925 resultados para sudden infant death syndrome
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EMOND, Alan et al. The effectiveness of community-based interventions to improve maternal and infant health in the Northeast of Brazil. Revista Panamericana de Salud Pública/ Pan American Journal of Public Health , v.12, n.2, p.101-110, 2002
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1. This experiment was carried out to evaluate the productive and physiological consequences of a slight but long term food restriction of male broiler chickens from 2 commercial strains.2. Cobb-500 and Ross chickens were submitted to a 20% food restriction from 8 to 21 d of age. Strain, food programme and their interactive effects were analysed in terms of consequences upon performance, mortality, incidence of sudden death syndrome (SDS) and ascites syndrome (AS), index of right cardiac hypertrophy and plasma concentrations of hormones related to metabolism and growth (T-3, T-4, T-3:T-4 ratio, IGF-I and GH).3. Although some catch-up growth was observed by refeeding previously restricted birds after 22 d of rearing, food restriction decreased (P less than or equal to 0.05) body weight at market age (42 d) irrespective of the strain, but improved (P less than or equal to 0.05) food conversion.4. The incidence of mortality was not high in non-restricted birds but SDS and AS caused more than 50% of deaths. Hypertrophic cardiac index was observed in chickens of both strains after 4 weeks of age and was higher in ad libitum fed birds.5. During the period of food restriction, plasma T-3 and IGF-I concentrations decreased whereas plasma T-4 and GH concentrations increased compared to those of the age-matched ad libitum fed counterparts. During the subsequent ad libitum feeding period, few differences in circulating hormone concentrations were observed, except for the higher mean CH litres in previously food-restricted chickens at 35 d of age.6. These results indicate that even a non-severe food restriction negatively affects body weight of 42-d-old male broilers but these are benefits with improved food efficiency and diminished mortality from metabolic disturbances. The hormone results suggest that the degree of food restriction applied was not severe because there was a very fast adaptive response with small and transient alterations in T-3, T-4 and GH plasma concentrations during the period of compensatory growth.
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The effect of feed restriction (0, 10, 20, 30, 40 and 50%) from 8 until 14 days post-hatching on performance, total mortality incidence and sudden death syndrome (SDS) rate was studied in male broilers during winter and summer.Ad libitum fed broilers had a better performance, but a higher total mortality rate (13.00% in winter, 3.67% in summer) and SDS (3.67% in winter, 0.67% in summer). All restricted groups had a lower mortality level in winter than the control group with a non linear response influenced by feed restriction. Birds submitted to 40% feed restriction showed the lowest mortality incidence (2.67%) followed by groups submitted to 30% (4.67%), 50% (5.33%) and 10% and 20% (7.67%) feed restriction. Birds fed ad libitum had the highest SDS incidence (3.67%, against .33, 1.00, .67, 1.33 and 1.33% at 10, 20, 30, 40, 50% feed restriction, respectively), but differences were not significant. In summer, incidences of total mortality and due to SDS were low and not influenced by feed restriction, either during the restrictive period itself (8 to 14 days) or during the total period of raising (1 to 49 days). In both seasons, the feed restricted birds showed compensatory gain only until three weeks post-restriction period. At 49 days, body weight and weight-gain were lower in feed restricted birds, but feed :gain ratio rate was improved. This resulted in better productivity index in winter, but not in summer. The feed restriction at 30 to 40% for seven days during the second week may decrease mortality in male broilers raised in winter without lowering productivity if the restriction is followed by at least three weeks of full feeding.
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Two trials were carried out to test the susceptibility for metabolic disturbances of different strains of male broilers. In Trial 1, 1,890 male chickens were allotted in a randomized block design with seven treatments (Arbor Acres, Avian Farms, Cobb-500, Hubbard-Peterson, ISA, Naked Neck, and Ross) and six blocks of 45 chickens. Trial 2 involved 2,184 male chickens of six strains (Arbor Acres, Avian Farms, Cobb 500, Hubbard-Peterson, ISA Naked Neck, and Ross) allotted in seven complete blocks of 52 birds. The same management system was adopted for all birds, reared up to 42 d in an open house during late winter (Trial 1) or late autumn (Trial 2). The most marked differences observed among the strains tested was the lower BW and higher feed conversion of Naked Neck broilers. Total percentage mortalities were high among the most productive broilers, being more than 50% due to sudden death (SDS) and ascites syndrome (AS). No Naked Neck birds died as a consequence of these disturbances and the total mortalities were significantly lower (P ≤ 0.05) than the other strains. The ratio of right ventricle weight to total ventricle weight of the dead birds was over 0.25, except for Naked Neck birds, which presented a nonhypertrophic ratio. The two trials confirmed the relationship between high productivity and high incidence of SDS and AS and indicated that Naked Neck male broilers are resistant to these metabolic disturbances.
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Seven male broiler strains (Arbor Acres, Avian Farms, Cobb-500, Hubbard-Peterson, ISA, Naked Neck, and Ross) were compared for their growth rate, feed efficiency, and mortality due to sudden death and ascites. In addition, weekly plasma levels of thyroid hormones [3,3′,5-triiodothyronine (T3) thyroxine (T4), T3: T4 ratio, growth hormone (GH), and insulin-like growth factor-I (IGF-I)] were determined. The highly productive, commercial strains were very similar in their endocrine profiles but differed markedly from the Naked Neck chickens. Naked Neck chickens were characterized by higher plasma T3 and lower T4 levels at similar ages as well as when compared on the same body weight basis. The present findings support the hypothesis that the slightly hypothyroid state of high productive broilers renders them more sensitive to metabolic disorders. Naked Neck chickens also had higher plasma GH levels than those of their age-matched commercial broilers. The coefficient of variation for GH was highest for Naked Neck chickens, which is indicative for an amplified GH burst amplitude. It may be stated that changes in plasma thyroid hormone concentration in indirect response to selection for low feed conversion and fast growth may be causatively linked to susceptibility for metabolic disturbances such as sudden death syndrome and ascites.
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Pós-graduação em Biotecnologia - IQ
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Background: Hypertrophic cardiomyopathy (HCM) is a common cardiac disease caused by a range of genetic and acquired disorders. The most common cause is genetic variation in sarcomeric proteins genes. Current ESC guidelines suggest that particular clinical features (‘red flags’) assist in differential diagnosis. Aims: To test the hypothesis that left ventricular (LV) systolic dysfunction in the presence of increased wall thickness is an age-specific ‘red flag’ for aetiological diagnosis and to determine long-term outcomes in adult patients with various types of HCM. Methods: A cohort of 1697 adult patients with HCM followed at two European referral centres were studied. Aetiological diagnosis was based on clinical examination, cardiac imaging and targeted genetic and biochemical testing. Main outcomes were: all-cause mortality or heart transplantation (HTx) and heart failure (HF) related-death. All-cause mortality included sudden cardiac death or equivalents, HF and stroke-related death and non-cardiovascular death. Results: Prevalence of different aetiologies was as follows: sarcomeric HCM 1288 (76%); AL amyloidosis 115 (7%), hereditary TTR amyloidosis 86 (5%), Anderson-Fabry disease 85 (5%), wild-type TTR amyloidosis 48 (3%), Noonan syndrome 15 (0.9%), mitochondrial disease 23 (1%), Friedreich’s ataxia 11 (0.6%), glycogen storage disease 16 (0.9%), LEOPARD syndrome 7 (0.4%), FHL1 2 (0.1%) and CPT II deficiency 1 (0.1%). Systolic dysfunction at first evaluation was significantly more frequent in phenocopies than sarcomeric HCM [105/409 (26%) versus 40/1288 (3%), (p<0.0001)]. All-cause mortality/HTx and HF-related death were higher in phenocopies compared to sarcomeric HCM (p<0.001, respectively). When considering specific aetiologies, all-cause mortality and HF-related death were higher in cardiac amyloidosis (p<0.001, respectively). Conclusion: Systolic dysfunction at first evaluation is more common in phenocopies compared to sarcomeric HCM representing an age-specific ‘red flag’ for differential diagnosis. Long-term prognosis was more severe in phenocopies compared to sarcomeric HCM and when comparing specific aetiologies, cardiac amyloidosis showed the worse outcomes.
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Many people with acute myocardial infarction die from sudden cardiac arrest before reaching the hospital. The current clinical understanding of the mechanisms and risk factors surrounding sudden cardiac death is limited. However, 2 factors related to sudden death, namely the occluded coronary vessel (right coronary, left circumflex, or left anterior descending artery) and the extent of collateral circulation, are of potential relevance. Recent data suggest that the risk differs between the different coronary arteries and that coronary collateral circulation seems to have an important protective 'antiarrhythmic' effect. This editorial will address possible mechanisms and potential implications in clinical practice.
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UNLABELLED The automatic implantable defibrillator (AID) is the treatment of choice for primary and secondary prevention of sudden death. At the Instituto Nacional de Cardiología, since October 1996 until January 2002, 25 patients were implanted with 26 AID. There were 23 men (92%) and the mean age of the whole group, was 51.4 years. Twenty-three patients (92%) presented structural heart disease, the most common was ischemic heart disease in 13 patients (52%), with a mean ejection fraction of 37.8%. One patient without structural heart disease had Brugada Syndrome. The most frequent clinical arrhythmia was ventricular tachycardia in 14 patients (56%). The mean follow-up was of 29.3 months during which a total of 30 events of ventricular arrhythmia were treated through AID; six of them were inappropriate due to paroxismal atrial fibrillation; 10 AID patients (34%) have not applied for therapy. Three patients (12%) of the group died due to congestive heart failure refractory to pharmacologic treatment. CONCLUSION The implant of the AID is a safe and effective measure for primary and secondary prevention of sudden death. World-wide experience evidences, that this kind of device has not modified the mortality rate due to heart failure in these patients, but it has diminished sudden arrhythmic death.
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OBJECTIVES This study aimed to demonstrate that the presence of late gadolinium enhancement (LGE) is a predictor of death and other adverse events in patients with suspected cardiac sarcoidosis. BACKGROUND Cardiac sarcoidosis is the most important cause of patient mortality in systemic sarcoidosis, yielding a 5-year mortality rate between 25% and 66% despite immunosuppressive treatment. Other groups have shown that LGE may hold promise in predicting future adverse events in this patient group. METHODS We included 155 consecutive patients with systemic sarcoidosis who underwent cardiac magnetic resonance (CMR) for workup of suspected cardiac sarcoid involvement. The median follow-up time was 2.6 years. Primary endpoints were death, aborted sudden cardiac death, and appropriate implantable cardioverter-defibrillator (ICD) discharge. Secondary endpoints were ventricular tachycardia (VT) and nonsustained VT. RESULTS LGE was present in 39 patients (25.5%). The presence of LGE yields a Cox hazard ratio (HR) of 31.6 for death, aborted sudden cardiac death, or appropriate ICD discharge, and of 33.9 for any event. This is superior to functional or clinical parameters such as left ventricular (LV) ejection fraction (EF), LV end-diastolic volume, or presentation as heart failure, yielding HRs between 0.99 (per % increase LVEF) and 1.004 (presentation as heart failure), and between 0.94 and 1.2 for potentially lethal or other adverse events, respectively. Except for 1 patient dying from pulmonary infection, no patient without LGE died or experienced any event during follow-up, even if the LV was enlarged and the LVEF severely impaired. CONCLUSIONS Among our population of sarcoid patients with nonspecific symptoms, the presence of myocardial scar indicated by LGE was the best independent predictor of potentially lethal events, as well as other adverse events, yielding a Cox HR of 31.6 and of 33.9, respectively. These data support the necessity for future large, longitudinal follow-up studies to definitely establish LGE as an independent predictor of cardiac death in sarcoidosis, as well as to evaluate the incremental prognostic value of additional parameters.
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The QT interval, an electrocardiographic measure reflecting myocardial repolarization, is a heritable trait. QT prolongation is a risk factor for ventricular arrhythmias and sudden cardiac death (SCD) and could indicate the presence of the potentially lethal mendelian long-QT syndrome (LQTS). Using a genome-wide association and replication study in up to 100,000 individuals, we identified 35 common variant loci associated with QT interval that collectively explain ∼8-10% of QT-interval variation and highlight the importance of calcium regulation in myocardial repolarization. Rare variant analysis of 6 new QT interval-associated loci in 298 unrelated probands with LQTS identified coding variants not found in controls but of uncertain causality and therefore requiring validation. Several newly identified loci encode proteins that physically interact with other recognized repolarization proteins. Our integration of common variant association, expression and orthogonal protein-protein interaction screens provides new insights into cardiac electrophysiology and identifies new candidate genes for ventricular arrhythmias, LQTS and SCD.
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There are large variations in the incidence, registration methods and reported causes of sudden cardiac arrest/sudden cardiac death (SCA/SCD) in competitive and recreational athletes. A crucial question is to which degree these variations are genuine or partly due to methodological incongruities. This paper discusses the uncertainties about available data and provides comprehensive suggestions for standard definitions and a guide for uniform registration parameters of SCA/SCD. The parameters include a definition of what constitutes an 'athlete', incidence calculations, enrolment of cases, the importance of gender, ethnicity and age of the athlete, as well as the type and level of sporting activity. A precise instruction for autopsy practice in the case of a SCD of athletes is given, including the role of molecular samples and evaluation of possible doping. Rational decisions about cardiac preparticipation screening and cardiac safety at sport facilities requires increased data quality concerning incidence, aetiology and management of SCA/SCD in sports. Uniform standard registration of SCA/SCD in athletes and leisure sportsmen would be a first step towards this goal.
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The long QT syndrome (LQTS) is a heritable disorder that predisposes to sudden cardiac death. LQTS is caused by mutations in ion channel genes including HERG and KCNE1, but the precise mechanisms remain unclear. To clarify this situation we injected adenoviral vectors expressing wild-type or LQT mutants of HERG and KCNE1 into guinea pig myocardium. End points at 48–72 h included electrophysiology in isolated myocytes and electrocardiography in vivo. HERG increased the rapid component, IKr, of the delayed rectifier current, thereby accelerating repolarization, increasing refractoriness, and diminishing beat-to-beat action potential variability. Conversely, HERG-G628S suppressed IKr without significantly delaying repolarization. Nevertheless, HERG-G628S abbreviated refractoriness and increased beat-to-beat variability, leading to early afterdepolarizations (EADs). KCNE1 increased the slow component of the delayed rectifier, IKs, without clear phenotypic sequelae. In contrast, KCNE1-D76N suppressed IKs and markedly slowed repolarization, leading to frequent EADs and electrocardiographic QT prolongation. Thus, the two genes predispose to sudden death by distinct mechanisms: the KCNE1 mutant flagrantly undermines cardiac repolarization, and HERG-G628S subtly facilitates the genesis and propagation of premature beats. Our ability to produce electrocardiographic long QT in vivo with a clinical KCNE1 mutation demonstrates the utility of somatic gene transfer in creating genotype-specific disease models.