Sudden death associated with anomalous coronary origin and obstructive coronary disease in the young

Sudden cardiac death in a young patient is a catastrophic occurrence. Anomalous coronary origin (ACO) is a significant cause of sudden cardiac death among individuals under the age of 35 years. We sought to define the premortem clinical and postmortem histopathologic findings in victims of sudden cardiac death resulting from either ACO or obstructive atherosclerotic coronary artery disease (CAD) among U.S. military recruits (ages 17-35 years). The autopsy records of all sudden cardiac deaths occurring among recruits during their basic military training period from 1977 through 2001 were reviewed. Twenty-one deaths were associated with ACO and 10 with CAD. Recruits with ACO were more likely to have prodromal symptoms of exertional syncope and/or chest pain (48% vs. 0%, P = 0.011). All sudden cardiac deaths resulting from ACO involved a left main coronary artery takeoff from the right coronary sinus with a course between the aorta and the right ventricular outflow tract and an otherwise normal distribution of the major epicardial coronary arteries. Myocardial fibrosis was seen equally in those with both CAD and ACO (30% vs. 20%, P = 0.66), but the finding of necrosis tended to be more common among recruits with CAD (50% vs. 15%, P = 0.08). In conclusion, review of autopsy data of sudden cardiac deaths among U.S. military recruits reveals myocardial fibrosis or necrosis occurred in 70% of cases with CAD and 35% of cases with ACO. Sudden cardiac deaths resulting from ACO were more likely to be associated with premortem exertional chest discomfort and/or syncope compared with deaths resulting from CAD.     

Sudden death risk in overt coronary heart disease: the Framingham Study

Over 30 years of surveillance of 5127 subjects free of CHD, 760 men and 574 women developed overt CHD, and there were 160 sudden deaths in men and 73 in women. Among those who sustained clinically manifest CHD, the sudden death risk was increased 6.7 times that of those without an interim event. Although the relative risk was comparable in the two sexes, CHD did not eliminate the female advantage over men. Myocardial infarction imposed a greater sudden death risk than angina pectoris, and silent infarctions were as dangerous as symptomatic infarctions. Onset of CHD put young and old at equal risk of sudden death. Some 40% of sudden deaths occurred in the 4% of the general population with overt CHD. The proportion of coronary attacks presenting as sudden death increased from 13% at ages 35 to 64 years to 20% at ages 65 to 94 years. The fraction of CHD deaths classified as sudden deaths was lower in those with than without interim CHD. In those with established CHD, factors reflecting ischemic myocardial damage and cardiac failure were the chief predictors of sudden death. The proportion of CHD deaths presenting as sudden deaths has not declined in subjects with prior CHD over three decades, despite a national decline in the overall CHD mortality rate.     

Sudden death in the general population in Okinawa: incidence and causes of death

Sudden unexpected death is generally considered to be caused by acute myocardial infarction and/or arrhythmia. To document the incidence and causes of sudden death in Japan, where the incidence of myocardial infarction is low, the present study examined death certificates, hospital records, the forensic medical records, and the police records of residents of the southern part of Okinawa island who died at the age of 20-74 years during a 3-year period from January 1, 1992 to December 31, 1994. Sudden death was defined as death within 24 h from the onset of unexpected symptoms. The study documented 126 (87 men and 39 women) sudden deaths. The crude incidence rate was 0.37/1,000 person per year (0.51 in men and 0.23 in women). According to the death certificates, 78 cases died of heart diseases. However, the cause of death could be determined by examination of all available records in only 64 cases: myocardial infarction in 10, non-ischemic heart diseases in 13, and stroke in 23 cases. Even when the analysis was limited to the cases who died within 1 h from the onset of symptoms, heart disease was the cause of death in only 22% of the cases while the cause of death could not be determined in 53% of the cases. Only 13% of those diagnosed as heart diseases on the death certificate were verified. The agreement rate between the diagnosis reached by the re-evaluation of the records and that on the death certificate was 82% for stroke and 33% for other diseases. In Okinawa, Japan, the frequencies of heart disease and stroke as the cause of sudden death may be similar. Except for stroke, the diagnosis appearing on the death certificate has substantial inaccuracy.     

Relationship between baseline electrocardiographic measurements and outcomes in patients with high-risk heart failure: Insights from the VerICiguaT Global Study in Subjects with Heart Failure with Reduced Ejection Fraction (VICTORIA) trial

Aims

Whether electrocardiographic (ECG) measurements predict mortality in chronic heart failure with reduced ejection fraction (HFrEF) is unknown.

Methods and results

We studied 4880 patients from the Vericiguat Global Study in Subjects with Heart Failure with Reduced Ejection Fraction (VICTORIA) trial with a baseline 12-lead ECG. Associations between ECG measurements and mortality were estimated as hazard ratios (HR) and adjusted for the Meta-Analysis Global Group in Chronic Heart Failure (MAGGIC) risk score, N-terminal pro-B-type natriuretic peptide, and index event. Select interactions between ECG measurements, patient characteristics and mortality were examined. Over a median of 10.8 months, there were 824 cardiovascular (CV) deaths (214 sudden) and 1005 all-cause deaths. Median age was 68 years (interquartile range [IQR] 60–76), 24% were women, median ejection fraction was 30% (IQR 23–35), 41% had New York Heart Association class III/IV, and median MAGGIC score was 24 (IQR 19–28). After multivariable adjustment, significant associations existed between heart rate (per 5 bpm: HR 1.02), QRS duration (per 10 ms: HR 1.02), absence of left ventricular hypertrophy (HR 0.64) and CV death, and similarly so with all-cause death (HR 1.02; HR 1.02; HR 0.61, respectively). Contiguous pathologic Q waves were significantly associated with sudden death (HR 1.46), and right ventricular hypertrophy with all-cause death (HR 1.44). The only sex-based interaction observed was for pathologic Q waves on CV (men: HR 1.05; women: HR 1.64, p_interaction = 0.024) and all-cause death (men: HR 0.99; women: HR 1.57; p_interaction = 0.010). Whereas sudden death doubled in females, it did not differ among males (male: HR 1.25, 95% confidence interval [CI] 0.87–1.79; female: HR 2.50, 95% CI 1.23–5.06; p_interaction = 0.141).

Conclusion

Routine ECG measurements provide additional prognostication of mortality in high-risk HFrEF patients, particularly in women with contiguous pathologic Q waves.     

The athlete's heart syndrome

The athlete's heart is a benign condition, associated with physiologic alterations that can be detected on physical and laboratory examination. Echocardiography is a particularly useful technique is quantitating cardiac adaptation to exercise training and in screening for cardiovascular disorders that can be deleterious to the athlete. Cardiomyopathies are common causes of sudden death in young athletes, and myocarditis in physically-active young military recruits. Coronary disease is usually implicated in middle-aged athletes such as distance runners. Recent well-publicized deaths in several athletes have focused more attention on the need to detect Marfan's syndrome and cocaine use. Published guidelines such as the 16th Bethesda Conference and recent medical advances like new antihypertensive and antiarrhythmic drugs assist the clinician in counseling and managing athletes with cardiovascular disorders.     

Can the mode of death be predicted in patients with angiographically documented coronary artery disease?

To determine whether sudden versus non-sudden cardiac death could be predicted in high risk patients, 1157 medical patients were followed for an average of 46 months after a diagnostic coronary angiogram and 18 clinical, hemodynamic, and angiographic variables known to be associated with a high risk of mortality were analyzed. The total group of 141 deaths was classified into 3 subgroups: (1) 82 sudden deaths (less than 1 hour after onset of symptoms); (2) 46 deaths due to acute myocardial infarction with or without heart failure, and (3) 13 deaths unrelated to cardiac symptoms. In a subset of 64 patients, the duration of electrical systole (QTc) was calculated before angiography and before death. A comparison was made of QTc measurements at entry with QTc values of subjects with normal coronary arteries and normal left ventricular function. Deaths from cardiac causes could often be predicted from older age, male sex, history of myocardial infarction, unstable angina, congestive heart failure, abnormal cardiothoracic ratio, multivessel disease, abnormal left ventricular contraction, and abnormal ejection fraction. However, these variables did not discriminate between sudden and nonsudden cardiac deaths and both modes of death were characterized by depressed left ventricular function and multivessel coronary disease. During follow-up the incidence of acute myocardial infarction was not different in patients with cardiac and noncardiac deaths and in long-term survivors. However, patients dying from cardiac causes had a higher incidence of heart failure. Patients dying suddenly did not present new infarctions during follow-up whereas patients dying from acute myocardial infarction had a 13% incidence of prior infarction and a higher incidence of heart failure. In addition, QTc at entry was longer in nonsurvivors than in normal subjects (p less than 0.0001) and patients experiencing sudden death exhibited the highest incidence of QTc prolongation (greater than or equal to 440 ms) during follow-up (p less than 0.05). We conclude that: (1) although the severity of coronary disease and left ventricular dysfunction are closely related to cardiac mortality, they do not discriminate between sudden and nonsudden cardiac deaths; (2) patients experiencing sudden death are characterized by a low incidence of new myocardial infarction or congestive heart failure and prolongation of the QTc interval during follow-up.     

Epidemiology of sudden coronary death: population at risk

Sudden coronary death is a major manifestation of clinical coronary artery disease which doubles in incidence with each decade of life after age 45, with women lagging behind men in incidence by 20 years. Some 14% of heart attacks present as sudden death, and 41% of deaths from coronary disease are sudden deaths. Half of all sudden coronary deaths occur in persons without prior overt coronary artery disease. Persons with established coronary disease are at a three- to fourfold increased risk of sudden death, but the proportion of coronary deaths due to sudden death is no higher. This report examines how sudden death evolves over the long term in the general population and in persons with overt coronary artery disease, and attempts to delineate prime candidates and modifiable predisposing factors using the Framingham Heart Study. In asymptomatic persons the risk of sudden death varies over a wide range in relation to risk factors such as systolic blood pressure, serum cholesterol, cigarette smoking, heart rate, electrocardiographic abnormality and relative weight. Multivariate combination of these risk factors identifies 38.6% of sudden deaths in men and 43.8% of sudden deaths in women in the upper quintile of multivariate risk, which are, respectively, 6.0 and 5.8 times greater than the proportion of sudden deaths in the lowest quintile. When overt coronary artery disease is manifest, the major risk factors have less influence on sudden death risk, which becomes determined chiefly by indicators of intrinsic myocardial damage. With cardiac failure there is an eightfold increased risk of sudden death in men, and cardiac failure without concomitant coronary artery disease imposes a 2.7-fold increased risk.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of increased left ventricular mass index to mortality and sudden death in patients with stable coronary heart disease (from the Heart and Soul Study)

Data are limited about the significance of left ventricular (LV) hypertrophy or mass in patients with coronary heart disease (CHD), particularly in the setting of normal ejection fraction (EF). The association of LV mass index with all-cause mortality and sudden death in a cohort with CHD was evaluated. Using transthoracic echocardiography, LV mass normalized to body surface area was measured in 1,016 subjects with stable CHD. Cox proportional hazards models were used to examine the association of LV mass index and LV hypertrophy (LV mass index >95 g/m(2) in women and >115 in men) with time to death and time to sudden or arrhythmic death. Mean LV mass index was 101 +/- 27 g/m(2) in men and 88 +/- 23 in women. During a mean follow-up of 3.55 years, there were 146 deaths and 34 sudden or arrhythmic deaths. Total mortality was higher in subjects with LV hypertrophy (25% vs 11%, p <0.001), as was mortality from sudden or arrhythmic death (6.7% vs 2.2%, p = 0.001). After adjustment for age, gender, cardiovascular risk factors, and medical therapy, LV hypertrophy was associated with both all-cause mortality (hazard ratio 2.0, p <0.001) and sudden or arrhythmic death (hazard ratio 3.1, p = 0.003). Findings were similar in the subgroup with EF > or =55% (mortality hazard ratio 1.8, p = 0.02; sudden and arrhythmic death hazard ratio 3.1, p = 0.02). Analyzed as a continuous variable, every 20-unit increase in LV mass index increased the adjusted hazard of death by 22% (p = 0.001) and adjusted hazard of sudden or arrhythmic death by 40% (p = 0.004). In conclusion, in patients with stable CHD, increased LV mass index was independently associated with all-cause mortality and sudden or arrhythmic death, even in subjects with normal EF.     

Kidney dysfunction and sudden cardiac death among women with coronary heart disease

We evaluated the association between kidney dysfunction and sudden cardiac death risk among ambulatory women with coronary heart disease. The Heart and Estrogen Replacement Study evaluated the effects of hormone treatment on cardiovascular events among 2763 postmenopausal women with coronary heart disease. Kidney dysfunction was categorized by estimated glomerular filtration rate (eGFR) using the Modification of Diet in Renal Disease equation. Multivariate proportional hazards models were used to adjust for cardiovascular risk factors, congestive heart failure, and myocardial infarction. At baseline, 37% (n=1027) had an eGFR of >60 mL/min, 54% (n=1503) had an eGFR of 40 to 60 mL/min, and 8% (n=230) had an eGFR of <40 mL/min. During the 6.8-year follow-up period, there were 136 adjudicated sudden cardiac deaths. The rate of sudden cardiac death was higher in those with lower kidney function (0.5% per year among those with an eGFR >60; 0.6% per year with an eGFR between 40 and 60; and 1.7% per year with an eGFR <40 mL/min; P for trend <0.001). After multivariate analysis with baseline risk factors, eGFR at 40 to 60 mL/min was not a significant predictor, but eGFR at <40 mL/min remained strongly associated with sudden cardiac death (hazard ratio: 3.2; 95% CI: 1.9 to 5.3); adjustment for incident congestive heart failure and myocardial infarction during follow-up diminished this association (hazard ratio: 2.3; 95% CI: 1.3 to 3.9), suggesting that congestive heart failure and myocardial infarction mediated only part of the association between kidney dysfunction and sudden cardiac death. Advanced kidney dysfunction is an independent predictor of sudden cardiac death among women with coronary heart disease.     

Patterns of coronary heart disease morbidity and mortality in the sexes: a 26-year follow-up of the Framingham population

A population-based survey, using data from the Framingham study, assessed sex-specific patterns of coronary heart disease occurring over a 26-year period of time. Among subjects ages 35 to 84 years, men have about twice the total incidence of morbidity and mortality of women. The sex gap in morbidity tends to diminish during the later years of the age range, mainly because of a surge in growth of female morbidity after age 45 years, while by that age, the growth in the male rate begins to taper off. An approximate 10-year difference between the sexes persists in mortality rates throughout the life span. The relative health advantage that is possessed by women, however, is buffered by a case fatality rate from coronary attacks that exceeds the male rate (32% vs 27%). Coronary disease manifestations differ between the sexes. Myocardial infarction is more likely to be unrecognized in women than in men (34% vs 27%). Angina pectoris in women more frequently is uncomplicated (80%), whereas in men angina tends to evolve out of infarction (66%). Also, sudden death comprises a greater proportion of male deaths than female deaths (50% vs 39%). Because women maintain a lesser probability of the disease than do men at any level of the major cardiovascular risk factors, distinctions in their risk factor profiles do not explain completely the observed disease patterns.     

Impact of converting enzyme inhibition on progression of chronic heart failure: results of the Munich Mild Heart Failure Trial.

OBJECTIVE--Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure. DESIGN AND PATIENTS--170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years. MAIN OUTCOME MEASURES--Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death. RESULTS--Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87). CONCLUSIONS--Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.     

A survey of sudden death among school children in Osaka Prefecture

For 2 years, from January 1985 to December 1986, we carried out a thorough investigation of sudden death or apparent sudden death in a population between 5 and 19 years of age in Osaka Prefecture. Sudden death (unexpected death caused by intrinsic factors within 24 h after the onset of symptoms) occurred in 62 boys and 30 girls, with an annual sudden death rate of 3.0 per 100,000 for boys and 1.5 per 100,000 for girls. Of these 92 deaths, 64 occurred among school children (elementary or high school students), and it was these that were subjected to further analyses. Of the school children deaths, 29.7% seemed to be apparent sudden cardiac death (based on circumstances immediately before death, although there was no definite evidence for sudden cardiac death), and 29.7% were sudden death clearly attributable to underlying heart diseases (hence, sudden cardiac death in the usual meaning of this term accounted for about 60% of the 64 sudden deaths). In addition, 17.2% of the 64 cases were sudden death from bronchial asthma. Analysis of seasonal variation in the incidence of sudden death showed that apparent sudden cardiac death frequently occurred in summer, while sudden death clearly attributable to underlying cardiac diseases often took place in winter, sudden death from bronchial asthma occurred chiefly in summer and fall. Of the total number of sudden deaths, death occurred during exercise in 29.7%, and during sleep in 18.8% of individuals. The percentage of sudden deaths occurring during school hours was as low as 23.4% (15/64). Analysis of the physical condition of the 64 sudden death cases immediately before death disclosed the presence of respiratory infection in 10.9%, fatigue in 21.9%, lack of sleep in 4.7% and other conditions in 4.7%. Thus, the percentage of sudden deaths which occurred under ordinary physical conditions was 57.8% (37/64), of which 14 deaths (21.9% of the total) were associated with exercise.     

Impact of converting enzyme inhibition on progression of chronic heart failure: results of the Munich Mild Heart Failure Trial.

OBJECTIVE--Neurohormonal activation has major impact on the pathophysiology of congestive heart failure. The Munich Mild Heart Failure Trial was designed to test the hypothesis that interference with the renin-angiotensin system by angiotensin converting enzyme inhibition favourably influences the natural history of heart failure. DESIGN AND PATIENTS--170 patients, median New York Heart Association (NYHA) class II, were randomised to double blind treatment with 25 mg captopril twice a day or placebo in addition to standard treatment for a median observation period of 2.7 years. MAIN OUTCOME MEASURES--Progression of heart failure to NYHA class IV on an optimally adjusted standard treatment, death due to progressive heart failure, and sudden death. RESULTS--Heart failure progressed to class IV in nine patients (10.8%) treated with captopril and in 23 patients (26.4%) treated with placebo (p = 0.01). The mean survival time until this end point was 223 days longer in the captopril group (Kaplan-Meier life table analysis; p = 0.02). Also, progressive deterioration to severe heart failure was a powerful predictor of total mortality and death from heart failure; 80% of deaths due to progressive heart failure occurred after this end point. There were fewer deaths caused by progressive heart failure in the captopril group than in the placebo group (4 v 11; p = 0.10) but similar numbers of sudden deaths (11 v 10). Progressive heart failure was the cause of death in 18.2% of all deaths in the captopril group and 50% in the placebo group. Total heart failure events (the end point on which power calculation was based) were also more common in the placebo group (19 v 32 events) but not significantly so. Total mortality was similar to both groups (22 of 83 v 22 of 87). CONCLUSIONS--Angiotensin converting enzyme inhibition in conjunction with standard therapy early in the course of congestive heart failure slowed the progress of heart failure and thus favourably altered the natural history of the disease.     

Sudden coronary death in the United States: 1980-1985

To describe patterns of an indicator of sudden coronary death, data from the National Center for Health Statistics were examined for deaths occurring out of hospital and in the emergency room (OH/ER) from 1980 to 1985 in 40 states. In 1985, 56% of ischemic heart disease deaths occurred OH/ER among persons aged 35-74 years. The percentage occurring OH/ER declined with age, was higher in men than women, and higher in blacks than whites. At age 55-64, 61% of ischemic heart disease deaths in white and 66% in black men occurred OH/ER. Between 1980 and 1985, age-adjusted death rates in white men aged 35-74 years declined 19% for OH/ER and 18% for in-hospital ischemic heart disease deaths. The percentage of deaths in ER increased. The decline in deaths occurring OH/ER accounted for 61% of the total absolute decline in ischemic heart disease death rate in white men, 55% in white women, and about 70% in nonwhites. The decline in rates of death OH/ER should encourage further efforts at preventing coronary heart disease and improving emergency medical services.     

Sudden Unexpected Death in Children with Heart Disease

Objective. To review a mortality database, and identify all sudden unexpected deaths in patients followed by the cardiac program. Design. Retrospective review of prospectively maintained database. Results. Over 8 years, we identified 80 sudden unexpected deaths, among which there were sufficient data in 69 (24 females). Patients died at a median age of 17.2 months (28 days?18.8 years). Forty‐six patients had 2 functional ventricles and 23 had received palliation for a single‐functional ventricle. Patients with a single ventricle died at a younger age (median 120 days; 28 days?17.2 years) and sooner after last assessment (median 27 days; 1–146 days) than patients in the biventricular group (median age 2 years; 43 days?18.8 years; median time since last assessment 49 days, 1 days?1 year) (P < .01; P = .01). Thrombosis was the most common cause (61%) of death in the single‐ventricle group. Arrhythmia or presumed arrhythmia was the most common cause (46%) of death in the biventricular group. Fifty‐one patients had undergone surgery. Six patients had primary electrophysiological disease, and 5 had cardiomyopathy. Eight deaths occurred in patients with pulmonary vascular disease. Conclusion. Our study demonstrates that sudden unexpected death occurred at a frequency of at least 10 patients per year over an 8‐year period with 55 730 patient encounters. We were able to determine a clinical cause of death in most patients. Arrhythmias (30%) and pulmonary vascular disease (13%) are important causes of sudden death. Simple aortic valve disease and hypertrophic cardiomyopathy are rare (4%) causes of sudden death in childhood. Infants and young children with surgical shunts comprise 23% of sudden unexpected deaths that occur within a month of the last evaluation. Close surveillance of these patients is warranted.     

The molecular autopsy: an indispensable step following sudden cardiac death in the young?

Annually thousands of sudden deaths involving young individuals (<?35?years of age) remain unexplained following a complete medicolegal investigation that includes an autopsy. In fact, epidemiological studies have estimated that over half of sudden deaths involving previously healthy young individuals have no morphological abnormalities identifiable at autopsy. Cardiac channelopathies associated with structurally normal hearts such as long QT syndrome (LQTS), catecholaminergic polymorphic ventricular tachycardia (CPVT), and Brugada syndrome (BrS), leave no evidence to be found at autopsy, leaving investigators to only speculate that a lethal arrhythmia might lie at the heart of a sudden unexplained death (SUD). In cases of autopsy-negative SUD, continued investigation, through the use of a cardiological and genetic evaluation of first- or second-degree relatives and/or a molecular autopsy, may pinpoint the underlying mechanism attributing to the sudden death and allow for the identification of living family members with the pathogenic substrate that renders them vulnerable to an increased risk for cardiac events, including sudden death.     

Circadian rhythm in sudden cardiac death: a retrospective study of 2,665 cases

Several studies have reported a circadian variation in sudden cardiac death. The aim of this study was to determine whether in northern Greece sudden cardiac death shows a circadian rhythm and/or a weekly and seasonal distribution. We studied 2,665 sudden deaths due to coronary heart disease from 13,832 sudden deaths that merited autopsy; 1,429 (53.6%) of them were due to acute myocardial infarction (AMI) and 1,236 (46.4%) to chronic ischemic heart disease (IHD). The time of death was determined on the basis of autopsy results and witness interviews. There was a circadian rhythm of sudden cardiac death (p<0.010), with a low incidence during the hours 04.00-08.00 (13.1%) and an increased incidence during 20.00-24.00 (19.8%) (p<0.05). Women did not show the same significant circadian variation. Time of occurrence of sudden cardiac death attributed either to AMI or to IHD showed a similar 24-hour distribution (lowest incidence during 04.00-08.00 hours, 12.8% and 13.5%, respectively, and higher during 20.00-24.00, 19.5% and 20.3%, respectively). Weekday distribution of sudden cardiac death showed a significant statistical variation (p<0.005) with the highest frequency on Monday (21.1%) and the lowest on Sunday (7.5%). The same distribution was observed in men, whereas in women the lower frequency was also on Sunday but the higher was on Tuesday. Sudden cardiac death was evenly distributed over the months of the year, with the highest incidence in summer (27.3%) and the lowest in autumn (22%). Sudden cardiac death shows a circadian rhythm and a significant variation during the week.     

Ventricular fibrillation in chronic heart disease

The objective of the work was to describe in subjects with spontaneous ventricular fibrillation, after elimination of acute cardiac disease, the strategy of antiarrhythmic treatment and to evaluate, based on prospective follow-up, the effectiveness of this treatment. The authors included in the group 36 patients (30 men and 6 women) within the range from 34 to 78 years (mean age 58 +/- 11 years) with spontaneous ventricular fibrillation. They divided the group into a subgroup (15 subjects) without revascularization of the heart muscle, into a subgroup (17 subjects) with revascularization of the myocardium (coronary angioplasty and bypasses) and a subgroup (4 subjects) where ischaemic heart disease was ruled out (mostly cardiomyopathies). In all subgroups they used programmed ventricular stimulation (apparatuses of Quinton Co. USA, Biotronik Co. GFR), in the subgroup with revascularization within 3 months. During the diagnostic procedure of ventricular stimulation they tested antiarrhythmic drugs most frequently amiodarone per os (for 4 weeks). An implantable cardioverter--defibrillator was implanted in 17 patients (8 subjects without revascularization, 6 subjects with revascularization, 3 subjects without ischaemic heart disease). All patients were followed up till death, maximum 24 months. The authors evaluated the rate of cardiac deaths (death on cardiac grounds, incl. sudden arrhythmic death) and sudden arrhythmic deaths (within one hour after the onset of symptoms or the first malignant ventricular tachyarrhythmia recorded after implantation of the defibrillator). In the subgroup without revascularization with electric instability of the ventricles according to programmed stimulation 66.7% they described seven cardiac deaths (46.7%) and 6 sudden "arrhythmic" deaths (40%) incl. 5 subjects with ineffective testing of antiarrhythmic drugs. Conversely in the subgroup with revascularization and with diagnostic programmed stimulation in 47.1% they found 3 cardiac deaths (17.7%), one sudden "arrhythmic" death (5.9%)--a subject with ineffective testing. In the subgroup without ischaemic heart disease they recorded cardiac and sudden "arrhythmic" deaths in half the subjects, in all instances in subjects without inducible ventricular tachyarrhythmia. The authors found in the course of a two-year investigation a relapse of cardiac arrest in 25% of subjects after spontaneous ventricular fibrillation. A third of these subjects (all without a cardioverter-defibrillator) died. They confirm the benefit of implantation of a defibrillator for all subjects regardless of the basic diagnosis and revascularization of the heart muscle.     

Mode of death in patients with newly diagnosed heart failure in the general population

BACKGROUND: Early prognosis for incident (new) heart failure (HF) patients in the general population is poor. Clinical trials suggest approximately half of chronic HF patients die suddenly but mode of death for incident HF cases in the general population has not been evaluated. AIMS: To describe mode of death in the first six months after a new diagnosis in the general population. METHODS: Two-centre UK population-based study. RESULTS: 396 incident HF patients were prospectively identified. Overall mortality rates were 6% [3-8%], 11% [8-14%] and 14% [11-18%] at 1, 3 and 6months respectively. There were 59 deaths over a median follow-up of 10months; 86% (n = 51) were cardiovascular (CV) deaths. Overall, the mode of death was progressive HF in 52% (n = 31), sudden death (SD) in 22% (n = 13), other CV death in 12% (n = 7), and non-CV death in 14% (n = 8). On multivariable analysis, progressive HF deaths were associated with older age, lower serum sodium, systolic hypotension, prolonged QRS duration at baseline and absence of ACE inhibitor therapy at the time of discharge or death. CONCLUSION: Early prognosis after a new diagnosis of HF in the general population is poor and progressive HF, rather than sudden death, accounts for the majority of deaths.     

Prediction of sudden death from QTc interval prolongation in patients with chronic ischemic heart disease

Although prolongation of QTc interval has been shown to increase the risk of sudden death after recent myocardial infarction, no data exist on the relationship between sudden death and QTc duration in patients with chronic ischemic heart disease. Furthermore, it is not known whether patients with long QTc intervals (greater than or equal to 440 units) have more prevalent coronary risk factors. Thus 141 nonsurvivors (128 with coronary death and 13 with noncoronary death) representing the follow-up deaths of a cohort of 1157 medically treated patients with ischemic heart disease over a four-year period were compared to 141 consecutive long-term survivors of the same cohort. Thirty-one patients were excluded because of drug interactions, bundle-branch block or atrial fibrillation. QTc duration was calculated on the ECG immediately prior to angiography in 62 patients with sudden death, 36 with intermediate death, 13 with noncoronary death and 140 long-term survivors with chronic ischemic heart disease. In addition, in 64 nonsurvivors (58%) in whom more than one yearly follow-up ECG was available, QTc was calculated in the last ECG preceding death (mean of four months before death). These data were compared to those obtained in 140 long-term survivors at the time of last ECG (mean 48 months after enrollment). At the time of angiography, mean QTc intervals were similar in patients who later died of ischemic heart disease and in long-term survivors (423 +/- 35 vs 421 +/- 25 units). No difference in QTc duration was apparent among nonsurvivors with ischemic heart disease. All study patients were divided into normal and long QTc subgroups.(ABSTRACT TRUNCATED AT 250 WORDS)