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Sudden Death (sudden + death)
Selected AbstractsRisk Factors in Sudden Death in Epilepsy (SUDEP): The Quest for MechanismsEPILEPSIA, Issue 5 2007Lina Nashef Summary:, People with epilepsy may die suddenly and unexpectedly without a structural pathological cause. Most SUDEP cases are likely to be related to seizures. SUDEP incidence varies and is <1:1,000 person-years among prevalent cases in the community and ,1:250 person years in specialist centres. Case,control studies identified certain risk factors, some potentially amenable to manipulation, including uncontrolled convulsive seizures and factors relating to treatment and supervision. Both respiratory and cardiac mechanisms are important. The apparent protective effect of lay supervision supports an important role for respiratory factors, in part amenable to intervention by simple measures. Whereas malignant tachyarrhythmias are rare during seizures, sinus bradycardia/arrest, although infrequent, is well documented. Both types of arrhythmias can have a genetic basis. This article reviews SUDEP and explores the potential of coexisting liability to cardiac arrhythmias as a contributory factor, while acknowledging that at present, bridging evidence between cardiac inherited gene determinants and SUDEP is lacking. [source] Urinary Antispasmodic Use and the Risks of Ventricular Arrhythmia and Sudden Death in Older PatientsJOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 1 2002DrPH, Philip S. Wang MD First page of article [source] The Mechanism of Sudden Death in the Wolff-Parkinson-White SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2005ALEXANDER MAZUR M.D. No abstract is available for this article. [source] Relatively Benign Clinical Course in Asymptomatic Patients with Brugada-Type Electrocardiogram Without Family History of Sudden DeathJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001SHIHO TAKENAKA M.D. Asymptomatic Brugada-Type ECG.Introduction: The incidence of sudden death or ventricular fibrillation (VF) in asymptomatic Brugada syndrome patients with a family history of sudden death is reported to be very high. However, there are few reports on the prognosis of asymptomatic Brugada syndrome patients without a family history of sudden death. Methods and Results: Eleven patients (all male; mean age 40.5 ± 9.6 years, range 26 to 56) with asymptomatic Brugada-type ECG who had no family history of sudden death were evaluated. The degrees of ST segment elevation and conduction delay on signal-averaged ECG (SAECG) before and after pilsicainide were evaluated in all 11 patients. VF inducibility by ventricular electrical stimulation also was evaluated in 8 of 11 patients. Patients were followed for a period of 9 to 84 months (mean 42.5 ± 21.6). The J point level was increased (V1 :0.19 ± 0.09 mV to 0.36 ± 0.23 mV; V2: 0.31 ± 0.12 mV to 0.67 ± 0.35 mV) by pilsicainide. Conduction delay was increased (total QRS: 112.2 ± 6.3 msec to 131 7 ± 6.3 msec; under 40 , V: 42.0 ± 8.5 msec to 52.7 ± 12.7 msec; last 40 msec: 17.4 ± 5.9 , V to 10.4 ± 6.1 , V) on SAECG by pilsicainide. VF was induced in only 1 of 8 patients. None of the patients had syncope or sudden death during a mean follow-up of 42.5 ± 21.6 months. Conclusion: This study suggests that asymptomatic patients with Brugada-type ECG who have no family history of sudden death have a relatively benign clinical course. [source] Three Unusual Neuropathologic-Related Causes of Sudden Death,JOURNAL OF FORENSIC SCIENCES, Issue 3 2008Dennis J. Chute M.D. Abstract:, We discuss the autopsy findings of three medico-legal cases of sudden death associated with uncommon neuropathologic findings of which the general forensic pathologist may not be familiar. Case 1 was a 43-year-old man who died of a seizure due to malignant melanoma of the temporal lobe associated with neurocutaneous melanosis (NCM). Case 2 was a 57-year-old woman with a history of mental retardation and incoordination because of chronic lead poisoning, who died of a pulmonary thromboembolism due to deep venous thrombosis status post left leg fracture after a fall down a staircase. Autopsy revealed atrophy and gliosis of her cerebellum as a result of childhood lead poisoning. The third patient was a 75-year-old woman who died as a result of acute bacterial leptomeningitis at the cervico-medullary junction with acute inflammation of the connective tissue of her upper cervical spinal column associated with subluxation of her atlantoaxial (AA) joint, also known as Grisel's syndrome. [source] The Role of Environmental Factors in the Causation of Sudden Death in Infants: Two Cases of Sudden Unexpected Death in Two Unrelated Infants Who Were Cared for by the Same BabysitterJOURNAL OF FORENSIC SCIENCES, Issue 6 2007Bennet I. Omalu M.D., M.P.H. Abstract:, We report two cases of sudden unexpected death in two unrelated African American female infants, 2 months and 4 months old. Both infants were attended to by the same babysitter in the same apartment and died 39 days apart in the same bed and in the same bedroom. The autopsy of the first infant revealed sudden unexplained death in an infant. Toxicologic analysis for carbon monoxide (CO) was not performed because it was not suspected. When the second infant died, investigation into the ambient air quality within the apartment revealed high levels of CO emanating from a poorly ventilated and defective hot water heater, which was located across a hallway from the bedroom where the two babies died. CO saturation levels in the postmortem blood samples of the two babies were elevated and were similar (13% and 14%). Nicotine and cotinine were not detected in the blood sample of the two infants. Cherry-red livor mortis was absent. Acute CO intoxication was determined to be the underlying cause of these two unexpected deaths. These two cases underscore the need to integrate ambient air analysis and postmortem CO analysis as routine components of the comprehensive death investigation of infants who die suddenly and unexpectedly. [source] Sudden Death from Tubercular MyocarditisJOURNAL OF FORENSIC SCIENCES, Issue 3 2006Enrico Silingardi M.D. ABSTRACT: Tuberculous myocarditis is a rare finding. We present the case of a 33-year-old woman who was in good health and who died suddenly at home. Autopsy and histopathologic examinations revealed granulamatous lesions in the myocardium, lungs, lymph nodes, liver, and spleen. No fast acid bacilli were demonstrated on histological examination. The presence of a Mycobacterium tuberculosis DNA complex was identified using a polymerase chain reaction (PCR) on formalin-fixed paraffin-embedded histological samples. An HIV test carried out on the blood obtained during the autopsy was negative according to the DNA amplification technique (PCR) and enzyme-linked immunosorbent assay serological test. We hypothesize that the mechanism of death was severe ventricular arrhythmia due to granulomatous proliferation in the structures of the interventricular septum. [source] Application of a Cardiac Arrest Score in Patients with Sudden Death and ST Segment Elevation for Triage to Angiography and InterventionJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2002PETER A. MCCULLOUGH M.D. The aim of this study was to test a previously validated, prognostic, cardiac arrest score in patients with ST segment elevation acute myocardial infarction (AMI) who suffereda witnessed cardiac arrest and survived to emergency department admission. A consecutive series constructed retrospectively from a sudden death database (n= 22) of patients with ST segment elevation AMI resuscitated from cardiac arrest underwent angiography and angioplasty of the culprit vessel within 24 hours of presentation. A cardiac arrest score was assigned to each case by explicit criteria present on evaluation. Primary outcomes were survival to hospital discharge and the degree of neurological recovery during the hospitalization. All patients underwent successful coronary angioplasty and 77% received adjunctive intraaortic balloon counterpulsation. The overall rate of survival to discharge was 41%. For cardiac arrest scores of 0, 1, 2, and 3, respectively, the rates of neurologic recovery were 0 (0%) of 4 (95% CI 0,53%), 3 (50%) of 6 (95% CI 15,85%), 2 (67%) of 3 (95% CI 13,98%), and 9 (100%) of 9 (95% CI 72,100%), and the rates of survival to discharge were 0(0%) of 4, (95% CI 0,53%), 2 (33%) of 6 (95% CI 6,74%), 2 (67%) of 3 (95% CI 13,98%), and 9 (100%) of 9 (95% CI 72,100%), P<0.01 for both outcomes over ascending scores. These results suggest appropriate patients for primary angioplasty after cardiac arrest are those with ST segment elevation AMI and an emergency department cardiac arrest score of ,2, thus predicting a11 (92%) of 12 (95% CI 65,100%) chance of survival to discharge. [source] Effect of n -3 Polyunsaturated Fatty Acids on Risk Reduction of Sudden DeathNUTRITION REVIEWS, Issue 12 2002Article first published online: 16 SEP 200 Two recent reports confirm the role ofn -3 polyunsaturated fatty acid (PUFA) consumption in risk reduction for sudden death. The mechanism likely involves an antiarrhythmic effect, further supporting the role of dietaryn -3 PUFA in maintenance of human health. [source] Brugada Pattern Electrocardiogram Associated with Supratherapeutic Phenytoin Levels and the Risk of Sudden DeathPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007BASEL AL ALOUL M.D. The emergence of Brugada pattern on electrocardiogram in response to class IA or IC antiarrhythmic agents is widely utilized to diagnose concealed Brugada syndrome and recognized as a risk factor for sudden death. Phenytoin, a class IB antiarrhythmic agent, has not been reported to induce Brugada pattern. We report a patient who presented with Brugada electrocardiogram at supratherapeutic phenytoin level. Considering that patients with syncope may falsely be labeled to have seizures and some epilepsy patients are at increased risk of sudden death, all patients with supratherapeutic phenytoin level should be evaluated with an electrocardiogram for emergence of Brugada pattern. [source] Sudden Death in Heart Failure Associated with Reduced Left Ventricular Function: Substrates, Mechanisms, and Evidence-Based Management, Part IIPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001MICHAEL O. SWEENEY First page of article [source] Athletes' Heart and Echocardiography: Athletes' HeartECHOCARDIOGRAPHY, Issue 7 2008B.Sc., Martin Stout M.Sc. Sudden death of competitive athletes is rare. However, they continue to have an impact on both the lay and medical communities. These deaths challenge the perception that trained athletes represent the healthiest segment of modern society. There is an increasing frequency of such reported deaths worldwide and the visibility of this issue is underlined by the high-profile nature of each case. Differential diagnosis between pathological and the physiologic (nonpathological) responses to high levels of physical training has become clinically more important. The purpose of this review is to highlight the main echocardiograph characteristics related to different types of training/sports participation and to highlight already recognized and newer concepts in their clinical assessment. [source] Results of pacemaker implantation in 104 dogsJOURNAL OF SMALL ANIMAL PRACTICE, Issue 1 2007M. S. Johnson Objectives: To document the outcome, survival and complications involved in pacemaker implantation in dogs in a retrospective study. Methods: Case records for all dogs in which pacemaker implantation was performed were reviewed. Results: A total of 104 dogs underwent pacemaker implantation. Dogs were presented with atrioventricular (AV) block (71), sick sinus syndrome (25) or vasovagal syncope (eight). Age at presentation varied from six months to 13 years with a median age of seven years and two months. The Labrador was the most commonly represented breed (17 cases). All but one dog survived pacemaker implantation, with 93 showing resolution of their clinical signs while 10 dogs showed intermittent residual signs. One-, three- and five-year survival estimates were 86, 65 and 39 per cent, respectively. Major complications after implantation were documented in 15 dogs and three of these led to fatalities. Minor complications were noted in 23 dogs. Sudden death occurred in six dogs three to 55 months following successful pacemaker implantation. Clinical Significance: Transvenous pacemaker implantation was successful in reducing or eliminating clinical signs in over 90 per cent of dogs with third-degree atrioventricular (AV) block or sick sinus syndrome. In dogs with vasovagal syncope, six of eight dogs had greatly reduced frequency of collapse and two became asymptomatic. Although the procedure was associated with complications, these were rarely life threatening and good survival was documented in the majority of cases. [source] Functional neuroanatomy of the human pre-Bötzinger complex with particular reference to sudden unexplained perinatal and infant deathNEUROPATHOLOGY, Issue 1 2008Anna M. Lavezzi The authors are the first to identify in man the pre-Bötzinger complex, a structure of the brainstem critical for respiratory rhythmogenesis, previously investigated only in rats. The evaluation of the neurokinin 1 receptors and somatostatin immunoreactivity in a total of 63 brains from 25 fetuses, nine newborns and 29 infants, allowed to delineate the anatomic structure and the boundaries of this human neural center in a restricted area of the ventrolateral medulla at the obex level, ventral to the semicompact ambiguus nucleus. The neurons of the pre-Bötzinger complex were roundish in fetuses before 30 gestational weeks and lengthened after birth, embedded in a dendritic system belonging to the reticular formation. Besides, structural and/or functional alterations of the pre-Bötzinger complex were present in a high percentage of sudden deaths (47%), prevalent in late fetal deaths. In particular, different developmental defects (hypoplasia with a decreased neuronal number and/or dendritic hypodevelopment of the reticular formation, abnormal neuronal morphology, immunonegativity of neurotransmitters, and agenesis) were found. The authors suggest that the pre-Bötzinger complex contains a variety of neurons not only involved in respiratory rhythm generation, but more extensively, essential to the control of all vital functions. Sudden death and in particular sudden unexpected fetal death could therefore be ascribed to a selective process when developmental alterations of the pre-Bötzinger complex arise. [source] Sudden death caused by chronic Chagas disease in a non-endemic country: Autopsy reportPATHOLOGY INTERNATIONAL, Issue 3 2010Fumiko Satoh Chagas disease is a tropical disease that is prevalent in Latin America. Described herein is an autopsy case of the sudden death of a 48-year-old Brazilian man who had stayed in Japan for 7 years. The man, who had a history of Chagas disease, collapsed unexpectedly at work. Because the cause of death was unknown, forensic autopsy examination was performed. As gross findings, the heart was dilated and rounded with an increase in size and weight. The esophagus and large intestine were dilated moderately, with extensive interstitial inflammatory infiltration in the cardiac muscle, but no apparent parasite nest was observed in various tissues. On post-mortem laboratory examinations, indirect immunofluorescence antibody test indicated the presence of IgG antibody specific to Trypanosoma cruzi in the serum. Subsequent polymerase chain reaction amplification using DNA extracted from blood yielded the specific product derived from T. cruzi genomic DNA. These examinations indicate that the infection had resulted from the Tripanosoma parasite. The cause of death was judged to be chronic cardiomyopathy caused by Chagas disease. It is important for pathologists to know the possible involvement of chronic Chagas disease in sudden unexpected deaths in the current globalized society of Japan. [source] Sudden death due to dissecting aortic aneurysm in an adolescent without any underlying diseasePEDIATRICS INTERNATIONAL, Issue 6 2002Takashi Hishitani No abstract is available for this article. [source] Causes and place of death in Italian patients with amyotrophic lateral sclerosisACTA NEUROLOGICA SCANDINAVICA, Issue 3 2010R. Spataro Spataro R, Lo Re M, Piccoli T, Piccoli F, La BellaV. Causes and place of death in Italian patients with amyotrophic lateral sclerosis. Acta Neurol Scand: 122: 217,223. © 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Objectives,,, To determine the causes and place of death in a cohort of Italian patients with amyotrophic lateral sclerosis (ALS). A better understanding of the likely causes of death in ALS might improve the palliative care at the end-of-life, whereas knowing the place of death will help to verify the need for highly specialized care services, e.g. hospice and nursing home. Patients and methods,,, Between 2000 and 2008, 182 ALS patients (onset: spinal, 127; bulbar, 55; M/F: 1.6) were followed in a single ALS Tertiary Centre in Palermo, Sicily, Italy until death. Medical data for each individual patient were recorded in a large database throughout the disease course. Information concerning causes and place of death were obtained by consultation with relatives or the family physician. Results,,, Respiratory failure (terminal respiratory insufficiency, pneumonia) was the most frequent cause of death (81.3%), which included six cases (3.3%) who requested a terminal sedation. Sudden death and death during sleep accounted for by 6.0% and 6.6% of all deaths, respectively. Heart-related causes of death were relatively infrequent in our cohort, accounting for by 7.1% of all deaths (i.e. sudden death: 6.0% and myocardial infarct: 1.1%). Patients (85.2%) died at home. Conclusions,,, The leading cause of death in ALS remains the respiratory failure, followed by the sudden death and death during sleep. Most patients in our cohort died at home, a choice that might be only partially driven by cultural factors. These findings might have a great impact on the development of the advanced and end-of-life palliative care and in the planning of specialized care services, as hospice and nursing home. [source] Aneurysm-related mortality during late follow-up after endovascular aneurysm repair of infrarenal aortaBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2001S. R. Vallabhaneni Background: Aneurysm-related mortality (ARM) accounts for around 1·5 per cent of all deaths following open aneurysm repair. The incidence of ARM following endovascular aneurysm repair (EVAR) is unknown. The aim was to examine all causes of death, including ARM, during late follow-up after EVAR. ARM was defined as death resulting directly from rupture of the repaired aneurysm or another complication of the aneurysm, more than 30 days after repair, or death within 30 days of a secondary intervention undertaken solely to rectify a complication of repair. Methods: Preoperative and follow-up data on 2194 patients from 88 European centres were collected prospectively on to a database. Survival up to 48 months after EVAR was analysed by means of Kaplan,Meier survival analysis. The causes of death during this period were noted. Results: There were 161 deaths between 1 and 48 months after EVAR. The cumulative rate of secondary intervention for this cohort at 4 years was 33 per cent. The causes of death were: cardiac 28·6 per cent, malignancy 18·6 per cent, cerebrovascular 6·8 per cent, respiratory 3·1 per cent, renal 1·8 per cent, other 22·3 per cent and ARM 11·8 per cent. There were 19 deaths from aneurysm-related causes. Nine patients died following proven rupture of the aneurysm, three died from presumed rupture of the aneurysm and a further seven died following late conversion (three patients), graft sepsis (two) and secondary intervention (two). Sudden death of uncertain cause occurred in ten patients in whom rupture of AAA was a possibility. Conclusion: Non-aneurysm-related causes of death were comparable to those in published reports of survival after open repair. However, the proportion of aneurysm-related deaths (11·8 per cent) was appreciably higher than that reported after open repair. These results may reflect the learning curve experience of the teams involved in the study, but continued caution is advisable regarding expectations of outcome following EVAR. © 2001 British Journal of Surgery Society Ltd [source] Female Gender and the Risk of Rupture of Congenital Aneurysmal Fistula in AdultsCONGENITAL HEART DISEASE, Issue 1 2008Salah A.M. Said MD ABSTRACT Aims., To delineate the risk factors for rupture of congenital aneurysmal fistulas in adult patients. Methods., We conducted a literature search of the Medline database using Pubmed search interface to identify reports dealing with rupture of congenital aneurysmal fistulas in an adult population. The search included the English and non-English languages between 1963 and 2005. Results., Fourteen adult patients (12 females) with serious and life-threatening complications secondary to aneurysmal fistulas were reported. Mean age was 62.9 years. The ethnic origins of these 14 patients were 9 Asian and 5 Caucasian. Most patients have had no other cardiac malformations. Five patients had a history of hypertension. One patient was asymptomatic. In 13 symptomatic patients, the clinical presentation was cardiac tamponade, pericardial effusion, syncope, heart failure, chest pain, dyspnea, fatigue, distal thromboembolic events with infarction, shock, and/or sudden death. Aneurysmal fistulas were identified in 10 patients; of these 6 were of the saccular type. Rupture occurred in 9 patients (8 females and 1 male). Eleven patients were treated surgically with 1 late death. Two male subjects experienced sudden unexpected cardiac death. Conclusion., Rupture of congenital aneurysmal fistulas occurred more often in females. Identified risk factors for rupture, hemopericardium, tamponade, and death were among others saccular aneurysm, Asian ethnic race, origin of the aneurysmal fistulas from the left coronary artery and a history of hypertension may play a role. In this article, we present a literature review of congenital aneurysmal fistulas associated with or without rupture and a case report of a woman with unruptured aneurysmal fistula. [source] Pulmonary Regurgitation after Tetralogy of Fallot Repair: Clinical Features, Sequelae, and Timing of Pulmonary Valve ReplacementCONGENITAL HEART DISEASE, Issue 6 2007Naser M. Ammash MD ABSTRACT Pulmonary regurgitation following repair of tetralogy of Fallot is a common postoperative sequela associated with progressive right ventricular enlargement, dysfunction, and is an important determinant of late morbidity and mortality. Although pulmonary regurgitation may be well tolerated for many years following surgery, it can be associated with progressive exercise intolerance, heart failure, tachyarrhythmia, and late sudden death. It also often necessitates re-intervention. Identifying the appropriate timing of such intervention could be very challenging given the risk of prosthetic valve degeneration and the increased risk of reoperation. Comprehensive informed and regular assessment of the postoperative patient with tetralogy of Fallot, including evaluation of pulmonary regurgitation, right heart structure and function, is crucial to the optimal care of these patients. Pulmonary valve replacement performed in an experienced tertiary referral center is associated with low operative morbidity and mortality and very good long-term results. Early results of percutaneous pulmonary valve replacement are also promising. [source] Left Coronary Artery Arteriovenous Malformation Presenting as a Diastolic Murmur with Exercise Intolerance in a Child with a Suspected Familial Vascular Malformation SyndromeCONGENITAL HEART DISEASE, Issue 3 2007Valerie A. Schroeder MD Abstract Objective., Intracardiac arteriovenous malformations are rare and may be associated with sudden death in adults. This case report describes an intracardiac left coronary arteriovenous malformation in a 7-year-old boy with a suspected familial cutaneous vascular malformation syndrome. The patient presented with a diastolic murmur, exercise intolerance, chest pain, and a left ventricular mass. Methods., The left ventricular mass was initially identified by echocardiography. Subsequently, a computed tomography scan revealed the vascular nature of the lesion. We hypothesized that the lesion represented either an arteriovenous malformation (AVM) or a hemangioma. These lesions are thought to cause coronary steal and myocardial dysfunction. Skin biopsies of the patient's cutaneous lesions revealed capillary hyperplasia, which was not consistent with either hemangioma or AVM. Thus, a surgical biopsy and partial resection of the mass was performed. Results., The surgical pathology of the cardiac mass was consistent with an AVM. Within 6 months following partial resection of the mass, the patient unexpectedly developed a left ventricular pseudoaneurysm at the resection site and required re-operation. Although a portion of the mass remains, both the patient's chest pain and exercise tolerance have improved subjectively. Conclusion., Patients with cutaneous vascular malformations and diastolic murmurs, as well as cardiac symptoms, should undergo echocardiography or alternative imaging modalities to screen for treatable pathological myocardial vascular malformations. [source] Zebrafish as a model for long QT syndrome: the evidence and the means of manipulating zebrafish gene expressionACTA PHYSIOLOGICA, Issue 3 2010I. U. S. Leong Abstract Congenital long QT syndrome (LQT) is a group of cardiac disorders associated with the dysfunction of cardiac ion channels. It is characterized by prolongation of the QT-interval, episodes of syncope and even sudden death. Individuals may remain asymptomatic for most of their lives while others present with severe symptoms. This heterogeneity in phenotype makes diagnosis difficult with a greater emphasis on more targeted therapy. As a means of understanding the molecular mechanisms underlying LQT syndrome, evaluating the effect of modifier genes on disease severity as well as to test new therapies, the development of model systems remains an important research tool. Mice have predominantly been the animal model of choice for cardiac arrhythmia research, but there have been varying degrees of success in recapitulating the human symptoms; the mouse cardiac action potential (AP) and surface electrocardiograms exhibit major differences from those of the human heart. Against this background, the zebrafish is an emerging vertebrate disease modelling species that offers advantages in analysing LQT syndrome, not least because its cardiac AP much more closely resembles that of the human. This article highlights the use and potential of this species in LQT syndrome modelling, and as a platform for the in vivo assessment of putative disease-causing mutations in LQT genes, and of therapeutic interventions. [source] QTc-interval abnormalities in a forensic populationCRIMINAL BEHAVIOUR AND MENTAL HEALTH, Issue 2 2007Sobhi Girgis Background,Antipsychotic drugs have been linked to sudden death among psychiatric patients, with a suggestion that prolongation of the QT-interval detectable on a standard electrocardiogram may be linked to fatal cardiac arrhythmias in these circumstances. Patients in secure forensic psychiatric facilities may be particularly likely to be on high-dose antipsychotic medication, and yet, as far as the authors are aware, no study of QT-intervals among such patients has been reported. Aim,To investigate the prevalence of QT-interval abnormalities and associated known risk factors for fatal cardiac arrhythmias in a sample of forensic patients. Method,Participants had a 12-lead electrocardiogram taken at 50 mm/s. Information was collected on their age, gender, psychiatric diagnosis, history of cardiovascular, liver and kidney diseases, and smoking, on all medications and on history of seclusion over the previous 12 months. Analysis was carried out using binary logistic regression. Results,Lower rates of QT-interval abnormalities than might be expected for this population were found. It was also found that a high dose of antipsychotics was associated with QTc prolongation (Adjusted OR = 9.5, 95% CI 2.6,34.2), a result consistent with previous literature. Conclusion,Forensic patients need not be at increased risk of QTc abnormality provided risk factors are properly managed. A high dose of antipsychotic medication increases the risk of QTc prolongation. Copyright © 2007 John Wiley & Sons, Ltd. [source] Heart rate and QT variability in children with anxiety disorders: A preliminary reportDEPRESSION AND ANXIETY, Issue 2 2001Vikram K. Yeragani M.B.B.S. Abstract This study compared beat-to-beat heart rate and QT variability in children with anxiety disorders (n=7) and normal controls (n=15) by using an automated algorithm to compute QT intervals. An increase in QT variability appears to be associated with a higher risk for sudden cardiac death. A decrease in heart rate variability is also linked to significant cardiovascular events. Supine detrended QT variability, QT variability corrected for mean QT interval, and QTvi (a log ratio of QT variance normalized for mean QT over heart rate variability normalized for mean heart rate) were significantly higher in children with anxiety compared to controls (P<0.05). The largest Lyapunov Exponent (LLE) of heart rate time series was significantly lower (P<0.05) in children with anxiety compared to controls. These findings suggest a relative increase in sympathetic activity and a relative decrease in cardiac vagal activity in children with anxiety disorders, and are discussed in the context of the effects of tricyclics on cardiac autonomic function in children, and the rare occurrence of sudden death during tricyclic antidepressant treatment. Depression and Anxiety 13:72,77, 2001. © 2001 Wiley-Liss, Inc. [source] Brainstem mechanisms underlying the sudden infant death syndrome: Evidence from human pathologic studiesDEVELOPMENTAL PSYCHOBIOLOGY, Issue 3 2009Hannah C. Kinney Abstract The brainstem hypothesis is one of the leading hypotheses concerning the sudden infant death syndrome (SIDS). It states that SIDS, or an important subset of SIDS, is due to abnormal brainstem mechanisms in the control of respiration, chemosensitivity, autonomic regulation, and/or arousal which impairs the infant's response to life-threatening, but often occurring, stressors during sleep (e.g., hypoxia, hypercarbia, asphyxia, hyperthermia) and leads to sudden death in a vulnerable developmental period. In this review, we summarize neuropathologic evidence from SIDS cases that support this hypothesis, beginning with the seminal report of subtle brainstem gliosis three decades ago. We focus upon recent neurochemical studies in our laboratory concerning the neurotransmitter serotonin (5-HT) and its key role in mediating protective responses to homeostatic stressors via medullary circuits. The possible fetal origin of brainstem defects in SIDS is reviewed, including evidence for adverse effects of prenatal exposure to maternal cigarette smoking and alcohol upon the postnatal development of human brainstem 5-HT pathways. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 223,233, 2009 [source] Hyperglycaemia induced QT interval duration: a key to the increased risk of sudden death in diabetic patients?DIABETIC MEDICINE, Issue 8 2008G. Andrássy No abstract is available for this article. [source] Prediabetes and the big baby,DIABETIC MEDICINE, Issue 1 2008D. R. Hadden Abstract The concept of prediabetes has come to the fore again with the worldwide epidemic of Type 2 diabetes. The careful observations of W. P. U. Jackson and his colleagues in Cape Town, South Africa 50 years ago still deserve attention. Maternal hyperglycaemia cannot be the only cause of fetal macrosomia, and the pathophysiological reason for the unexplained stillbirth in late diabetic pregnancy still eludes us. The biochemical concepts of ,facilitated anabolism' and ,accelerated starvation' were developed by Freinkel as explanations of the protective mechanisms for the baby during the stresses of pregnancy. Some of these nutritional stresses may also occur in the particular form of early childhood malnutrition known in Africa as kwashiorkor, where subcutaneous fat deposition, carbohydrate intolerance, islet hyperplasia and sudden death may follow a period of excess carbohydrate and deficient protein intake. Different feeding practices in different parts of the world make comparisons uncertain, but there is evidence for insulin resistance in both the macrosomic fetus of the hyperglycaemic mother and in the child with established kwashiorkor. These adaptive changes in early development may play both a physiological and a pathological role. Worldwide studies of hyperglycaemia in pregnancy are gradually establishing acceptable diagnostic criteria, appropriate screening procedures and an evidence base for treatment. Nevertheless the challenge of prediabetes and the big baby is still with us,in Jackson's words,,diabetes mellitus is a fascinating condition,the more we know about it the less we understand it'. [source] A new approach to long QT syndrome mutation detection by Sequenom MassARRAY® systemELECTROPHORESIS, Issue 10 2010Catarina Allegue Abstract Congenital long QT syndrome is an inherited cardiac disorder characterized by a prolonged QT interval and polymorphic ventricular arrhythmias that could result in recurrent syncope, seizures or sudden death as the most dramatic event. Until now QT interval mutations have been described in 12 genes, where the majority of mutations reside in three genes KCNQ1, KCNH2, and SCN5A. Diagnosis and prognosis are directly related with the gene and mutation involved. We have developed a diagnostic approach for long QT syndrome and Brugada syndrome based on published mutations and Sequenom MassArray® system. Three diagnostic tests have been developed, oriented to each of the three most prevalent genes in the long QT syndrome. A total of 433 mutations are analyzed in 38 multiplex reactions, allowing their detection in about 48,h. Tests were validated on 502 samples from individuals with different clinical conditions and family history. The average call rates obtained for each of the tests were 93, 83, and 73% in KCNQ1, KCNH2, and SCNA, respectively. Sequenom MassARRAY mutation detection is a reliable, highly flexible, and cost-efficient alternative to conventional methods for genetic testing in long QT syndrome and Brugada syndrome, facilitating flexible upgrades of the version of the test presented here with the inclusion of new mutations. [source] Study of laryngopharyngeal pathology in Thoroughbred horses in southern CaliforniaEQUINE VETERINARY JOURNAL, Issue 9 2009S. DIAB Summary Reasons for performing study: There is increasing anecdotal evidence among horse owners, trainers and equine clinicians of a high prevalence of subepiglottic ulcers, suggested to have a negative effect on racing performance. Objectives: To provide a prevalence study and pathological characterisation of laryngopharyngeal lesions with emphasis in the subepiglottic area and, in particular, subepiglottic ulcers. Methods: The study was carried out on 91 Thoroughbred racehorses received for post mortem examination from 4 major Southern California racetracks. The most common reason for submission was catastrophic musculoskeletal injury, but others include sudden death, laminitis, colic, colitis, neurological disorders, pleuropneumonia and arytenoid chondropathy. Laryngopharyngeal specimens were collected and examined grossly; selected cases were also examined histopathologically. Results: Thirteen horses (14.3%) had at least one type of laryngopharyngeal abnormality, 7 horses (7.7%) had lesions in the subepiglottic soft tissues, including 4 subepiglottic ulcers, 2 soft palate ,kissing lesions' and one 'subepiglottic scar'. Eight horses (8.8%) had lesions elsewhere in the laryngopharynx, including mucosal ulcerations, arytenoid chondropathy, epiglottic entrapment and partial absence of arytenoid cartilage. Conclusions and potential relevance: Lesions in the subepiglottic area were among the most prevalent in this study, suggesting that an important percentage of laryngopharyngeal abnormalities may be missed during routine endoscopy of the standing horse, which often does not include the examination of subepiglottic tissues. Pathologically, subepiglottic ulcers were chronic-active with viable hyperplastic epithelial margins, suggesting that proper healing and re-epithelialisation should occur with appropriate treatment. In most cases, the lesions observed do not necessarily indicate a clinical problem and more extensive prevalence studies and correlation between abnormalities found and performance are needed to assess the clinical relevance of subepiglottic soft tissue lesions accurately. [source] Use of morphine and 6-monoacetylmorphine in blood for the evaluation of possible risk factors for sudden death in 192 heroin usersADDICTION, Issue 4 2003Anna Fugelstad Abstract Aims, To detect risk factors for sudden death from heroin injection. Design, Evaluation of data from forensic investigations of all fatal cases of suspected heroin death in a metropolitan area. Only cases with detectable morphine and 6-monoacetylmorphine (6-MAM) in blood were included in order to select heroin intoxication cases. Setting, Stockholm, Sweden. Measurements, Autopsy investigation and toxicological analysis of blood and urine; and police reports. Findings, In two-thirds of the 192 cases, death occurred in public places, and mostly without any time delay. Blood concentrations of morphine ranged from 50 to 1200 ng/g, and of 6-MAM from 1 to 80 ng/g. Codeine was detected in 96% of the subjects. In the majority of cases the forensic investigation indicated polydrug use, the most common additional findings being alcohol and benzodiazepines. However, in one-quarter of the cases other drug combinations were found. Previous abstinence from heroin and use of alcohol were identified as risk factors. For 6-MAM there was also a correlation with the presence of THC and benzodiazepines. Despite a high frequency of heart abnormalities (e.g. myocarditis and focal myocardial fibrosis), these conditions did not correlate with morphine or 6-MAM blood concentrations. Conclusions, We confirm that alcohol intake and loss of tolerance are risk factors for death from heroin use, whereas no connection to heart pathology was observed. Further, prospective, studies should focus on other possible risk factors. [source] | |||||||||||||||||||||||||||||||||||||