Relative Risk Of Sudden Death Research Articles

Sudden Death in Young Brazilian Athletes: Isn't It Time We Created a Genuinely National Register?

Young competitive athletes (≤ 35 years old) with or without a previous diagnosis of cardiovascular disease may suddenly die in competitive activities, potentially leading to an impact in society through the media. Although the relative risk for sudden death (SD) in athletes is twice as high as for their counterparts, the absolute incidence is low. While there is consensus among medical societies worldwide that early detection of causal factors is highly desirable, there is debate among different screening schemes to that end. In Brazil, the recommendations of the Brazilian Society of Cardiology mirror the guidelines of the European Society of Cardiology (ESC), which indicate a clinical examination combined with a 12-lead resting electrocardiogram, regardless of the presence of risk factors. The possibility of genetic screening is also plausible, since most clinical entities that cause SD in young competitive athletes are related to genotype. Finally, considering the diversity of practiced sports, and the population miscegenation, we emphasize the need to a national registry of cases.

Performance of 2014 NICE defibrillator implantation guidelines in heart failure risk stratification

ObjectiveDefine the real-world performance of recently updated National Institute for Health and Care Excellence guidelines (TA314) on implantable cardioverter-defibrillator (ICD) use in people with chronic heart failure.MethodsMulticentre prospective cohort study...

ECG risk score: A powerful predictor of sudden death in hypertrophic cardiomyopathy - genotype correlates

Background: An ECG risk score, scoring amplitudes and morphological abnormalities, which predicts a very high relative risk of sudden death if the point score is >5 has been described. The genotype-phenotype relationships, and correlation with sudden death have been studied in a geographical cohort of patients diagnosed with HCM < 19 yrs of age in the West Götaland Region, Sweden. Methods: Diagnosis was established with echocardiography, and ECG risk score was quantified from a 12-lead ECG according to Eur.Heart J 2010;31:439. DNA was analysed at international commercial laboratories. Results: 67 patients had ECG and echocardiographic data, 64% male. 45 (67%) had familial disease, and 12 Noonan-spectrum dysmorphology. Based on ECG-risk score 28 patients were high-risk (>5 points), and 39 low-risk (<6 points). The risk score correlated with death (correlation coefficient 0.57, p < 0.0001); there were 7 sudden deaths in the high-risk group and none in the low risk group (p = 0.0005). Familial disease was more common in the low-risk (85%) than in the high-risk group (37%), but a higher proportion of genotyped individuals had positive findings in the high-risk (81%) than in the low-risk group (67%). MYH7 mutations were more common than MYBPC3 (29% versus 19%) in the high-risk group, whereas in the low-risk group MYBPC was predominant (33%). Additional genes affected in the high-risk group were ACTC, MYL, MYPN, LAMP2, RAF 1 and PTNP11. Conclusions: The simple inexpensive ECG risk score effectively pinpoints high-risk individuals who require urgent full risk assessment, and where the yield of genetic testing is particularly high.

Syncope and Risk of Sudden Death in Hypertrophic Cardiomyopathy

The prognostic significance of syncope has not been investigated systematically in hypertrophic cardiomyopathy, and treatment strategies have been based largely on intuition and experience. We assessed the relationship between syncope and sudden death in 1511 consecutive patients with hypertrophic cardiomyopathy. Unexplained (n=153) or neurally mediated (n=52) syncope occurred in 205 patients (14%). Over a 5.6+/-5.2-year follow-up, 74 patients died suddenly. Relative risk of sudden death was 1.78 (95% confidence interval 0.88 to 3.51, P=0.08) in patients with unexplained syncope and 0.91 (95% confidence interval 0.00 to 3.83, P=1.0) in those with neurally mediated syncope compared with patients without syncope. In multivariable analysis, the temporal proximity of unexplained syncope to initial patient evaluation was independently associated with risk of sudden death (P=0.006). Patients with unexplained syncope within 6 months before the initial evaluation showed a 5-fold increase in risk compared with patients without syncope (adjusted hazard ratio 4.89, 95% confidence interval 2.19 to 10.94), a relationship that was maintained throughout all age groups (<18, 18 to 39, and > or =40 years). Older patients (> or =40 years of age) with remote episodes of syncope (>5 years before initial evaluation) did not show an increased risk of sudden death (adjusted hazard ratio 0.38, 95% confidence interval 0.05 to 2.74). In the present large cohort of patients with hypertrophic cardiomyopathy, unexplained syncope was a risk factor for sudden death. Patients with syncopal events that occurred in close temporal proximity to the initial evaluation showed a substantially higher risk of sudden death than patients without syncope. Older patients with remote syncopal events did not show an increased risk.

Abstract 4683: Risk Stratification in Hypertrophic Cardiomyopathy: Evidence that Syncope is a Marker for Sudden Death

Risk stratification and identification of those patients with hypertrophic cardiomyopathy (HCM) at the highest risk for sudden death is a major issue for patient management, given the effective option of the implantable defibrillator in this disease. For example, the prognostic significance of syncope has not been investigated systematically in large HCM cohorts, and therefore treatment strategies related to this symptom have been based largely on intuition and experience. We assessed the relationship between syncope and sudden death in 1511 consecutive HCM patients. Unexplained (n=153) or neurally-mediated (n=52) syncope occurred in 205 (14%) of patients. Over a 5.6±5.2 year follow-up, 74 patients died suddenly. Relative risk of sudden death was 1.78 (95% CI 0.88 –3.51; p=0.08) in patients with unexplained syncope, and 0.91 (95% CI 0.00 –3.83; p=1.0) in those with neurally-mediated syncope, compared to patients without syncope. However, the time interval between unexplained syncope and initial patient evaluation proved to have a strong impact on sudden death risk. Patients with recent syncope (≤6 months from initial evaluation) showed a 5-fold increase in risk compared to patients without syncope (adjusted HR=4.89; CI 2.19 –10.94; p=0.006), a relationship maintained throughout all age groups (&lt;18, 18 –39 and ≥40 years). Conversely, adult patients (18 –39 and ≥40 years) with remote syncope (&gt;6 months from evaluation) showed no increase in sudden death rate (4.8; 95% CI 0.1–26.7 and 3.2; 95% CI 0.1–17.8 per 1000 person-years, respectively), compared to patients of similar age without syncope (11.8; 95% CI 7.6 –17.6 and 5.7%; 95% CI 3.8 – 8.3 per 1000 person-years). Left ventricular outflow obstruction was not associated with sudden death risk (p=0.29). In this large HCM cohort, unexplained syncope proved to be a risk factor for sudden death. In addition, the temporal proximity of syncopal events to patient evaluation is of clinical relevance. Recent unexplained syncope is associated with an increased risk for sudden death in all age groups, while remote syncopal events do not convey increased risk to adult patients.

The Relative Risk of Sudden Death in Children with Cardiomyopathy

uncertain that thecohortmost at risk is correctly identified. Further prospective studies are required. doi:10.1016/j.hlc.2008.05.468 468 The Relative Risk of Sudden Death in Children with Cardiomyopathy Tara Bharucha ∗, Andrew Davis, Alan Nugent, Piers Daubeney, Christian Turner, Terry Robertson, Jim Ramsay, Patty Chondros, Ingrid King, Robert Weintraub The National Australian Childhood Cardiomyopathy Study, Melbourne, Australia Background: The incidence and risk factors for sudden death in children (SCD) with cardiomyopathy (CM) have not been well defined. Methodology: The National Australian Childhood Cardiomyopathy Study comprises all children in Australia with primary CM who were diagnosed at age 0–10 years, between 1987 and 1997. Sudden cardiac deathwas defined as sudden andunexpected death in childrenwho survived at least 30 days from presentation were not hospitalized and not in congestive heart failure. Indexed echocardiographic measurements at latest follow-up were compared between surviving subjects and those with SCD. Results: There were 264 subjects, with mean follow-up of 7 (

Myocardial Disease Mortality in Children and Young Adults. A Population-Based Observational Study

Few studies have investigated death due to myocardial disease in children and young adults. The aim of this study was to analyze the epidemiological, clinical, and pathologic characteristics of death in these cases. Population-based observational study of all deaths in individuals aged 1-35 years in the Spanish province of Biscay over a period of 12 years. Forty deaths from myocardial disease occurred in 29 males and 11 females (mean age 25.3 years): 30 sudden and 10 non-sudden deaths. The mortality rate was 0.64 per 100,000 persons-year. The relative risk of sudden death was significantly greater than that of non-sudden death, particularly in adolescents and young males. The cause of death was myocarditis in 12 cases (83.3% sudden death), dilated cardiomyopathy in 10 (80% non-sudden death), arrhythmogenic cardiomyopathy in seven, hypertrophic cardiomyopathy in six, and idiopathic concentric left ventricular hypertrophy in five (100% sudden death). Myocardial disease was diagnosed before sudden death in only three cases. Ten subjects had symptoms and electrocardiogram abnormalities but their cardiomyopathy had not been diagnosed. Six individuals had a comorbid condition (morbid obesity in four), six had prodromal symptoms, and 11 had arrhythmic triggering factors (sporting activity in seven). Ventricular fibrillation was frequently observed during cardiopulmonary resuscitation. Mortality due to myocardial disease in children and young adults is uncommon. Most deaths are sudden. However, some may be preventable. Preventative measures should be aimed at sudden death in adolescents and young males. There was a noticeable association between arrhythmogenic cardiomyopathy and sporting activity.

Day-Night Pattern of Sudden Death in Obstructive Sleep Apnea

Background The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep. Methods We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea–hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during...

Day–Night Pattern of Sudden Death in Obstructive Sleep Apnea

The risk of sudden death from cardiac causes in the general population peaks from 6 a.m. to noon and has a nadir from midnight to 6 a.m. Obstructive sleep apnea is highly prevalent and associated with neurohormonal and electrophysiological abnormalities that may increase the risk of sudden death from cardiac causes, especially during sleep. We reviewed polysomnograms and the death certificates of 112 Minnesota residents who had undergone polysomnography and had died suddenly from cardiac causes between July 1987 and July 2003. For four intervals of the day, we compared the rates of sudden death from cardiac causes among people with obstructive sleep apnea and the following: the rates among people without obstructive sleep apnea, the rates in the general population, and the expectations according to chance. For each interval, we assessed the median apnea-hypopnea index and the relative risk of sudden death from cardiac causes. We similarly analyzed sudden death from cardiac causes during three time intervals that correlate with usual sleep-wake cycles. From midnight to 6 a.m., sudden death from cardiac causes occurred in 46 percent of people with obstructive sleep apnea, as compared with 21 percent of people without obstructive sleep apnea (P=0.01), 16 percent of the general population (P<0.001), and the 25 percent expected by chance (P<0.001). People with sudden death from cardiac causes from midnight to 6 a.m. had a significantly higher apnea-hypopnea index than those with sudden death from cardiac causes during other intervals, and the apnea-hypopnea index correlated directly with the relative risk of sudden death from cardiac causes from midnight to 6 a.m. For people with obstructive sleep apnea, the relative risk of sudden death from cardiac causes from midnight to 6 a.m. was 2.57 (95 percent confidence interval, 1.87 to 3.52). The analysis of usual sleep-wake cycles showed similar results. People with obstructive sleep apnea have a peak in sudden death from cardiac causes during the sleeping hours, which contrasts strikingly with the nadir of sudden death from cardiac causes during this period in people without obstructive sleep apnea and in the general population.

Does sports activity enhance the risk of sudden death in adolescents and young adults?

ObjectivesWe sought to assess the risk of sudden death (SD) in both male and female athletes age 12 to 35 years. BackgroundLittle is known about the risk of SD in adolescents and young adults engaged in sports. MethodsWe did a 21-year prospective cohort study of all young people of the Veneto Region of Italy. From 1979 to 1999, the total population of adolescents and young adults averaged 1,386,600 (692,100 males and 694,500 females), of which 112,790 (90,690 males and 22,100 females) were competitive athletes. An analysis by gender of risk of SD and underlying pathologic substrates was performed in the athletic and non-athletic populations. ResultsThere were 300 cases of SD, producing an overall cohort incidence rate of 1 in 100,000 persons per year. Fifty-five SDs occurred among athletes (2.3 in 100,000 per year) and 245 among non-athletes (0.9 in 100,000 per year), with an estimated relative risk (RR) of 2.5 (95% confidence interval [CI] 1.8 to 3.4; p < 0.0001). The RR of SD among athletes versus non-athletes was 1.95 (CI 1.3 to 2.6; p = 0.0001) for males and 2.00 (CI 0.6 to 4.9; p = 0.15) for females. The higher risk of SD in athletes was strongly related to underlying cardiovascular diseases such as congenital coronary artery anomaly (RR 79, CI 10 to 3,564; p < 0.0001), arrhythmogenic right ventricular cardiomyopathy (RR 5.4, CI 2.5 to 11.2; p < 0.0001), and premature coronary artery disease (RR 2.6, CI 1.2 to 5.1; p = 0.008). ConclusionsSports activity in adolescents and young adults was associated with an increased risk of SD, both in males and females. Sports, per se, was not a cause of the enhanced mortality, but it triggered SD in those athletes who were affected by cardiovascular conditions predisposing to life-threatening ventricular arrhythmias during physical exercise.

Blood levels of long-chain n-3 fatty acids and the risk of sudden death.

Experimental data suggest that long-chain n-3 polyunsaturated fatty acids found in fish have antiarrhythmic properties, and a randomized trial suggested that dietary supplements of n-3 fatty acids may reduce the risk of sudden death among survivors of myocardial infarction. Whether long-chain n-3 fatty acids are also associated with the risk of sudden death in those without a history of cardiovascular disease is unknown. We conducted a prospective, nested case-control analysis among apparently healthy men who were followed for up to 17 years in the Physicians' Health Study. The fatty-acid composition of previously collected blood was analyzed by gas-liquid chromatography for 94 men in whom sudden death occurred as the first manifestation of cardiovascular disease and for 184 controls matched with them for age and smoking status. Base-line blood levels of long-chain n-3 fatty acids were inversely related to the risk of sudden death both before adjustment for potential confounders (P for trend = 0.004) and after such adjustment (P for trend = 0.007). As compared with men whose blood levels of long-chain n-3 fatty acids were in the lowest quartile, the relative risk of sudden death was significantly lower among men with levels in the third quartile (adjusted relative risk, 0.28; 95 percent confidence interval, 0.09 to 0.87) and the fourth quartile (adjusted relative risk, 0.19; 95 percent confidence interval, 0.05 to 0.71). The n-3 fatty acids found in fish are strongly associated with a reduced risk of sudden death among men without evidence of prior cardiovascular disease.

Association of elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone with cardiac mortality risk in chronic hemodialysis patients.

Hyperphosphatemia is highly prevalent among patients with end-stage renal disease (ESRD) and is associated with increased mortality risk in hemodialysis (HD) patients. The mechanism through which this mortality risk is mediated is unclear. Data from two national random samples of HD patients (n = 12,833) was used to test the hypothesis that elevated serum PO(4) contributes mainly to cardiac causes of death. During a 2-yr follow-up, the cause-specific relative risk (RR) of death for patients was analyzed separately for several categories of cause of death, including coronary artery disease (CAD), sudden death, and other cardiac causes, cerebrovascular and infection. Cox regression models were fit for each of the eight cause of death categories, adjusting for patient demographics and non-cardiovascular comorbid conditions. Time at risk for each cause-specific model was censored at death that resulted from any of the other causes. Higher mortality risk was seen for patients in the high PO(4) group (>6.5mg/dl) compared with the lower PO(4) group (< or =6.5mg/dl) for death resulting from CAD (RR 1.41; P < 0.0005), sudden death (RR 1.20; P < 0.01), infection (RR 1.20; P < 0.05), and unknown causes (RR 1.25; P < 0.05). Patients in the high PO(4) group also had non-significantly increased RR of death from other cardiac and cerebrovascular causes of death. The RR of sudden death was also strongly associated with elevated Ca x PO(4) product (RR 1.07 per 10 mg(2)/dl(2); P < 0.005) and serum parathyroid hormone levels greater than 495 pg/ml (RR 1.25; P < 0.05). This study identifies strong relationships between elevated serum PO(4), Ca x PO(4) product, and parathyroid hormone and cardiac causes of death in HD patients, especially deaths resulting from CAD and sudden death. More vigorous measures to reduce the prevalence of these factors in HD patients may result in improved survival.

Triggering of Sudden Death from Cardiac Causes by Vigorous Exertion

Retrospective and cross-sectional data suggest that vigorous exertion can trigger cardiac arrest or sudden death and that habitual exercise may diminish this risk. However, the role of physical activity in precipitating or preventing sudden death has not been assessed prospectively in a large number of subjects. We used a prospective, nested case-crossover design within the Physicians' Health Study to compare the risk of sudden death during and up to 30 minutes after an episode of vigorous exertion with that during periods of lighter exertion or none. We then evaluated whether habitual vigorous exercise modified the risk of sudden death that was associated with vigorous exertion. In addition, the relation of vigorous exercise to the overall risk of sudden death and nonsudden death from coronary heart disease was assessed. During 12 years of follow-up, 122 sudden deaths were confirmed among the 21,481 male physicians who were initially free of self-reported cardiovascular disease and who provided information on their habitual level of exercise at base line. The relative risk of-sudden death during and up to 30 minutes after vigorous exertion was 16.9 (95 percent confidence interval, 10.5 to 27.0; P<0.001). However, the absolute risk of sudden death during any particular episode of vigorous exertion was extremely low (1 sudden death per 1.51 million episodes of exertion). Habitual vigorous exercise attenuated the relative risk of sudden death that was associated with an episode of vigorous exertion (P value for trend=0.006). The base-line level of exercise was not associated with the overall risk of subsequent sudden death. These prospective data from a study of U.S. male physicians suggest that habitual vigorous exercise diminishes the risk of sudden death during vigorous exertion.

Predicting sudden death in the population: the Paris Prospective Study I.

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. 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). 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.

Need for a Revision of the Normal Limits of Resting Heart Rate

The current definition of sinus tachycardia is a heart rate >100 beats per minute (bpm).1 This limit was set arbitrarily when heart rate was not yet regarded as a risk factor for cardiovascular disease, probably with the main purpose of distinguishing between a disease state (fever, thyrotoxicosis, anemia, congestive heart failure, etc) and a normal condition. In recent years, interest has been aroused by the awareness that fast heart rate is a potent precursor of hypertension, atherosclerosis, and their sequelae.2 3 4 5 6 7 8 9 10 In addition, many leading epidemiological studies have shown that tachycardia is associated with an increased risk of death from cardiovascular and noncardiovascular causes. This relationship has been found in general populations,3 4 5 6 7 in elderly individuals,9 and in hypertensive cohorts.10 In all of these studies, the heart rate value above that in which a significant increase in risk was observed was below the 100 bpm threshold (Table 1⇓). Only in the study by Levy et al3 was tachycardia defined as a heart rate >99 bpm, but in that study the cutoff between normal and high heart rate was chosen arbitrarily, and the highest heart rate value measured during the examination was taken to define the subject’s heart rate. In all the other studies, the threshold level between normal and fast heart rate was between 79 and 90 bpm. View this table: Table 1. Heart Rate Values Above Which a Significant Increase in Risk Was Found: Data From 9 Epidemiological Studies The normalcy limits of a clinical variable can be established according to different criteria. For many parameters, such as most biochemical indexes, the 95% confidence interval is calculated to identify the upper normal limit of the variable. This statistical approach does not appear suitable for those clinical variables …

Effects of propranolol in patients entered in the Beta-Blocker Heart Attack Trial with their first myocardial infarction and persistent electrocardiographic ST-segment depression

Objective/Background It has been shown that patients with an acute myocardial infarction and persistent electrocardiographic ST-segment depression are at high risk for subsequent cardiac events. The purpose of this retrospective analysis was to examine the long-term effects of propranolol therapy in patients with their first acute myocardial infarction and persistent electrocardiographic ST-segment depression. Methods The outcomes of 2877 patients enrolled in the Beta-Blocker Heart Attack Trial (BHAT) with their first myocardial infarction (75% of patients in BHAT) were reviewed. Patients were divided into three groups on the basis of presence or absence of ≥1 mm ST-segment depression in two contiguous leads of the 12-lead electrocardiogram obtained soon after admission or at the time of randomization, which occurred 10.1 ± 3.5 days after the index myocardial infarction. Group 1 included 774 patients (392 randomly assigned to placebo and 382 to propranolol) with no ST-segment depression; group 2 included 1447 patients (713 placebo, 734 propranolol) with ST-segment depression at admission or at the time of randomization (labeled as transient); and group 3 included 656 patients (339 placebo and 317 propranolol) who had electrocardiographic ST-segment depression from the time of admission to the time of randomization (labeled as persistent). Results In group 3, patients with persistent electrocardiographic ST depression, the mortality rate in patients randomly assigned to placebo was 13.6% compared with 7.6% in patients with propranolol ( p = 0.012; log rank test). Sudden death in the placebo arm was 9.7% compared with 4.7% in the propranolol group ( p = 0.012, log rank test). The results of the Cox regression analysis, adjusting for all baseline variables with p values <0.25, showed the relative risk of overall mortality rate and the relative risk of sudden death were 2.13 (1.22, 3.70) and 2.56 (1.27, 5.26), respectively, for the placebo group compared with the propranolol group. Patients with persistent ST-segment depression had the greatest benefit from propranolol (47.2 fewer events [deaths/reinfarctions] per 1000 person-years compared with 7.8 and 2.1 fewer events in patients with transient and no ST-segment depression, respectively). Conclusions It appears that the greatest benefit for β-blocker therapy in patients after myocardial infarction is observed in patients with persistent ST-segment depression who are at greatest risk for death and reinfarction. Definitive conclusions regarding therapy with β-adrenergic blocking agents in patients with persistent ST-segment depression cannot be made because our analysis, given its retrospective nature, is only hypothesis generating. (Am Heart J 1998;135:261-7.)

Fish consumption and risk of sudden cardiac death.

Dietary fish intake has been associated with a reduced risk of fatal cardiac end points, but not with nonfatal end points. Dietary fish intake may have a selective benefit on fatal arrhythmias and therefore sudden cardiac death. To investigate prospectively the association between fish consumption and the risk of sudden cardiac death. Prospective cohort study. The US Physicians' Health Study. A total of 20 551 US male physicians 40 to 84 years of age and free of myocardial infarction, cerebrovascular disease, and cancer at baseline who completed an abbreviated, semiquantitative food frequency questionnaire on fish consumption and were then followed up to 11 years. Incidence of sudden cardiac death (death within 1 hour of symptom onset) as ascertained by hospital records and reports of next of kin. There were 133 sudden deaths over the course of the study. After controlling for age, randomized aspirin and beta carotene assignment, and coronary risk factors, dietary fish intake was associated with a reduced risk of sudden death, with an apparent threshold effect at a consumption level of 1 fish meal per week (P for trend=.03). For men who consumed fish at least once per week, the multivariate relative risk of sudden death was 0.48 (95% confidence interval, 0.24-0.96; P=.04) compared with men who consumed fish less than monthly. Estimated dietary n-3 fatty acid intake from seafood also was associated with a reduced risk of sudden death but without a significant trend across increasing categories of intake. Neither dietary fish consumption nor n-3 fatty acid intake was associated with a reduced risk of total myocardial infarction, nonsudden cardiac death, or total cardiovascular mortality. However, fish consumption was associated with a significantly reduced risk of total mortality. These prospective data suggest that consumption of fish at least once per week may reduce the risk of sudden cardiac death in men.

United States Perspective on Definitions and Classifications

Interest in sudden unexpected and unexplained death in individuals with epilepsy (SUDEP) was rekindled in the United States by Jay and Leestma during the early 1980s and more recently by antiepileptic drug (AED) trials and medicolegal issues. The incidence of SUDEP has been and is being evaluated in North America and the United Kingdom. Specific criteria for the classification of definite, probable, possible, and unlikely SUDEP implemented in United States epidemiologic studies are presented. Evidence for the increased relative risk for sudden death in epilepsy compared with the general population is also discussed.

Ventricular tachycardia rate variability as a new predictor of sudden death in patients with remote myocardial infarction.

Clinical data have shown that evaluation of sinus rhythm variability is a useful test for selection of high-risk patients after myocardial infarction. The purpose of this study was to test the hypothesis that measures of ventricular rate variability (VRV) during non-sustained ventricular tachycardia (NSVT) may be helpful in predicting sudden death in patients with a remote myocardial infarction. The study group comprised 162 patients with remote myocardial infarction who showed NSVT on 24 h ECG recording. Temporal changes in up to 10 beat-to-beat V-V intervals of NSVT episodes were assessed. The following parameters of VRV-NSVT were calculated: average value of successive differences in V-V intervals (ADVV); normalized average value of successive differences in V-V intervals (nADVV). During a mean follow-up of 4 years, 57 patients (35%) had died; sudden death was identified in 34 (21%). Patients who died suddenly had significantly (P < 0.001) lower values of ADVV and nADVV variables compared with survivors or those whose death was not sudden. The incidence of sudden death was assessed in the group of patients with more stable cycle durations in the episodes of NSVT (expected to be at high risk) and in the group with more variable cycle durations (expected to be at low risk). The relative risk of sudden death for patients with ADVV values less than 30 ms was 3.2 compared with those with ADVV values of at least 30 ms (P < 0.001), and that for patients with nADVV values less than 6% was 3.0 compared with those with nADVV values of at least 6% (P < 0.001). These results indicate a relationship between regularity of NSVT rhythm and risk of sudden death. The assessment of VRV-NSVT can be used to identify patients with NSVT who remain at high risk after myocardial infarction.

1023-111 Effects of Propranolol in Patients with Their First Acute Myocardial Infarction and Persistent Electrocardiographic ST Segment Depression in the Beta Blocker Heart Attack Trial

The available data suggest that patients (pts) recovering from an acute my ocardial infarction (AMI) who have persistent electrocardiographic (ECG) ST segment depression (STD) are at high risk for future cardiac events when compared with AMI pts without STD. There are little data on the long term effects of medical therapy on acute MI pts with STD. The objectives of this retrospective analysis were to examine in the Beta Blocker Heart Attack Trial (BHAT) the effects of propranolol in this high risk group. Of the 2877 first MI BHAT pts, 656 pts had persistent ECG STD from the time of admission until randomization (9.7 ± 3.1 days after index MI). Of these, 317 pts were randomized to the propranolol and 339 pts to placebo. There were no significant baseline differences (p &lt; 0.05) between the two groups. The median follow up was 24.6 months. Follow-up Events Propranolol Placebo p-value (n = 317) (n = 339) (Cox regression) Overall mortality 7.6% 13.6% 00078 Sudden death 4.7% 9.7% 00094 Definite or probable MI 3.8% 7.7% 0.037 MI andlor mortality 9.2% 17.4% 0.0011 Cox regression analysis, adjusting for baseline variables showed the relative risk of mortality and the relative risk of sudden death were 2.13 (1.22, 3.70) and 2.56 (1.27, 5.26) respectively in the placebo, compared to the propranolol group. It appears that propranolol therapy is effective in reducing cardiac events in pts recovering from an AMI with ECG STD.