7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Overview of sudden cardiac arrest and sudden cardiac death : Philip J Podrid, MD, FACC : Brian Olshansky, MD, Scott Manaker, MD, PhD : Nisha Parikh, MD, MPH All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Jan 27, 2023. INTRODUCTION Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity. These events mostly occur in patients with structural heart disease (that may not have been previously diagnosed), particularly coronary heart disease. (See "Pathophysiology and etiology of sudden cardiac arrest".) The event is referred to as SCA (or aborted SCD) if an intervention (eg, defibrillation) or spontaneous reversion restores circulation, and the event is called SCD if the patient dies [1]. However, the use of SCD to describe both fatal and nonfatal cardiac arrest persists by convention. The specific causes of SCA vary with the population studied and patient age ( table 1). SCA most commonly results from hemodynamic collapse due to primary ventricular fibrillation (VF) or polymorphic or monomorphic ventricular tachycardia (VT) degenerating into VF. This usually occurs in the setting of structural heart disease ( waveform 1) [2]. Less commonly, SCA may occur with bradycardia/asystole or pulseless electrical activity or electromechanical dissociation. (See "Pathophysiology and etiology of sudden cardiac arrest".) The outcome following SCA depends upon numerous factors including the underlying cause and the rapidity of resuscitation. (See "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest" and "Prognosis and outcomes following sudden cardiac arrest in adults".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 1/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate A patient is more likely to be resuscitated if they have ventricular tachycardia or VF rather than asystole or pulseless electrical activity. However, if the patient has a poorly tolerated cardiac rhythm, this may be the inevitable consequence of a dying heart. Thus, even early resuscitation may not be successful. Most individuals suffering from SCA become unconscious within seconds to minutes as a result of insufficient cerebral blood flow. There are usually no premonitory symptoms. If symptoms are present, they are nonspecific and include chest discomfort, palpitations, shortness of breath, and weakness. DEFINITIONS Various criteria have been used to define SCA and SCD [3]. Difficulties in deriving a specific definition include the following: Events are witnessed in only one-third of cases, making the diagnosis difficult to establish in many instances [4]. It is not possible to restrict the definition of SCA to documented cases of VT-VF or VF since the cardiac rhythm at clinical presentation is unknown in many cases. The duration of symptoms prior to SCA generally defines the suddenness of death. However, the duration of symptoms is unknown in approximately one-third of cases. For these reasons, operational criteria for SCA and SCD have been proposed that do not rely upon the cardiac rhythm at the time of the event. The criteria focus on the out-of-hospital occurrence of a presumed sudden pulseless condition and the absence of evidence of a noncardiac condition (eg, central airway obstruction, intracranial hemorrhage, pulmonary embolism) as the cause of cardiac arrest. The 2006 American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) to establish data standards for electrophysiology included definitions to guide documentation in research and clinical practice. The following definitions of SCA and SCD were presented: "[Sudden] cardiac arrest is the sudden cessation of cardiac activity so that the victim becomes unresponsive, with no normal breathing and no signs of circulation. If corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by CPR and/or defibrillation or https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 2/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate cardioversion, or cardiac pacing. Sudden cardiac death should not be used to describe events that are not fatal." Throughout this topic we will use the terms SCA and SCD as defined in the 2006 ACC/AHA/HRS document. However, many continue to use SCD to describe both fatal and nonfatal cardiac arrest. EPIDEMIOLOGY Death certificate data suggest that SCD accounts for approximately 13 to 15 percent of the total mortality in the United States and other industrialized countries [5,6]. However, death certificate data may overestimate the prevalence of SCD [7,8]. In a prospective evaluation of deaths in one county in Oregon, SCD was implicated in 5.6 percent of annual mortality [7]. In absolute terms, the number of sudden cardiac deaths in the United States in 2019 was approximately 370,000 [6]. Despite advances in the treatment of heart disease, the outcome of patients experiencing SCA remains poor, although the prognosis varies significantly according to the initial rhythm and underlying cardiovascular disease. (See "Prognosis and outcomes following sudden cardiac arrest in adults".) The risk of SCA is dependent on several factors [5,8,9]. The incidence increases dramatically with age and underlying cardiovascular disease, as well as specific comorbidities (eg, diabetes) ( figure 1 and figure 2). In addition, men are two to three times more likely to experience SCA than women ( figure 1). Among 161,808 postmenopausal women participating in the Women's Health Initiative who were followed for an average of 10.8 years, the rate of SCD was 2.4 per 10,000 women/year. Nearly half who had SCD did not have clinically recognized coronary heart disease [10]. The magnitude of the influence of cardiovascular disease on the risk of SCA is illustrated by several observations: The risk of SCA is increased 6- to 10-fold in the presence of clinically recognized heart disease, and two- to four-fold in the presence of coronary heart disease (CHD) risk factors [8,11]. SCD is the mechanism of death in over 60 percent of patients with known CHD [5,12,13]. In addition, SCA is the initial clinical manifestation of CHD in approximately 15 percent [14]. ETIOLOGY https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 3/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate SCA usually occurs in people with some form of underlying structural heart disease, most notably CHD ( table 1). The etiologies of SCA are discussed in detail separately, but will be briefly reviewed here. (See "Pathophysiology and etiology of sudden cardiac arrest".) Coronary heart disease The majority of SCAs have been attributed to CHD. Among patients with CHD, SCA can occur both during an acute coronary syndrome (ACS) and in the setting of chronic, otherwise stable CHD (often such patients have had prior myocardial damage and scar that serves as a substrate for SCA) [4]. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and "Incidence of and risk stratification for sudden cardiac death after myocardial infarction".) The arrhythmic mechanisms and the implications for SCA survivors are different in these two settings. (See "Prognosis and outcomes following sudden cardiac arrest in adults".) Other structural heart disease Other forms of structural heart disease, both acquired and hereditary, account for approximately 10 percent of cases of SCA. Examples of such disorders include the following: Heart failure and dilated cardiomyopathy of any etiology in which SCD is responsible for approximately one-third of deaths. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy".) Left ventricular hypertrophy due to hypertension or other causes. (See "Left ventricular hypertrophy and arrhythmia".) Myocarditis. Infiltrative cardiomyopathy (eg, cardiac sarcoid, cardiac amyloid). (See "Management and prognosis of cardiac sarcoidosis" and "Management and prognosis of cardiac sarcoidosis", section on 'Management of arrhythmias and conduction system disease' and "Amyloid cardiomyopathy: Treatment and prognosis".) Hypertrophic cardiomyopathy. (See "Hypertrophic cardiomyopathy: Risk stratification for sudden cardiac death".) Arrhythmogenic right ventricular cardiomyopathy. (See "Arrhythmogenic right ventricular cardiomyopathy: Pathogenesis and genetics".) Congenital coronary artery anomalies. (See "Congenital and pediatric coronary artery abnormalities".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 4/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Mitral valve prolapse. (See "Natural history of chronic mitral regurgitation caused by mitral valve prolapse and flail mitral leaflet".) Valvular heart disease (eg, aortic stenosis). Congenital heart disease (eg, tetralogy of Fallot). Absence of structural heart disease In different reports, approximately 10 to 12 percent of cases of SCA among subjects under age 45 without defined structural heart disease [15,16], while a lower value of about 5 percent has been described when older patients are included [17,18]. San Francisco County between February 2011 and March 2014 suggested greater than 40 percent of clinically-defined SCD was non-arrhythmic in origin, due to causes including occult overdose, neurologic disorders, infection, etc [4]. (See "Approach to sudden cardiac arrest in the absence of apparent structural heart disease".) SCA can occur due to: Brugada syndrome (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".) Idiopathic VF, also called primary electrical disease (See "Approach to sudden cardiac arrest in the absence of apparent structural heart disease", section on 'Idiopathic VF'.) Congenital or acquired long QT syndrome ( table 2) (See "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Acquired long QT syndrome: Definitions, pathophysiology, and causes".) Familial polymorphic ventricular tachycardia, also called "catecholaminergic polymorphic VT" (See "Catecholaminergic polymorphic ventricular tachycardia".) Familial SCD of uncertain cause Wolff-Parkinson-White syndrome (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Ventricular fibrillation and sudden death'.) Acute triggers In addition to the presence of the underlying disorders of structural heart disease, superimposed triggers for SCA appear to play a major role. These include ischemia, electrolyte disturbances (particularly hypokalemia and hypomagnesemia), proarrhythmic effects of some antiarrhythmic drugs, autonomic https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 5/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate nervous system activation, and psychosocial factors. (See "Pathophysiology and etiology of sudden cardiac arrest", section on 'Transient or reversible causes'.) Commotio cordis SCA can also result from commotio cordis in which VF is precipitated by direct trauma over precordium. (See "Approach to sudden cardiac arrest in the absence of apparent structural heart disease", section on 'Commotio cordis'.) Circadian pattern SCA has a circadian pattern with a reported peak during the waking hours of 7 to 11 am [19-21]. Among 5200 Framingham Heart Study participants over a 38- year period, 429 cases of SCD were 70 percent higher at 7 to 9 am than they were at other times of day or night [21]. A separate study of 1200 in- and out-of-hospital arrests in Pittsburgh showed the lowest risk of SCA was during early morning sleep hours, between 12 and 6 am [22]. The circadian pattern of SCD mirrors that of other cardiac issues (such as angina, heart failure, and other arrhythmias) that are also more common in the morning [23]. The circadian pattern may result from pineal gland secretion of melatonin-stimulating hormone, resulting in increased melatonin levels and from a morning cortisol surge. Melatonin increases vagal tone, causing lower sympathetic tone and a slower heart rate at night. Melatonin levels are lower in morning (when natural light hits retina suppressing pineal activity) and hence vagal tone is lower. At the same time, the morning cortisol surge also increases as a result of increased sympathetic tone. Warning symptoms "Warning" symptoms may precede the SCA event in a large number of patients, but symptoms may be unrecognized or minimized by patients, and subsequent ascertainment of symptoms is often limited, particularly in patients who do not survive the event. In addition, patients who have SCA and are resuscitated often have a retrograde amnesia and hence do not remember events or symptoms that may have been present. In a community- based study of 839 patients with SCA between 2002 and 2012 in whom symptom assessment could be ascertained (either from the surviving patient or from family members, witnesses at the scene of the event, or medical records from the four weeks leading up to the event), 430 patients (51 percent) were identified as having warning symptoms within four weeks preceding SCA [24]. Eighty percent of patients experienced symptoms at least one hour before SCA, with 34 percent having symptoms more than 24 hours before SCA. Chest pain (46 percent) and dyspnea (18 percent) were the most common symptoms, with women more likely to have experienced dyspnea than chest pain (31 versus 24 percent). Patients with symptoms concerning for cardiac disease, particularly new or unstable symptoms, should seek prompt medical care for potentially life-saving evaluation and treatment. (See "Outpatient evaluation of the adult with chest pain", https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 6/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate section on 'Cardiac conditions' and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".) As symptoms are nonspecific and may reflect benign conditions, and as these symptoms may not necessarily occur before all episodes of cardiac arrest (insensitive), their presence may not be of value in helping offset or prevent episodes. A causal or temporal relationship between symptoms and sudden death has not been established. RISK FACTORS A number of clinical characteristics and other factors are associated with an increased risk of SCA among persons without prior clinically recognized heart disease [25-30]. It should be noted that these risk factors are neither specific nor highly sensitive for SCA prediction. Most risk factors for CHD are also risk factors for SCA. These include dyslipidemia, hypertension, cigarette smoking, physical inactivity, obesity, diabetes mellitus, and a family history of premature CHD or myocardial infarction ( figure 3) [10,25-27,31,32]. (See "Overview of established risk factors for cardiovascular disease".) Cigarette smoking Current cigarette smoking and the number of cigarettes smoked per day among current smokers are strongly related to the risk of SCA in patients with CHD. As an example, among 101,018 women followed for 30 years in the Nurses' Health Study, current smokers had a significantly greater risk of SCD than women who had never smoked (adjusted hazard ratio 2.44, 95% CI 1.80-3.31), and there was an increased risk even among those women who smoked 1 to 14 cigarettes per day (adjusted hazard ratio 1.84, 95% CI 1.16-2.92) [33]. For women in this study who stopped smoking, the risk of SCD declined over time in a linear fashion; these women had the same risk of SCD as never smokers 20 years after quitting [33]. Based upon the observations that the risk of SCA is particularly high among current smokers and declines rapidly after stopping smoking, smoking cessation should be viewed as a critical component of efforts to reduce the risk of SCA as well as a multitude of other complications. (See "Cardiovascular risk of smoking and benefits of smoking cessation" and "Overview of smoking cessation management in adults".) Exercise The risk of SCA is transiently increased during and up to 30 minutes after strenuous exercise compared to other times [27,34]. However, the actual risk during any one episode of vigorous exercise is very low (1 per 1.51 million episodes of exercise) [34]. Furthermore, the magnitude of the transient increase in risk during acute exercise is lower among men who are regular exercisers compared with men for whom exercise is unusual [27,34]. (See "The benefits and risks of aerobic exercise".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 7/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate The small transient increase in risk during exercise is outweighed by a reduction in the risk of SCA at other times [25,35]. Regular exercise is associated with a lower resting heart rate and increased heart rate variability, characteristics associated with a reduced risk of SCD. (See "Exercise and fitness in the prevention of atherosclerotic cardiovascular disease".) One exception to the lower overall risk associated with intensive exercise occurs in patients with certain, often unrecognized underlying heart diseases. Examples include hypertrophic cardiomyopathy, anomalous coronary artery of wrong sinus origin, myocarditis, and arrhythmogenic right ventricular cardiomyopathy [36,37]. (See "Athletes: Overview of sudden cardiac death risk and sport participation".) Family history of SCA A family history of SCA, either alone or with myocardial infarction, is associated with a 1.5 to 1.8-fold increased risk of SCA [26,32]. The increase in risk is not explained by traditional risk factors that tend to aggregate in families, such as hypercholesterolemia, hypertension, diabetes mellitus, and obesity. The magnitude of the increase in risk associated with the presence of a family history is modest compared to the two- to five-fold increase in risk associated with other modifiable risk factors such as physical inactivity and current cigarette smoking. Few studies have examined potential gene-environment interactions related to the risk of SCD. Nevertheless, it is likely that interactions of mutations or polymorphisms in specific genes and environmental factors influence this risk. Diabetes Among patients with diabetes, type 1 diabetes was more strongly associated with SCA compared with type 2 diabetes and had less favorable outcomes following resuscitation. In a community-based case-control study, 2771 people with SCA were compared with 8313 demographic-matched controls [38]. The following findings were noted: People with diabetes were associated with 1.5 times higher odds of SCA. Among those with diabetes, the odds of having SCA were 2.41 times higher in type 1 than in type 2 diabetes (95% CI 1.53-3.80; p<0.001). People with SCA with type 1 diabetes were more likely to have an unwitnessed arrest, less likely to receive resuscitation, and less likely to survive compared with those with type 2 diabetes. Serum CRP Chronic inflammation, as manifested in part by higher serum concentrations of C- reactive protein (CRP), has been implicated as a risk factor for a variety of cardiovascular https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 8/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate diseases (including acute coronary syndromes and stroke). Elevated serum CRP is also associated with an increased risk of SCA [39]. (See "C-reactive protein in cardiovascular disease".) Excess alcohol intake Moderate alcohol intake (eg, one to two drinks per day and avoidance of binge drinking) may decrease the risk of SCD [40,41]. In comparison, heavy alcohol consumption (four to six or more drinks per day) or binge drinking increases the risk for SCD. This may be a result of alcohol withdrawal that occurs with heavy alcohol use or binge drinking (which has been termed the "holiday heart syndrome"). Alcohol withdrawal is associated with an elevation of sympathetic neural activity and circulating catecholamines. Each specific type of alcoholic drink (eg, beer, wine, spirits) may have different associations with SCD. In a study from the United Kingdom Biobank, 408,712 middle-aged participants were followed for a median of 12 years for the development of SCD [40]. There were 2044 SCD events. Total alcohol consumption had a U-shaped association with SCD, with the lowest-risk group reporting <26 drinks per week. Consumption of greater amounts of beer, cider, and spirits were associated with increasing SCD risk, whereas increasing wine intake was associated with reduced risk. The association of alcohol with other cardiovascular disease is discussed separately. (See "Cardiovascular benefits and risks of moderate alcohol consumption".) Psychosocial factors Clinical observations have suggested a possible relation between acutely stressful situations and the risk of SCA. Major disasters, such as earthquakes and war, result in a rapid transient increase in the rate of SCA in populations [28,29]. The level of educational attainment and social support from others may alter the risk associated with stressful life events. (See "Psychosocial factors in sudden cardiac arrest".) Caffeine Excessive caffeine intake has been investigated as a potential risk factor for SCA [42]. In the limited data available, no significant association between caffeine intake and SCA have been found. Fatty acids Elevated plasma nonesterified fatty acid (free fatty acid) concentrations were associated with ventricular arrhythmias and SCD after a myocardial infarction [43]. However, nonesterified fatty acids were not associated with SCD in the Cardiovascular Health Study, a population-based cohort of older adults [44]. In addition, in a population-based case-control study among persons without prior clinically recognized heart disease, SCA cases had higher concentrations of trans isomers of linoleic acid in red blood cell membranes [45]. (See "Dietary fat".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 9/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate In contrast, a higher dietary intake and higher levels of long-chain n-3 polyunsaturated fatty acids (eicosapentaenoic acid and docosahexaenoic acid) in plasma and the red blood cell membrane are associated with a lower risk of SCD [30,46-48]. (See 'Fish intake and fish oil' below.) MANAGEMENT The acute management of cardiac arrest is discussed in detail separately. (See "Initial assessment and management of the adult post-cardiac arrest patient".) Management issues for survivors of SCA include the following: Identification and treatment of acute reversible causes Evaluation for structural heart disease In patients without obvious arrhythmic triggers or cardiac structural abnormalities, an evaluation for primary electrical diseases Neurologic and psychologic assessment In selected patients with a suspected or confirmed heritable syndrome, evaluation of family members These issues are discussed in detail separately. (See "Cardiac evaluation of the survivor of sudden cardiac arrest".) PRIMARY PREVENTION The optimal approach to the primary prevention of SCA varies depending on the patient group, as discussed in the sections below. General population There are two approaches to reduce the risk of SCA in the general population: Screening and risk stratification to identify high-risk individuals who may benefit from specific interventions (eg, stress testing, screening ECGs). Interventions that may be expected to reduce SCA risk in any individual (eg, smoking cessation or other lifestyle modifications). Such interventions generally target the underlying disorders that predispose to SCA. https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 10/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Screening and risk stratification Among populations already known to be at an elevated risk of SCA (eg, patients with a prior myocardial infarction), further risk stratification with a variety of tests can identify subgroups that benefit from specific therapies, such as primary prevention with an ICD, particularly those with an ischemic cardiomyopathy and left ventricular ejection fraction <35 percent. (See 'Ischemic heart disease' below and "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".) However, in the general population without known cardiovascular disease, there is no evidence that routine screening with any test (eg, 12-lead electrocardiography, exercise stress testing, or Holter monitoring) effectively identifies populations at an increased risk of SCA. With regard to risk stratification of the general population, we suggest the following: Screening for risk factors for cardiovascular disease according to standard guidelines. (See "Screening for lipid disorders in adults".) The USPSTF clinical practice guideline for screening for high blood pressure, as well as other USPSTF guidelines, can be accessed through the website for the Agency for Healthcare Research and Quality at www.uspreventiveservicestaskforce.org/. Screening for CHD as appropriate in selected patients, according to standard guidelines. (See "Screening for coronary heart disease".) Routine additional testing for the purpose of SCA risk stratification is not recommended. An issue that merits special consideration is the pre-participation evaluation of athletes. This is a complex issue and there are conflicting opinions regarding whether to screen and, if so, the appropriate nature of a screening evaluation, such as with an electrocardiogram or echocardiogram. (See "Screening to prevent sudden cardiac death in competitive athletes".) Risk factor reduction Many of the traditional risk factors associated with the development of CHD are also associated with SCA. (See 'Risk factors' above and "Overview of primary prevention of cardiovascular disease".) Thus, management of these risk factors may reduce the incidence of SCA in the general public. Such interventions include: Effective treatment of hypercholesterolemia Effective treatment of hypertension Adoption of a heart-healthy diet Regular exercise Smoking cessation https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 11/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Moderation of alcohol consumption Effective treatment of diabetes These interventions are generally in agreement with guidelines published in 2001 by a task force of the European Society of Cardiology [49]. There is no definitive evidence that risk factor reduction in the general population lowers the rate of SCA. However, a number of studies have demonstrated that interventions to treat risk factors can lower total cardiovascular and coronary mortality. Since the majority of CHD mortality is due to SCD, these results suggest that interventions to reduce risk factors will reduce SCA rates as well. (See "Overview of primary prevention of cardiovascular disease".) As an example, a multifactorial, controlled, randomized trial from the Belgian component of the World Health Organization evaluated the effect of efforts aimed at reducing serum cholesterol (via dietary changes), increasing physical activity, and controlling smoking, hypertension, and weight (in those who were overweight) on risk factors and mortality [50]. Compared to the control group, the intervention group had significant reductions in the incidence of CHD and coronary mortality. Moderate alcohol intake Excess alcohol intake increases the risk of SCA, while light-to- moderate alcohol consumption (ie, 2 drinks per day) is associated with a lower risk of coronary heart disease and cardiovascular mortality [41,51]. (See 'Excess alcohol intake' above.) It is reasonable to expect that moderate alcohol intake will also reduce SCA. This effect was documented by the Physicians Health Study, which evaluated 21,537 men who were free of known cardiovascular disease [41]. Compared to men who rarely or never drank, those who had two to four drinks per week or five to six drinks per week had a significantly reduced risk for SCD (relative risks 0.40 and 0.21, respectively); the risk approached unity at 2 drinks per day. (See "Cardiovascular benefits and risks of moderate alcohol consumption".) Regular exercise There are no data from long-term exercise intervention trials among apparently healthy persons that focus upon major disease end points. Nevertheless, regular exercise should be encouraged for the primary prevention of CHD and SCA. Although there is a small transient increase in risk during and shortly after strenuous exercise, there is an overall reduction in SCD among exercisers compared with sedentary men [25,27,35,52]. It is unclear if more exercise (higher intensity or longer duration) is better than less (non-strenuous physical activity, such as walking for exercise 30 minutes most days). (See 'Exercise' above and "The benefits and risks of aerobic exercise" and "Exercise and fitness in the prevention of atherosclerotic cardiovascular disease".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 12/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Patients should be advised to pay attention to potential symptoms of CHD, even if they have engaged in regular exercise without limitations for an extended period of time. In addition, patients with known heart disease should be encouraged to engage in regular exercise in a supervised setting such as a cardiac rehabilitation program. (See "Cardiac rehabilitation programs".) Fish intake and fish oil In observational studies of populations at low cardiovascular risk, greater dietary fatty fish intake was associated with lower cardiac mortality [30,47,48,53,54]. This benefit is due in part to a reduced risk of SCD. Based upon these results, subsequent randomized trials evaluated the benefit of fish oil supplements in various high-risk populations [55,56]. These issues are discussed in detail separately. (See "Fish oil: Physiologic effects and administration".) For most individuals, there is little evidence that the pharmacologic doses of n-3 polyunsaturated fatty acids found in fish oil supplements (approximately 10 to 20 times the nutritional dose from fish) provide more protection than the intake of one to two servings of fatty fish (eg, salmon) per week. The pharmacologic use of fish oils supplements should be restricted to patients with refractory hypertriglyceridemia and, in such patients, the periodic monitoring of apolipoprotein B levels is recommended. (See "Healthy diet in adults" and "Hypertriglyceridemia in adults: Management", section on 'Treatment goals'.) Ischemic heart disease Patients who have ischemic heart disease, particularly those who have had an MI, are at an increased risk of SCA. However, among post-MI patients, this risk varies significantly according to a number of factors. The approach to the prevention of SCA in such patients includes the following: Standard medical therapies. Both beta blockers and ACE inhibitors (or angiotensin II receptor blockers) reduce overall mortality after an MI and are routinely administered. These agents also lower the incidence of SCD. However, the benefit may be limited to three years post MI. Beta blockers post-MI are useful for a longer period of time in patients with post-MI heart failure or ongoing chronic angina. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF", section on 'Guideline-directed medical therapy' and "Acute myocardial infarction: Role of beta blocker therapy".) Risk stratification to identify those patients at the highest risk of SCA. (See "Incidence of and risk stratification for sudden cardiac death after myocardial infarction".) https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 13/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate ICD implantation in selected patients, ie, those with an ischemic cardiomyopathy and LVEF <35 percent. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF".) Heart failure and cardiomyopathy Patients with heart failure and left ventricular systolic dysfunction, regardless of the etiology, are at an increased risk of SCA. Primary prevention with an ICD is recommended in selected patients with either ischemic or nonischemic cardiomyopathy, although recent studies have shown less if any benefit of an ICD in those with a nonischemic cardiomyopathy. (See "Primary prevention of sudden cardiac death in patients with cardiomyopathy and heart failure with reduced LVEF", section on 'Use of an ICD'.) In addition, as with patients with CHD, standard medical therapies for HF (beta blockers, ACE inhibitors or angiotensin II receptor blockers, and aldosterone inhibitors such as spironolactone or eplerenone) may lower the risk of SCA. (See "Ventricular arrhythmias: Overview in patients with heart failure and cardiomyopathy", section on 'Heart failure therapy'.) Inherited arrythmia syndromes Patients with one of the congenital disorders associated with an increased risk of SCA (eg, Brugada syndrome, congenital long QT syndrome, Wolff- Parkinson-White syndrome) are at increased risk for SCA. (See "Brugada syndrome: Clinical presentation, diagnosis, and evaluation" and "Congenital long QT syndrome: Epidemiology and clinical manifestations" and "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis".) Counseling patients and families Given the mounting evidence related to the primary prevention of SCA, it now is clear that primary care clinicians can influence the occurrence of these events. As discussed above, there are clinical recommendations for those at risk of SCA that are likely to reduce risk. (See 'Risk factor reduction' above.) SECONDARY PREVENTION ICD therapy An implantable cardioverter-defibrillator (ICD) is the preferred therapeutic modality in most survivors of SCA. The ICD does not prevent the recurrence of malignant ventricular arrhythmias, but it effectively terminates these arrhythmias when they do recur. The role of the ICD in survivors of SCA is presented separately. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy".) ICD patients who have frequent arrhythmia recurrences and device discharges may benefit from adjunctive therapies, such as antiarrhythmic drugs or catheter ablation. (See "Secondary prevention of sudden cardiac death in heart failure and cardiomyopathy", section on https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 14/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate 'Antiarrhythmic drugs' and "Pharmacologic therapy in survivors of sudden cardiac arrest", section on 'Treatment of breakthrough arrhythmias' and "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Radiofrequency catheter ablation'.) Other antiarrhythmic therapies Antiarrhythmic drugs are less effective than an ICD for secondary prevention of SCD. Thus, their use in this setting is limited to the adjunctive role described above, or in patients who do not want or are not candidates for an ICD (eg, due to marked comorbidities or end-stage heart failure that make death likely). Patients in whom ventricular arrhythmias result in recurrent shocks despite antiarrhythmic medications may be candidates for catheter ablation in an effort to reduce the arrhythmic burden. (See "Pharmacologic therapy in survivors of sudden cardiac arrest" and "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis", section on 'Radiofrequency catheter ablation'.) INFORMATION FOR PATIENTS UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." th th The Basics patient education pieces are written in plain language, at the 5 to 6 grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more th th sophisticated, and more detailed. These articles are written at the 10 to 12 grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon. Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.) Basics topics (see "Patient education: Sudden cardiac arrest (The Basics)") SUMMARY AND RECOMMENDATIONS The following summary and recommendations address general issues related to sudden cardiac arrest (SCA) and sudden cardiac death (SCD). https://www.uptodate.com/contents/overview-of-sudden-cardiac-arrest-and-sudden-cardiac-death/print 15/32 7/6/23, 1:40 PM Overview of sudden cardiac arrest and sudden cardiac death - UpToDate Background SCA and SCD refer to the sudden cessation of cardiac activity with hemodynamic collapse. Events that are successfully treated with patient survival are referred to as SCA, while those that lead to death are referred to as SCD. (See 'Definitions' above.) Epidemiology SCD is common, accounting for up to 15 percent of total mortality in industrialized countries, based upon review of death certificate data. Smaller prospective studies, however, have suggested a lower incidence. (See 'Epidemiology' above.) Etiology SCA is most commonly due to ventricular tachyarrhythmias (ie, ventricular