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• W2053508869 abstract "HomeCirculationVol. 123, No. 25Sudden Cardiac Arrest Without Overt Heart Disease Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBSudden Cardiac Arrest Without Overt Heart Disease Simon Modi, MBBS and Andrew D. Krahn, MD Simon ModiSimon Modi From the Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada. Search for more papers by this author and Andrew D. KrahnAndrew D. Krahn From the Division of Cardiology, Department of Medicine, University of Western Ontario, London, Ontario, Canada. Search for more papers by this author Originally published28 Jun 2011https://doi.org/10.1161/CIRCULATIONAHA.110.981381Circulation. 2011;123:2994–3008The topic of sudden unexplained cardiac arrest without overt heart disease is a highly emotive and important subject with a rapidly advancing knowledge base. The correct identification of those conditions predisposing to cardiac arrest is paramount, and is part of the role of every practicing cardiologist. This review article is designed to give the practicing cardiologist an up-to-date insight into a subspecialized field of cardiac electrophysiology and cardiac genetics. It seeks to help to formulate diagnoses with advanced electrophysiological testing and genetic profiling and also with a reminder of basic clinical presentations and pathophysiological features of the conditions in question. This article seeks to encapsulate the field in general and at the same time to provide a select amount of useful detail, both contemporary and historical, and to provide references from a resource of excellent reviews in the literature. We hope that the reader will develop confidence in identifying rare causes of cardiac arrest and an insight into the sort of patients that should be referred to subspecialist clinics.Structural or coronary heart disease is by far the most common cause of sudden cardiac arrest.1 Once overt heart disease has been excluded in the cardiac arrest survivor, the differential diagnosis includes manifest or latent primary electrical disease and latent structural causes (Tables 1 and 2). These conditions predispose the patient to recurrent ventricular arrhythmia and cardiac arrest without overt heart disease. The overriding immediate concern in these patients is recurrence of unheralded ventricular tachycardia or fibrillation. Every effort must be made to define the underlying pathophysiology in order to understand prognosis, direct therapy, and identify family members who may be at risk if the culprit is an inherited condition.Table 1. Causes of Sudden Cardiac ArrestCardiac arrest with overt structural heart diseaseCoronary diseaseIschemic heart diseaseAnomalous coronary circulationCoronary spasmCardiomyopathiesIschemic cardiomyopathyHypertrophic cardiomyopathyDilated cardiomyopathyInfiltrative (eg, sarcoid, amyloid)Arrhythmogenic right ventricular cardiomyopathyTakotsubo cardiomyopathyLeft ventricular noncompaction cardiomyopathyMyocarditisCorrected congenital cardiomyopathyOtherWolff-Parkinson-White syndromeCommotio cordisCardiac arrest without overt heart diseasePrimary electricLong-QT syndromesShort-QT syndromesBrugada syndromesEarly repolarization syndromesCatecholaminergic polymorphic ventricular tachycardiaIdiopathic ventricular fibrillationMetabolic imbalanceHyperkalemia/hypokalemiaHypocalcemiaHypomagnesemiaAcidosisDrug overdoseConcealed structuralArrhythmogenic right ventricular cardiomyopathyMyocarditisCoronary spasmSarcoidosisNoncardiacAcute intracranial hemorrhageMassive pulmonary embolusEpilepsyTable 2. Summary of Conditions Causing Sudden Cardiac Arrest Without Overt Heart DiseaseConditionFeaturesDiagnosisCommentsLong-QT syndromesAbnormally long and/or morphologically abnormal QT/T wave (>440 ms male, >460 ms female)History, ECGs, exercise, and adrenaline provocation and genetic testingSee long-QT syndrome (Table 3)Brugada syndromeAbnormal ST elevation in precordial leadsHistory, ECGs, and sodium channel blockers provocation testingGenetic testing low yieldCatecholaminergic polymorphic ventricular tachycardiaNormal resting ECG but exercise/adrenergic-induced ectopy and ventricular tachycardia (bidirectional or polymorphic)History, exercise, and adrenaline provocation and genetic testingGenetic testing may be usefulEarly repolarization syndromeST elevation or J-point slurring in inferolateral leadsECGNo reliable provocation testShort-QT syndromeShortened QT interval with peaked T wave; consider if QTc <360 msQT on ECG, peaked T waveUsually QTc <320 msCoronary spasmTransient regional ST elevation and myocardial dysfunction with normal or near-normal epicardial coronary arteriesHistory and ECGs; small marker rise; provocation testing (ergonovine or acetylcholine)Often mild coronary disease in smokersArrhythmogenic right ventricular cardiomyopathyFeatures of right ventricular dilatation, thinning, fibrosis, and aneurysm formation, often not seen on echocardiogram; epsilon waves, right bundle branch block; may have ventricular tachycardia originating in the right ventricleECGs, imaging especially MRI, genetic testing, electroanatomic voltage map, biopsy in select casesOften has structural change evidentMyocarditisRecent viral illness or chronic systemic inflammatory condition; regional or global ventricular dysfunction together with small marker riseECGs, imaging especially MRI with gadolinium, biopsy where availableOften will show evidence of ventricular dysfunctionSarcoidosisOther signs of systemic sarcoidosis (eg, pulmonary, ocular)Imaging especially MRI, biopsy where available (may be extracardiac if systemic involvement)Commonly associated with systemic involvementMRI indicates magnetic resonance imaging.The conditions in question are largely those causing abnormalities in cardiac depolarization or repolarization, usually due to inherited, drug-, metabolic-, or electrolyte-induced ion channel dysfunction. They have loosely been termed the channelopathies or primary electric diseases. Often included in the category of cardiac arrest without overt heart disease are patients with subclinical structural diseases such as myocarditis, coronary spasm, arrhythmogenic right ventricular cardiomyopathy (ARVC), and sarcoidosis.2 Although these conditions may be readily diagnosed with overt evidence of a structural cause of cardiac arrest, structural abnormalities may be subtle or even undetectable with standard testing early in their course, requiring a high index of suspicion to discern.Survivors of cardiac arrest without overt heart disease typically come under the care of an electrophysiologist because of the need for implantation of an implantable cardioverter-defibrillator (ICD). Care is ideally delivered by a team of individuals with expertise in genetics, electrophysiology, and cardiomyopathies, with input from imaging experts as well. This team deals with survivors of cardiac arrest, their family members when an inherited cause is identified, and the less fortunate families when sudden death occurs without overt heart disease and families are sent for screening.3–6 This is often referred to as cascade family screening.4,7 It should be recognized, however, that even when each of the known causes of cardiac arrest without overt heart disease has been systematically excluded with in-depth testing, nearly half of the causes of cardiac arrest in these patients will remain unexplained.2Investigation of the Sudden Cardiac Arrest SurvivorSurvivors of cardiac arrest require a comprehensive clinical review with an in-depth sequential testing strategy (Figure 1). This includes a detailed presenting history with witness statements as well as comprehensive family and drug histories. Family history should inquire not only about sudden death, but also about events such as drowning, fatal single-vehicle accidents, sudden infant death syndrome, and frequent miscarriages, all potential signs of an inherited predisposition to sudden death. Baseline electrolyte and metabolic testing should be undertaken to look for reversible causes of cardiac channel instability, along with markers of cardiac injury. These are infrequent explanatory mechanisms of cardiac arrest but may be substantial triggers in predisposed individuals. Further biochemical, immunologic, and serological testing should be undertaken if findings are suggestive of cardiac involvement of systemic disease, such as amyloid, sarcoid, autoimmune disease, and viremia.Download figureDownload PowerPointFigure 1. A, Investigation cascade in the patient with cardiac arrest without overt heart disease. SAECG indicates signal-averaged ECG; CMR, cardiac magnetic resonance; CT, computed tomography; EP, electrophysiological; and RV, right ventricular. B, Investigation schematic to approach family members.Structural and electric testing should then be routinely performed. The term overt heart disease is open to a degree of subjectivity. For the vast majority of settings, it is defined as the absence of a clear structural or electric cause of cardiac arrest on coronary angiography, echocardiography, and resting ECG. Further imaging with cardiac magnetic resonance imaging (MRI) and drug provocation should be included in the new standard approach to investigation of this population.2,8,9Resting 12-lead ECGs and monitored telemetry strips should be reviewed both during the acute admission and historically (if available), with the clinician looking for evidence of repolarization abnormalities, coronary ischemia or spasm, preexcitation, or ventricular ectopy, all of which may play a significant etiologic role in cardiac arrest. Postresuscitation ECGs can often display changes in depolarization and repolarization, and patients undergoing postarrest hypothermic protocols in the intensive care setting are equally subjected to transient ECG changes, including Osborne J waves and transient QT prolongation. Many patients in the intensive care setting will receive either sympathomimetic infusions or drugs that affect repolarization that can provide clues to an underlying diagnosis. ECG findings in these metabolically deranged states should only be used as a guide to investigation or diagnosis once normal physiology returns rather than as a definitive diagnosis.Coronary imaging, usually with coronary angiography, is required to exclude coronary artery disease, particularly in those patients with a history of chest pain or known risk factors. In the younger population, coronary angiography is principally used to rule out congenital coronary anomalies. Although coronary spasm may occur as a result of catheter positioning, this commonly occurs in the proximal portion of the major coronary vessels. Coronary spasm elsewhere in the vessel, particularly if imaging is undertaken during an acute presentation with ST elevation, is highly likely to be significant. If coronary atheroma is observed but is nonocclusive in nature, this should be noted because it may represent a possible substrate for coronary spasm. We typically advocate consideration of ergonovine or acetylcholine challenge in patients with suspicion of coronary spasm, acknowledging the associated recognized remote risk of myocardial infarction and ventricular arrhythmias.Echocardiography is routinely recommended even when left ventriculography has been performed at cardiac catheterization. Specific attention should be paid to the presence of chamber hypertrophy, dilatation, and systolic function. Apparent left ventricular apical hypertrophy can be observed in patients with left ventricular noncompaction cardiomyopathy, and care must be taken to visualize endocardial borders and noncompaction channels, usually with contrast media. Changes in the right ventricle can be difficult to assess with echocardiography. Nevertheless, attempts should be made to look for thinning and aneurysm formation in the right ventricular free wall, apex, and outflow tract as well as chamber dilatation. Echocardiographic changes of myocarditis are notoriously subjective but should still be investigated.Subsequent testing in the absence of clear pathology at this stage should include treadmill testing and a signal-averaged ECG. Treadmill testing serves as a provocation test for catecholaminergic polymorphic ventricular tachycardia (CPVT)2 as well as some idiopathic outflow tract ventricular tachycardias. It is also used to uncover subtle clues leading to a diagnosis of long-QT syndrome (LQTS), such as inadequate QT shortening, postural T-wave change, and exercise-related T-wave notching.10,11 The QT interval can be difficult to assess during exercise because of motion artifact, and bicycle testing is often substituted to provide clearer definition. An ECG performed immediately after the patient is in recovery often provides a useful surrogate to inspect peak exercise QT changes. Signal-averaged ECG testing is primarily used to look for evidence of late potentials, which is helpful in the screening of ischemic cardiomyopathy, subclinical arrhythmogenic right ventricular cardiomyopathy, and Brugada syndrome.Drug provocation to unmask a primary electric cause of cardiac arrest plays a key role when the diagnosis remains unclear or to further risk stratify phenotypically suggestive patterns. Provocation testing protocols, including sympathomimetic or sodium channel–blocking drug infusions, are primarily used to unmask phenotypes of LQTS, Brugada syndrome, and CPVT. They are usually performed in a coronary care unit, monitored investigation unit, or electrophysiology laboratory and can be safely performed as day case investigations. Their diagnostic yield varies between conditions and will be discussed in more detail later in this review.Advanced imaging such as gated cardiac MRI or computed tomographic scanning should be considered unless a clear diagnosis has been obtained. The key purpose is to detect subclinical ARVC, sarcoidosis, myocardial injury from coronary spasm, and myocarditis. Detailed discussion of the optimal imaging sequences to detect these conditions is beyond the scope of this review.When the diagnosis remains unclear at this juncture, further testing is exploratory and unlikely to offer a definitive result. Additional tests to be considered in elusive cases are electrophysiology studies with voltage mapping and cardiac biopsy. Genetic testing is indicated when an inherited phenotype (ARVC, Brugada, CPVT, or LQTS) is detected, both for diagnosis and to aid family screening. The role of blanket genetic screening in phenotypically ambiguous or negative patients is unclear but clearly remains a research tool at present.This diagnostic strategy has been applied in a registry of patients with apparently unexplained cardiac arrest after exclusion of coronary artery disease, left ventricular dysfunction, and manifest LQTS or Brugada syndrome2 (Figure 1). This study assessed survivors of cardiac arrest defined as documented cardiovascular collapse with ventricular tachycardia or fibrillation requiring direct current cardioversion or defibrillation with an ejection fraction >50%. Patients were excluded if they had a coronary stenosis >50%, an abnormal resting QT interval (male QTc <460 ms, female QTc <480 ms), and diagnostic Brugada ST segments.2 Patients were predominantly white, with 60% men and a mean age of 43 years. A clinical diagnosis was reached in 56% of patients, with an inherited cause found in 40% (Figure 2). The underlying diagnoses included a range of conditions that will be described in further detail below. This registry is limited by its exclusion of patients with manifest repolarization disorders such as LQTS or Brugada syndrome and its setting in a specialty referral network in Canada. Of importance, this strategy is predicated on access to costly advanced diagnostic tools such as MRI and genetic testing. The author's perspective is that deployment of these resources is warranted, given the typical young patient with an otherwise excellent prognosis and the implications for family screening and further prevention of cardiac arrest and sudden death. This perspective is clearly contextual.Download figureDownload PowerPointFigure 2. Diagnostic yield of comprehensive testing in unexplained cardiac arrest patients without overt heart disease. ARVC indicates arrhythmogenic right ventricular cardiomyopathy; CPVT, catecholaminergic polymorphic ventricular tachycardia; LQTS, long-QT syndrome; and Repol, repolarization. Adapted from Krahn et al 2with permission of the publisher. Copyright © 2009, Lippincott Williams & Wilkins.Therapy for the cardiac arrest survivor depends largely on the underlying diagnosis, typically combining condition-specific medication with an ICD, which is discussed in more detail below.Relatives of the Sudden Cardiac Arrest SurvivorThe management of families is driven by the outcome of thorough evaluation of the index cardiac arrest survivor. The focus is on exclusion of known phenotypes/genotypes or, alternatively, the blind workup of a relative of an undiagnosed cardiac arrest. This may involve reevaluation of postmortem studies or accessing prior health records to look for historical ECGs from the deceased index case. Occasionally, it may be pertinent to obtain a postmortem genotype in cases of high clinical suspicion. This technique of molecular autopsy has been shown to provide genetic clues in up to 30% of both young adult and childhood sudden unexplained death in which the standard autopsy is negative. It has proven most helpful for genetic mutations in LQTS or CPVT. Many experts in the field would advocate this in their standard patient workup, especially in cases in which the infrastructure for testing exists.12,13 In situations in which the index case diagnosis is unclear, a tiered approach to screening is usually offered, including ECG, echocardiogram, exercise testing, signal-averaged ECGs, and Holter monitoring. Cardiac MRI, electrophysiology studies, and cardiac biopsy are reserved for diagnostic uncertainties. The depth to which screening should permeate through family lineage is often considered and is aided significantly with positive genotyping. In this often-asymptomatic group, discussion is commonly centered on education and therapy for new phenotypically or genotypically positive family members, together with consideration of drug and/or ICD therapy. Counseling, particularly in the setting of infant or young adult death, clearly plays an important role, with achievement of closure being significantly helped when a unifying diagnosis is reached.12Causes of Sudden Cardiac Arrest Without Overt Heart DiseaseThis review will now focus on the most common causes of cardiac arrest without overt heart disease, detailing important clues to diagnosis as well as reviewing recommended and novel diagnostic and therapeutic options.Long-QT SyndromePresentation and DiagnosisOur understanding of LQTS has been driven by extensive molecular and genetic research combined with outstanding natural history data from the International LQT Registry established by Schwartz and Moss in 1979.14,15 Initial descriptions of congenital LQTS with or without congenital deafness have grown into 12 individual subtypes (Table 3), with an estimated prevalence of 1:2000.16,17 More than 95% of cases represent abnormalities in the rectifier potassium channels (IKr, IKs) or inward sodium channels corresponding to LQT types 1 to 3.18 At some point, 30% to 50% of patients are symptomatic, typically presenting with syncope. The lifetime risk of cardiac arrest is in the order of 3% to 5%, with cardiac arrest as the initial manifestation in a small proportion of these patients.19,20 The hallmark arrhythmia is torsades de pointes (pause-dependent, oscillatory polymorphic ventricular tachycardia). Index events are noted to occur at any age, but often present in prepubescent males or postpubescent females with LQT1.21,22 Gene-specific triggers of symptoms have been reported and should be sought in the history, including swimming- or exercise-related events in LQT1, auditory or emotional triggers in LQT2, and resting- or sleep-related events in LQT3.23 The postpartum stage in females is also noted as a high-risk period.24 Arrhythmia in LQTS may also present as unexplained accidents or drowning (given its relation to swimming),25 sudden infant death syndrome,26 and epilepsy.27Table 3. The Long-QT SyndromesLong-QT TypeGenotypeCharacteristic QT MorphologyClinical PhenotypeIncidence, %Comments1KCNQ1Broad based, symmetrical T waveAdrenergic triggers (swimming, emotion, or exercise)30–35Most common but least severe; homozygotes have severe phenotype with congenital deafness (Jervell and Lange-Nielsen); β-blockers efficacious2KCNH2/HERGBifid T waveCommonly drug induced; auditory stimuli25–30Second most common; β-blockers largely efficacious3SCN5ADelayed-onset/asymmetrical T waveRest/sleep5–10Little β-blocker effect; may respond to sodium channel blockers4ANK2Exercise<15KCNE1Exercise and emotion<1Homozygotes have severe phenotype with congenital deafness (Jervell and Lange-Nielsen)6KCNE2Rest, drugs, or exercise<17KCNJ2Prominent U waves with pseudo QT prolongationRest or exercise<1Linked to Andersen-Tawil syndrome; periodic paralysis, skeletal muscle deformity, and hypokalemia8CACNA1CProminent and widely split T-U waves; prolonged terminal T-wave slope and minimal QT prolongationExercise<1Timothy syndrome; congenital heart disease, autism, syndactyly, and immune deficiency; early-onset, malignant arrhythmic course; some response to calcium channel blockers9CAV3Rest or sleep<1Possible limb-girdle myodystrophy link10SCN4BExercise<0.1Atrioventricular block11AKAP9Exercise<0.112SNTA1BifidRest<0.1Concerns should also be raised when syncope or cardiac arrest occurs in the setting of new medication. Current literature reports hundreds of drugs with definite or potential effects on the QT interval, which are summarized at http://www.qtdrugs.org. In addition, QT prolongation in the absence of congenital LQTS is often evident in the patient with myocardial infarction or cerebral anoxia and during hypothermia protocols.28,29The 12-lead ECG is the cornerstone of LQTS diagnosis. It is now generally recognized that the absolute QT interval should be measured from the start of the QRS to the end of the T wave, preferably in either lead II or V5, over an average of 3 to 5 cycles on standard 25-mm/s and 10-mm/mV calibration ECG paper. The duration of the normal versus pathological QT duration is open to interpretation. Corrected QT intervals >440 ms in men and >460 ms in women are widely considered prolonged, and at times a further 20-ms zone is considered borderline. Central to accurate QT interval measurement is defining the end of the T wave, particularly when the T wave is low amplitude or has a complex morphology. Interoperator error and variability are well reported,30 and therefore standardization of measurement techniques should be attempted. Techniques involve the creation of a threshold level of the T-wave amplitude or the use of the projected slope of the T wave.31 Our practice involves the use of the projected maximum slope to baseline intersection (Figure 3). It must be noted that mutations affecting the latter part of repolarization (IKs) can often change the trajectory of the terminal portion of the T wave, making this tangential method less accurate. The U wave should generally be ignored when the T-wave end is defined. Secondary deflections of equal or higher amplitude to the T wave are classified as a bifid T wave, not as a U wave, and should be incorporated into the QT measurement.10 QT correction for heart rate commonly involves the widely used Bazett's formula (QTc=QT/√R-R [seconds]), which is less accurate at extremes of heart rate, although numerous alternative correction methods are reported.32 The ECG also allows assessment of morphological differences in the T wave. To date, type-specific T-wave morphology has been suggested in LQT1 to LQT333,34 (Figure 4).Download figureDownload PowerPointFigure 3. Measurement of the QT interval. A, Use of the maximum slope technique to establish the end of the T wave in an ECG with normal T-wave morphology. B, Twelve-lead ECG of a young woman who suffered a cardiac arrest during a stressful situation. C, Magnified lead V2 of the ECG in B. This shows a notched T wave. The patient was subsequently diagnosed with type 2 long-QT syndrome. For further discussion, see Reference 31.Download figureDownload PowerPointFigure 4. Long-QT syndrome ECGs. Long-QT type 1 (LQT1) has a broad T wave, long-QT type 2 (LQT2) has a notched T wave with an asymmetrical appearance, and long-QT type 3 (LQT3) has a long isoelectric segment with a normal symmetrical T wave. Absolute QT intervals seen here are unimpressive until correction for heart rate is performed. The upper 2 ECGs were obtained after standing, known to unmask QTc prolongation. As a general principle, a T wave terminating within the latter half of the same R-R interval is highly suspicious for long-QT syndrome.34QT prolongation is not always manifest on the resting ECG in LQTS, and there is often a disparate relationship between symptoms, genotype, and QT interval.35 The repolarization reserve hypothesis helps to explain this. This theory posits that cardiac repolarization is a multifactorial entity requiring the interplay of a number of factors for correct function. Thereby, if a single potassium channel is genetically defective, other factors may compensate to produce apparently normal repolarization. Further imbalance within the reserve, created, for example, by electrolyte- or drug-induced disturbance, will lead to phenotypic abnormalities of repolarization.36 It is this severance of genotype and phenotype that provocation testing helps to unite. Testing usually involves exercise protocols or infusion of sympathomimetic agents. With exercise protocols, the combination of posture- and exercise-related QT change, including failed QT shortening, has been shown to reliably predict the LQT1 genotype.11 Epinephrine (adrenaline) testing is now in widespread use, and both continuous infusion and bolus protocols have demonstrated high sensitivity and specificity for unmasking both concealed LQT1 and possibly LQT2.37,38 Other novel protocols have included intravenous erythromycin, facial immersion, and adenosine boluses39–41Prognosis and TherapyPrognosis has improved significantly with early identification, family screening programs, and drug therapy. Sudden cardiac death is increasingly rare in the era of antiadrenergic therapy and patient education.42 As noted, of the 3 common LQTS subtypes, LQT3 and LQT2 appear to confer a worse cardiac arrest prognosis, which may be related to the highly efficacious use of adrenergic blockade in the LQT1 group.43 Therapy in LQTS centers on education, specifically β-blocker compliance,42 avoidance of triggers, and, at times, exercise restriction. Triggers may be exercise related (eg, swimming in LQT1), noise related (eg, alarm clocks in LQT2), or metabolic (eg, hypokalemia in LQT2),44 and are known to be related to an increase in subtype-specific cardiac events. Patients should also be educated about avoidance of QT-prolonging medications. β-Blockers are the mainstay of therapy in LQT1 and LQT2, and although they are classically believed to be less efficacious in LQT3, recent data suggest a reasonable effect of adrenergic blockade.45 The use of sodium channel blockers such as flecainide and mexiletine is also beneficial in LQT3.46,47 Rarely, more aggressive interventions such as sympathetic denervation surgery or implantable defibrillators are needed in high-risk cases, such as the cardiac arrest survivor, patients with persistent symptoms despite β-blocker therapy, patients with QTc intervals persistently >550 ms, or symptomatic patients with >1 genotype (compound heterozygotes).48,49 Although sympathetic denervation surgery has traditionally been used as an adjunct to defibrillator therapy, its safety and therapeutic success in the era of minimally invasive thoracoscopic surgery have raised its profile, and it should now be considered as a therapeutic option before ICD implantation in drug-refractory cases.50Brugada SyndromePresentation and DiagnosisThe Brugada syndrome, first identified by Martini et al in 1989,51 was subsequently described by the Brugada brothers in 1992 as an abnormal persistent ST elevation with right bundle-branch block pattern in a small cohort of cardiac arrest survivors with structurally normal hearts.52 The original ECG pattern, now known as type 1, was associated with polymorphic ventricular tachycardia or ventricular fibrillation usually during sleep, particularly in young men from Southeast Asia.53–55 Although initially believed to be a common cause of cardiac arrest without overt heart disease, recent data suggest a prevalence of no more than 5% in cases of sudden cardiac arrest without overt heart disease.2,56 Fever, autonomic factors, sodium channel–blocking drugs, and a full stomach are all reported to precipitate the characteristic ECG pattern and/or arrhythmia.57–60 The syndrome has also been linked with atrial fibrillation, supraventricular tachycardia, and bradyarrhythmias.61The ECG is again the cornerstone of diagnosis. Three Brugada ECG patterns are recognized: a type 1 Brugada pattern is characterized by ≥2 mV coved ST elevation with T-wave inversion in 2 contiguous precordial leads, usually V1 through V2, with standard ECG lead positions. Varying degrees of right bundle branch block are commonly seen.52,62 Type 2 and 3 patterns have a saddleback appearance, with a markedly less concerning natural history unless a type 1 ECG ca" @default.
• W2053508869 created "2016-06-24" @default.
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• W2053508869 date "2011-06-28" @default.
• W2053508869 modified "2023-09-24" @default.
• W2053508869 title "Sudden Cardiac Arrest Without Overt Heart Disease" @default.
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