Omega-3 consumption and sudden cardiac death in schizophrenia

People with schizophrenia show a two- to three-fold increased risk to die prematurely. Mortality is accounted for by a combination of factors (patients’ life style, suicide, premature cardiovascular disease, metabolic syndromes and, not so often mentioned, sudden death). The cause of sudden death in schizophrenia is unknown, but cardiac arrhythmia plays a potential role. Patients with schizophrenia are at high risk for cardiovascular disease, and some antipsychotics may be associated with cardiovascular adverse events (e.g., electrocardiograph QT interval prolongation), suggesting that this could lead to sudden cardiac death. Animal and clinical studies have shown that omega-3 fatty acids could be useful in the prevention and treatment of schizophrenia. As omega-3 fatty acids have been considered a cardioprotector agent, reducing cardiac arrhythmias and hence sudden cardiac deaths and given their relative safety and general health benefits, our update article summarizes the knowledge by the possible positive effects of omega-3 supplementation and fish consumption against sudden cardiac death in patients with schizophrenia. However, fish species should be selected with caution due to contamination with toxic methylmercury.     

Endpiece: Genius (1815)

ObjectiveTo examine the proposition that a used infant mattress is associated with an increased risk of sudden infant death syndrome.DesignCase-control study.SettingScotland (population 5.1 million, with about 53 000 births a year).Participants131 infants who died of sudden infant death syndrome between 1 January 1996 and 31 May 2000 and 278 age, season, and obstetric unit matched control infants.ResultsRoutine use of an infant mattress previously used by another child was significantly associated with an increased risk of sudden infant death syndrome (multivariate odds ratio 3.07, 95% confidence interval 1.51 to 6.22). Use of a used infant mattress for last sleep was also associated with increased risk (6.10, 2.31 to 16.12). The association was significantly stronger if the mattress was from another home (4.78, 2.08 to 11.0) than if it was from the same home (1.64, 0.64 to 4.2).ConclusionA valid significant association exists between use of a used infant mattress and an increased risk of sudden infant death syndrome, particularly if the mattress is from another home. Insufficient evidence is available to judge whether this relation is cause and effect.

What is already known about this topic

The major risk factors for sudden infant death syndrome are sleeping prone and parental smokingOne study has suggested that the syndrome is associated with sleeping on an infant mattress previously used by another child

What this study adds

New case-control data show that the association between a previously used infant mattress and sudden infant death syndrome is validWhen source of used mattress is categorised, the association is significant only if the mattress is from another homeInsufficient evidence is available to judge whether this is a cause and effect relation     

Bed sharing,smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group.

OBJECTIVES--To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption. DESIGN--Nationwide case-control study. SETTING--Region of New Zealand with 78% of all births during 1987-90. SUBJECTS--Home interviews were completed with parents of 393 (81.0% of total) infants who died from the sudden infant death syndrome in the postneonatal age group, and 1592 (88.4% of total) controls who were a representative sample of all hospital births in the study region. RESULTS--Maternal smoking interacted with infant bed sharing on the risk of sudden infant death. Compared with infants not exposed to either risk factor, the relative risk for infants of mothers who smoked was 3.94 (95% confidence interval 2.47 to 6.27) for bed sharing in the last two weeks and 4.55 (2.63 to 7.88) for bed sharing in the last sleep, after other confounders were controlled for. The results for infants of non-smoking mothers were inconsistent with the relative risk being significantly increased for usual bed sharing in the last two weeks (1.73; 1.11 to 2.70) but not for bed sharing in the last sleep (0.98; 0.44 to 2.18). Neither maternal alcohol consumption nor the thermal resistance of the infant''s clothing and bedding interacted with bed sharing to increase the risk of sudden infant death, and alcohol was not a risk factor by itself. CONCLUSION--Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.     

Alcohol intemperance and sudden death.

Ten years after a health screening examination was offered to 50 year old men 32 of the 2322 participants and 12 of the 454 nonparticipants had died of ischaemic heart disease. Of these, 26 and 11 respectively had suffered sudden death, for which necropsy was performed. Half of the men who had died suddenly had been registered for alcohol intemperance up to 1973, which was four times the prevalence of such registrations in the general population. Registration at both the Swedish Temperance Board and the Bureau of Social Services was associated with an odds ratio of 3.74 for sudden death as compared with not being registered at either. Logistic analysis including the classical risk factors for ischaemic heart disease together with registration for alcohol intemperance and at the Bureau of Social Services showed only the two types of registration and systolic blood pressure to be independent risk factors. On the other hand, there was no overrepresentation of subjects entered in the registers among those surviving a myocardial infarction. For non-fatal myocardial infarction blood pressure and serum triglyceride concentration were significant risk factors and serum cholesterol concentration, smoking, and body mass index probable risk factors; the two types of registration were not independent risk factors. Alcohol intemperance is strongly associated with an increased risk of sudden death after myocardial infarction.     

Risk stratification and subclinical phenotyping of dilated and/or arrhythmogenic cardiomyopathy mutation-positive relatives: CVON eDETECT consortium

In relatives of index patients with dilated cardiomyopathy and arrhythmogenic cardiomyopathy, early detection of disease onset is essential to prevent sudden cardiac death and facilitate early treatment of heart failure. However, the optimal screening interval and combination of diagnostic techniques are unknown. The clinical course of disease in index patients and their relatives is variable due to incomplete and age-dependent penetrance. Several biomarkers, electrocardiographic and imaging (echocardiographic deformation imaging and cardiac magnetic resonance imaging) techniques are promising non-invasive methods for detection of subclinical cardiomyopathy. However, these techniques need optimisation and integration into clinical practice. Furthermore, determining the optimal interval and intensity of cascade screening may require a personalised approach. To address this, the CVON-eDETECT (early detection of disease in cardiomyopathy mutation carriers) consortium aims to integrate electronic health record data from long-term follow-up, diagnostic data sets, tissue and plasma samples in a multidisciplinary biobank environment to provide personalised risk stratification for heart failure and sudden cardiac death. Adequate risk stratification may lead to personalised screening, treatment and optimal timing of implantable cardioverter defibrillator implantation. In this article, we describe non-invasive diagnostic techniques used for detection of subclinical disease in relatives of index patients with dilated cardiomyopathy and arrhythmogenic cardiomyopathy.     

A Case of Inappropriate Therapies for Atrial Flutter From a Subcutaneous ICD

Hypertrophic cardiomyopathy’s (HCM) association with sudden cardiac death is well recognised. The risk of sudden cardiac death is known to increase when there is a history of unexplained syncope, abnormal blood pressure response during exercise, severe left ventricular hypertrophy or a family history of unexplained death.Implantable Cardioverter Defibrillator (ICD) implantation has been widely used for primary and secondary prevention of sudden cardiac death (SCD) in people with HCM. Subcutaneous ICD (S-ICD) therapy has been developed to overcome some of the problems associated with the transvenous leads used in conventional ICDs.In this article, we report the use of S-ICD in a patient with HCM and multiple risk factors for sudden cardiac death, this device had to be extracted due to recurrent inappropriate shocks caused by over sensing of atrial flutter and failure to treat a VT episode. We are not aware of any reports of inappropriate shocks caused by atrial flutter in people with a S-ICD.     

Electrophysiological evaluation of Wolff-Parkinson-White syndrome

Sudden death might complicate the follow-up of symptomatic patients with the Wolff-Parkinson-White syndrome (WPW) and might be the first event in patients with asymptomatic WPW. The risk of sudden death is increased in some clinical situations. Generally, the noninvasive studies are unable to predict the risk of sudden death correctly . The electrophysiological study is the best means to detect the risk of sudden death and to evaluate the nature of symptoms. Methods used to define the prognosis of WPW are well-defined. At first the maximal rate of conduction through the accessory pathway is evaluated; programmed atrial stimulation using 1 and 2 extrastimuli delivered at different cycle lengths is then used to determine the accessory pathway refractory period and to induce a supraventricular tachycardia. These methods should be performed in the control state and repeated in adrenergic situations either during exercise test or more simply during a perfusion of small doses of isoproterenol. The induction of an atrial fibrillation with rapid conduction through the accessory pathway (> 240/min in control state, > 300/min after isoproterenol) is the sign of a form of WPW at risk of sudden death.     

Cardiovascular disease and long-chain omega-3 fatty acids

PURPOSE OF REVIEW: Of all known dietary factors, long-chain omega-3 fatty acids may be the most protective against death from coronary heart disease. New evidence has confirmed and refined the cardioprotective role of these fatty acids. RECENT FINDINGS: Omega-3 fatty acid supplementation reduces the risk of sudden cardiac death and death from any cause within 4 months in post-myocardial infarction patients. Evidence continues to accrue for benefits in the primary prevention of coronary heart disease and stroke, and an anti-arrhythmogenic mechanism is emerging as the most likely explanation. SUMMARY: Current evidence suggests that individuals with coronary artery disease may reduce their risk of sudden cardiac death by increasing their intake of long-chain omega-3 fatty acids by approximately 1 g per day.     

Inherited cardiomyopathies and sports participation

Competitive sports activity is associated with an increased risk of sudden cardiovascular death in adolescents and young adults with inherited cardiomyopathies. Many young subjects aspire to continue competitive sport after a diagnosis of cardiomyopathy and the clinician is frequently confronted with the problem of eligibility and the request of designing specific exercise programs. Since inherited cardiomyopathies are the leading cause of sudden cardiovascular death during sports performance, a conservative approach implying disqualification of affected athletes from most competitive athletic disciplines is recommended by all the available international guidelines. On the other hand, we know that the health benefits of practicing recreational sports activity can overcome the potential arrhythmic risk in these patients, provided that the type and level of exercise are tailored on the basis of the specific risk profile of the underlying cardiomyopathy. This article will review the available evidence on the sports-related risk of sudden cardiac death and the recommendations regarding eligibility of individuals affected by inherited cardiomyopathies for sports activities.     

Risk of death due to chronic chagasic cardiopathy

In this longitudinal study 5,710 people were included. The inclusion criteria were two positive serological results for Trypanosoma cruzi infection, 15 and 50 years old and no other demonstrable disease at the time of study. In the five year follow up 1,117 patients were lost. The follow up involved yearly evaluation of serology, clinical examination, X-ray of thorax, and ECG, for 4,593 patients and 263 were contacted at home because they did not assist for their clinical consultant. Time average of follow up was 5.3 years. Eighty nine (1.5%) of the 4,593 patients died during the follow-up period, 63 (71%) by cardiac insufficiency (CI) and 26 (29%) by severe ventricular arrhythmias. Diagnosis of cardiomegaly was present in all the patients with diagnosis of CI and in 15 (5%) of the patients with diagnosis of arrhythmias. The ECG alterations of these patients show 61 right bundle branch block (RBBB), associated or not with left anterior hemiblock (LAHB), 47 pathological Q wave and 70 primary repolarization alterations; 61 had polyfocal ventricular arrhythmia. The death rate was similar in the sexes and was more frequent between 40 and 50 years of age. Information on 1,380 recuperated patients shows that 15 died with no previous symptoms and without medical assistance and were interpreted as sudden death. The latest ECG in three follow-up of these patients indicates (before death) that only one had normal study and 14 presented 12 RBBB; 9 LAHB; 7 isolated ventricular arrhythmia; 10 repolarize alterations; 2 pathological Q wave, 10 patients of them with RBBB and repolarize alterations. In all the cases we had people between 35 and 43 years old, 9 men and 6 women. This study shows that in Chagas disease is possible to differentiate two risk groups. A low risk death group that have normal ECG and clinical evaluation during the follow up, and a high risk group associate ECG with RBBB and primary alterations of repolarization and/or inactivation zones with not annual clinical evaluation.     

Malignant familial hypertrophic cardiomyopathy in a family with a 453Arg→Cys mutation in the β-myosin heavy chain gene: Coexistence of sudden death and end-stage heart failure

Recent genotype-phenotype correlation studies in familial hypertrophic cardiomyopathy (FHC) have revealed that some mutations in the β-myosin heavy chain (BMHC) gene may be associated with a high incidence of sudden death and a poor prognosis. Coexistence of sudden death and end-stage heart failure in several families with FHC has recently being reported; however, the genetic basis of such families has not been clearly demonstrated. A three-generation Chinese familial hypertrophic cardiomyopathy (FHC) family (family HL1) with two cases of end-stage heart failure and three cases of sudden death was analyzed. The average age of death in the affected members in this family was 34 years old. Genetic linkage analysis using polymorphisms in the α- and β-myosin heavy chain genes revealed that FHC in this family is significantly linked to the BMHC gene without recombinations. Single-strand conformation polymorphism analysis of exons 8, 9 and 13 to 23 in the BMHC gene showed a polymorphic band on exon 14 that is in complete linkage with the disease status in this family. DNA sequencing analysis in the affected members revealed an 453Arg→Cys mutation in the BMHC gene. To our knowledge this is the first reported mutation of FHC in Chinese. Our data suggest that the 453Arg→Cys mutation is associated with a malignant clinical course in FHC due not only to sudden death but also to end-stage heart failure. Received: 6 July 1995 / Revised: 20 September 1995     

Antiarrhythmic effects of n-3 fatty acids: evidence from human studies

PURPOSE OF REVIEW: N-3 fatty acids from fish reduce cardiovascular mortality including sudden cardiac death. In this paper, the authors discuss the results of human studies with regard to the hypothesis that n-3 fatty acids reduce the risk of fatal coronary heart disease through antiarrhythmic effects. RECENT FINDINGS: Results from two recent clinical trials do not support a protective effect of n-3 fatty acids. In light of the earlier published bulk of evidence that n-3 fatty acids reduce cardiovascular mortality and sudden cardiac death, it is hard to explain these findings. Two recent observational studies confirmed that intake of n-3 fatty acids from fish is associated with less cardiovascular disease in the general population. They indicated that the protective effect of a fish meal may depend on the n-3 fatty acid content or preparation method and suggested a protective effect on arrhythmia rather than on atherosclerosis. Intervention studies on electrophysiological predictors of arrhythmia do not clearly confirm a beneficial effect of n-3 fatty acids. However, most of these studies were small or performed in healthy populations. SUMMARY: The available evidence still suggests that n-3 fatty acids may prevent fatal cardiac arrhythmia, but more conclusive studies are urgently needed.     

Apollo, sudden death, and Homer's "Odyssey": a warning from the past that we may be unable to eradicate coronary artery disease

Over recent years there has been a gratifying decrease in the incidence of recorded deaths from coronary artery disease in the Western world. The common view is that coronary artery disease is a recent phenomenon, that we have been subject to an epidemic in the mid-20th century that is now tailing off, and that with appropriate risk modification we may eradicate this disease or make it very rare. However, this article examines the cases of sudden, nontraumatic death described in Homer's Odyssey, which dates from c. 800 BCE. The results suggest that a high incidence of death from coronary artery disease may not be a recent phenomenon. Together with other described evidence, this study casts doubt on the view that coronary artery disease is a modern epidemic that can be eradicated.     

Hypertrophic cardiomyopathy in daily practice: an introduction on diagnosis,prognosis and treatment

Hypertrophic cardiomyopathy (HCM) is a complex, inherited cardiac disease that has been subject to intense investigation since it was first described in 1957. Over the past 40 years, understanding has evolved regarding the diagnosis, prognosis and treatment of HCM. Analyses of HCM populations from nonreferral centres have refined the insights into the natural history and the occurrence of sudden cardiac death, which is the most devastating component of its natural history. Therapeutic strategies are diverse and may vary during the course of the disease. Optimal therapy depends on symptoms, haemodynamic findings and the presence of risk factors for sudden cardiac death. At present, invasive therapy for patients with obstructive HCM and drug-refractory symptoms includes surgery or percutaneous transluminal septal myocardial ablation.This report summarises the diagnostic criteria, clinical course and therapeutic management of HCM. Attention is also paid to certain issues of special interest in this disease.     

Electrical storms in Brugada syndrome successfully treated with isoproterenol infusion and quinidine orally

Brugada syndrome is an inherited cardiac disease and is associated with a peculiar pattern on the electrocardiogram and an increased risk of sudden death. Electrical storm is a malignant but rare phenomenon in symptomatic patients with Brugada syndrome. We describe a patient who presented with repetitive ICD discharges during two episodes of recurrent VF. After the initiation of isoproterenol infusion and oral quinidine, the ventricular tachyarrhythmias were successfully suppressed. (Neth Heart J 2007;15:151-4.)     

Subdiaphragmatic murine electrophysiological studies: sequential determination of ventricular refractoriness and arrhythmia induction

Programmed electrical stimulation (PES) is a crucial aspect of the evaluation of the risk of arrhythmias in cardiac patients and provides a powerful tool for understanding the mechanisms of arrhythmia in experimental models. Whereas PES in the mouse is well characterized, the procedures allowing for follow-up studies in the same animal have not been developed. In this report, we describe a novel subdiaphragmatic approach that allows for repeat electrophysiological studies in the mouse. Under inhaled anesthesia, PES was performed in 36 wild-type mice via a stimulating electrode introduced through an epigastric incision and placed directly into the diaphragmatic surface of the heart. The procedure was repeated 7 days later. Ventricular effective refractory periods (VERP) did not change significantly between the initial and follow-up trials. Chronic treatment with amiodarone, however, was associated with a 70% prolongation in VERP from initial to follow-up studies (P < or = 0.001). In addition, PES of a genetically modified strain with sudden cardiac death, the connexin43 conditional knockout mouse consistently induced lethal polymorphic ventricular tachycardia. Thus sequential PES in mice is feasible with the use of a subdiaphragmatic approach, yields reproducible VERP values, and can be used to follow pharmacologically induced changes in VERP and identify mice at risk of lethal ventricular arrhythmias.     

Clinical aspects and physiopathology of Brugada syndrome: review of current concepts

Brugada syndrome (BS) is an inherited cardiac disorder characterized by typical electrocardiographic patterns of ST segment elevation in the precordial leads, right bundle branch block, fast polymorphic ventricular tachycardia in patients without any structural heart disease, and a high risk of sudden cardiac death. The incidence of BS is high in male vs. female (i.e., 8-10/1: male/female). The disorder is caused by mutations in the SCN5A gene encoding Nav1.5, the cardiac sodium channel, which is the only gene in which mutations were found to cause the disease. Mutations in SCN5A associated with the BS phenotype usually result in a loss of channel function by a reduction in Na+ currents. We review the clinical aspects, risk stratification, and therapeutic management of this important syndrome.     

The Prognostic Value of Family History for the Estimation of Cardiovascular Mortality Risk in Men: Results from a Long-Term Cohort Study in Lithuania

Aim

To evaluate the additional prognostic value of family history for the estimation of cardiovascular (CVD) mortality risk in middle-aged urban Lithuanian men.

Methods

The association between family history of CVD and the risk of CVD mortality was examined in a population-based cohort of 6,098 men enrolled during 1972–1974 and 1976–1980 in Kaunas, Lithuania. After up to 40 years of follow-up, 2,272 deaths from CVD and 1,482 deaths from coronary heart disease (CHD) were identified. Multivariate Cox proportional hazards models were used to estimate hazard ratios (HR) for CVD and CHD mortality.

Results

After adjustment for traditional CVD risk factors, the HR for CVD mortality was 1.24 (95% CI 1.09–1.42) and for CHD mortality 1.20 (1.02–1.42) in men with first-degree relatives having a history of myocardial infarction (MI), compared to men without positive family history. A significant effect on the risk of CVD and CHD mortality was also observed for the family history of sudden cardiac death and any CVD. Addition of family history of MI, sudden death, and any CVD to traditional CVD risk factors demonstrated modest improvement in the performance of Cox models for CVD and CHD mortality.

Conclusions

Family history of CVD is associated with a risk of CVD and CHD mortality significantly and independently of other risk factors in a middle-aged male population. Addition of family history to traditional CVD risk factors improves the prediction of CVD mortality and could be used for identification of high-risk individuals.     

Approach to the asymptomatic patients with Brugada syndrome

Brugada syndrome is an arrhythmogenic disease characterized by an ECG pattern of coved-type ST segment elevation in the right precordial leads and an increased risk of sudden cardiac death (SCD) as a result of polymorphic ventricular tachyarrhythmia or ventricular fibrillation (VF). Data from large patient studies and a meta-analysis of previous reports have shown that patients with a history of syncope or SCD and a spontaneous type 1 Brugada type ECG are at high risk for SCD. However, risk stratification of asymptomatic patients with Brugada type ECG is still a challenge. In particular, the use of electrophysiological study (EPS) for risk stratification remains controversial. Although some investigators have reported the possibility of use of EPS for distinguishing between high- and low-risk patients with Brugada type ECG, no precise predictor of risk for SCD in asymptomatic patients has yet been determined. The approach to treatment of these patients is thus still unclear. Large clinical prospective studies with uniform diagnostic criteria and protocols for EPS as well as extended follow-up periods of over ten years are required for prediction of SCD.