A handbook for clinical practice - part 4 docx

Traditional risk factors and the incidence of sudden coronary death with and without coronary thrombosis in blacks.. Characteristics of the resuscitated out-of-hospital cardiac arrest v

Silvia: “chap06” — 2005/10/6 — 22:32 — page 81 — #8

Clinical characteristics of SCD victims 81

Vigorous exertion

Although there are many well-established cardiovascular benefits of exercise,

it is also well known that SCD appears to occur with a higher than averagefrequency during or shortly after vigorous exertion In various case series,from 6% to as high as 30% of SCDs occur in association with acute exertion

In Rhode Island, an examination of mortality records revealed 12-recordedcases of SCD during jogging during a 6-year period The authors assessed thecommunity exposure to jogging, and estimated that the age-adjusted relativerisk of SCD during jogging was 7 (95% CI= 4–26) compared with the risk dur-ing sedentary activities [36] These findings were extended using a prospectivenested case-crossover design within the Physicians’ Health Study [37] Menwho exercised less than weekly had a 74-fold increased risk of SCD in theperiod during and 30 min after exertion compared to the risk observed dur-ing other activities In comparison, men who exercised at least five times perweek had an 11-fold increased risk However, this risk was still significantlyelevated compared to the risk during periods of lesser exertion A retrospectivecase–control study involving cardiac arrest victims in Seattle and King Countycame to similar conclusions [38]

The effect of vigorous exertion on the sympathetic nervous system and/orplaque vulnerability could account for both the transiently increased risk ofSCD during a bout of exertion and the ability of habitual vigorous exercise

to modify this excess risk In an autopsy study of men with CHD who diedsuddenly, the findings showed that men who died during exertion were morelikely to have plaque rupture than those who died at rest [39] Alternatively,chronic exercise has known beneficial effects on lipids that may improveplaque stability and also has direct electrophysiologic effects through thesympathetic nervous system Acute bouts of exercise, decrease vagal activ-ity leading to an acute increase in susceptibility to VF, whereas habitualexertion increases basal vagal tone resulting in increased cardiac electricalstability

Reassuringly, the absolute risk of SCD during any particular episode of orous exertion is extremely low in all studies (e.g 1 SCD per 1.51 millionepisodes in the Physicians’ Health Study [38]) So, despite large magnitudeincreases in the relative risk, SCD during vigorous exertion is a rare event.Little is currently known about whether more moderate levels of exer-tion might trigger SCD Preliminary data from the Triggers of VentricularArrhythmia Study suggest that both moderate and vigorous exertion maytrigger shocks for ventricular tachyarrhythmias among ICD patients

Silvia: “chap06” — 2005/10/6 — 22:32 — page 82 — #9

Figure 6.3 Daily numbers of sudden deaths related to CHD from January 10 through

23, 1994 On January 17, the day of the earthquake, there were 24 cases of sudden

death related to atherosclerotic cardiovascular disease (p < 001) (Reproduced from

Reference 41 with permission from Massachusetts Medical Society.)

studies have found increases in informant-reported objective life stresses, such

as death of a spouse and loss of job, either acutely or during the weeks beforethe SCD [40] On a population level, acute increases in the incidence of SCDhave been documented after disasters such as earthquakes or wars One suchexample is, the Northridge earthquake; there was a sharp increase in the num-ber of sudden deaths due to CHD on the day of the earthquake followed by

an unusually low incidence of such deaths in the week after [41] (Figure 6.3).This “natural experiment” exemplifies how emotional stress may precipit-ate cardiac events in those who may be predisposed to such events Of thetypes of mental stress, anger may be a particularly potent trigger of ventricu-lar arrhythmias One small study of 49 ICD patients found that anger was theonly emotion associated with ICD shocks for ventricular arrhythmias [42].Recently, mental stress induced by anger recall and mental arithmetic hasbeen demonstrated to induce cardiac electrical instability by increasing T-wavealternans among ICD patients with CHD Interestingly, these same stressorsdid not increase T-wave alternans among controls [43] Therefore, as sug-gested by the earthquake example, an underlying arrhythmic vulnerability isalso required for these potentially “triggering” events/emotions to result inlife-threatening arrhythmias

With respect to chronic mental stresses, depression, anxiety, and social tion have all been linked to increases in CHD mortality in diverse populations;and anxiety has been directly linked to SCD risk in three separate popula-tions [44] In the US Health Professionals Follow-up Study, high levels ofphobic anxiety as measured by the Crown-Crisp Index were associated with

isola-a three-fold increisola-ase in risk of CHD deisola-ath, which wisola-as entirely due to isola-a six-foldincrease in SCD [45] We have found similar results among women enrolled

in the Nurses’ Health Study, but the magnitude of the risk elevation was less

Silvia: “chap06” — 2005/10/6 — 22:32 — page 83 — #10

Clinical characteristics of SCD victims 83

(RR= 1.6; p = 03) Individuals with high levels of anxiety have reduced heart

rate variability compared to normal subjects, and the mechanism underlyingthe increased risk of SCD is again thought to involve alterations in autonomictone [44] similar to those described above for other triggers

Sleep

Along with the morning peak in SCD incidence, most studies have reported anadir during the nighttime sleeping hours [31,34] In one review, only 12% ofSCDs occurred during sleep [40] This would be less than half of the number ofcases expected to occur if the events were uniformly distributed throughoutthe 24-h period However, since deaths that occur during the usual hours

of sleep are less likely to be witnessed, these deaths are also less likely to

be classified as sudden Temporal patterns of ventricular tachyarrythmias inICD patients should be free from this potential bias, and most studies havedocumented a similar decrease in ventricular tachyarrhythmias during sleep[29,32] Since vagal tone and ventricular refractory periods are the highestduring sleep, the mechanism underlying the majority of the 12% of SCDsthat occur during sleep is unclear Some of the rare forms of SCD not associ-ated with structural heart disease described above occur preferentially duringsleep These include long QT3, where ventricular arrhythmias appear to betriggered by bradycardia, and Brugada syndrome Mutations in the cardiac

sodium channel gene, SCN5A, have been described in both of these disorders

and have also been linked to cases of sudden infant death syndrome, whichalso occur during sleep [46]

Pharmacologic agents and SCD

In addition to other activities, pharmacologic agents can also trigger lar arrhythmias and SCD The classic example of a drug-induced arrhythmia is

ventricu-torsades de pointes (TdP), a potentially lethal polymorphic ventricular

tachycar-dia seen in the setting of QT-prolongation Antiarrhythmic drugs (class IA andclass III agents) and nonantiarrhythmic drugs that prolong the QT interval caninduce this arrhythmia Examples of nonantiarrhythmic drugs that can pro-long the QT interval include macrolide antibiotics, antipsychotics, histaminereceptor antagonists (Terfenadine), and cholinergic antagonists (Cisapride)[47] A full listing is available at www.qtdrugs.org Although TdP second-ary to nonantiarrhythmic drugs is exceedingly rare (<1 case per 10 000 or

100 000 exposures) [48], rates of TdP in association with antiarrhythmicdrugs range from 2% to as high as 8% in association with Quinidine [47].Again, as for psychological triggers, the underlying vulnerability to ventriculararrhythmias influences risk Patients with structural heart disease, partic-ularly left ventricular systolic dysfunction and/or hypertrophy, are at anelevated risk of drug-induced TdP In addition, there may be genetic factorsthat influence risk Poorly penetrant mutations and/or polymorphisms inthe genes that result in congenital long-QT syndrome have been found in10–15% of patients with drug-associated long QT [49] Therefore, there may

Silvia: “chap06” — 2005/10/6 — 22:32 — page 84 — #11

84 Chapter 6

be individuals carrying silent mutations and/or predisposing polymorphisms

on LQTS genes who may manifest ventricular arrhythmias only when the

arrhythmogenic substrate is destabilized further by QT-prolonging drugs.Type IC antiarrhythmic agents can result in proarrhythmia through othermechanisms not dependent on QT-prolongation Although these agents aresafely utilized in younger patients without structural heart disease for a vari-ety of supraventricular arrhythmias, the same agents can result in devastatingconsequences when used in patients with known ischemic heart disease Inthis setting, otherwise nonfatal ischemic events can result in fatal ventricu-lar arrhythmias and SCD [50] Other classes of pharmacologic agents thatcan induce ventricular arrhythmias and SCD through a variety of mechan-isms include sympathomimetic agents (cocaine, amphetamines, etc.), digoxin,diuretics, and heavy alcohol consumption (>5 drinks/day).

References

1 Priori SG, Aliot E, Blomstrom-Lundqvist C et al Task force on sudden cardiac death

of the European Society of Cardiology Eur Heart J 2001; 22: 1374–1450.

2 Burke AP, Farb A, Pestaner J et al Traditional risk factors and the incidence of sudden coronary death with and without coronary thrombosis in blacks Circulation

2002; 105: 419–424.

3 Jouven X, Desnos M, Guerot C, Ducimetiere P Predicting sudden death in the

population: the Paris Prospective Study I Circulation 1999; 99: 1978–1983.

4 Albert CM, Chae CU, Grodstein F et al Prospective study of sudden cardiac death

among women in the United States Circulation 2003; 107: 2096–2101.

5 Weijenberg MP, Feskens EJ, Kromhout D Blood pressure and isolated systolic hypertension and the risk of coronary heart disease and mortality in elderly men

(the Zutphen Elderly Study) J Hypertens 1996; 14: 1159–1166.

6 Albert CM, Ma J, Rifai N, Stampfer MJ, Ridker PM Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac

death Circulation 2002; 105: 2595–2599.

7 Burke AP, Tracy RP, Kolodgie F et al Elevated C-reactive protein values and

atherosclerosis in sudden coronary death: association with different pathologies.

Circulation 2002; 105: 2019–2123.

8 Gorgels AP, Gijsbers C, de Vreede-Swagemakers J, Lousberg A, Wellens HJ hospital cardiac arrest – the relevance of heart failure The Maastricht Circulatory

Out-of-Arrest Registry Eur Heart J 2003; 24: 1204–1209.

9 Bowker TJ, Wood DA, Davies MJ et al Sudden, unexpected cardiac or unexplained

death in England: a national survey Quart J Med 2003; 96: 269–279.

10 Doolan A, Langlois N, Semsarian C Causes of sudden cardiac death in young

Australians Med J Aust 2004; 180: 110–112.

11 Maron BJ, Carney KP, Lever HM et al Relationship of race to sudden cardiac death

in competitive athletes with hypertrophic cardiomyopathy J Am Coll Cardiol 2003;

41: 974–980.

12 Goldstein S, Landis JR, Leighton R et al Characteristics of the resuscitated

out-of-hospital cardiac arrest victim with coronary heart disease Circulation 1981; 64:

977–984.

Silvia: “chap06” — 2005/10/6 — 22:32 — page 85 — #12

Clinical characteristics of SCD victims 85

13 Cobbe SM, Dalziel K, Ford I, Marsden AK Survival of 1476 patients

ini-tially resuscitated from out of hospital cardiac arrest Brit Med J 1996; 312:

1633–1637.

14 de Vreede-Swagemakers JJ, Gorgels AP, Dubois-Arbouw WI et al Circumstances and causes of out-of-hospital cardiac arrest in sudden death survivors Heart 1998;

79: 356–361.

15 Schaffer WA, Cobb LA Recurrent ventricular fibrillation and modes of death

in survivors of out-of-hospital ventricular fibrillation N Engl J Med 1975; 293:

259–262.

16 Weaver WD, Lorch GS, Alvarez HA, Cobb LA Angiographic findings and prognostic

indicators in patients resuscitated from sudden cardiac death Circulation 1976; 54:

895–900.

17 Lo YS, Cutler JE, Blake K, Wright AM, Kron J, Swerdlow CD Angiographic

coronary morphology in survivors of cardiac arrest Am Heart J 1988; 115:

781–785.

18 Mangi AA, Boeve TJ, Vlahakes GJ et al Surgical coronary revascularization and antiarrhythmic therapy in survivors of out-of-hospital cardiac arrest Ann Thorac

Surg 2002; 74: 1510–1516.

19 Maron BJ, Gohman TE, Aeppli D Prevalence of sudden cardiac death during

com-petitive sports activities in Minnesota high school athletes J Am Coll Cardiol 1998;

32: 1881–1884.

20 Phillips M, Robinowitz M, Higgins JR, Boran KJ, Reed T, Virmani R Sudden cardiac

death in Air Force recruits A 20-year review JAMA 1986; 256: 2696–2699.

21 Elliott PM, Poloniecki J, Dickie S et al Sudden death in hypertrophic

cardi-omyopathy: identification of high risk patients J Am Coll Cardiol 2000; 36:

23 Chugh SS, Chung K, Zheng ZJ, John B, Titus JL Cardiac pathologic findings reveal

a high rate of sudden cardiac death of undetermined etiology in younger women.

Am Heart J 2003; 146: 635–639.

24 Wever EF, Robles de Medina EO Sudden death in patients without structural heart

disease J Am Coll Cardiol 2004; 43: 1137–1144.

25 Chugh SS, Senashova O, Watts A et al Postmortem molecular screening in

unexplained sudden death J Am Coll Cardiol 2004; 43: 1625–1629.

26 Muller JE, Ludmer PL, Willich SN et al Circadian variation in the frequency of

sudden cardiac death Circulation 1987; 75: 131–138.

27 Cohen MC, Rohtla KM, Lavery CE, Muller JE, Mittleman MA Meta-analysis of

the morning excess of acute myocardial infarction and sudden cardiac death Am J

Cardiol 1997; 79: 1512–1516.

28 Willich SN, Goldberg RJ, Maclure M, Perriello L, Muller JE Increased onset of

sudden cardiac death in the first three hours after awakening Am J Cardiol 1992;

70: 65–68.

29 Englund A, Behrens S, Wegscheider K, Rowland E (for the European 7219 Jewel Investigators) Circadian variation of malignant ventricular arrhythmias in patients with ischemic and nonischemic heart disease after cardioverter defibrillator

implantation J Am Coll Cardiol 1999; 34: 1560–1568.

Silvia: “chap06” — 2005/10/6 — 22:32 — page 86 — #13

86 Chapter 6

30 Peters RW, Muller JE, Goldstein S, Byington R, Friedman LM (for the BHAT Study Group) Propranolol and the morning increase in the frequency of sudden cardiac

death (BHAT Study) Am J Cardiol 1989; 63: 1518–1520.

31 Peckova M, Fahrenbruch CE, Cobb LA, Hallstrom AP Circadian variations in

the occurrence of cardiac arrest: initial and repeat episodes Circulation 1998; 98:

31–39.

32 Kozak M, Krivan L, Semrad B Circadian variations in the occurrence of ventricular

tachyarrhythmias in patients with implantable cardioverter defibrillators Pacing

Clin Electrophysiol 2003; 26: 731–735.

33 Peckova M, Fahrenbruch CE, Cobb LA, Hallstrom AP Weekly and seasonal

variation in the incidence of cardiac arrests Am Heart J 1999; 137: 512–515.

34 Arntz HR, Willich SN, Schreiber C, Bruggemann T, Stern R, Schultheiss HP Diurnal, weekly and seasonal variation of sudden death Population-based analysis of 24,061

consecutive cases Eur Heart J 2000; 21: 315–320.

35 Muller D, Lampe F, Wegscheider K, Schultheiss HP, Behrens S Annual

distribu-tion of ventricular tachycardias and ventricular fibrilladistribu-tion Am Heart J 2003; 146:

1061–1065.

36 Thompson PD, Funk EJ, Carleton RA, Sturner WQ Incidence of death

dur-ing joggdur-ing in Rhode Island from 1975 through 1980 JAMA 1982; 247:

2535–2538.

37 Albert CM, Mittleman MA, Chae CU, Lee I-M, Hennekens CH, Manson JE

Trig-gering of sudden cardiac death by vigorous exertion N Engl J Med 2000: 343:

1351–1361.

38 Siscovick DS, Weiss NS, Fletcher RH, Lasky T The incidence of primary cardiac

arrest during vigorous exercise N Engl J Med 1984; 311: 874–847.

39 Burke AP, Farb A, Malcom GT, Llang Y-H, Smialek J, Virmani R Plaque rupture

and sudden death related to exertion in men with coronary artery disease JAMA

1999; 281: 921–926.

40 Willich SN, Maclure M, Mittleman M, Arntz H-R, Muller JE Sudden cardiac death:

support for a role of triggering in causation Circulation 1993; 87: 1442–1450.

41 Leor J, Poole WK, Kloner RA Sudden cardiac death triggered by an earthquake.

N Engl J Med 1996; 334: 413–419.

42 Lampert R, Joska T, Burg MM, Batsdord WP, McPherson CA, Jain D

Emo-tional and physical precipitants of ventricular arrhythmia Circulation 2002; 106:

1800–1805.

43 Kop WJ, Krantz DS, Nearing BD et al Effects of acute mental stress and exercise

on T-wave alternans in patients with implantable cardioverter defibrillators and

controls Circulation 2004; 109: 1864–1869.

44 Kubzansky LD, Kawachi I Going to the heart of the matter: negative emotions and

coronary heart disease J Psychosom Res 2000; 48: 323–337.

45 Kawachi I, Colditz GA, Ascherio A et al Coronary heart disease/myocardial

infarc-tion: prospective study of phobic anxiety and risk of coronary heart disease in men.

Circulation 1994; 89: 1992–1997.

46 Moric E, Herbert E, Trusz-Gluza M, Filipecki A, Mazurek U, Wilczok T The

implic-ations of genetic mutimplic-ations in the sodium channel gene (SCN5A) Europace 2003;

5: 325–334.

47 Viskin S Long QT syndromes and torsade de pointes Lancet 1999; 354: 1625–1633.

48 Haverkamp W, Breithardt G, Camm AJ et al The potential for QT prolongation and

proarrhythmia by non-antiarrhythmic drugs: clinical and regulatory implications.

Silvia: “chap06” — 2005/10/6 — 22:32 — page 87 — #14

Clinical characteristics of SCD victims 87

Report on a policy conference of the European Society of Cardiology Eur Heart J

2000; 21: 1216–1231.

49 Yang P, Kanki H, Drolet B et al Allelic variants in long-QT disease genes

in patients with drug-associated torsades de pointes Circulation 2002; 105:

Silvia: “chap06” — 2005/10/6 — 22:32 — page 88 — #15

Silvia: “chap07” — 2005/10/6 — 22:32 — page 89 — #1

Section two:

Disease states and special

populations

Silvia: “chap07” — 2005/10/6 — 22:32 — page 90 — #2

CHAPTER 7

Ischemic heart disease

William Wijns and Elliott M Antman

Epidemiology/scope of problem

Although considerable advances have occurred in the management of patientswith cardiovascular diseases over the last 50 years, it still remains the singlemost common cause of natural death in industrialized countries It is difficult

to obtain precise estimates of the worldwide incidence of sudden cardiac death(SCD), but it is generally accepted that about 50% of cardiovascular deaths

in industrialized countries are due to SCD [1] Therefore, extension of thepandemic of ischemic heart disease to developing countries may lead to anincrease in the incidence of SCD in developing nations of the world as well.Epidemiologic studies have established ventricular tachycardia/ventricularfibrillation (VT/VF) as the typical sequence of electrical events leading to SCD.The pathophysiologic construct that has been proposed to explain SCD holdsthat patients experiencing SCD have an underlying high-risk substrate uponwhich certain triggers are superimposed (transient ischemia, hemodynamicfluctuations, neurocardiovascular influences, environmental factors) followed

by precipitation of the fatal sequence of electrical events Ischemic heart ease is estimated to be the cause of the high-risk underlying substrate in 80%

dis-of patients suffering from SCD [1,2] (Figure 7.1) Two broad patterns dis-of tiation of the fatal arrhythmia have been reported in patients with ischemicheart disease: (1) acute myocardial ischemia triggers a ventricular tachyar-rhythmia in patients who may or may not have a preexisting myocardial scar,and (2) a ventricular tachyarrhythmia occurs in the setting of a myocardial scarfrom a previous infarction but without evidence of acute myocardial ischemiaoccurring at the time of the ventricular tachyarrhythmia

ini-The important factors for identification of patients at risk when ing strategies for prevention of SCD in patients with ischemic heart diseaseinclude: (1) the size of the population subgroup at risk and (2) the timedependence of risk of SCD Figure 7.2 illustrates the challenge of predict-ing and managing patients at risk of SCD [3] While the overall incidence ofSCD in the adult population is low, the large denominator of patients in thatsubgroup results in a large contribution to the total number of SCD eventsper year Similarly, patients at high risk, such as those with a previous out-of-hospital cardiac arrest or those with a previous myocardial infarction (MI),reduced ejection fraction, and history of VT/VF, have a higher incidence of SCD

consider-91

Silvia: “chap07” — 2005/10/6 — 22:32 — page 92 — #4

92 Chapter 7

Uncommon

causes

Genetic factors, hypertension

Sudden death

Typical sequence of electrical events:

Sinus rhythm Ventricular tachycardia Ventricular fibrillation Asystole

Triggers of cardiac arrest:

transient ischemia, hemodynamic fluctuations, neurocardiovascular influences, environmental factors

Dilated cardiomyopathy

Chronic myocardial scar caused by infarction

Acute plaque destabilization: rupture, fissure, hemorrhage, thrombosis

Genetic factors, infection, others

Cardiomyopathy

Coronary atherosclerosis

Risk factors for coronary atherosclerosis: older age, male sex, hyperlipidemia, smoking, hypertension, diabetes

Figure 7.1 Pathophysiology and epidemiology of sudden death from cardiac causes Reproduced from Reference 1 (p 1475), with permission from the Massachusetts Medical Society.

when considered as a specific subgroup, but the smaller absolute number ofpatients relative to the overall adult population results in a relatively smallercontribution to the total number of sudden cardiac events per year

The risk of SCD following a major cardiovascular (CV) event varies in anonlinear fashion after the acute event The idealized survival curves shown

in Figure 7.3 emphasize that the highest risk of mortality is in the first6–18 months after which the slope of the survival curve in high-risk patientsappears to be roughly parallel to the slope of the survival curve for low-risk patients Of note, the data on which these curves are based may notreflect the impact of contemporary interventions in patients with ischemicheart disease For example, aggressive interventions at limitation of infarctsize in patients with ST elevation myocardial infarction (STEMI) theoretic-ally would decrease the proportion of patients with a large myocardial scar,putting them at risk for a VT On the other hand, the increasing age of the

Silvia: “chap07” — 2005/10/6 — 22:32 — page 93 — #5

Ischemic heart disease 93

Convalescent phase VT/VF after MI

EF < 30%

heart failure Any prior coronary event High coronary risk subgroup Overall incidence

in adult population

Out-of-hospital cardiac arrest survivors

3.3%

11.2%

EF (<35%)

(a)

(b)

Sudden

Sudden Nonsudden

Nonsudden

Figure 7.2 Incidence of sudden and nonsudden cardiac deaths in population

subgroups, and the relation of total number of events per year to incidence figures Approximations of subgroup incidence figures, and the related population pool from which they are derived, are presented Approximately 50% of all cardiac deaths are sudden and unexpected The incidence triangle on the left (“percent/year”) indicates the approximate percentage of sudden and nonsudden deaths in each of the

population subgroups indicated, ranging from the lowest percentage in unselected adult populations (0.1–2% per year) to the highest percentage in patients with VT or

VF during convalescence after an MI (approximately 50% per year) The triangle on the right indicates the total number of events per year in each of these groups, to reflect incidence in context with the size of the population subgroups The highest risk categories identify the smallest number of total annual events, and the lowest incidence category accounts for the largest number of events per year (EF = ejection fraction; VT = ventricular tachycardia; VF = ventricular fibrillation; MI = myocardial infarction) Reproduced from Reference 3 (p 1620), with permission from the McGraw-Hill Company.

Silvia: “chap07” — 2005/10/6 — 22:32 — page 94 — #6

94 Chapter 7

Low-risk subgroup, free of major CV events High-risk subgroup, after major CV events

Figure 7.3 Idealized curves of survival from sudden death are shown for a population

of patients with known cardiovascular disease but at low risk because of freedom from major cardiovascular (CV) events (top curve) and for populations of patients who have survived a major cardiovascular event (bottom curve) Attrition over time

is accelerated in both absolute and relative terms for the initial 6–18 months after the major cardiovascular event After the initial attrition, the slopes of the curves for the high-risk and low-risk populations parallel each other, highlighting both the early attrition and the attenuation of risk after 18–24 months These relations have been observed in diverse high-risk subgroups (cardiac arrest survivors, post-myocardial infarction patients with high-risk markers, recent onset of heart failure), and

highlight the changing risk pattern as a function of time and the importance of the time dimension for recognition and intervention in strategies designed to alter outcome Reproduced from Reference 4 with permission from Elsevier.

population results in an expanding epidemiologic cohort at increased riskfor SCD events Finally, the impact of primary prevention strategies with

an implantable cardioverter-defibrillator (ICD) is not reflected in the curvesshown in Figure 7.3

Diagnostic modalities

Table 7.1 shows a summary of clinical markers that have been identified asplacing patients at increased risk of SCD [1] With the exception of specificECG abnormalities indicative of the Brugada or Wolff–Parkinson–White syn-dromes, all of the markers listed are applicable to evaluation of patients withischemic heart disease However, a fundamental problem in using the indic-ators listed in the table is the unsatisfactory predictive power in an individualpatient While the indicators shown in Table 7.1 are valid when discussingrisk from a broad population perspective, the sensitivity and specificity of theindicators in an individual patient are far from ideal This has inspired clini-cians to continue in their search for additional indicators of risk of SCD andalso to seek alternative treatment strategies, especially those that focus on

Silvia: “chap07” — 2005/10/6 — 22:32 — page 95 — #7

Ischemic heart disease 95 Table 7.1 Indicators of an increased risk of sudden death from arrhythmia.

Conventional coronary risk factors

Low power to discriminate the individual person

at risk for sudden death from arrhythmia Clinical markers

NYHA functional class

Ejection fraction

Extent of structural disease

High power to predict death from cardiac causes; relatively low specificity at predictors of death from arrhythmia Ambient ventricular arrhythmia

other variables Higher predictive power, with low ejection fraction

death from arrhythmia Specific abnormalities

(e.g prolonged QT interval,

right bundle-branch block plus

ST-segment elevation in

lead V1 (Brugada syndrome),

ST-segment and T-wave

abnormalities in leads V1

and V2 (right ventricular

dysplasia), delta waves

(Wolff–Parkinson–White

syndrome))

High degree of accuracy

in identifying specific electrical abnormalities

High resolution ECG

(Continued)