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Author(s): V. Chhor [sup.1] [sup.2], A. Follin [sup.1], J. Joachim [sup.1], B. Champigneulle [sup.1], J. Chatelon [sup.1], G. Favé [sup.1], A. Neuschwander [sup.1], J. Mantz [sup.1], Romain Pirracchio [sup.1] [sup.3] [...]

Objective Brain injury is well established as a cause of early mortality after out-of-hospital cardiac arrest (OHCA), but postresuscitation shock also contributes to these deaths. This study aims to describe the respective incidence, risk factors, and relation to mortality of post-cardiac arrest (CA) shock and brain injury. Design Retrospective analysis of an observational cohort. Setting 24-bed medical intensive care unit (ICU) in a French university hospital. Patients All consecutive patients admitted following OHCA were considered for analysis. Post-CA shock was defined as a need for infusion of vasoactive drugs after resuscitation. Death related to brain injury included brain death and care withdrawal for poor neurological evolution. Intervention None. Measurements and main results Between 2000 and 2009, 1,152 patients were admitted after OHCA. Post-CA shock occurred in 789 (68 %) patients. Independent factors associated with its onset were high blood lactate and creatinine levels at ICU admission. During the ICU stay, 269 (34.8 %) patients died from post-CA shock and 499 (65.2 %) from neurological injury. Age, raised blood lactate and creatinine values, and time from collapse to restoration of spontaneous circulation increased the risk of ICU mortality from both shock and brain injury, whereas a shockable rhythm was associated with reduced risk of death from these causes. Finally, bystander cardiopulmonary resuscitation (CPR) decreased the risk of death from neurological injury. Conclusions Brain injury accounts for the majority of deaths, but post-CA shock affects more than two-thirds of OHCA patients. Mortality from post-CA shock and brain injury share similar risk factors, which are related to the quality of the rescue process., Author(s): Virginie Lemiale [sup.1] [sup.5] [sup.7], Florence Dumas [sup.2] [sup.6], Nicolas Mongardon [sup.1] [sup.5], Olivier Giovanetti [sup.6], Julien Charpentier [sup.1] [sup.5], Jean-Daniel Chiche [sup.1] [sup.5], Pierre Carli [sup.4] [sup.5], Jean-Paul [...]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2010.06.012 Byline: James M. Peacock (a), Tetsuya Ohira (b), Wendy Post (c)(d), Nona Sotoodehnia (e), Wayne Rosamond (f), Aaron R. Folsom (a) Abstract: We hypothesized that serum magnesium (Mg) is associated with increased risk of sudden cardiac death (SCD). Author Affiliation: (a) Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, Minneapolis, MN (b) Department of Social and Environmental Medicine, Graduate School of Medicine, Osaka University, Suita, Japan (c) Division of Cardiology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD (d) Department of Epidemiology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD (e) Cardiovascular Health Research Unit, Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA (f) Department of Epidemiology, School of Public Health, University of North Carolina, Chapel Hill, NC Article History: Received 21 October 2009; Accepted 4 June 2010

We have previously shown that a newly developed calpain inhibitor, SNJ-1945 (SNJ), with good aqueous solubility prevents the heart from KCI arrest-reperfusion injury associated with the impairment of total [Ca.sup.2+] handling by inhibiting the proteolysis of [alpha]-fodrin as a cardioplegia. The aim of the present study was to investigate certain actions of this calpain inhibitor, SNJ, on left ventricular (LV) mechanical work and energetics in cross-circulated excised rat hearts undergoing blood perfusion with 40 [micro]M SNJ. Mean end-systolic pressure at midrange LV volume and systolic pressure-volume area (PVA) at mLVV (a total mechanical energy/beat) were significantly increased by SNJ perfusion (P < 0.01). Mean myocardial oxygen consumption per beat ([[??]o.sub.2]) intercepts ([[??]o.sub.2] for the total [Ca.sup.2+] handling in excitation-contraction coupling and basal metabolism) of [[??]o.sub.2]-PVA linear relations were significantly increased (P < 0.01) with unchanged mean slopes of [Vo.sub.2]-PVA linear relations. Pretreatment with the selective [[beta].sub.1]-blocker landiolol (10 [micro]M) blocked these effects of SNJ perfusion. There were no significant differences in mean basal metabolic oxygen consumption among normal, 40 [micro]M SNJ, and 10 [micro]M landiolol + 40 [micro]M SNJ groups. Our results indicate that water-soluble SNJ exerted positive actions on mechanical work and energetics mediated via [[beta].sub.1]-adrenergic receptors associated with the enhancement of total [Ca.sup.2+] handling in excitation-contraction coupling and with unchanged contractile efficiency. In clinical settings, this pharmacological action of SNJ is beneficial as an additive agent for cardioplegia. cardiac function; systolic pressure-volume area; oxygen consumption; [[beta].sub.1]-adrenergic receptor doi: 10.1152/ajpheart.00153.2010.

Therapeutic hypothermia (TH) cardioprotection has recently been associated with increased Akt signaling in a rat model of cardiac arrest. However, it is not known whether Akt is required for this beneficial effect of TH. We used a mouse model of cardiac arrest demonstrating TH cardioprotection to study the response of mice deficient in an Aktl allele. We hypothesized that Aktl mediates TH cardioprotection and that decreases in Aktl content would diminish such protection. Adult C57BL/6 wildtype (WT) mice underwent an 8-min cardiac arrest. After 6 min, the mice were randomized to normothermia ([WT.sub.NT], 37[degrees]C) or TH ([WT.sub.TH], 30[degrees]C). Following cardiopulmonary resuscitation and the return of spontaneous circulation (ROSC), the animals were hemodynamically monitored for 240 min (R240). At R240, cardiac tissue Akt content and phosphorylation were assayed. Studies were repeated in Aktl heterozygous ([Aktl.sup.+/-]) mice. As a result, baseline characteristics and ROSC rates were equivalent across groups. At R240, [WT.sub.TH] mice exhibited lower heart rate, larger stroke volume, and higher cardiac output than [WT.sub.NT] animals (P < 0.05). Cardioprotection in [WT.sub.TH] at R240 was associated with increased cardiac Akt phosphorylation at Ser473 and Thr308 compared with that in [WT.sub.NT] (P < 0.05). TH-associated alterations in Akt phosphorylation, stroke volume, heart rate, and cardiac output were abrogated in [Aktl.sup.+/-] animals. In conclusion, TH improves post-ROSC cardiac function and increases Akt phosphorylation in WT, but not [Aktl.sup.+/-], mice. The Aktl isoform appears necessary for TH-mediated cardioprotection. sudden cardiac death; asystole; cardiopulmonary resuscitation; therapeutic hypothermia; protein kinase B doi: 10.1152/ajpheart.00187.2010.

The Cardiac Arrhythmia Suppression Trial demonstrated that antiarrhythmic drugs not only fail to prevent sudden cardiac death, but actually increase overall mortality. These findings have been confirmed in additional trials. The 'proarrhythmic' effects of most currently available antiarrhythmic drugs makes it essential that we investigate novel strategies for the prevention of sudden cardiac death. Targeted ablation of cardiac sympathetic neurons may become a therapeutic option by reducing sympathetic activity. Thus cholera toxin B subunit (CTB) conjugated to saporin (a ribosomal inactivating protein that binds to and inactivates ribosomes; CTB-SAP) was injected into both stellate ganglia to test the hypothesis that targeted ablation of cardiac sympathetic neurons reduces the susceptibility to ischemia-induced, sustained ventricular tachycardia in conscious rats. Rats were randomly divided into three groups: 1) control (no injection); 2) bilateral stellate ganglia injection of CTB; and 3) bilateral stellate ganglia injection of CTB-SAP. CTB-SAP rats had a reduced susceptibility to ischemiainduced, sustained ventricular tachycardia. Associated with the reduced susceptibility to ventricular arrhythmias were a reduced number of stained neurons in the stellate ganglia and spinal cord (segments [T.sub.1]-T4), as well as a reduced left ventricular norepinephrine content and sympathetic innervation density. Thus CTB-SAP retrogradely transported from the stellate ganglia is effective at ablating cardiac sympathetic neurons and reducing the susceptibility to ventricular arrhythmias. cholera toxin B subunit; stellate ganglion; neurotoxin; saporin; sympathectomy doi: 10.1152/ajpheart.00955.2009.

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2009.08.015 Byline: Stephanie E. Chiuve (a)(c), Eric B. Rimm (a)(b)(e), JoAnn E. Manson (b)(c), William Whang (f), Dariush Mozaffarian (a)(b)(d)(e), Meir J. Stampfer (a)(b)(e), Walter C. Willett (a)(b)(e), Christine M. Albert (c)(d) Abstract: Total intake of trans fat is associated with coronary heart disease (CHD), and recent reports in primarily male populations suggest that blood levels of specific trans isomers may have different effects on risk, particularly risk of sudden cardiac death (SCD). Author Affiliation: (a) Department of Nutrition, Harvard School of Public Health, Boston, MA (b) Department of Epidemiology, Harvard School of Public Health, Boston, MA (c) Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (d) Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (e) Channing Laboratory, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA (f) Columbia University, New York, NY Article History: Received 14 May 2009; Accepted 18 August 2009

Sudden cardiac death resulting from ventricular tachyarrhythmias remains the leading cause of death in industrially developed countries, accounting for between 300,000 and 500,000 deaths each year in the United States. Yet, despite the enormity of this problem, both the identification of factors contributing to ventricular fibrillation as well as the development of safe and effective antiarrhythmic agents remain elusive. Subnormal cardiac parasympathetic regulation coupled with an elevated cardiac sympathetic activation may allow for the formation of malignant ventricular arrhythmias. In particular, myocardial infarction can reduce cardiac parasympathetic regulation and alter [beta]-adrenoceptor subtype expression enhancing [beta]-adrenoceptor sensitivity that can lead to intracellular calcium dysregulation and arrhythmias. As such, myocardial infarction can induce a remodeling of cardiac autonomic regulation that may be required to maintain cardiac pump function. If alterations in cardiac autonomic regulation play an important role in the genesis of life-threatening arrhythmias, then one would predict that interventions designed to either augment parasympathetic activity and/or reduce cardiac adrenergic activity would also protect against ventricular fibrillation. Recently, studies using a canine model of sudden death demonstrate that endurance exercise training (treadmill running) enhanced cardiac parasympathetic regulation (increased heart rate variability), restored a more normal [beta]-adrenoceptor balance (i.e., reduced [beta]-adrenoceptor sensitivity and expression), and protected against ventricular fibrillation induced by acute myocardial ischemia. Thus exercise training may reverse the autonomic neural remodeling induced by myocardial infarction and thereby enhance the electrical stability of the heart in individuals shown to be at an increased risk for sudden cardiac death. sympathetic nervous system; parasympathetic nervous system; [beta]-adrenergic receptors; myocardial infarction; ventricular fibrillation doi: 10.1152/ajpheart.00534.2009

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ahj.2009.07.023 Byline: Jari A. Laukkanen (a)(b), Timo H. Makikallio (b)(c), Jussi Kauhanen (a), Sudhir Kurl (a) Abstract: Adrenoceptors mediate contraction of vascular smooth muscle and induce coronary vasoconstriction in humans. A deletion variant of the human [alpha].sub.2B-adrenoreseptor of glutamic acid residues has been associated with impaired receptor desensitization. This receptor variant could, therefore, be involved in cardiovascular diseases associated with enhanced vasoconstriction. Our aim was to study whether an insertion/deletion (I/D) polymorphism in the [alpha].sub.2B-adrenoceptor gene is associated with the risk for sudden cardiac death. Author Affiliation: (a) Research Institute of Public Health, School of Public Health and Clinical Nutrition, University of Kuopio, Kuopio, Finland (b) Department of Internal Medicine, Lapland Central Hospital, Rovaniemi, Finland (c) Division of Cardiology, Department of Internal Medicine, University of Oulu, Oulu, Finland Article History: Received 22 April 2009; Accepted 10 July 2009 Article Note: (footnote) The US National Heart, Lung, and Blood Institute grant HL44199.

Byline: Brendan G. Carr (1,2,4,5), Munish Goyal (2,3), Roger A. Band (2), David F. Gaieski (2,3), Benjamin S. Abella (2,3), Raina M. Merchant (1,2,3,4), Charles C. Branas (5), Lance B. Becker (2,3), Robert W. Neumar (2,3) Abstract: Purpose We sought to generate national estimates for post-cardiac arrest mortality, to assess trends, and to identify hospital factors associated with survival. Methods We used a national sample of US hospitals to identify patients resuscitated after cardiac arrest from 2000 to 2004 to describe the association between hospital factors (teaching status, location, size) and mortality, length of stay, and hospital charges. Analyses were performed using logistic regression. Results A total of 109,739 patients were identified. In-hospital mortality was 70.6%. A 2% decrease in unadjusted mortality from 71.6% in 2000 to 69.6% in 2004 (OR 0.96, P < 0.001) was observed. Mortality was lower at teaching hospitals (OR 0.58, P = 0.001), urban hospitals (OR 0.63, P = 0.004), and large hospitals (OR 0.55, P < 0.001). Conclusion Mortality after in-hospital cardiac arrest decreased over 5 years. Mortality was lower at urban, teaching, and large hospitals. There are implications for dissemination of best practices or regionalization of post-cardiac arrest care. Author Affiliation: (1) The Robert Wood Johnson Clinical Scholars Program, University of Pennsylvania School of Medicine, 932 Blockley Hall, 423 Guardian Drive, Philadelphia, PA, 19104-6021, USA (2) Department of Emergency Medicine, University of Pennsylvania School of Medicine, Philadelphia, USA (3) Center for Resuscitation Science, University of Pennsylvania School of Medicine, Philadelphia, USA (4) The Leonard Davis Institute of Health Economics, University of Pennsylvania, Philadelphia, USA (5) Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania School of Medicine, Philadelphia, USA Article History: Registration Date: 08/10/2008 Received Date: 28/04/2008 Accepted Date: 26/09/2008 Online Date: 21/10/2008

Two mechanisms are generally proposed to explain right precordial ST-segment elevation in Brugada syndrome: 1) right ventricular (RV) subepicardial action potential shortening and/or loss of dome causing transmural dispersion of repolarization; and 2) RV conduction delay. Here we report novel mechanistic insights into ST-segment elevation associated with a [Na.sup.+] current ([I.sub.Na]) loss-of-function mutation from studies in a Dutch kindred with the COOH-terminal SCN5A variant p.Phe2004Leu. The proband, a man, experienced syncope at age 22 yr and had coved-type ST-segment elevations in ECG leads V1 and V2 and negative T waves in V2. Peak and persistent mutant [I.sub.Na] were significantly decreased. [I.sub.Na] closed-state inactivation was increased, slow inactivation accelerated, and recovery from inactivation delayed. Computer-simulated [I.sub.Na]-dependent excitation was decremental from endo- to epicardium at cycle length 1,000 ms, not at cycle length 300 ms. Propagation was discontinuous across the midmyocardial to epicardial transition region, exhibiting a long local delay due to phase 0 block. Beyond this region, axial excitatory current was provided by phase 2 (dome) of the M-cell action potentials and depended on L-type [Ca.sup.2+] current ('phase 2 conduction'). These results explain right precordial ST-segment elevation on the basis of RV transmural gradients of membrane potentials during early repolarization caused by discontinuous conduction. The late slow-upstroke action potentials at the subepicardium produce T-wave inversion in the computed ECG waveform, in line with the clinical ECG. arrhythmia (mechanisms); computer modeling; conduction (block); electrocardiogram; sodium channel

Long QT syndrome (LQTS) is a heritable disease associated with ECG QT interval prolongation, ventricular tachycardia, and sudden cardiac death in young patients. Among genotyped individuals, mutations in genes encoding repolarizing [K.sup.+] channels (LQT1:KCNQ1; LQT2:KCNH2) are present in approximately 90% of affected individuals. Expression of pore mutants of the human genes KCNQ1 (KvLQT1-Y315S) and KCNH2 (HERG-G628S) in the rabbit heart produced transgenic rabbits with a long QT phenotype. Prolongations of QT intervals and action potential durations were due to the elimination of [I.sub.Ks] and [I.sub.Kr] currents in cardiomyocytes. LQT2 rabbits showed a high incidence of spontaneous sudden cardiac death (>50% at 1 year) due to polymorphic ventricular tachycardia. Optical mapping revealed increased spatial dispersion of repolarization underlying the arrhythmias. Both transgenes caused downregulation of the remaining complementary [I.sub.Kr] and [I.sub.Ks] without affecting the steady state levels of the native polypeptides. Thus, the elimination of 1 repolarizing current was associated with downregulation of the reciprocal repolarizing current rather than with the compensatory upregulation observed previously in LQTS mouse models. This suggests that mutant KvLQT1 and HERG interacted with the reciprocal wild-type [alpha] subunits of rabbit ERG and KvLQT1, respectively. These results have implications for understanding the nature and heterogeneity of cardiac arrhythmias and sudden cardiac death., Introduction The long QT syndrome (LQTS) is a familial, usually autosomal dominant disease, characterized by prolongation of the QT interval in the surface ECG, spontaneous polymorphic ventricular tachycardia (VT, often [...]

The [Ca.sup.2+] release channel ryanodine receptor 2 (RyR2) is required for excitation-contraction coupling in the heart and is also present in the brain. Mutations in RyR2 have been linked to exercise-induced sudden cardiac death (catecholaminergic polymorphic ventricular tachycardia [CPVT]). CPVT-associated RyR2 mutations result in "leaky" RyR2 channels due to the decreased binding of the calstabin2 (FKBP12.6) subunit, which stabilizes the closed state of the channel. We found that mice heterozygous for the R2474S mutation in Ryr2 (Ryr2-R2474S mice) exhibited spontaneous generalized tonic-clonic seizures (which occurred in the absence of cardiac arrhythmias), exercise-induced ventricular arrhythmias, and sudden cardiac death. Treatment with a novel RyR2-specific compound (S107) that enhances the binding of calstabin2 to the mutant Ryr2-R2474S channel inhibited the channel leak and prevented cardiac arrhythmias and raised the seizure threshold. Thus, CPVT-associated mutant leaky Ryr2-R2474S channels in the brain can cause seizures in mice, independent of cardiac arrhythmias. Based on these data, we propose that CPVT is a combined neurocardiac disorder in which leaky RyR2 channels in the brain cause epilepsy, and the same leaky channels in the heart cause exercise-induced sudden cardiac death., Introduction Pharmacological seizure models have implicated abnormalities in intracellular [Ca.sup.2+] cycling of inhibitory interneurons and/or astrocytes as a mechanism of seizure generation (1), (2), and the inositol 1,4,5-trisphosphate receptor (IP3R), [...]

A study to record if the outcomes after a cardiac arrest in hospital differed during nights and weekends as against days or evening and weekdays is conducted. Results show lower survival rates from cardiac arrests during nights and weekends.

Reducing testosterone and estrogen levels with a luteinizing hormone-releasing hormone agonist such as Zoladex (i.e., chemical gonadectomy) is a common treatment for many prostate and breast cancer patients, respectively. There are reports of surgical gonadectomy inducing cardiac dysfunction, and exercise has been shown to be cardioprotective under these circumstances. Minimal research has been done investigating the effects of chemical gonadectomy and increased physical activity on cardiac function. The purpose of this investigation was to examine the effects of chemical gonadectomy and physical activity on cardiac function. Male (M) and female (F) Sprague-Dawley rats received either Zoladex treatment (Zol) that suppressed gonadal function for 8 wk or control implants (Con) and either were allowed unlimited access to voluntary running wheels (WR) or remained sedentary (Sed) throughout the treatment period. In vivo and ex vivo left ventricle (LV) function were then assessed, and myosin heavy chain (MHC) expression was analyzed to help explain LV functional differences. Hearts from M Sed+Zol exhibited significantly lower aortic blood flow velocity, developed pressure, and maximal rate of pressure development and higher [beta]-MHC expression than M Sed+Con. Hearts from F Sed+Zol exhibited significantly lower LV wall thicknesses, fractional shortening, and developed pressure and higher [beta]-MHC expression than F Sed+Con. This cardiac dysfunction was not evident in hearts from M or F WR+Zol, and this was associated with a preservation of the MHC isoform distribution. Thus an 8-wk chemical gonadectomy with Zoladex promoted cardiac dysfunction in male and female rats, and voluntary wheel running protected against this cardiac dysfunction. echocardiography; myosin heavy chain; orchiectomy; ovariectomy; sex hormones

The article examines Medicare beneficiaries at high risk of sudden cardiac death and finds significant sex differences in the use of ICD therapy.

Studies are conducted to determine the relationship between clinical risk profile and incidence and efficacy of the implantable cardioverter-defibrillator (ICD) intervention in hypertrophic cardiomyopathy (HCM). Results reveal that in a high-risk HCM cohort, ICD interventions for life-threatening ventricular tachyarrhythmias were frequent and highly effective in restoring normal rhythm.

The inhibition of cyclooxygenase (COX)-2 confers a small but absolute risk of cardiovascular events on patients taking nonsteroidal anti-inflammatory drugs (NSAIDs). This risk has been established by placebo-controlled trials of NSAIDs selective for COX-2; traditional NSAIDs seem to be heterogeneous with respect to cardiovascular risk. The American Heart Association (AHA) has proposed a 'stepped-care' approach to the use of NSAIDs in patients with cardiovascular disease, whereas the Food and Drug Administration (FDA) has failed to approve the COX-2-selective NSAID etoricoxib. In this article, these actions of the AHA and the FDA are interpreted in the light of current knowledge, prompting the formulation of scientific questions that might be addressed.

Emotional trauma and psychological stress can precipitate cardiac arrhythmia and sudden death through arrhythmogenic effects of efferent sympathetic drive. Patients with preexisting heart disease are particularly at risk. Moreover, generation of proarrhythmic activity patterns within cerebral autonomic centers may be amplified by afferent feedback from a dysfunctional myocardium. An electrocortical potential reflecting afferent cardiac information has been described, reflecting individual differences in interoceptive sensitivity (awareness of one's own heartbeats). To inform our understanding of mechanisms underlying arrhythmogenesis, we extended this approach, identifying electrocortical potentials corresponding to the cortical expression of afferent information about the integrity of myocardial function during stress. We measured changes in cardiac response simultaneously with electroencephalography in patients with established ventricular dysfunction. Experimentally induced mental stress enhanced cardiovascular indices of sympathetic activity (systolic blood pressure, heart rate, ventricular ejection fraction, and skin conductance) across all patients. However, the functional response of the myocardium varied; some patients increased, whereas others decreased, cardiac output during stress. Across patients, heartbeat-evoked potential amplitude at left temporal and lateral frontal electrode locations correlated with stress-induced changes in cardiac output, consistent with an afferent cortical representation of myocardial function during stress. Moreover, the amplitude of the heartbeat-evoked potential in the left temporal region reflected the proarrhythmic status of the heart (inhomogeneity of left ventricular repolarization). These observations delineate a cortical representation of cardiac function predictive of proarrhythmic abnormalities in cardiac repolarization. Our findings highlight the dynamic interaction of heart and brain in stress-induced cardiovascular morbidity. afferent homeostatic feedback | electroencephalography | heart beat-evoked potential | insula cortex | ischemia

The causes of sudden cardiovascular death in the young athletic population in the Veneto region of Italy and the changes in incidence rates after introduction of systematic preparticipation screening are analyzed. It is observed that the incidence of sudden vascular death in young athletes has significantly reduced since the implementation of the screening, as it is effective in identifying athletes with hypertrophic cardiomyopathy and in providing some protection against the risk of sudden death.

A study of 2772 participants was conducted to identify risk factors associated with aborted cardiac arrest and sudden cardiac death during adolescence in patients with clinically suspected long-QT syndrome (LQTS). Findings indicate that the timing and frequency of syncope, the degree of QTc prolongation and sex are independent predictors of life-threatening events in adolescents with LQTS.

The risk of sudden cardiac death in women during moderate to vigorous exertion is compared with the risk of sudden cardiac death during lighter or no exertion and the long-term association between moderate to vigorous exercise and sudden cardiac death are assessed. The results have shown that sudden cardiac death during exertion is an extremely rare event in women and exercising regularly might significantly minimize this small transient risk.

Joshua Oukrop, a Minnesota teenager with hypertrophic cardiomyopathy and a high risk of sudden death from ventricular fibrillation, received an implantable cardioverter-defibrillator (ICD) on October 4, 2001. Oukrop on March 14, 2005 collapsed and died as the device had short-circuited internally, while trying to deliver high-voltage therapy.

A study conducted to measure multiple parameters of in-hospital cardiopulmonary resuscitation (CPR) quality and to determine compliance with published American Heart Association and international guidelines is reported. The results revealed that the quality of multiple parameters of CPR was inconsistent and often did not meet published guideline recommendations, even when performed by well-trained hospital staff.

This controlled clinical trial was designed to assess the incremental value of prehospital advanced-life-support interventions. 5638 patients who had cardiac arrest outside the hospital were enrolled. The addition of advanced-life-support interventions did not improve the rate of survival after out-of-hospital cardiac arrest in a previously optimized emergency-medical-services system of rapid defibrillation.

This study shows that enhancing a well-developed, monitored, layperson-enacted cardiopulmonary resuscitation (CPR) response plan by adding automated external defibrillators (AEDS) and AED training can increase the number of survivors of out-of-hospital cardiac arrest in public locations. Training and equipping volunteers to attempt early defibrillation with in a structured response system can increase the number of survivors to hospital discharge after out-of-hospital cardiac arrest in public locations.

Sudden Cardiac arrest is primarily a problem in patients outside of the hospital; in fact, approximately 80 percent of cases of sudden death from cardiac causes occur at home. Studies confirm the importance of early access to defibrillation for improved survival in out-of-hospital cardiac arrest.

The importance of prophylactic implantation of an implantable cardioverter-defibrillator (ICD), to prevent sudden deaths in patients with nonischemic dilated cardiomyopathy, is evaluated with the help of a study.

Byline: Tobias Back (2), Thomas Hemmen (2), Olaf G. Schuler (1) Keywords: brain ischemia; MRI; cardiac arrest; stroke; pathophysiology; cerebral ischemia Abstract: Abstract. There is sound evidence from histopathological and magnetic resonance imaging (MRI) studies that focal ischemic brain lesions tend to increase in size over time. Considerable lesion growth was observed in models of animal stroke as well as in patients presenting with hemispheric stroke. In focal cerebral ischemia, lesions predominantly enlarge early within 12 hours after onset. Ischemic injury is caused by complete necrosis in most of the affected tissue. By contrast, in global cerebral ischemia as seen after cardiac arrest, lesions appear late (&gt 12 h) in selectively vulnerable brain regions such as the hippocampus, and neurons are damaged by apoptotic cell death. The high and regionally distinct vulnerability of the brain explains why prolonged periods of global ischemia result in widespread loss of energy metabolites combined with diffuse brain edema and global damage. Postulated mechanisms involved in lesion growth include among others excitotoxicity, periinfarct depolarizations, lactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling. Research in the field faces two main challenges. First,maturation phenomena of injury may require special imaging techniques to detect early ischemic changes. Second, the dynamic nature of the changes underlines the need to conduct longitudinal studies with a variety of imaging techniques (e. g., metabolic imaging, diffusion/perfusion MRI, positron emission tomography) that require a differentiated interpretation of the alterations observed. Author Affiliation: (1) Department of Neurology, Ludwig Maximilians University Munich, Marchioninistrasse 15, 81377, Munchen, Germany (2) Department of Neurology, Philipps University Marburg, R.-Bultmann-Str. 8, 35039, Marburg, Germany Article History: Registration Date: 01/01/2004 Received Date: 04/08/2003 Accepted Date: 15/01/2004

Byline: Roberto Imberti (1), Guido Bellinzona (1), Francesca Riccardi (1), Michele Pagani (1), Martin Langer (1) Keywords: Cardiac arrest Cardiopulmonary resuscitation Brain tissue partial pressure of oxygen Intracranial pressure Cerebral perfusion pressure Cerebral oxygen metabolism Abstract: Objective: To report on the effects of cardiopulmonary resuscitation (CPR) instituted immediately after a cardiac arrest on cerebral perfusion pressure (CPP) and cerebral tissue oxygen tension (PbrO.sub.2). Design: Case report. Setting: ICU of a university hospital. Patient: A head-injured 17-year-old man submitted to multimodal neurological monitoring underwent sudden cardiac arrest and successful CPR. Interventions: External chest compression, 100% oxygen ventilation, volume expansion and standard ACLS protocols. Measurements and results: Heart rate, ECG, mean arterial blood pressure (MABP), ETCO.sub.2,PaO.sub.2, intracranial pressure (ICP), CPP and PbrO.sub.2 were continuously monitored during CPR and data recorded at 15-s intervals by a dedicated personal computer. At the onset of the cardiac arrest, PbrO.sub.2 decreased to zero. The institution of CPR resulted in a progressive increase of MABP, CPP and PbrO.sub.2. Assuming, on the basis of previous experimental and clinical reports, 8 mmHg PbrO.sub.2 as a possible ischaemic/hypoxic threshold value, during the first 6.5 min of CPR, PbrO.sub.2 values were below this threshold (range 0--7 mmHg) and CPP values were 25 mmHg for 77.3% of the time. These values were associated with a PbrO.sub.2 >8 mmHg (range 8--28 mmHg) at all times. Conclusions: In the clinical setting of a witnessed cardiac arrest, immediate institution of CPR can be effective in generating PbrO.sub.2 values above a supposed ischaemic/hypoxic threshold when CPP is >25 mmHg. PbrO.sub.2 monitoring by the Licox system is sensitive and reliable, even at low values, and can be suitable for evaluating cerebral oxygenation during experimental CPR. Author Affiliation: (1) Servizio di Anestesia e Rianimazione II, IRCCS Policlinico S. Matteo, 27100, Pavia, Italy Article History: Received Date: 29/10/2002 Accepted Date: 18/02/2003 Article note: Electronic Publication