(Circulation. 1999;99:1978-1983.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Predicting Sudden Death in the Population
The Paris Prospective Study I
From Service de Cardiologie, Hôpital Boucicaut (X.J., M.D., C.G.,) and Unité INSERM 258 d'Epidémiologie Cardiovasculaire, Hôpital Broussais (P.D.), Paris, France.
Correspondence to Xavier Jouven, Service de Cardiologie, Hôpital Boucicaut, 78 Rue de la Convention, 75015 Paris, France. E-mail xavier.jouven{at}bcc.ap-hop-paris.fr
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Abstract |
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Background—Sudden death was found to share the same set of usual risk factors as coronary events and therefore could not be specifically predicted in the population. It appears, however, that parental history of sudden death has not been investigated yet as a risk factor for sudden death. Therefore, we assessed risk factors, including parental sudden death, associated with the occurrence of sudden death in a long-term cohort study.
Methods and Results—We included 7746 men employed by the city of Paris who were 43 to 52 years of age in 1967 to 1972 in the Paris Prospective Study I. Each subject underwent a physical examination and an ECG, provided blood for laboratory tests, and answered questionnaires administered by trained interviewers who paid particular attention to family medical history. Men with known ischemic cardiac disease were further excluded from analysis. For 95.5% of the men, vital status was obtained from specific inquiries until retirement, then by death certificates. Resting heart rate, systolic or diastolic blood pressure, tobacco consumption, body mass index, diabetes status, serum cholesterol, and parental history of sudden death were independent factors associated with sudden death during follow-up (23 years on average). When adjusted for confounding variables, including parental history of myocardial infarction, relative risk of sudden death associated with parental sudden death was 1.80 (95% CI, 1.11 to 2.88).
Conclusions—Parental sudden death is an independent risk factor for sudden death in middle-aged men. The existence of familial risk factors for sudden death may help provide better identification of subjects at high risk of and early prevention of sudden death.
Key Words: death, sudden • epidemiology • risk factors
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Introduction |
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Sudden death is a major problem in industrially developed countries. It is frequently an unexpected first (and last) clinical manifestation of coronary artery disease, but it has been reported that up to 50% of sudden deaths in men occur in persons without knowledge of prior coronary heart disease.1 Despite a decline in ischemic heart disease mortality2 and the progress has been made in resuscitation, treatment of sudden death victims is frequently unsuccessful.3 4 The ideal solution would be to prevent the disease process that causes the initial episode of cardiac arrest. Early identification of subjects at high risk of sudden death is therefore essential to propose preventive treatment strategies. But identifying long-term risk factors that predispose specifically to sudden death remains difficult. The usual risk factors associated with coronary heart disease are also predictive of sudden death: age, systolic blood pressure, serum cholesterol, vital capacity, cigarette smoking, relative weight, diabetes, heart rate, and ECG abnormalities.1 5 6 7 8 9 Elevated heart rate, arrhythmia,10 and tobacco consumption11 have been described as more highly associated with sudden death than with other cardiac end points. Family history of coronary heart disease is an independent risk factor for coronary heart disease,12 13 and when its definition includes both myocardial infarction and primary cardiac arrest in parents, it has been found to be an independent risk factor for primary cardiac arrest in a recently published case-control study.14 No information is available, however, on the specific association of parental history of sudden death with the occurrence of sudden death. Case-control studies are not very suitable because of a possible recall bias (family members may selectively and artificially report more familial sudden death events after the occurrence of 1 case of sudden death). Thus, we used the long follow-up period of the Paris Prospective Study I (>20 years) to assess the role of reported parental history of sudden death as a predisposing factor to sudden death in middle-aged men.
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Methods |
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Details of the Paris Prospective Study I recruitment, design, and procedures have been described elsewhere.15 Briefly, examination of 7746 native Frenchmen employed by the Paris Civil Service who were 43 to 52 years of age was carried out from 1967 to 1972. Subjects underwent ECG and physical examination conducted by a physician, provided blood samples for laboratory tests, and answered questionnaires administered by trained interviewers regarding sociodemographic factors, family and personal medical histories, and smoking habits. Subjects were asked for a parental myocardial infarction, for parental age at death, and whether the death was sudden or not. There were 3 measurements of diastolic and systolic blood pressures during the examination, and the mean of those measures was used for analysis. Diabetes status was defined as past or present reported diabetes, whether treated or not.
The administrative department in charge of the population provided a list of deceased subjects annually until participant retirement. All available data relevant to the causes of death were collected from specific inquiries, ie, medical records from hospital departments or general practitioners identified by relatives of the deceased. After retirement, causes of death were obtained from death certificates. The data were then reviewed by an independent medical committee (3 medical doctors not involved in the study), which assigned a principal cause of death for each case. The ninth revision of the International Classification of Diseases16 was used for coding. Sudden death (code 798.1) was defined as a natural death occurring within 1 hour of onset of acute symptoms. Fatal myocardial infarction (codes 410 through 414) was coded only if the death was found to be strictly related to a myocardial infarction.
The deadline for the follow-up period was January 1, 1994. Vital status could not be obtained for 355 subjects (4.6%). Men with a diagnosis of ischemic heart disease (myocardial infarction or angina) established at the beginning of the study on personal medical history, clinical examination, and ECG were excluded from analysis. The analysis was conducted on the remaining 7079 subjects.
Statistical Analysis
ANOVA and 
2 analysis were used
for global comparisons between groups. Because of the skewed
distribution of triglycerides, log-transformed values were
used in the analysis. Relative risks (RRs) of mortality were
adjusted for confounding factors and estimated by the Cox
proportional-hazard model. SAS procedures (Statistical Analysis
System) were used for analysis.
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Results |
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Among 7079 men followed for an average of 23 years, there were 2083 deaths, among which were 603 cardiovascular deaths distributed as follows: 118 sudden deaths (19.6%), 192 fatal myocardial infarctions (31.8%), 31 deaths caused by cardiac failure (5.1%), 110 deaths resulting from other cardiac causes (18.2%), 100 deaths caused by strokes (16.6%), and 52 deaths resulting from other vascular causes (8.6%).
At entry, 497 subjects declared a history of sudden death for their fathers and 281 for their mothers, providing 759 subjects with parental sudden death, including 19 subjects with sudden death for both parents.
In addition, 321 subjects reported myocardial infarction for their fathers and 162 for their mothers, providing 476 subjects who reported any parental history, including 7 subjects with myocardial infarction for both parents.
Characteristics of the subjects are given in Table 1
. All reported
parameters were significantly different between the 3
groups of subjects: those who died of sudden death, those who died of
myocardial infarction, and all other participants taken as control
subjects. A parental sudden death was found in 18.6% of the subjects
who died of sudden death (n=22), 9.9% of subjects who died of
myocardial infarction (n=19), and 10.6% of the control subjects
(n=718).
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Table 2 indicates the RR ratios for
sudden death and fatal myocardial infarction associated with each
parameter reported in Table 1
. Heart rate, systolic
and diastolic blood pressures, tobacco consumption,
triglycerides, and cholesterol level were risk
factors for both sudden death and fatal myocardial infarction. Relative
weight (body mass index) was a risk factor for sudden death but did not
reach significance for fatal myocardial infarction (P=0.06),
whereas diabetes status was a strong risk factor for sudden death (RR,
3.23; 95% CI, 1.64 to 6.37) but not for fatal myocardial infarction
(RR, 1.47; 95% CI, 0.69 to 3.12).
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Age at the time of death was 59.2±6.0 years for sudden death and 64.3±6.4 years for fatal myocardial infarction (P<0.0001).
Parental history of sudden death was a risk factor for the occurrence of sudden death (RR, 1.95; 95% CI, 1.23 to 3.10) but was not associated with the occurrence of fatal myocardial infarction (RR, 0.97; 95% CI, 0.60 to 1.55). Both mother's sudden death and father's sudden death were risk factors for the subject's sudden death but not for fatal myocardial infarction.
Conversely, parental history of myocardial infarction was a risk factor for the occurrence of fatal myocardial infarction (RR, 2.09; 95% CI, 1.36 to 3.20) but was not associated with the occurrence of sudden death (RR, 1.30; 95% CI, 0.68 to 2.49). Both mother's and father's myocardial infarctions were risk factors for fatal myocardial infarction but not for sudden death.
When age, body mass index, heart rate, systolic blood
pressure (or diastolic blood pressure), diabetes status,
tobacco consumption, cholesterol level,
triglyceride level, parental history of myocardial
infarction, and parental history of sudden death were
simultaneously entered into the survival model (Table 3), parental history of sudden death
remained an independent risk factor for sudden death (RR, 1.80; 95%
CI, 1.11 to 2.88) but not for fatal myocardial infarction (RR, 0.85;
95% CI, 0.52 to 1.39), whereas parental history of myocardial
infarction remained an independent risk factor for fatal myocardial
infarction (RR, 2.30; 95% CI, 1.47 to 3.60) but not for sudden death
(RR, 1.16; 95% CI, 0.60 to 2.25).
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There is a positive and significant correlation (r=0.52,
P=0.01) between the age of the parent and age of the progeny
(n=22) at the times of their sudden death (see the
Figure).
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When only deaths in participants <65 years of age were considered for
subjects (sudden death, n=93; fatal myocardial infarction, n=96) and
for their parents, the results did not change appreciably (Table 4), and the adjusted RR associated with
parental sudden death remained statistically significant for the
occurrence of sudden death (RR, 2.00; 95% CI, 1.02 to 3.90) but not
for the occurrence of fatal myocardial infarction (RR, 0.70; 95% CI,
0.26 to 1.81), whereas the adjusted RR associated with parental
myocardial infarction remained significant for the occurrence of fatal
myocardial infarction (RR, 3.42; 95% CI, 1.22 to 9.54) but not for the
occurrence of sudden death (RR, 1.73; 95% CI, 0.42 to 7.14).
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Despite the small number of subjects with both father's and mother's medical histories of sudden death (n=19), we looked for cumulative effects. The RR for sudden death of having 1 parental history of sudden death was 1.89, and the RR of having 2 parental histories of sudden deaths was 9.44 (P=0.01).
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Discussion |
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Risk Factors of Sudden Death
The usual risk factors associated with sudden death were confirmed in this long-term, prospective study of a middle-aged working male population.1 5 8 9 10 14 Parental history of myocardial infarction and other usual risk factors were also confirmed as risk factors for fatal myocardial infarction.12 13 In both univariate and multivariate analyses, diabetes status remained associated with sudden death7 but not with fatal myocardial infarction. It is likely that the propensity for sudden death in individuals with coronary disease may be enhanced by diabetes-associated autonomic neuropathy or microvascular disease affecting the conduction system of the heart. But subjects with diabetes or glucose intolerance are also prone to earlier development of extracoronary macrovascular (cerebral and peripheric) and microvascular diseases (kidney, retina, and nerves) that may contribute to the particular association with sudden death.
The original finding of this study concerned the role of parental history of sudden death as a predictor of sudden death. The correlation between age of the parent and that of the progeny at their time of sudden death appears to be a supplementary indication in favor of this relationship.
Possible Etiologic Pathways
Sudden death in the young does not have the same causes as in
adults; myocarditis, hypertrophic cardiomyopathy,
and conduction system abnormalities are the major underlying causes in
subjects <20 years of age.17 However, the prevalence of
coronary artery disease increases with age, and this condition
is the most frequent underlying cause in patients >30 years of
age.17 18 If parental history of coronary heart
disease is a well-known risk factor for coronary heart
disease,12 13 we were unable to find any study that
reported data on parental history of sudden death as a specific risk
factor for sudden death.
This result suggests a familial risk of sudden death distinct from the familial risk pattern of myocardial infarction. Because coronary disease is very frequent in sudden death patients >40 years of age,1 7 we can hypothesize that the expression and mechanisms of coronary disease may be under partial familial control, which may cause sudden death rather than fatal myocardial infarction for some subjects. According to Davis and Thomas,19 20 plaque fissure and intraintimal thrombosis are observed more commonly in patients with sudden ischemic death than in patients with nonsudden ischemic death.
But this familial risk may be related to noncoronary disease that can also be involved in the occurrence of sudden death. Some cases of hypertrophic21 22 and dilated cardiomyopathy23 24 are familial. Some long-QT syndromes are also familial,25 and some cardiomyopathies that may cause arrhythmia may be familial (certain forms of arrhythmogenic right ventricular dysplasia26 27 ). A genetic basis for idiopathic ventricular fibrillation has recently been described28 in 6 small families and a few sporadic patients with a peculiar ECG pattern consisting of right bundle-branch block and ST-segment elevation in leads V1 through V3.29 But because of the rare prevalence of familial forms of all those specific diseases in middle-aged men, it is difficult to hypothesize that they play a major role in the occurrence of sudden death. However, it currently is not possible to give specific weight to each of the 2 mechanisms; in particular, it is not possible to rule out either mechanism. In any case, the role of environmental and/or genetic factors in this association is unknown.
Study Limitations
It remains difficult to assess the impact of the definition of
sudden death on robustness of the results. Although sudden death may be
defined in various ways, the common working definition is a natural
death occurring within 1 hour of onset of acute symptoms. Although many
sudden deaths are instantaneous or unwitnessed, the elapsed time can be
at least roughly estimated.30 It is likely that we had
some inaccurate coding for sudden death from death certificates, mainly
because of imprecise knowledge of the elapsed time, and some inaccurate
coding for parental medical history of sudden death declared at the
screening interview. Sensibility and positive predictive value of death
certificates compared with autopsies range from 70% to 90%, and death
certificates generally underestimate the number of deaths from
ischemic cardiomyopathy.31 32 33 34
Thus, misclassification cases are likely to be conservative and might
tend to reduce the strength of the association between sudden death and
parental history of sudden death.
When the study setting is retrospective, relatives of men with recent sudden death may more frequently selectively report familial diseases (true or supposed) compared with control subjects, and this recall bias may exaggerate the findings. The recall bias can be ruled out in the present study.
The diagnosis of sudden death can be debatable and imprecise among older subjects who are susceptible to various medical disorders. Nevertheless, we found consistent results when an age limit of 65 years was given to both sudden death diagnosis in the cohort and the definition of family history of sudden death.
Conclusions
Besides heart rate, systolic or diastolic
blood pressure, relative weight, diabetes status, tobacco consumption,
and serum cholesterol, the existence of familial factors
for sudden death may help in early identification of subjects with high
risk of sudden death. It would therefore be useful to ask every patient
about a possible parental history of sudden death, as is frequently
done for familial history of myocardial infarction. It may then be
possible to reduce the risk of sudden death in secondary35
and primary prevention by correcting classic risk factors, eg, by
lowering cholesterol,36 losing weight, and
quitting smoking.37 Thus, the existence of a familial risk
factor for sudden death enhances the necessity to correct the other
modifiable risk factors, particularly those in high-risk
subjects.
Received August 18, 1998; revision received December 31, 1998; accepted January 11, 1999.
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A.-J. L.H.J. Aarnoudse, C. Newton-Cheh, P. I.W. de Bakker, S. M.J.M. Straus, J. A. Kors, A. Hofman, A. G. Uitterlinden, J. C.M. Witteman, and B. H.C. Stricker Common NOS1AP Variants Are Associated With a Prolonged QTc Interval in the Rotterdam Study Circulation, July 3, 2007; 116(1): 10 - 16. [Abstract] [Full Text] [PDF]
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J.-P. Empana, P. Duciemetiere, B. Balkau, and X. Jouven Contribution of the metabolic syndrome to sudden death risk in asymptomatic men: the Paris Prospective Study I Eur. Heart J., May 1, 2007; 28(9): 1149 - 1154. [Abstract] [Full Text] [PDF]
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G. F. Tomaselli A Failure to Adapt: Ankyrins in Congenital and Acquired Arrhythmias Circulation, January 30, 2007; 115(4): 428 - 429. [Full Text] [PDF]
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K. S. Kaikkonen, M.-L. Kortelainen, E. Linna, and H. V. Huikuri Family History and the Risk of Sudden Cardiac Death as a Manifestation of an Acute Coronary Event Circulation, October 3, 2006; 114(14): 1462 - 1467. [Abstract] [Full Text] [PDF]
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J. C. Lopshire and D. P. Zipes Sudden Cardiac Death: Better Understanding of Risks, Mechanisms, and Treatment Circulation, September 12, 2006; 114(11): 1134 - 1136. [Full Text] [PDF]
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L. R.C. Dekker, C. R. Bezzina, J. P.S. Henriques, M. W. Tanck, K. T. Koch, M. W. Alings, A. E.R. Arnold, M.-J. de Boer, A. P.M. Gorgels, H. R. Michels, et al. Familial Sudden Death Is an Important Risk Factor for Primary Ventricular Fibrillation: A Case-Control Study in Acute Myocardial Infarction Patients Circulation, September 12, 2006; 114(11): 1140 - 1145. [Abstract] [Full Text] [PDF]
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Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death--Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) J. Am. Coll. Cardiol., September 5, 2006; 48(5): 1064 - 1108. [Full Text] [PDF]
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Developed in Collaboration With the European Heart, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) J. Am. Coll. Cardiol., September 5, 2006; 48(5): e247 - e346. [Full Text] [PDF]
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D. P. Zipes, D. P. Zipes, A. J. Camm, M. Borggrefe, A. E. Buxton, B. Chaitman, M. Fromer, G. Gregoratos, G. Klein, A. J. Moss, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death--executive summary: A report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death) Developed in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. Eur. Heart J., September 1, 2006; 27(17): 2099 - 2140. [Full Text] [PDF]
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N. Sotoodehnia, D. S. Siscovick, M. Vatta, B. M. Psaty, R. P. Tracy, J. A. Towbin, R. N. Lemaitre, T. D. Rea, J. P. Durda, J. M. Chang, et al. {beta}2-Adrenergic Receptor Genetic Variants and Risk of Sudden Cardiac Death Circulation, April 18, 2006; 113(15): 1842 - 1848. [Abstract] [Full Text] [PDF]
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E. C. Stecker, C. Vickers, J. Waltz, C. Socoteanu, B. T. John, R. Mariani, J. H. McAnulty, K. Gunson, J. Jui, and S. S. Chugh Population-Based Analysis of Sudden Cardiac Death With and Without Left Ventricular Systolic Dysfunction: Two-Year Findings from the Oregon Sudden Unexpected Death Study J. Am. Coll. Cardiol., March 21, 2006; 47(6): 1161 - 1166. [Abstract] [Full Text] [PDF]
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F. Brigadeau, C. Kouakam, D. Klug, C. Marquie, A. Duhamel, F. Mizon-Gerard, D. Lacroix, and S. Kacet Clinical predictors and prognostic significance of electrical storm in patients with implantable cardioverter defibrillators Eur. Heart J., March 2, 2006; 27(6): 700 - 707. [Abstract] [Full Text] [PDF]
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Part 2: Adult Basic Life Support Circulation, November 29, 2005; 112(22_suppl): III-5 - III-16. [Full Text] [PDF]
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M. Shah, F. G. Akar, and G. F. Tomaselli Molecular Basis of Arrhythmias Circulation, October 18, 2005; 112(16): 2517 - 2529. [Abstract] [Full Text] [PDF]
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X. Jouven, R. N. Lemaitre, T. D. Rea, N. Sotoodehnia, J.-P. Empana, and D. S. Siscovick Diabetes, glucose level, and risk of sudden cardiac death Eur. Heart J., October 2, 2005; 26(20): 2142 - 2147. [Abstract] [Full Text] [PDF]
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M.-R. Movahed, M. Hashemzadeh, and M. M. Jamal Increased Prevalence of Third-Degree Atrioventricular Block in Patients With Type II Diabetes Mellitus Chest, October 1, 2005; 128(4): 2611 - 2614. [Abstract] [Full Text] [PDF]
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G. Thorgeirsson, G. Thorgeirsson, H. Sigvaldason, and J. Witteman Risk factors for out-of-hospital cardiac arrest: the Reykjavik Study Eur. Heart J., August 1, 2005; 26(15): 1499 - 1505. [Abstract] [Full Text] [PDF]
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X. Jouven, J.-P. Empana, P. J. Schwartz, M. Desnos, D. Courbon, and P. Ducimetiere Heart-Rate Profile during Exercise as a Predictor of Sudden Death N. Engl. J. Med., May 12, 2005; 352(19): 1951 - 1958. [Abstract] [Full Text] [PDF]
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A. Diaz, M. G. Bourassa, M.-C. Guertin, and J.-C. Tardif Long-term prognostic value of resting heart rate in patients with suspected or proven coronary artery disease Eur. Heart J., May 2, 2005; 26(10): 967 - 974. [Abstract] [Full Text] [PDF]
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J.P. Empana, P. Ducimetiere, M.A. Charles, and X. Jouven Sagittal Abdominal Diameter and Risk of Sudden Death in Asymptomatic Middle-Aged Men: The Paris Prospective Study I Circulation, November 2, 2004; 110(18): 2781 - 2785. [Abstract] [Full Text] [PDF]
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M. Josephson and H. J.J. Wellens Implantable Defibrillators and Sudden Cardiac Death Circulation, June 8, 2004; 109(22): 2685 - 2691. [Full Text] [PDF]
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D. E. Arking, S. S. Chugh, A. Chakravarti, and P. M. Spooner Genomics in Sudden Cardiac Death Circ. Res., April 2, 2004; 94(6): 712 - 723. [Abstract] [Full Text] [PDF]
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M. Naghavi, P. Libby, E. Falk, S. W. Casscells, S. Litovsky, J. Rumberger, J. J. Badimon, C. Stefanadis, P. Moreno, G. Pasterkamp, et al. From Vulnerable Plaque to Vulnerable Patient: A Call for New Definitions and Risk Assessment Strategies: Part II Circulation, October 14, 2003; 108(15): 1772 - 1778. [Abstract] [Full Text] [PDF]
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J. Dallongeville, J. Yarnell, P. Ducimetiere, D. Arveiler, J. Ferrieres, M. Montaye, G. Luc, A. Evans, A. Bingham, B. Hass, et al. Fish Consumption Is Associated With Lower Heart Rates Circulation, August 19, 2003; 108(7): 820 - 825. [Abstract] [Full Text] [PDF]
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H. V. Huikuri, T. H. Makikallio, M. J. P. Raatikainen, J. Perkiomaki, A. Castellanos, and R. J. Myerburg Prediction of Sudden Cardiac Death: Appraisal of the Studies and Methods Assessing the Risk of Sudden Arrhythmic Death Circulation, July 8, 2003; 108(1): 110 - 115. [Full Text] [PDF]
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A. P.M Gorgels, C. Gijsbers, J. de Vreede-Swagemakers, A. Lousberg, and H. J.J Wellens Out-of-hospital cardiac arrest-the relevance of heart failure. The Maastricht Circulatory Arrest Registry Eur. Heart J., July 1, 2003; 24(13): 1204 - 1209. [Abstract] [Full Text] [PDF]
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D. P. Zipes Less Heart Is More Circulation, May 27, 2003; 107(20): 2531 - 2532. [Full Text] [PDF]
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C. M. Albert, C. U. Chae, F. Grodstein, L. M. Rose, K. M. Rexrode, J. N. Ruskin, M. J. Stampfer, and J. E. Manson Prospective Study of Sudden Cardiac Death Among Women in the United States Circulation, April 29, 2003; 107(16): 2096 - 2101. [Abstract] [Full Text] [PDF]
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F. B. Hu, E. Cho, K. M. Rexrode, C. M. Albert, and J. E. Manson Fish and Long-Chain {omega}-3 Fatty Acid Intake and Risk of Coronary Heart Disease and Total Mortality in Diabetic Women Circulation, April 15, 2003; 107(14): 1852 - 1857. [Abstract] [Full Text] [PDF]
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M. Firouzi and W. A. Groenewegen Gene polymorphisms and cardiac arrhythmias Europace, January 1, 2003; 5(3): 235 - 242. [Full Text] [PDF]
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D. M. Roden The problem, challenge and opportunity of genetic heterogeneity in monogenic diseases predisposing to sudden death J. Am. Coll. Cardiol., July 17, 2002; 40(2): 357 - 359. [Full Text] [PDF]
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P. M. Spooner and D. P. Zipes Sudden Death Predictors: An Inflammatory Association Circulation, June 4, 2002; 105(22): 2574 - 2576. [Full Text] [PDF]
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S. G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, J. A. Camm, R. Cappato, S. M. Cobbe, C. Di Mario, et al. TASK FORCE ON SUDDEN CARDIAC DEATH, EUROPEAN SOCIETY OF CARDIOLOGY: Summary of Recommendations Europace, January 1, 2002; 4(1): 3 - 18. [Abstract] [PDF]
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H. V. Huikuri, A. Castellanos, and R. J. Myerburg Sudden Death Due to Cardiac Arrhythmias N. Engl. J. Med., November 15, 2001; 345(20): 1473 - 1482. [Full Text] [PDF]
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S.G. Priori, E. Aliot, C. Blomstrom-Lundqvist, L. Bossaert, G. Breithardt, P. Brugada, A.J. Camm, R. Cappato, S.M. Cobbe, C. Di Mario, et al. Task Force on Sudden Cardiac Death of the European Society of Cardiology Eur. Heart J., August 2, 2001; 22(16): 1374 - 1450. [PDF]
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P. M. Spooner, C. Albert, E. J. Benjamin, R. Boineau, R. C. Elston, A. L. George Jr, X. Jouven, L. H. Kuller, J. W. MacCluer, E. Marban, et al. Sudden Cardiac Death, Genes, and Arrhythmogenesis : Consideration of New Population and Mechanistic Approaches From a National Heart, Lung, and Blood Institute Workshop, Part II Circulation, May 22, 2001; 103(20): 2447 - 2452. [Abstract] [Full Text] [PDF]
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S. E. Kimmel, J. A. Berlin, C. Miles, J. Jaskowiak, J. L. Carson, and B. L. Strom Risk of acute first myocardial infarction and use of nicotine patches in a general population J. Am. Coll. Cardiol., April 1, 2001; 37(5): 1297 - 1302. [Abstract] [Full Text] [PDF]
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J. Mikkelsson, M. Perola, P. Laippala, A. Penttila, and P. J. Karhunen Glycoprotein IIIa PlA1/A2 polymorphism and sudden cardiac death J. Am. Coll. Cardiol., October 1, 2000; 36(4): 1317 - 1323. [Abstract] [Full Text] [PDF]
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