Search

Introduction: Ibutilide is a rapid-acting antiarrhythmic drug with worldwide use for conversion of recent-onset atrial fibrillation. Vernakalant is a novel drug, which is likewise used intravenously, with proven effectiveness and safety compared to placebo and amiodarone in randomized clinical trials. Hypothesis: We hypothesized that the time to sinus rhythm and the conversion rate within 90 minutes is different between vernakalant and ibutilide in patients with recent-onset atrial fibrillation. Methods: A randomized, controlled, open-label trial registered at clinicaltrials.gov (NCT01447862) was performed in one hundred patients with recent-onset atrial fibrillation treated at the emergency department of a tertiary care hospital. Patients received up to two short-infusions of vernakalant (n= 49; 3mg/kg, 2mg/kg) or ibutilide (n= 51; 1mg, 1mg) according to the manufacturer’s instructions. Clinical and laboratory variables, adverse events, conversion rates and time to conversion were recorded. Results: Time to conversion of AF to sinus rhythm was significantly shorter in the vernakalant group compared to the ibutilide group (median time: 10min vs. 26min, p=0.02), and likewise the conversion success within 90 minutes was significantly higher (69% vs. 43%, p=0.01) in the vernakalant group. In both groups no serious adverse events occurred. Conclusion: Vernakalant was significantly faster and more effective in converting recent-onset atrial fibrillation to sinus rhythm at the emergency department.

Background: Based on demographic changes in the western world, the number of patients with cardiac arrest due to a cardiovascular event is continuously rising. A large variety of factors impacting on favorable neurological outcome (CPC 1-2) and the 6-month survival, are well established. The question whether the knowledge about these predictive factors result in improved outcome over the last 20 years, has not been proven within a long-term study so far. Methods: We prospectively identified 2670 patients (out-of hospital [OOH], n = 1822; in-hospital [IH], n = 848) with cardiac arrest of cardiac etiology and ventricular fibrillation as a first rhythm treated at our emergency department between January 1992 and December 2012. Chi-square test and Cochran-Mantel-Haenszel test have been used to assess differences in CPC and 6-month survival within the observation-period. Results: Within our total cohort, 2189 patients (82.0%) survived the initial event. After a follow-up period of 6 months, 1007 patients (46%) with ROSC deceased. A favorable CPC (1-2) after 6 months has been detected in 1197 patients (54.7%). Within the last 20 years there was an improvement of favorable neurological outcome (CPC 1-2) (p Independently in patients with IH cardiac arrest, 78.5% (n=666) survived the initial event, but the 6-month survival rate (n=381, 57.2%) and the favorable CPC outcome (n=443, 66.5%) were approximately higher. Independently within IH cardiac arrest patients a reduction of 6-month mortality rates (p=0.048) was found. Still there were constantly high rates of favorable neurological outcome (CPC 1-2) after 6 months, but there was no improvement within the past 20 years (p=0.665). Conclusion: We were able to demonstrate, that outcome of patients with cardiac arrest of a cardiac etiology has improved significantly within the last 20 years. This gives the impression, that critical care medicine on a high level for patients with cardiac arrest even in the emergency department could be important for outcome. If such specific cardiac arrest centers merged with emergency departments prove to be valuable for ideal patient care has to be further evaluated in detail.

Background —International guidelines recommend differentiation between cardiac and noncardiac causes of cardiac arrest. The aim of this study was to find the rate of agreement between primarily postulated and definitive causes of cardiac arrest. Methods and Results —We retrospectively analyzed the primarily presumed cause of cardiac arrest as determined by the emergency room physician on admission in all patients admitted to the emergency department of one urban tertiary care hospital. This was compared with the definitive cause as established by clinical evidence or autopsy. Within 4 years, the initially presumed cause was unclear in 24 (4%) of 593 patients. In the remaining 569 patients, the presumed cause was correct in 509 (89%) and wrong in 60 (11%) cases. Cardiac origin was presumed in 421 (71%) and the definitive cause in 408 (69%) cases. Noncardiac origin was presumed in 148 (25%) and the definitive cause in 185 (31%) patients. Presumed cardiac cause was sensitive (96%) but less specific (77%). Noncardiac causes such as pulmonary embolism, cerebral disorders, or exsanguination were those most frequently overlooked. Asystole occurred significantly more often in patients in whom presumed cause remained undetermined or differed from the definitive cause. Conclusions —Cause of cardiac arrest is not as easily recognized as anticipated, especially when the initial rhythm is different from ventricular fibrillation. This might affect comparability of study results, therapeutic strategies, prognosis, and outcome. Patients in whom the presumed cause was confirmed as being correct had significantly better survival and neurological outcome.

To The Editor: With interest we have read the article by Kitamura and colleagues about bystander initiated rescue breathing for out-of-hospital cardiac arrest of noncardiac origin.1 The authors included a large number of patients from a population based registry and concluded that rescue breathing has an incremental benefit for out-of-hospital cardiac arrests of noncardiac origin. We would like to discuss some aspects of the study design: The main question was a comparison between compression-only CPR to conventional CPR including …

Purpose: The aim of our study was to assess the effect of hypothermia on histological damage in 19 brain regions after prolonged cardiac arrest in pigs. Methods: Pigs were anaesthetized and mechanically ventilated. After stabilisation of pulmonary artery temperature (Tpa) at 38.5±0.2 °C, ventricular fibrillation (VF) was induced and 10 min of untreated VF were followed by 8 min of cardiopulmonary resuscitation (mechanical chest compressions, two doses of vasopressin 0.4 IE/kg). At 8 min of CPR, up to 3 countershocks were delivered. Pigs that had return of spontaneous circulation (ROSC) were randomized to one of 2 groups (control, hypothermia). Pigs in the hypothermia group were cooled to Tpa 33.0±1.0 °C with a surface cooling device (LRS Thermosuit™) circulating ice water over most of the skin surface. Pigs in the control group were kept at 38.5±1.0 °C throughout the experiment. After 14 hours of hypothermia, pigs were rewarmed, weaned and brought to the stable. At day 9 of the experiment, final neurologic examination was performed. After that the animals were sacrificed and perfused with 4 liters of saline, followed by 1 liter of paraformaldehyde (3%, pH 7.4). The brain was removed and 19 different regions of the brain were examined by means of lightmicroscopy using a histopathologic damage score that was used in previous studies. Following damage qualities were considered: edema, eosinophilic necrosis (oncosis), vacuolar degeneration and malacia. The total numeric histological damage score (HDS) was the sum of all area scores. Data are presented as median and interquartile range, group comparison was done with a Mann-Whitney-U test. Results: 16 (29 –35 kg) pigs were randomized. The time to reach target temperature in the hypothermia group (n = 8) was 9.0 (5.3; 11.9) min. Total HDS in the hypothermia group was 71 (61; 84), in the control group 132 (124; 174; p Conclusions: Histological damage after prolonged cardiac arrest was improved significantly in cooled animals compared to control animals. Not all brain regions could benefit to the same extent.

Background: The prognosis of patients with cardiac arrest is still poor, and hardly any specific therapeutic options exist to improve outcome. Platelet activation has been observed in patients undergoing cardiopulmonary resuscitation (CPR). This may contribute to impairment of microcirculatory function and overall poor outcome despite return of spontaneous circulation. Data on direct platelet function in cardiac arrest are scarce. Platelets of patients with myocardial infarction are hyperfunctional, which predicts the degree of myocardial necrosis. Thus, we hypothesized that platelets may be even more hyper-functional in patients whose myocardial infarction causes cardiac arrest. We determined platelet function under high shear rates of patients with cardiac arrest and were further interested whether this may be related to the cause of cardiac arrest. Methods: We conducted a prospective study in 77 cardiac arrest patients at the Emergency Department of a tertiary care hospital. Collagen adenosine diphosphate closure time (CADP-CT) was assessed by the FDA-approved platelet function analyzer (PFA-100). In addition, plasma levels of von Willebrand factor (vWf:RiCo) were measured by turbidometry. Independent staff members of the emergency department not otherwise involved in this trial diagnosed the origin of cardiac arrest. Results: More than half of cardiac arrests were caused by myocardial ischemia. CADP-CT values (54s; 95%CI: 48–60s in 3.8% citrate) were much shorter in these patients as compared to patients with other causes of cardiac arrest (110s; 95%CI: 84–135s, p Conclusion: Patients with myocardial ischemia triggered cardiac arrest displayed the highest degree of platelet hyper-function under high shear rates, which was not solely due to increased vWF. Those patients may benefit from a rapid, more aggressive anti-platelet therapy than currently performed or an anti-vWF targeted therapy.

Background— The purpose of this study was to determine whether implementation of recent guidelines improves in-hospital mortality from acute ST-elevation myocardial infarction (STEMI) in a metropolitan area. Methods and Results— We organized a network that consisted of the Viennese Ambulance Systems, which is responsible for diagnosis and triage of patients with acute STEMI, and 5 high-volume interventional cardiology departments to expand the performance of primary percutaneous catheter intervention (PPCI) and to use the fastest available reperfusion strategy in STEMI of short duration (2 to 3 hours from onset of symptoms), either PPCI or thrombolytic therapy (TT; prehospital or in-hospital), respectively. Implementation of guidelines resulted in increased numbers of patients receiving 1 of the 2 reperfusion strategies (from 66% to 86.6%). Accordingly, the proportion of patients not receiving reperfusion therapy dropped from 34% to 13.4%, respectively. PPCI usage increased from 16% to almost 60%, whereas the use of TT decreased from 50.5% to 26.7% in the participating centers. As a consequence, in-hospital mortality decreased from 16% before establishment of the network to 9.5%, including patients not receiving reperfusion therapy. Whereas PPCI and TT demonstrated comparable in-hospital mortality rates when initiated within 2 to 3 hours from onset of symptoms, PPCI was more effective in acute STEMI of >3 but Conclusions— Implementation of recent guidelines for the treatment of acute STEMI by the organization of a cooperating network within a large metropolitan area was associated with a significant improvement in clinical outcomes.

Background— Platelet activation is a hallmark of acute coronary syndromes. Numerous lines of evidence suggest a mechanistic link between von Willebrand factor or platelet hyperfunction and myocardial damage in patients with acute coronary syndromes. Thus, we assessed whether platelet function under high shear rates (collagen adenosine diphosphate closure times [CADP-CTs]) measured with the platelet function analyzer (PFA-100) may be enhanced in patients with myocardial infarction (MI) and whether it may predict the extent of myocardial damage as measured by creatine kinase (CK-MB) or troponin T (TnT) levels. Methods and Results— Patients with acute chest pain or symptoms suggestive of acute coronary syndromes (n=216) were prospectively examined at an emergency department. CADP-CT was significantly shorter in patients with MI, particularly in those with an ST-segment-elevation MI (STEMI) compared with the other patient groups (unstable angina, stable coronary artery disease, or controls). Furthermore, CADP-CT and collagen epinephrine–CT at presentation were independent predictors of myocardial damage as measured by CK-MB or TnT. Patients with MI whose CADP-CT values fell in the first quartile had 3-fold higher CK-MB and TnT levels than those in the fourth quartile. Conclusions— Patients with STEMI have significantly enhanced platelet function when measured under high shear rates. CADP-CT is an independent predictor of the severity of MI, as measured by markers of cardiac necrosis. Measurement of platelet function with the PFA-100 may help in the risk stratification of patients presenting with MI.