, survival to hospital discharge for bystander-witnessed events in which individuals presented with VF exceeded 50%.9 Prevention of OHCA These coordinated efforts to provide rapid response to SCD individuals are complemented by approaches to prevent SCD. Prevention requires a synergy of efforts, including proper medical therapy and ICD placement in appropriate high-risk individuals. The work by Hulleman et al4 is important because it, specifically, places into context the role of ICDs in reducing VF-OHCA in light of important changes in the epidemiology of disease and other factors in north Holland. Because ICD use explained only 33% of the reduced incidence of VF-OHCA in this study, the implication is that additional factors are significant contributors to the decline in VF-OHCA incidence. Medication Use Improved use of medical therapies such as -blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, potassium-sparing diuretics, and polyunsaturated fatty acids that may affect SCD likely have had an impact on the declining incidence of VF-OHCA. These therapies most likely confer their antiarrhythmic potential indirectly by inhibiting or delaying adverse structural remodeling in a diseased heart, and by modulating upstream inflammatory and neurohormonal pathways, thereby contributing to electrophysiological stability.13 Specifically, Hulleman et al4 point out that -blocker use, which has been reported to decrease sudden death by as much as 50%, may have reduced the incidence of VF. Yet, there are potentially important ramifications of these therapies, particularly in light of the reported increase in non-VF-OHCA. Individuals taking -blockers who experienced OHCA were 5 times more likely to present with non-VF than VF as the first documented rhythm. A recent trial using implantable loop recorders in myocardial infarction patients with left ventricular dysfunction reported that VF and bradyarrhythmias accounted for equal proportions of recordings at the time of death. Even though VT/VF was the terminal rhythm and was associated primarily with SCD, intermittent high- degree atrioventricular block was also a strong predictor of cardiac death.14 It is conceivable that -blockers not only reduce the incidence of VT/VF, but also may alter the electrophysiological milieu in such a manner as to convert VF-OHCA events to non-VF events. Further efforts to ensure proper medical therapy and to understand the interactions of medical therapy with the diverse mechanisms of SCD are necessary. Declines in Coronary Heart Disease Rates A second potential reason for reduction in VF-OHCA incidence is a concomitant decline in coronary heart disease (CHD) burden over time. This decline can likely be explained by improvements in diagnosis and treatment of comorbidities associated with CHD, such as diabetes mellitus, hypertension, and dyslipidemia, and improved targeted therapies and interventions for CHD. Because CHD is the leading cause of SCD in the world, a decline in CHD rates should parallel the reduction in VF-OHCA rates to some degree. As Hulleman et al4 note, the decline in VF-OHCA may also be attributed to other changing biological mechanisms in the population at risk for VF. Future Approaches to OHCA The impact of the ICD in reducing the population-based problem of SCD is clearly significant, but is far from enough. Certainly one of the factors limiting the population impact of ICDs is the consistent finding that most individuals who experience SCD fall outside the current guidelines for consideration of an ICD. Substantial impact on VF-OHCA can be achieved by improving our ability to identify individuals at risk for SCD prior to them experiencing a life-threatening event. More important, enhancing our risk stratification armamentarium of tools, genetic markers, and other techniques to provide adequate discriminatory power to manage individuals requires rigorous and ongoing research.15 Although the field of risk stratification for the prevention of SCD is currently focused on using certain approaches to identify appropriate ICD candidates, the importance of this research endeavor transcends this specific treatment. Individuals found to be at significant risk for SCD could be treated with a host of therapies, including lifestyle modifications (ie, exercise, diet), more aggressive medical therapy, and newer medical or other novel therapies. Examples of the latter could include vagus nerve stimulators or spinal cord stimulators meant to modulate the autonomic nervous system effects on the heart. The final challenge in addressing the vast public health problem of SCD is that, in a sizable percentage of individuals, SCD is the first manifestation of cardiac disease.16 Improved public education and screening for cardiovascular disease are modalities that may impact SCD in this subpopulation. Because of the number of susceptible individuals who would not be identified as candidates for an ICD using current guideline approaches, it remains important to continue to focus on rapid identification and efficient response systems to OHCA, and successful restoration of spontaneous circulation. Continued improvements in this field, such as greater dissem- Ilkhanoff and Goldberger Out-of-Hospital Cardiac Arrest 795 Figure. The universe of out-of-hospital cardiac arrest (OHCA) is divided into those with ventricular fibrillation (VF) and non-VF arrest, with slightly higher prevalence of the latter based on Hulleman et al.4 Within each major mode of OHCA, there are opportunities for improved prevention (the middle slices) and improved response (the top 2 slices), with some of the potential approaches listed. In some cases (the bottom 2 slices), OHCA is a terminal event for which no preventive or response measures could be effective (Zone of futility). The size of the slices are meant to be relative, not absolute. For example, more non-VF-OHCAs are likely terminal events than VF-OHCAs, and there is greater opportunity for prevention of VF-OHCA than nonVF-OHCA. EMS indicates emergency medical services; AED, automated external defibrillator; CPR, cardiopulmonary resuscitation; and ACLS, advanced cardiac life support. Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017 ination of automated external defibrillators, rapid and early cardiopulmonary resuscitation, the development and implementation of hypothermia protocols, and other systems of care will also further impact SCD outcomes and lead to improved survival rates in OHCA.9,10 In Philadelphia, for example, a comprehensive multidisciplinary treatment protocol for patients resuscitated from OHCA and its implementation led to survival rates that improved from 22% to ⬎50%.9 The future clearly holds significant opportunity to reduce the population burden of OHCA (Figure). Our greatest opportunity appears to stem from unlocking the mechanisms and triggering events leading to VF in at-risk individuals and disseminating appropriate therapies to limit this risk. Our greatest challenge may be in preventing and treating non-VF-OHCA, for which the triggering events for SCD remain elusive. Because non-VF-OHCA represents a sizable portion of all OHCAs, a better understanding of this mode of SCD and its precursors is required to have a tangible impact. The future, as suggested by Hulleman et al,4 may bring further shifts in OHCA from VF to non-VF cases. Improvements in risk stratification and identification of individuals as appropriate candidates for medical and device therapy, advancements in medical therapy to limit progression of cardiac disease, and enhancements in resuscitative services collectively will lead to incremental and continued declines in the incidence of VF-OHCA and overall SCD rates. Further studies are necessary to continue to track the epidemiological impact of all these efforts on OHCA. Disclosures Dr Goldberger is director of the Path to Improved Risk Stratification, a not-for-profit think tank on risk stratification for prevention of sudden cardiac death, which has received unrestricted educational grants from Medtronic, Boston Scientific, and St. Jude Medical. Dr Goldberger has received past honoraria from Medtronic, Biotronik and St. Jude Medical. Dr Ilkhanoff has received past honoraria from Biotronik and St. Jude Medical. References 1. Zipes DP, Rubart M. Neural modulation of cardiac arrhythmias and sudden death. Heart Rhythm. 2006;3:108 –113. 2. Cummins RO, Ornato JP, Thies WH, Pepe PE. Improving survival from sudden cardiac arrest: the “chain of survival” concept. Circulation. 1991; 83:1833–1847. 3. Rubart M, Zipes DP. Mechanisms of sudden death. J Clin Invest. 2005; 115:2305–2315. 4. Hulleman M, Berdowski J, de Groot JR, van Dessel PFHM, Borleffs CJW, Blom MT, Bardai A, de Cock CC, Tan HL, Tijssen JGP, Koster RW. Implantable cardioverter-defibrillators have reduced the incidence of resuscitation for out-of-hospital cardiac arrest caused by lethal arrhythmias. Circulation. 2012;126:815– 821. 5. Cobb LA, Fahrenbruch CE, Olsufka M, Copass MK. Changing incidence of out-of-hospital ventricular fibrillation, 1980 –2000. JAMA. 2002;288: 3008 –3013. 6. Bunch TJ, White RD, Friedman PA, Kottke TE, Wu LA, Packer DL. Trends in treated ventricular fibrillation out-of-hospital cardiac arrest: a 17-year population-based study. Heart Rhythm. 2004;1:255–259. 7. Herlitz J, Andersson E, Bang A, Engdahl J, Holmberg M, Lindqvist J, Karlson BW, Waagstein L. Experiences from treatment of out-of-hospital cardiac arrest during 17 years in Goteborg. Eur Heart J. 2000;21: 1251–1258. 8. Kuisma M, Repo J, Alaspaa A. The incidence of out-of-hospital ventricular fibrillation in Helsinki, Finland, from 1994 to 1999. Lancet. 2001; 358:473– 474. 9. Neumar RW, Barnhart JM, Berg RA, Chan PS, Geocadin RG, Luepker RV, Newby LK, Sayre MR, Nichol G. Implementation strategies for improving survival after out-of-hospital cardiac arrest in the United States: consensus recommendations from the 2009 American Heart Association Cardiac Arrest Survival Summit. Circulation. 2011;123: 2898 –2910. 10. McNally B, Robb R, Mehta M, Vellano K, Valderrama AL, Yoon PW, Sasson C, Crouch A, Perez AB, Merritt R, Kellerman A. Out-of-hospital cardiac arrest surveillance: Cardiac Arrest Registry to Enhance Survival (CARES), United States, October 1, 2005–December 31, 2010. Morbid Mortal Wkly Rep. 2011;60:1–19. 11. Caffrey SL, Willoughby PJ, Pepe PE, Becker LB. Public use of automated external defibrillators. N Engl J Med. 2002;347:1242–1247. 12. Bunch TJ, White RD, Gersh BJ, Meverden RA, Hodge DO, Ballman KV, Hammill SC, Shen W-K, Packer DL. Long-term outcomes of out-ofhospital cardiac arrest after successful early defibrillation. N Engl J Med. 2003;348:2626 –2633. 13. Ilkhanoff L, Kadish AH, Jacobson JT. Non-antiarrhythmic drugs in sudden death prevention. In: Gussak I, Antzelevitch C, eds. Electrical Diseases of the Heart, II. Springer Publishing; 2012. In press. 14. Bloch Thomsen PE, Jons C, Raatikainen MJ, Moerch Joergensen R, Hartikainen J, Virtanen V, Boland J, Anttonen O, Gang UJ, Hoest N, Boersma LV, Platou ES, Becker D, Messier MD, Huikuri HV, Cardiac Arrhythmias and Risk Stratification After Acute Myocardial Infarction (CARISMA) study group. Long-term recording of cardiac arrhythmias with an implantable cardiac monitor in patients with reduced ejection fraction after acute myocardial infarction: the Cardiac Arrhythmias and 796 Circulation August 14, 2012 Risk Stratification After Acute Myocardial Infarction (CARISMA) study. Circulation. 2010;122:1258 –1264. 15. Goldberger JJ, Buxton AE, Cain M, Costantini O, Exner DV, Lloyd-Jones DM, Kadish AH, Knight BP, Lee B, Moss A, Myerburg R, Olgin J, Passman R, Rosenbaum D, Stevenson W, Zareba W, Zipes DP. Risk stratification for sudden cardiac death: identifying the roadblocks. Circulation. 2011;123:2423–2430. 16. Myerberg RJ, Juntilla J. Sudden cardiac death caused by coronary heart disease. Circulation. 2012;125:1043–1052. KEY WORDS: Editorials 䡲 death 䡲 ventricular tachycardia 䡲 sudden 䡲 ventricular fibrillation Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017 Out-of-Hospital Cardiac Arrest: Getting Beyond the Tip of the Iceberg Leonard Ilkhanoff and Jeffrey J. Goldberger Circulation. 2012;126:793-796; originally published online August 6, 2012; doi: 10.1161/CIRCULATIONAHA.112.123588 Downloaded from http://circ.ahajournals.org/ by guest on June 15, 2017 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2012 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circ.ahajournals.org/content/126/7/793 Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. 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