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Sudden Cardiac Death (sudden + cardiac_death)
Selected AbstractsIncidence and Predictors of Sudden Cardiac Death in Patients with Diastolic Heart FailureJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2007M.H.S., SANA M. AL-KHATIB M.D. Introduction: Although it is known that patients with diastolic heart failure are at an increased risk of death, their mode of death has not been clearly defined. We conducted this study to examine the incidence and predictors of sudden cardiac death (SCD) in patients with isolated diastolic heart failure. Methods and Results: Using the Duke Databank for Cardiovascular Disease, we identified patients with a history of congestive heart failure (CHF) and an ejection fraction of greater than 50% who were enrolled in the database from 1995 through 2004. Mode of death was adjudicated by two independent reviewers. Of the 1,941 patients who met our inclusion criteria, 548 (28%) died (40 were SCD). Using a Cox proportional hazards model, five variables were found to be independently associated with a significant increase in the risk of SCD. These variables include diabetes mellitus (P < 0.01), the presence of mild mitral regurgitation (P < 0.01), severity of CHF (P < 0.01), the occurrence of a myocardial infarction within 3 days prior to the date of the index cardiac catheterization (P = 0.01), and severity of coronary artery disease (P = 0.02). Conclusions: SCD is not uncommon in patients with isolated diastolic heart failure. We identified some clinical variables that are associated with a significant increase in the risk of SCD and that may be used in the risk stratification of patients for SCD. Studies are needed to validate our findings. [source] Sudden Cardiac Death and Inherited Arrhythmia SyndromesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005ANDREA SARKOZY M.D. Sudden cardiac death (SCD) at youth is rare and is often caused by inherited cardiac disorders. This review focuses on the genetic background of inherited primary electrical diseases, the so-called "channelopathies." Following a short clinical description of each syndrome, the recent findings in the genetics of long QT syndrome, short QT syndrome, isolated cardiac conduction defect, familial sick sinus syndrome, familial atrial fibrillation, cathecholaminergic polymorphic ventricular tachycardia, familial Wolff-Parkinson-White (WPW) syndrome, and Brugada syndrome are discussed. The currently proposed theoretical model of overlapping phenotypes in SCN5A sodium channel mutations is presented. The recent data indicate that advances in molecular genetics, experimental and clinical electrophysiology shed some light on the genetic background of primary electrical diseases. However, it is also becoming clear that the process from a mutation of a gene to the clinical presentation of a patient is currently only partially understood and extremely complex. [source] Phytanic Acid Accumulation Is Associated with Conduction Delay and Sudden Cardiac Death in Sterol Carrier Protein-2/Sterol Carrier Protein-x Deficient MiceJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2004GEROLD MÖNNIG M.D. Introduction: The sterol carrier protein-2 gene encodes two functionally distinct proteins: sterol carrier protein-2 (SCP2, a peroxisomal lipid carrier) and sterol carrier protein-x (SCPx, a peroxisomal thiolase known as peroxisomal thiolase-2), which is involved in peroxisomal metabolism of bile acids and branched-chain fatty acids. We show in this study that mice deficient in SCP2 and SCPx (SCP2null) develop a cardiac phenotype leading to a high sudden cardiac death rate if mice are maintained on diets enriched for phytol (a metabolic precursor of branched-chain fatty acids). Methods and Results: In 210 surface and 305 telemetric ECGs recorded in wild-type (C57BL/6; wt; n = 40) and SCP2 null mice (n = 40), no difference was observed at baseline. However, on diet, cycle lengths were prolonged in SCP2 null mice (262.9 ± 190 vs 146.3 ± 43 msec), AV conduction was prolonged (58.3 ± 17 vs 42.6 ± 4 ms), and QRS complexes were wider (19.1 ± 5 vs 14.0 ± 4 ms). In 11 gene-targeted Langendorff-perfused hearts isolated from SCP2 null mice after dietary challenge, complete AV blocks (n = 5/11) or impaired AV conduction (Wenckebach point 132 ± 27 vs 92 ± 10 msec; P < 0.05) could be confirmed. Monophasic action potentials were not different between the two genotypes. Left ventricular function studied by echocardiography was similar in both strains. Phytanic acid but not pristanic acid accumulated in the phospholipid fraction of myocardial membranes isolated from SCP2 null mice. Conclusion: Accumulation of phytanic acid in myocardial phospholipid membranes is associated with bradycardia and impaired AV nodal and intraventricular impulse conduction, which could provide an explanation for sudden cardiac death in this model. [source] Colocalization of Tenascin and Sympathetic Nerves in a Canine Model of Nerve Sprouting and Sudden Cardiac DeathJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2000ANGELA C. LAI B.A. Tenascin and Cardiac Nerve Sprouting. Introduction: Sympathetic nerve sprouting after myocardial infarction (MI) may contribute significantly to the occurrence of ventricular arrhythmia and sudden cardiac death. Tenascin-X (TnX), a matrix protein known to be associated with nerve growth in central and peripheral nerves, also may play a role in cardiac nerve sprouting after MI. Methods and Results: Immunocytochemical staining techniques were used to identify nerves in 5-,m serial sections from 6 normal dogs and 11 dogs with MI. Among the dogs with MI, 4 also received nerve growth factor infusion to the left stellate ganglion. The time between MI to tissue harvest averaged 35.7 ± 14.4 days. Tyrosine hydroxylase (TH) stain was used to identify sympathetic nerves, and growth-associated protein-43 (GAP-43) was used to identify growing nerves. Polyclonal antibody was obtained for use in identifying TnX. Nerves were evident in both the infarcted and noninfarcted areas. Many nerves were found around blood vessels. A total of 181 nerves in 69 slides were examined: 89 were from noninfarcted myocardium, 4 from infarct, 13 from infarct horder zone, and 75 from perivascular regions. Except in normal dogs, all nerves stained positive for TH also stained positive for GAP-43, indicating sympathetic nerve sprouting after MI. In all dogs, the nerves that stained positive for TH also stained positive for TnX. Conclusion: There is a colocalization of TnX, GAP-43, and TH in sprouted cardiac nerves. These results suggest that TnX is important not only in the existing normal myocardial nerve cells but also in cardiac sympathetic nerve sprouting after MI. [source] Sudden Cardiac Death due to Giant Cell Inflammatory Processes,JOURNAL OF FORENSIC SCIENCES, Issue 4 2007Rebecca A. Hamilton M.D. Abstract:, Granulomatous inflammation of the myocardium may occur in a number of systemic disease processes including those with infectious etiologies such as fungal, mycobacterial and parasitic infections, as well as hypersensitivity reactions, and rarely autoimmune disorders. In many of these disorders, giant cells are components of the inflammatory infiltrate. Systemic granulomatous processes of unknown pathogenesis, most notably sarcoidosis, may also be associated with involvement of the myocardium. Occasionally, these disorders are associated with sudden death due to pathologic involvement of the heart. In contrast, giant cell myocarditis, also known as idiopathic myocarditis, a rare, frequently fulminant and fatal disorder of unknown etiology, is isolated to the heart and lacks systemic involvement. This disorder is most commonly diagnosed at autopsy. We present two cases in which sudden death resulted from a giant cell inflammatory process affecting the myocardium. Both individuals lacked antemortem diagnoses and collapsed at their respective places of employment. These cases compare and contrast the clinical and pathologic issues involved in the differential diagnoses of the subgroup of sudden cardiac deaths resulting from giant cell inflammatory processes that affect the myocardium, as well as the value of histologic examination and immunohistochemical studies. [source] Sudden Cardiac Death in Children and Adolescents: Introduction and OverviewPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009STUART BERGER M.D. First page of article [source] Implantable Cardioverter Defibrillator Criteria for Primary and Secondary Prevention of Pediatric Sudden Cardiac DeathPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009CHARLES I. BERUL M.D. The implantable cardioverter defibrillator is established as life-saving in specific adult populations. However, the precise indications and criteria for defibrillator implantation in children are less well defined. This article provides a succinct review of the indications and implantation criteria in pediatric populations at risk for sudden cardiac death, including specific disease substrates such as cardiomyopathies, inherited arrhythmias, and congenital heart disease. [source] Sudden Cardiac Death with Left Main Coronary Artery Occlusion in a Patient Whose Presenting ECG Suggested Brugada SyndromePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2003TADAYOSHI HATA This article describes a patient who died suddenly during Holter ECG monitoring. A ventricular premature systole with an extremely short coupling interval of 240 ms was immediately followed by torsades de pointes, soon degenerating into ventricular fibrillation. Retrospective survey of the patient's medical records revealed an incomplete right bundle branch block (iRBBB) configuration with fluctuating saddle back-type ST elevation in leads V1 and V2, these suggesting Brugada syndrome. Autopsy showed complete thrombotic occlusion of the left main coronary artery. (PACE 2003; 26:2175,2177) [source] ST Segment "Hump" during Exercise Testing and the Risk of Sudden Cardiac Death in Patients with Hypertrophic CardiomyopathyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009Andreas P. Michaelides M.D., F.A.C.C., F.E.S.C. Background: The appearance of a discrete upward deflection of the ST segment termed "the ST hump sign" (STHS) during exercise testing has been associated with resting hypertension and exaggerated blood pressure response to exercise. Objective: We investigated the prevalence and clinical significance of this sign in a population of patients with hypertrophic cardiomyopathy. Methods: Eighty-one patients with hypertrophic cardiomyopathy (HCM) who underwent cardiopulmonary exercise testing were followed in a retrospective cohort study for a mean period of 5.3 years. Results: The appearance of the STHS at the peak of exercise testing was observed in 42 patients (52%), particularly in the inferior and the lateral leads. Patients with the STHS had higher fractional shortening and maximum left ventricular wall thickness and exhibited more frequently outflow tract gradient >30 mmHg at rest. Furthermore, the presence of STHS was a strong independent predictor of the risk of sudden cardiac death (SCD), as the latter occurred in eight of the patients with this sign (8/42, 19%) and in none of the patients without it (0/39, 0%) (P < 0.001). Conclusion: The appearance of a "hump" at the ST segment during exercise testing appears to be a risk factor for SCD in patients with HCM. However, further studies are necessary to validate this finding in larger populations and to elucidate the mechanism of the appearance of the "hump." [source] The Future of Sudden Cardiac DeathANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2009Henry Greenberg M.D. No abstract is available for this article. [source] Annual Scientific Meeting of ASCEPT, 1999 Careful Screening To Target Interventions To Prevent Sudden Cardiac DeathCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2001Allan D Struthers SUMMARY 1. Cardiac death is due not only to coronary artery disease, but also to left ventricular (LV) abnormalities (fibrosis, dysfunction) and arrhythmogenic triggers, such as autonomic imbalance. 2. Nitric oxide deficiency could be a key mediator leading not only to coronary atherosclerosis, but also to LV abnormalities and autonomic imbalance. 3. It may be possible to screen for the above abnormalities (e.g. echocardiography and brain natriuretic peptide levels for LV abnormalities, 24 h tapes for autonomic imbalance and QT interval analysis). 4. Once individuals are identified as being at high risk, a range of interventions is possible (e.g. intensive statin therapy or angiotensin-converting enzyme inhibitors if LV abnormalities or autonomic imbalance are found). [source] Coronary Slow Flow Phenomenon and Risk for Sudden Cardiac Death Due to Ventricular Arrhythmias: A Case Report and Review of LiteratureCLINICAL CARDIOLOGY, Issue 8 2008Dr. Shoaib Saya Abstract We report a case of coronary slow flow phenomenon (CSFP) in a patient who underwent coronary angiography due to anginal chest pain and recurrent syncope with complete normalization of flow after intracoronary adenosine. He was noted to have multiple episodes of nonsustained ventricular tachycardia on holter monitor and increased QTc dispersion on surface electrocardiogram (EKG). He responded very well to oral dipyridamole therapy with complete resolution of his symptoms and no episodes of ventricular tachycardia on the event recorder at 3 months. We review the diagnosis and clinical features of CSFP and its association with increased QTc dispersion and the role of oral dipyridamole therapy in this condition. Copyright © 2007 Wiley Periodicals, Inc. [source] Editorial: Sudden cardiac death , the challenge to cardiologyFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 5 2010Keld Kjeldsen No abstract is available for this article. [source] The pathology of hypertrophic cardiomyopathyHISTOPATHOLOGY, Issue 5 2004S E Hughes Sudden cardiac death (SCD) is devastating at any age, but even more so when the individual affected is young and asymptomatic, and the death is entirely unexpected. SCD is a catastrophic complication of hypertrophic cardiomyopathy (HCM) and may be the first manifestation of this disease. HCM is an inherited intrinsic disease of the myocardium characterized by left ventricular hypertophy without chamber dilatation, in the absence of either a systemic or other cardiac disease, which may cause a similar magnitude of hypertrophy. HCM may be a clinically silent disease. Indeed, the pathologist may be the first to encounter a case of HCM at autopsy. HCM has wide-ranging implications for affected families, who will require cardiac screening and genetic counselling even if mutations are not known. Therefore, prompt and accurate diagnosis of HCM is vital. This review article will focus on the pathological diagnosis of HCM, recent advances in the genetics of this disease, and common pitfalls which may arise, leading to diagnostic uncertainty. [source] Predictors of All-Cause Mortality for Patients with Chronic Chagas' Heart Disease Receiving Implantable Cardioverter Defibrillator TherapyJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2007AUGUSTO CARDINALLI-NETO M.D., Ph.D. Background: Implantable Cardioverter Defibrillators (ICD) have sporadically been used in the treatment of either Sustained Ventricular Tachycardia (VT) or Ventricular Fibrillation (VF) in Chagas' disease patients. This study aimed at determining predictors of all-cause mortality for Chagas' disease patients receiving ICD therapy. Methods and Results: Ninety consecutive patients were entered the study. Mean left ventricular ejection fraction was 47 ± 13%. Twenty-five (28%) patients had no left ventricular systolic dysfunction. After device implantation, all patients were given amiodarone (mean daily dose = 331, 1 ± 153,3 mg), whereas a B-Blocking agent was given to 37 (40%) out of 90 patients. Results: A total of 4,274 arrhythmias were observed on stored electrogram in 64 (71%) out of 90 patients during the study period; SVT was observed in 45 out of 64 (70%) patients, and VF in 19 (30%) out of 64 patients. Twenty-six (29%) out of 90 patients had no arrhythmia. Fifty-eight (64%) out of 90 patients received appropriate shock, whereas Antitachycardia Pacing was delivered to 58 (64%) out of 90 patients. There were 31 (34%) deaths during the study period. Five patients were lost to follow up. Sudden cardiac death affected 2 (7%) out of 26 patients, whereas pump failure death was detected in the remaining 24 (93%) patients. Number of shocks per patient per 30 days was the only independent predictor of mortality. Conclusion: Number of shocks per patient per 30 days predicts outcome in Chagas' disease patients treated with ICD. [source] Sudden Cardiac Death and Inherited Arrhythmia SyndromesJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2005ANDREA SARKOZY M.D. Sudden cardiac death (SCD) at youth is rare and is often caused by inherited cardiac disorders. This review focuses on the genetic background of inherited primary electrical diseases, the so-called "channelopathies." Following a short clinical description of each syndrome, the recent findings in the genetics of long QT syndrome, short QT syndrome, isolated cardiac conduction defect, familial sick sinus syndrome, familial atrial fibrillation, cathecholaminergic polymorphic ventricular tachycardia, familial Wolff-Parkinson-White (WPW) syndrome, and Brugada syndrome are discussed. The currently proposed theoretical model of overlapping phenotypes in SCN5A sodium channel mutations is presented. The recent data indicate that advances in molecular genetics, experimental and clinical electrophysiology shed some light on the genetic background of primary electrical diseases. However, it is also becoming clear that the process from a mutation of a gene to the clinical presentation of a patient is currently only partially understood and extremely complex. [source] Validation of diagnostic codes for outpatient-originating sudden cardiac death and ventricular arrhythmia in Medicaid and Medicare claims data,PHARMACOEPIDEMIOLOGY AND DRUG SAFETY, Issue 6 2010Sean Hennessy PharmD Abstract Purpose Sudden cardiac death (SD) and ventricular arrhythmias (VAs) caused by medications have arisen as an important public health concern in recent years. The validity of diagnostic codes in identifying SD/VA events originating in the ambulatory setting is not well known. This study examined the positive predictive value (PPV) of hospitalization and emergency department encounter diagnoses in identifying SD/VA events originating in the outpatient setting. Methods We selected random samples of hospitalizations and emergency department claims with principal or first-listed discharge diagnosis codes indicative of SD/VA in individuals contributing at least 6 months of baseline time within 1999,2002 Medicaid and Medicare data from five large states. We then obtained and reviewed medical records corresponding to these events to serve as the reference standard. Results We identified 5239 inpatient and 29,135 emergency department events, randomly selected 100 of each, and obtained 119 medical records, 116 of which were for the requested courses of care. The PPVs for an outpatient-originating SD/VA precipitating hospitalization or emergency department treatment were 85.3% (95% confidence interval [CI],=,77.6,91.2) overall, 79.7% (95%CI,=,68.3,88.4) for hospitalization claims, and 93.6% (95%CI,=,82.5,98.7) for emergency department claims. Conclusions First-listed SD/VA diagnostic codes identified in inpatient or emergency department encounters had very good agreement with clinical diagnoses and functioned well to identify outpatient-originating events. Researchers using such codes can be confident of the PPV when conducting studies of SD/VA originating in the outpatient setting. Copyright © 2009 John Wiley & Sons, Ltd. [source] Circadian and Gender Effects on Repolarization in Healthy Adults: A Study Using Harmonic Regression AnalysisANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2010Kenneth A. Mayuga M.D. Background: Sudden cardiac death and myocardial infarction have a circadian variation with a peak incidence in the early morning hours. Increased dispersion of repolarization facilitates the development of conduction delay necessary to induce sustained arrhythmia. Both QT-dispersion and T-wave peak to T-wave end (TpTe) have been proposed as markers of dispersion of myocardial repolarization. Methods: Forty healthy adults (20 women), age 35,67 years old, with normal EKGs, echocardiograms, stress tests, and tilt-table tests were analyzed during a 27-hour hospital stay. EKGs were done at eight different time points. QT-intervals, QT-dispersion, and TpTe were measured at each time point. Harmonic regression was used to model circadian periodicity, P < 0.05 was considered significant. Results: The composite QT-interval was longer in women than in men (416 ± 17 msec vs 411 ± 20 msec, respectively, P = 0.006). The QT-dispersion among all leads was greater in men than women (37 ± 13 msec vs 30 ± 11 msec, respectively, P < 0.0001); a similar difference was found in the precordial leads. Harmonic regression showed that QT-dispersion had a significant circadian variation, primarily in men. In men, the maximum QT-dispersion occurred at 6 AM (45 ± 15 msec). TpTe also had a significant circadian variation that was not affected by gender in the majority of leads. Conclusions: A circadian variation exists in the dispersion of myocardial repolarization, as measured by both TpTe and QT-dispersion. Men and women have a different circadian variation pattern. Further studies regarding the mechanisms and clinical implications are needed. Ann Noninvasive Electrocardiol 2010;15(1):3,10 [source] T-Wave Variability Detects Abnormalities in Ventricular Repolarization: A Prospective Study Comparing Healthy Persons and Olympic AthletesANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2009Lara Heinz M.D. Background: Sudden cardiac death in athletes is more common than in the general population. Routine screening procedures are performed to identify competitors at risk. A new Holter-based parameter analyzes variation of the ventricular repolarization (TVar). The aim of this study was to evaluate differences in electrocardiogram (ECG), Echo, and Holter (H) in competitive athletes compared to a healthy control group consisting of medical students (MS). Methods: A total of 40 athletes (19 females, Olympic team, Luxembourg) and 40 MS (22 females) were examined by means of a resting ECG, treadmill exercise (TE), echocardiogram (Echo), as well as H recordings during a routine screening visit. To analyze TVar, a 20-minute H recording at rest (sampling rate 1000 per second) was performed. Moreover, heart rate variability (HRV) as well as HR turbulence (HRT) was computed. Results: No differences in demographic variables were detected. Quantification of HRV detected a significant increase in the vagal component of autonomic cardiac modulation. In contrast, no differences for HRT were found. Echo parameter demonstrated a thicker septal wall without differences of the posterior wall. TVar values were normal in range, but did differ significantly between the two groups. No correlation between TVar and echo as well as Holter parameters was detected. Conclusions: TVar was able to demonstrate significant differences in terms of alterations of ventricular activation. This might indicate an early change of myocardial repolarization representing a substrate for life-threatening arrhythmia. Larger studies on the predictive value of TVar including follow-up are necessary to confirm this preliminary finding. [source] Adrenergic Nervous System Influences on the Induction of Ventricular TachycardiaANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2002Oscar A. Pellizzón M.D. Background: Sudden cardiac death is a major cause of mortality in western countries and the ventricular tachyarrhythmias are mainly involved in this regard. The adrenergic autonomic nervous system has influences in provoking life-threatening arrhythmias, and the prevention of such arrhythmias with beta-blockers supports this viewpoint. To evaluate the effect of the adrenergic nervous system and some catecholamine-releasing stimuli on the induction of ventricular tachycardia, we decided to explore the occurrence of ventricular tachycardia in patients subjected to three consecutive tests, exercise testing, isoproterenol infusion, and mental stress. Methods: Nineteen subjects who experienced exercise test-induced ventricular tachycardia were subjected to an isoproterenol infusion and mental stress. All but one patient had cardiac disease, with 70% due to Chagas'disease. Seventeen of the 19 study subjects had normal ventricular function. Results: Exercise test-induced ventricular tachycardia was nonsustained in 17 patients and sustained in 2 cases. Isoproterenol infusion induced nonsustained ventricular tachycardia in 9 of 19 patients. Mental stress, on its own, was able to induce nonsustained ventricular tachycardia in 2 of 19 patients. Conclusions: Among patients preselected for exercise-induced ventricular tachycardia, almost half could be induced into ventricular tachycardia by isoproterenol infusion. Mental stress was a less powerful inducer of ventricular arrhythmias in this study group. A.N.E. 2002;7(4):281,288 [source] Epidemiology and stratification of risk for sudden cardiac deathCLINICAL CARDIOLOGY, Issue S1 2005Philip J. Podrid M.D. Abstract Sudden cardiac death (SCD) is a major cause of mortality in the United States. Approximately 65% of cases of SCD occur in patients with underlying acute or chronic ischemic heart disease. The incidence of SCD increases 2- to 4-fold in the presence of coronary disease and 6- to 10-fold in the presence of structural heart disease. Ventricular fibrillation (VF) precipitated by ventricular tachycardia (VT) is a common mechanism of cardiac arrest leading to SCD. Triggers for SCD include electrolyte disturbances, heart failure, and transient ischemia. Although a large percentage of patients with out-of-hospital SCD do not survive, successful resuscitation to hospitalization has improved in recent years. One of the challenges for preventing SCD lies in identifying individuals at highest risk for SCD within a lower-risk population. The progression from conventional risk factors of coronary artery disease to arrhythmogenesis and SCD can be represented as a cascade of changes associated with levels of increasing risk. At the first level is atherogenesis, followed by changes in atherosclerotic plaque anatomy, which may be mediated by inflammatory processes. Disruption of active plaque formed during a transitional state initiates the thrombotic cascade and acute occlusion, after which acute changes in myocardial electrophysiology become the immediate trigger for arrhythmogenesis and SCD. Each level of the cascade offers different opportunities for risk prediction. Among the classes of risk predictors are clinical markers, such as ECG measures and ejection fraction. Transient risk markers, such as inflammatory markers, are potentially useful for identifying triggers for SCD. In the future, genetic profiling is expected to allow better assessment of individual risks for SCD. [source] Implantable cardioverter defibrillators for prevention of sudden cardiac DeathCLINICAL CARDIOLOGY, Issue 1 2007Rishi Sukhija M.D. Abstract Despite the multiple advances in the field of cardiovascular medicine, the incidence of sudden cardiac death (SCD) continues to rise. Of all SCDs, <25% occur in individuals deemed at high risk by current risk-stratification algorithms; hence, these risk-stratification algorithms are not satisfactory. Until better markers are identified to risk stratify patients, we will see an increasing use of implantable cardioverter defibrillators (ICDs). However, even with the increase in defibrillator use, the impact on overall incidence of SCD may only be modest, as many individuals experience SCD as the first manifestation of cardiovascular disease. Another important challenge is widespread availability of automated external defibrillators and effective utilization of public access defibrillation programs for timely and appropriate management of out-of-hospital victims with cardiac arrest. This review discusses the current understanding on SCD, risk stratification, and management aimed at reducing SCD, particularly with the use of ICDs. Copyright © 2007 John Wiley & Sons, Ltd. [source] Patient and Physician Determinants of Implantable Cardioverter Defibrillator Use in the Heart Failure PopulationCONGESTIVE HEART FAILURE, Issue 4 2010Sanders H. Chae MD Recent studies report surprisingly low rates of implantable cardioverter defibrillator (ICD) placement for primary prevention against sudden cardiac death among patients with heart failure and left ventricular systolic dysfunction. Reasons for the low rates of utilization are not well understood. The authors examined ICD implantation rates at a university-based tertiary care center and used multivariable analysis to identify independent factors associated with ICD utilization. The ICD implantation rate for 850 eligible patients was 70%. Forty-seven (18%) patients refused implantation; women were twice as likely to refuse compared to men (8% vs 4%, P=.013). Race was not associated with utilization. On multivariable analysis, independent predictors of implantation included having a heart failure specialist (odds ratio [OR], 8.13; P<.001) or general cardiologist (OR, 2.23; P=.13) managing care, age range 70 to 79 (OR, 0.55; P<.001) or 80 and older (OR, 0.26; P<.001), female sex (OR, 0.49; P<.001), QRS interval (OR, 1.016; P<.001), diastolic blood pressure (OR, 0.979; P=.011), cerebrovascular disease (OR, 0.44; P=.007), and dementia (OR, 0.13; P=.002). Our registry of patients with cardiomyopathy and heart failure reveals that high rates of utilization are possible. Factors closely associated with ICD utilization include type of physician coordinating care, age, and comorbidities. Congest Heart Fail. 2010;16:141,146. © 2010 Wiley Periodicals, Inc. [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] Pulmonary Artery Dissection: Echocardiographic Findings and DiagnosisECHOCARDIOGRAPHY, Issue 4 2003Daniel Areco Pulmonary artery dissection is a rare but life-threatening event, predisposing to sudden cardiac death or cardiogenic shock. It is often associated with underlying congenital disorders predisposing to pulmonary hypertension. Rarely, it is diagnosed by echocardiography or other image techniques. We present a case report of a pulmonary artery dissection, diagnosed primarily by echocardiography. The patient died soon after refusing any interventional approach after a short period under medication. (ECHOCARDIOGRAPHY, Volume 20, May 2003) [source] Cardiac Dysrhythmia Associated with the Immediate Postictal State after Maximal Electroshock in Freely Moving RatEPILEPSIA, Issue 4 2002Olivier Darbin Summary: ,Purpose: Cardiac autonomic changes accompany complex partial seizures and generalized tonic,clonic seizures, and participate, at least partially, in the sudden and unexpected death in epilepsy (SUDEP). The analysis of the heart rate variability (HRV) is one of the simplest ways of providing insight into autonomic functions. The entropy quantifies the repetition of complex patterns in a signal and refers to systems randomness, regularity, and predictability. Clinical investigations have reported that entropy decreases in patients with a high risk of sudden cardiac death. The goal of this study was to evaluate the effects of the maximal electroshock (MES) on the entropy of HRV, monitored in the immediate postictal stage in the model of the freely moving rat. Methods: Entropy changes were correlated with the high and low frequencies of spectral analysis, which reflect the participation of the sympathetic and parasympathetic activities. Results: MES-induced arrhythmia is characterized by an HRV increase, an imbalance in favor of the parasympathetic activity, and a decrease in the entropy. Entropy decrease was restricted to the duration of the arrhythmia, suggesting that the postictal arrhythmia may be associated with a higher risk of lethal cardiac complications. Nevertheless, entropy changes did not correlate with spectral changes. Conclusions: The results suggest that the imbalance demonstrated in the spectral domain explains only partially the contribution of each autonomic system in the complexity of the heart rate during the postictal state. [source] Hypertrophic cardiomyopathy: from genetics to treatmentEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2010Ali J. Marian Eur J Clin Invest 2010; 40 (4): 360,369 Abstract Background, Hypertrophic cardiomyopathy (HCM) is the prototypic form of pathological cardiac hypertrophy. HCM is an important cause of sudden cardiac death in the young and a major cause of morbidity in the elderly. Design, We discuss the clinical implications of recent advances in the molecular genetics of HCM. Results, The current diagnosis of HCM is neither adequately sensitive nor specific. Partial elucidation of the molecular genetic basis of HCM has raised interest in genetic-based diagnosis and management. Over a dozen causal genes have been identified. MYH7 and MYBPC3 mutations account for about 50% of cases. The remaining known causal genes are uncommon and some are rare. Advances in DNA sequencing techniques have made genetic screening practical. The difficulty, particularly in the sporadic cases and in small families, is to discern the causal from the non-causal variants. Overall, the causal mutations alone have limited implications in risk stratification and prognostication, as the clinical phenotype arises from complex and often non-linear interactions between various determinants. Conclusions, The clinical phenotype of ,HCM' results from mutations in sarcomeric proteins and subsequent activation of multiple cellular constituents including signal transducers. We advocate that HCM, despite its current recognition and management as a single disease entity, involves multiple partially independent mechanisms, despite similarity in the ensuing phenotype. To treat HCM effectively, it is necessary to delineate the underlying fundamental mechanisms that govern the pathogenesis of the phenotype and apply these principles to the treatment of each subset of clinically recognized HCM. [source] SARS-coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARSEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2009G. Y. Oudit Abstract Background, Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1,7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction. Materials and methods, We studied mice infected with the human strain of the SARS-CoV and encephalomyocarditis virus and examined ACE2 mRNA and protein expression. Autopsy heart samples from patients who succumbed to the SARS crisis in Toronto (Canada) were used to investigate the impact of SARS on myocardial structure, inflammation and ACE2 protein expression. Results, Pulmonary infection with the human SARS-CoV in mice led to an ACE2-dependent myocardial infection with a marked decrease in ACE2 expression confirming a critical role of ACE2 in mediating SARS-CoV infection in the heart. The SARS-CoV viral RNA was detected in 35% (7/20) of autopsied human heart samples obtained from patients who succumbed to the SARS crisis during the Toronto SARS outbreak. Macrophage-specific staining showed a marked increase in macrophage infiltration with evidence of myocardial damage in patients who had SARS-CoV in their hearts. The presence of SARS-CoV in the heart was also associated with marked reductions in ACE2 protein expression. Conclusions, Our data show that SARS-CoV can mediate myocardial inflammation and damage associated with down-regulation of myocardial ACE2 system, which may be responsible for the myocardial dysfunction and adverse cardiac outcomes in patients with SARS. [source] Myocardial perfusion defects in Bartter and Gitelman syndromesEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2008R. Scognamiglio ABSTRACT Background, Normotensive hypokalaemic tubulopathies (Bartter and Gitelman syndromes (BS/GS)) are genetic diseases that are considered benign. However, QT prolongation, left ventricular dysfunction and reduction of cardiac index upon exercise leading to arrhythmias and sudden cardiac death have been reported in these patients. Hence, we aimed to verifying whether an isometric exercise could represent a useful tool for the identification of patients at risk for future cardiac events. Patients and methods, Myocardial function (MF) and perfusion, evaluated as myocardial blood flow (MBF) of 10 BS/GS patients and 10 healthy controls, were investigated at rest and during isometric exercise. MF and MBF were evaluated using quantitative two-dimensional and myocardial contrast echocardiography. Results, BS/GS patients had normal baseline MF and MBF. During exercise in BS/GS patients, corrected QT (QTc) was prolonged to peak value of 494 ± 9·1 ms (P < 0·001). In controls, MF increased from resting to peak exercise (left ventricular ejection fraction: 65 ± 4% to 78 ± 5%, P < 0·003) while in seven BS/GS patients (Group 1) it declined (64 ± 5% to 43 ± 9%, P < 0·001). Myocardial perfusion increased upon exercise in controls as shown by changes of its markers: , (a measure of myocardial flow velocity; 0·89 ± 0·12 vs. 0·99 ± 0·12, P < 0·001) and myocardial blood volume (14·4 ± 2 vs. 20·2 ± 0·25, P < 0·001), while in Group 1 BS/GS it decreased (0·87 ± 0·15 vs. 0·67 ± 0·15, P < 0·001; and 14·5 ± 1·9 vs. 8·3 ± 0·22, P < 0·001, respectively). Conclusions, Our results document for the first time that exercise induce coronary microvascular and myocardial defects in BS/GS patients. Therefore, this may challenge the idea that BS/GS are benign diseases. In addition, the diagnostic approach to these syndromes should include an in-depth cardiac assessment in order to identify patients at higher risk. [source] Increased QT variability in young asymptomatic patients with ,-thalassemia majorEUROPEAN JOURNAL OF HAEMATOLOGY, Issue 4 2007Damiano Magrě Abstract Background:, Despite recent progress in iron chelation therapy, sudden cardiac death due to malignant ventricular arrhythmias remains a vexing, clinical problem in patients with ,-thalassemia major (TM). In this study we assessed whether the major indices of QT variability, emerging tools for risk stratification of sudden cardiac death, differ in young asymptomatic patients with TM and healthy persons. Methods: Thirty patients with TM and 30 healthy control subjects underwent a 5-min electrocardiography recording to calculate the following variables: QT variance (QTv), QTv normalized for mean QT (QTVN) and QT variability index (QTVI). All subjects also underwent a two-dimensional and Doppler echocardiography study and magnetic resonance imaging (MRI) to determine cardiac and hepatic T2* values. Results: No differences were observed in clinical and conventional echo-Doppler findings in healthy control subjects and patients with TM whereas QTv, QTVN and QTVI values were significantly higher in patients than those in controls (QTv, P < 0.001; QTVN, P < 0.05 and QTVI, P < 0.001) and cardiac T2* and hepatic MRI T2* values were significantly lower in patients with TM (P < 0.001). The indices of temporal QT variability correlated significantly with MRI data. Conclusions: Young asymptomatic patients with TM have increased cardiac repolarization variability as assessed by QT variability indices, probably due to cardiac iron deposition. These easily assessed, non-invasive markers could be used to identify increased myocardial repolarization lability early in asymptomatic patients with TM. 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