Sudden Cardiac Death

Notes on sudden cardiac deathCopyright Dr Richard Jones 2006

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Notes on Sudden Cardiac Death

Definitions

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Unexpected natural death from a cardiac cause within a shorttime period (generally demise from cardiovascular collapse<= 1 hour from onset of symptoms according to FraminghamHeart Study) in a person without any prior condition thatwould appear fatal (Zipes and Wellens 1998; 98:2334-2351)(Leor et al NEJM 1996; 334:413-419) (Marks and GreeneCardiac Arrhythmias 1995)

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Other researchers use WHO definition of sudden death asdeath occurring within 24 hours of the onset of acutesymptoms (Myers and Dewar Br Heart J 1975 37:1133-1143)

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Prodromal symptoms often non-specific, and chest pain(ischaemia), palpitations (tachyarrhythmia) or dyspnoea(cardiac failure) are suggestive only. (Zipes and Wellens1998; 98:2334-2351)

Epidemiology

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Sudden cardiac death accounts for 300-400,000 deaths peryear in US, and is most common and often the firstpresentation of CHD responsible for >50% of the mortalityfrom cardiovascular disease in US (Zipes and Wellens 1998;98:2334-2351) or between 200,000 and 600,000 p.a. in US(Marks and Greene Cardiac Arrhythmias 1995) (Hirsch andAdams Spitz and Fisher) 80-90% of sudden cardiac deathpatients have significant CAD (Chugh et al Circulation 2000102(6):649-654)

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Sudden cardiac death in those with structurally normal heart– 20% of sudden cardiac deaths (Brugada et al 2004Circulation 109:30-35) 50% (Chugh et al Circulation 2000102(6):649-654) 80% have CHD – smaller amount of non-atherosclerotic coronary artery causes e.g. arteritis,embolism, dissection and malformations such as anomalousleft coronary artery origin (Zipes and Wellens 1998; 98:2334-2351)

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In Paris study, 72% of sudden cardiac death victims had nocardiac history. 83% occurred at home (and at rest), 30% of those were sleeping. Sudden cardiac death usually occurredon a background of severe coronary disease with multivesselsstenosed, but rarely thrombosed (15%) (Fornes et al Journalof Forensic Sciences 1993 38(5))

Notes on sudden cardiac deathCopyright Dr Richard Jones 2006

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Davies and Popple (Histopathology 1979 3:255-277) statedthat 33% have recent occlusive thrombus, whilst 66% havestenosis only. Occlusive thrombus present in 30% cases of sudden cardiac death, mural thrombus in 43% and plaquefissuring in 8%. Davies 1992 Circulation 85: (Supl 1) 19-24).New thrombotic event underlies 50-70% of sudden deathscaused by IHD. (Davies Heart 2000 83:361-366) Occlusivethrombus recognised by hospital pathologists in 23% of cases,recent MI in 20% and old MI scar in 56%. Occlusive thrombusmore common in those with prodromal chest pain. 25% of non-fatal infarctions are silent and medically unattended.(Norris Heart 2000 83:726-730)50-75% of sudden death cases have thrombus (remainderhave >75% cross sectional area luminal narrowing) (KolodgieHeart 2004 90: 1385-1391) New coronary plaque ruptureindependent of old MI is major cause of sudden death in thosewith old MI (recent thrombus/ plaque rupture in 55%,arrhythmia in 24%, pump failure in 14%) (Takada et al LegalMedicine 2003 5:S292-294)

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4.1% in 16-64 age-group are unexplained (SuddenArryhthmic Death Syndrome) (Behr et al 2003 Lancet362:1457-59)

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Incidence of sudden cardiac death in England in healthypeople 16-64 years is 11 per 100,000 (3500 deaths) per year(Behr et al 2003 Lancet 362:1457-59)

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Most people who die of SADS are young males who die whileinactive or in sleep (Behr et al 2003 Lancet 362:1457-59)

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Ventricular fibrillation is the main mechanism of suddencardiac death – vast majority have structural heart disease,those who do not have ‘idiopathic VF’. (Gaita F et alCirculation 2003; 108:965-970)

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80% occur at home and 40% are unwitnessed (Maastrichtstudy) (Zipes and Wellens 1998; 98:2334-2351)

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First-degree relatives of those suffering sudden cardiac deathidentified 7 families with familial cardiac disease, withprobable Long QT syndrome predominating. (Behr et al 2003Lancet 362:1457-59)

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Familial history of sudden cardiac death is associated withmajor (resuscitated cardiac arrest, syncope) and minor(palpitations, dizziness, atrial fibrillation) arrhythmic eventsand inducible VF at programmed stimulation (Gaita F et alCirculation 2003; 108:965-970)

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Myocardial fibrosis provides a predisposition to electricalinstability, re-entry circuits and fatal arrhythmias. (Lecomte Det al Journal of Forensic Sciences 2003; 38(3)? Page)

Notes on sudden cardiac deathCopyright Dr Richard Jones 2006

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Sudden death due to primary VF without evidence of structural heart disease occurs in approximately 5% of cases.(Zipes and Wellens 1998; 98:2334-2351)

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33% of people present with CAD present with sudden cardiacdeath (Chi and Kloner stress and MI)

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in sudden cardiac death 95% of hearts have an abnormality,although in 30% this abnormality is non-specific e.g..Interstitial fibrosis (Chugh et al Circulation 2000 102(6):649-654)

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acute MI was the underlying mechanism of sudden cardiacarrest (out-of-hospital) in 24/47 patients; ischaemic event orprimary arrhythmia due to old MI in 19/47 (de Vreede-Swagemakers JJM et al Heart 1998 79:356-361)

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new thrombotic event underlies 50-70% of sudden deathscaused by Ischaemic Heart Disease (Davies Heart 200083:361-366)

Risk Factors

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Generally identify risk of structural heart disease underlyingsudden cardiac death rather than the proximate precipitatorof the event. 80% of those who suffer sudden cardiac deathhave CHD (Zipes and Wellens 1998; 98:2334-2351)

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Incidence of sudden cardiac death increases with

age

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sex variation

M>F (3-4 times higher), white=black (becauseincidence of heart disease increases with age)

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Among people with CHD, the proportion of sudden deathsdecreases with age. Peaks of incidence birth-6 months (SIDS)and 45-75 due to CHD

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Physical activity

controversial. Vigorous activity – can triggersudden death and MI (increased platelet adhesiveness) butdecreased in moderate activity. Regular exercise in dogsincreases vagal activity and reduces ischaemia induced VFand death. Vigorous activity in untrained people may haveadverse effects – relative risk in men with low levels of habitual activity = 56 (95% CI 23-131) whilst in those withhigh levels of habitual activity = 5 (95% CI 2-14) MyocardialInfarction Onset Study 5 fold increase of risk of MI on heavyexertion and 2 fold increase in Triggers and Mechanisms of Myocardial Infarction Study (TRIMM) (Willich et al Circulation1993 87(5):1442-1450). Maastricht Sudden Death study –67% of sudden deaths were inactive at time of event. Sexualactivity doubles risk of MI (Chi and Kloner stress and MI)

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Anatomy

– acute changes in plaque morphology (thrombus,plaque disruption or both >50% of sudden cardiac deaths).Plaque erosion is common. Rupture >older women. ?role of