Sudden cardiac death: definition, mechanisms and risk factors

Sudden cardiac death is defined as natural death due to cardiac causes, heralded by abrupt loss of consciousness within one hour after the onset of symptoms. The mechanisms are the following: 1. ventricular fibrillation, 2. ventricular tachycardia and flutter with subsequent ventricular fibrillation, 3. torsade de pointe, 4. bradyarrhythmias and asystolic arrest. White the main risk factor is the presence of coronary artery disease, any organic or functional disease of the heart can predispose for sudden cardiac death. To evaluate the risk of sudden cardiac death noninvasive (Holter, echocardiography, exercise test and signal averaged (ECG) and often invasive (electrophysiological study) tests are necessary. The therapy is based on drugs (mainly beta blockers and amiodarone), coronary revascularization, catheter ablation techniques and the implantation of a cardioverter defibrillator; the latter appears to be the most promising approach.     

Routine microbiological testing in sudden and unexpected infant death

We reviewed 187 depth recorded seizures in 33 patients with non-lesional temporal lobe complex partial seizures. All patients had a minimum of 1 year follow-up following temporal lobectomy. We classified seizure onset pattern as rhythmic activity, attenuation, or repetitive spikes or spike wave complexes. The most common pattern of seizure onset was rhythmic activity and the next most common pattern was repetitive spikes. Seventy-five seizures (49%) had only one seizure onset pattern, and 79 seizures (51%) had a combination of seizure onset patterns. The degree of hippocampal gliosis strongly predicted the type of seizure onset pattern (Chi square = 24.07, 2 d.f., P < 0.01). The rhythmic activity pattern was associated with mild gliosis, and the repetitive spike pattern was associated with severe gliosis. We classified seizure onset as focal or regional based on the number of electrode contacts that were involved by the ictal EEG. A focal seizure onset was associated with an excellent outcome following temporal lobectomy.     

Sudden, unexpected death of infants and electromagnetic fields (author's transl)

The examination of 337 cases of Sudden Infant Death Syndorme (SIDS) ro Crib Deaths in Philadelphia, Penn., USA, and 294 cases in Hamburg, Federal Republic of Germany, shows regional concentrations which are close to uncommon magnetic fields or stray electric currents in the ground. The risk in the cellar and first floor of houses is higher than in the other floors. Therefore a possible causal relationship between electromagnetic fields and SIDS cases must be considered and checked by on-site measurements, animal experiments, and by more research on magnetic fields as stressor for infants.     

Sudden unexpected cardiac death: methods and results of a national pilot survey

In order to develop a methodology for measuring the occurrence and circumstances of sudden unexpected adult deaths due to cardiac and to unidentified causes throughout England, a stratified random pilot sample of 12 of the 133 coroner's jurisdictions in England was invited to survey prospectively a quota sample of 78 consecutive white Caucasians, aged from 16 to 64 years, with no history of ischaemic heart disease, who were last seen alive within 12 h of being found dead, and for whom a coroner's post-mortem examination found either a cardiac or no identifiable cause of death. Eleven (92%) coroners participated. In a median of 105 days (range 21-169), 65 cases (83% of the quota) were ascertained (54 (83%) males). Of the ascertained cases, registration forms were received on 62 (95%), tissue specimens on 63 (97%), and post-mortem reports on 58 (89%). Death was witnessed in 58%, of which 35% were 'instantaneous'. The median time from symptom onset to death was 40 min. In unwitnessed deaths, the median time since last being seen alive was 90 min. Sixty-eight per cent of all deaths were attended--by a relative in 34%, passer-by (8%), ambulance crew (32%), nurse (11%), doctor (38%), and police (9%). Cardio-pulmonary resuscitation was attempted in 38 of the 42 attended deaths. Sixty-seven per cent were taken ill at home, 12% at work, 12% in a public place, and 10% elsewhere. The certified cause of death was ischaemic heart disease in 89%, in whom coronary thrombosis and/or myocardial damage was absent in 6 cases (9%). In the remainder, the certified cause was hypertensive heart disease (5%), hypertrophic obstructive cardiomyopathy (3%), 'cardiomegaly' (1.5%) and 'sudden cardiac arrhythmia' alone (1.5%). A retrospective audit of coroner's records revealed the median case ascertainment rate was 75%. This approach to surveying sudden unexpected adult death nationally resulted in a high response rate (92%) from coroners, consultant pathologists and their staff, the identification of a large proportion of eligible cases, and complete information in most of the identified cases. In from 2% to 15% of cases, death may have been either purely dysrhythmic or due to a sudden adult death syndrome.     

Sudden unexpected death in infancy: epidemiologically determined risk factors related to pathological classification

OBJECTIVE: Gestational diabetes is associated with increased risk of developing noninsulin-dependent diabetes (NIDDM) later in life. By the time that a diagnosis of NIDDM is established, functional disturbances in the vascular system may be observed. This study was planned to assess macro- and microvascular function in nonpregnant women without signs of diabetes two to four years after a pregnancy complicated with gestational diabetes. DESIGN: Cross-sectional study. SETTING: Vascular research laboratory in the obstetric unit of a university hospital. PARTICIPANTS: Seventeen nonpregnant, healthy women with a history of gestational diabetes and 20 nonpregnant control women of similar age without previous diabetes. METHODS: For quantification of the mechanical properties in large arterial vessels the wall movements of the abdominal aorta and left common carotid artery were recorded with an ultrasonic tracking system. Microvascular perfusion in the skin of the hand and foot was recorded by a laser Doppler technique to assess the vasodilatory response induced by transcutaneous acetylcholine. RESULTS: Women in the gestational diabetes group showed evidence of increased wall stiffness in the common carotid artery and a lower maximum incremental velocity of the pulsatile vessel diameter change in both aorta and carotid artery compared with controls. Acetylcholine induced vasodilatation in both hand and foot was lower in women with previous gestational diabetes compared with controls. CONCLUSION: Abnormal vascular function was found in asymptomatic women with a history of gestational diabetes. It is speculated that these abnormalities might be early evidence of vascular complications associated with subsequent NIDDM.     

A clinical and pathological study of 46 cases of sudden and unexpected death

A series of 46 autopsied adult cases of sudden and unexpected natural death were investigated. In this study, sudden and unexpected death was defined as any death occurring with 24 hours of onset of symptoms in a person with or without probable cause of death suggested by medical history. The cases included 31 males and 15 females aged 26 to 85 years (mean 66.6 years). Age distribution peaked in seventies. The lesions causing sudden and unexpected death according to the most frequent organ systems were, diseases of the heart (acute myocardial infarction with or without old infarct, 20; old myocardial infarction without acute infarction, 2; dilated cardiomyopathy, 2; sarcoidosis, 1; amyloidosis, 2; and valvular disease, 2), the aorta (ruptured aneurysm, 6; dissecting aneurysm, 2), the respiratory tract (pulmonary embolism, 7; pulmonary hypertension, 1), the alimentary tract (intestinal obstruction, 1), and other diseases (cause unknown, 1). The cardiovascular lesions were found in 78.2% of cases autopsied. The sudden and unexpected death caused by acute myocardial infarction was found in 47.8%, and acute myocardial infarction seemed to play a major role in cardiac sudden death in these series. The respiratory lesions were found in 17.4%. Four of seven cases with pulmonary embolism died in two weeks after surgical operation. The most common underlying disease was post-operative condition.     

Causes of sudden unexpected cardiac death in the first two decades of life

Sudden, unexpected cardiac death in the age group 1 to 21 years usually is due to myocarditis, hypertrophic cardiomyopathy, aortic valvar stenosis, and coronary arterial abnormalities. The hearts of 70 patients <21 years of age who died suddenly were reviewed. Twenty patients were <1 year of age and 50 were 1 to 21 years old. The cardiac findings were compared with those in 68 age-matched controls with known cardiac disease who did not die suddenly. Significant cardiac abnormalities were present in 13 (65%) of the 20 infants; 10 (50%) had anomalies of the aortic origin of the coronary arteries. Among the 50 older patients, cardiac abnormalities were found in 40 (80%), among whom coronary arterial anomalies existed in 12 (24%). Anomalies of aortic origin more frequently involved the left main than the right coronary artery in both groups.     

The incidence of sudden unexpected death in epilepsy (SUDEP) in South Dublin and Wicklow

The binding of cocaine (COC) and cocaethylene (CE) to whole human liver homogenates in vitro was studied by equilibrium dialysis. Drugs were measured by high-pressure liquid chromatography. Up to 32% of COC and up to 43% of CE were bound. Scatchard analysis suggested a high-affinity, low-capacity binder for both COC (Ka, 4.69 x 10(4) L/mol; Bo, 1.08 x 10(-5) mol/L) and CE (Ka, 4.38 x 10(4) L/mol; Bo, 1.54 x 10(-5) mol/L). In addition, low-affinity, high-capacity binders for COC (Ka, 2.93 x 10(3) L/mol; Bo, 1.32 x 10(-4) mol/L) and CE (Ka, 6.50 x 10(3) L/mol; Bo, 1.11 x 10(-4) mol/L) were noted. Finally, for both compounds, very low-affinity, high-capacity binding, which was likely nonspecific in nature, was defined as follows: COC, Ka, 8.00 x 10(2) L/mol; Bo, 5.45 x 10(-4) mol/L and CE, Ka, 2.10 x 10(3) L/mol; Bo, 3.71 x 10(-4) mol/L. The binding profiles of COC and CE in liver were compared with those in human serum and placenta studied previously by this laboratory.     

Risk stratification and prediction of sudden death following myocardial infarction

Accurate and reliable identification of those survivors of acute myocardial infarction who are at high risk of sudden death remain an important and challenging problem. This review summarises the current state-of-the-art of the risk stratification techniques and lists achievements in this field. The review comments in detail on individual factors used in risk stratification. Residual ischemia may be considered as one of the main triggering factors of post-infarction arrhythmia. Depressed left ventricular ejection fraction indicates deterioration of ventricular function. Electrical instability of the myocardium reflects the potential substrate of arrhythmia. Frequent ventricular ectopic activity provides triggers of ventricular tachycardia and/or fibrillation when acting on a suitable substrate. Impaired autonomic status of the heart may lead to the loss of vagal antiarrhythmic protection. Further, the tests used for risk stratification are discussed. Ventriculography provides estimates of left ventricular ejection fraction. Holter monitoring is used for the assessment of ventricular ectopic activity and heart rate variability. Exercise testing is used to address residual ischemia. Programmed ventricular stimulation and the analysis of signal averaged electrocardiograms estimate electrical instability of the myocardium. Baroreflex sensitivity is a measure of cardiac parasympathetic reflexes. The design and results of different experimental and clinical studies which utilised these tests are also discussed.     

Prevention of sudden cardiac death by the atypical neuroleptic acepromazine following status epilepticus in rats

Normal male rats in which status epilepticus has been induced by injecting 30 mg/kg of pilocarpine after a single systemic administration of lithium (sufficient to produce blood levels of 0.2 mEq/L) invariably die within 24 hr. Real-time monitoring indicated sudden cardiac death; it was preceded by progressive intensification of arrhythmia. A single systemic injection (25 mg/kg) of the atypical phenothiazine acepromazine prevented the mortality and virtually eliminated the cardiac instability.     

Sudden death in implantable cardioverter-defibrillator recipients: clinical context, arrhythmic events and device responses

Reports regarding the effect of all-trans-retinoic acid (RA) on the cell growth of retinal pigment epithelial cells (RPE) have been contradictory. The aims of this study are to clarify the in vitro effect of RA on RPE cells and to examine polyamine metabolism after RA stimulation. A 4-day incubation of fetal-calf-serum (FCS)-stimulated RPE cells with 10 or 25 microM RA significantly increased both cell number and [3H]thymidine incorporation. RPE cells grown over an extended period for 8 days also increased in number and reached full confluency. However, if the incubation was further extended to 12 days, no further increase in cell number was detected. RA treatment of FCS-stimulated RPE cells shifted the peak of ornithine decarboxylase (ODC) activity from 16 to 4 h. S-adenosylmethionine decarboxylase (SAMDC) activity and spermidine/spermine N1-acetyltransferase (SAT) activity of RA-treated RPE cells were significantly greater until 8 and 16 h after incubation, respectively. The putrescine content was significantly increased in RA-treated RPE cells up until 24 h, while spermidine, spermine and N1-acetylspermidine contents were significantly increased until 16 h. Our findings suggest that RA treatment increases the intracellular polyamine concentration of RPE cells via activation of ODC, SAMDC and SAT and that this results in the promotion of RPE cell growth until the cells reach full confluency.     

Histiocytoid cardiomyopathy: a cause of sudden death in infancy

We report the case of an infant aged of 14 months deceased of sudden death. The diagnosis of histiocytoid cardiomyopathy was made on a necropsic basis. The pathologic examination showed a cardiac hypertrophy characterized by yellowish areas with irregular outlines, disseminated in the myocardium, and made of histiocyte-like cells with foamy or granular cytoplasm. These cells reacted positively with desmin and myoglobin labels, and had rare and disorganised myofibrils in electron microscopy, proving their muscular origin. The illness affects infants and usually causes severe cardiac troubles leading to death without treatment. This case is the fourteenth associated with sudden death.     

Sudden death in the laboratory rat: cardiac function, sensory, and experiental factors in swimming deaths

Three reported charateristics of sudden death in the wild rat, (1) bradycardia, (2) decreased survival without whiskers, and (3) increased suvival with preexposure to the stressor, are demonstrated in the domestic rat. Differences in sudden death between wild and domestic rats are discussed as well as possible interpretations of the phenomenon.     

Minor inflammatory lesions and sudden infant death: cause, coincidence, or epiphenomena?

Minor inflammatory changes are often found in tissues of infants who die suddenly. Recently it has been proposed that these infiltrates signal significant underlying infectious disease and are responsible for death. Currently there is no unanimity about the percentage of cases in which inflammatory infiltrates occur and no international consensus in regard to the minimal criteria required for their diagnosis or their significance. We recommend that the presence of minor inflammatory infiltrates should not detract from the diagnosis of sudden infant death syndrome (SIDS) until further study has determined otherwise.