Similarities and Differences in Extracellular Vesicle Profiles between Ischaemic Stroke and Myocardial Infarction.

Extracellular vesicles (EVs) are involved in intercellular signalling through the transfer of molecules during physiological and pathological conditions, such as ischaemic disease. EVs might therefore play a role in ischaemic stroke (IS) and myocardial infarction (MI). In the present study, we analysed the similarities and differences in the content of circulating EVs in patients with IS and MI. This prospective observational study enrolled 140 participants (81 patients with IS, 37 with MI and 22 healthy controls [HCs]). We analysed the protein and microRNA content from EVs using proteomics and reverse transcription quantitative real-time polymerase chain reaction and compared it between the groups. In the patients with IS and MI, we identified 14 common proteins. When comparing IS and MI, we found differences in the protein profiles (apolipoprotein B, alpha-2-macroglobulin, fibronectin). We also found lower levels of miR-340 and miR-424 and higher levels of miR-29b in the patients with IS and MI compared with the HCs. Lastly, we found higher miR-340 levels in IS than in MI. In conclusion, proteomic and miRNA analyses suggest a relationship between circulating EV content and the patient's disease state. Although IS and MI affect different organs (brain and heart) with distinct histological characteristics, certain EV proteins and miRNAs appear to participate in both diseases, while others are present only in patients with IS.

Cinética de la enolasa neuroespecífica: una herramienta adicional para el pronóstico neurológico después de una parada cardiaca / Neuron-specific enolase kinetics: an additional tool for neurological prognostication after cardiac arrest

INTRODUCCIÓN Y OBJETIVOS: Analizar la cinética de la enolasa neuroespecífica (EN) como biomarcador de pronóstico neurológico de los pacientes que sobreviven a una parada cardiaca tratados con control de temperatura. MÉTODOS: Análisis retrospectivo de pacientes ingresados tras sufrir una parada cardiaca dentro o fuera del hospital entre septiembre de 2006 y mayo de 2018 en un centro terciario y enfriados a 32-34°C durante 24 h. Las muestras de EN se tomaron al ingreso hospitalario y a las 24, 48 y 72 h del retorno a circulación espontánea (RCE). El estado neurológico se evaluó a los 3 meses mediante la escala Cerebral Performance Category (CPC) y se categorizó como favorable (CPC 1-2) o desfavorable (CPC 3-5). RESULTADOS: De los 451 pacientes, 320 cumplían los criterios de inclusión (el 80,3% varones; media de edad, 61+/-14,1 años). De estos, 174 (54,4%) sobrevivieron con una evolución neurológica favorable. Los pacientes con estado neurológico desfavorable tenían valores de EN más altos al ingreso hospitalario y a las 24, 48 y 72 h del RCE. A las 48 y las 72 h, los valores de EN predijeron un estado neurológico desfavorable, con áreas bajo la curva de 0,85 (IC95%, 0,81-0,90) y 0,88 (IC95%, 0,83-0,93). Además, el área bajo la curva de los valores delta de EN entre las 72 h y el ingreso hospitalario fue de 0,90 (IC95%, 0,85-0,95), y en el análisis multivariante resultó predictor independiente (p <0,001). CONCLUSIONES: En pacientes que sobrevivieron a una parada cardiaca tratados con control de la temperatura, se ha demostrado que los valores delta de EN entre las 72 h del RCE y el ingreso hospitalario son un potente predictor de resultado neurológico desfavorable

INTRODUCTION AND OBJECTIVES: To analyze neuron-specific enolase (NSE) kinetics as a prognostic biomarker of neurological outcome in cardiac arrest survivors treated with targeted temperature management. METHODS: We performed a retrospective analysis of patients resuscitated from in- or out-of-hospital cardiac arrest admitted from September 2006 to May 2018 in a single tertiary care center and cooled to 32°C to 34°C for 24 hours. Blood samples for measurement of NSE values were drawn at hospital admission and at 24, 48, and 72hours after return of spontaneous circulation (ROSC). Neurological outcome was evaluated by means of the Cerebral Performance Category (CPC) score at 3 months and was characterized as good (CPC 1-2) or poor (CPC 3-5). RESULTS: Of 451 patients, 320 fulfilled the inclusion criteria and were analyzed (80.3% male, mean age 61+/-14.1 years). Among these, 174 patients (54.4%) survived with good neurological status. Poor outcome patients had higher median NSE values at hospital admission and at 24, 48 and 72 hours after ROSC. At 48 and 72 hours after ROSC, NSE predicted poor neurological outcome with areas under the receiver-operating characteristic curves of 0.85 (95%CI, 0.81-0.90) and 0.88 (95%CI, 0.83-0.93), respectively. In addition, delta NSE values between 72hours after ROSC and hospital admission predicted poor neurological outcome with an area under the receiver-operating characteristic curve of 0.90 (95%CI, 0.85-0.95) and was an independent predictor of unfavorable outcome on multivariate analysis (P <.001). CONCLUSIONS: In cardiac arrest survivors treated with targeted temperature management, delta NSE values between 72 hours after ROSC and hospital admission strongly predicted poor neurological outcome

Neuron-specific enolase kinetics: an additional tool for neurological prognostication after cardiac arrest.

INTRODUCTION AND OBJECTIVES: To analyze neuron-specific enolase (NSE) kinetics as a prognostic biomarker of neurological outcome in cardiac arrest survivors treated with targeted temperature management. METHODS: We performed a retrospective analysis of patients resuscitated from in- or out-of-hospital cardiac arrest admitted from September 2006 to May 2018 in a single tertiary care center and cooled to 32°C to 34°C for 24 hours. Blood samples for measurement of NSE values were drawn at hospital admission and at 24, 48, and 72hours after return of spontaneous circulation (ROSC). Neurological outcome was evaluated by means of the Cerebral Performance Category (CPC) score at 3 months and was characterized as good (CPC 1-2) or poor (CPC 3-5). RESULTS: Of 451 patients, 320 fulfilled the inclusion criteria and were analyzed (80.3% male, mean age 61±14.1 years). Among these, 174 patients (54.4%) survived with good neurological status. Poor outcome patients had higher median NSE values at hospital admission and at 24, 48 and 72 hours after ROSC. At 48 and 72 hours after ROSC, NSE predicted poor neurological outcome with areas under the receiver-operating characteristic curves of 0.85 (95%CI, 0.81-0.90) and 0.88 (95%CI, 0.83-0.93), respectively. In addition, delta NSE values between 72hours after ROSC and hospital admission predicted poor neurological outcome with an area under the receiver-operating characteristic curve of 0.90 (95%CI, 0.85-0.95) and was an independent predictor of unfavorable outcome on multivariate analysis (P <.001). CONCLUSIONS: In cardiac arrest survivors treated with targeted temperature management, delta NSE values between 72 hours after ROSC and hospital admission strongly predicted poor neurological outcome.

Long term clinical outcomes in survivors after out-of-hospital cardiac arrest.

INTRODUCTION AND OBJECTIVES: Information regarding long-term outcomes in patients surviving out-of-hospital cardiac arrest (OHCA) is scarce. Our aim was to study the long-term clinical outcomes of a large cohort of OHCA patients surviving until hospital discharge and to identify predictors of mortality and cardiovascular events. METHODS: Consecutive OHCA patients admitted in the Acute Cardiac Care Unit who survived at least until hospital discharge between 2007 and 2019 were included. All received therapeutic hypothermia according to the local protocol. Pre- and intra-hospital clinical and analytical variables were analyzed, as well as the clinically relevant events during follow-up. RESULTS: A total of 201 patients were included, with a mean age of 57.6 ± 14.2 years, 168 (83.6%) were male. Thirty-six (17.9%) died during a median follow-up of 40.3 months (18.9-69.1), the most frequent causes of death being cardiovascular and neurological, followed by cancer. We calculated a predictive model for mortality during follow-up using Cox regression that included the following variables: poor neurological outcome [HR 3.503 (1.578-7.777)], non-shockable rhythm [HR 2.926 (1.390-6.163)], time to onset of CPR [HR 1.063 (0.997-1.134)], older age [1.036 (1.008-1.064)) and worse ejection fraction at discharge [1.033 (1.009-1.058)]. CONCLUSIONS: Even though few patients experience recurrent cardiac arrest events, survivors after OHCA face high morbidity and mortality during long-term follow-up. Therefore, they may benefit from multidisciplinary teams providing an integral management and ensuring continuity of care.

Dataset regarding baseline and follow-up characteristics of out-of-hospital cardiac arrest patients focused on neurological outcomes.

This data article contains the data related to the research article entitled "Long-term neurological outcomes in out-of-hospital cardiac arrest patients treated with targeted-temperature management" (Caro-Codón et al., 2018). In this dataset, we report details regarding the flow chart of the included patients and the specific exclusion criteria. We also include information on the difference between the patients who attended the structured personal interview (and therefore were finally included in the study) and those who did not attend. Neuropsychiatric and functional data before and after cardiac arrest are also reported. Finally, we list all the "de novo" focal neurological deficits identified after cardiac arrest in the related population.

A multicentre randomized pilot trial on the effectiveness of different levels of cooling in comatose survivors of out-of-hospital cardiac arrest: the FROST-I trial.

PURPOSE: To obtain initial data on the effect of different levels of targeted temperature management (TTM) in out-of-hospital cardiac arrest (OHCA). METHODS: We designed a multicentre pilot trial with 1:1:1 randomization to either 32 °C (n = 52), 33 °C (n = 49) or 34 °C (n = 49), via endovascular cooling devices during a 24-h period in comatose survivors of witnessed OHCA and initial shockable rhythm. The primary endpoint was the percentage of subjects surviving with good neurologic outcome defined by a modified Rankin Scale (mRS) score of ≤ 3, blindly assessed at 90 days. RESULTS: At baseline, different proportions of patients who had received defibrillation administered by a bystander were assigned to groups of 32 °C (13.5%), 33 °C (34.7%) and 34 °C (28.6%; p = 0.03). The percentage of patients with an mRS ≤ 3 at 90 days (primary endpoint) was 65.3, 65.9 and 65.9% in patients assigned to 32, 33 and 34 °C, respectively, non-significant (NS). The multivariate Cox proportional hazards model identified two variables significantly related to the primary outcome: male gender and defibrillation by a bystander. Among the 43 patients who died before 90 days, 28 died following withdrawal of life-sustaining therapy, as follows: 7/16 (43.8%), 10/13 (76.9%) and 11/14 (78.6%) of patients assigned to 32, 33 and 34 °C, respectively (trend test p = 0.04). All levels of cooling were well tolerated. CONCLUSIONS: There were no statistically significant differences in neurological outcomes among the different levels of TTM. However, future research should explore the efficacy of TTM at 32 °C. CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov unique identifier: NCT02035839 ( http://clinicaltrials.gov ).

Long-term neurological outcomes in out-of-hospital cardiac arrest patients treated with targeted-temperature management.

BACKGROUND: This study aimed to assess long-term cognitive and functional outcomes in out-of-hospital cardiac arrest (OHCA) patients treated with targeted-temperature management, investigate the existence of prognostic factors that could be assessed during initial admission and evaluate the usefulness of classic neurological scales in this clinical scenario. METHODS: Patients admitted due to OHCA from August 2007 to November 2015 and surviving at least one year were included. Each patient completed a structured interview focused on the collection of clinical, social and demographic data. All available information in clinical records was reviewed and a battery of neurocognitive and psychometric tests was performed. RESULTS: Seventy-nine patients were finally included in the analysis. Forty-three patients (54.4%) scored below the usual cut-off points for the diagnosis of mild cognitive impairment, even though most of these deficits went unnoticed when patients were assessed using CPC and modified Rankin scale. Nineteen (24%) developed certain degree of impairment in their attention capacity and executive functions. A significant proportion developed new memory-related disorders (43%), depressive symptoms (17.7%), aggressive/uninhibited behavior (12.7%) and emotional lability (8.9%). A greater number of weekly hours of intellectual activity and a qualified job were independent protective factors for the development of cognitive impairment. However, being older at the time of the cardiac arrest was identified as a poor prognostic factor. CONCLUSIONS: There is a high prevalence of long-term cognitive deficits and functional limitations in OHCA survivors. Most commonly used clinical scales in clinical practice are crude and lack sensitivity to detect most of these deficits.

Influence of the temperature on the moment of awakening in patients treated with therapeutic hypothermia after cardiac arrest.

INTRODUCTION: Target temperature management (TTM) has shown to reduce brain damage after an out-of-hospital cardiac arrest (CA), but the time to neurological recovery is not defined yet. We sought to determine the time these patients need to regain consciousness, as well as factors associated with a late post-arrest awakening. METHODS: We performed a retrospective analysis of patients cooled to 32-34°C during 24h after CA, who regained neurological responsiveness after rewarming. We measured the time until awakening, defined as obedience to verbal commands. RESULTS: We included 163 CA survivors (84.7% male, 60.2 years) who regained consciousness after TTM: target temperature was either 32°C (36.2%), 33°C (56.4%) or 34°C (6.7%). Mean time of awakening was 3.8 days. Thirty-four patients (20.9%) regained neurological responsiveness after 5 days after CA. All of them had been cooled to either 32°C (18 patients) or 33°C (16), and no patient cooled to 34°C awakened after day 5. A lower target temperature was associated with a later awakening (p<0.001). The time to advanced cardiopulmonary resuscitation (CPR) was shorter among the early awakers (p=0.04), but we found no other predictors of an earlier awakening. CONCLUSIONS: A high proportion of CA survivors induced to TTM regained consciousness after 5 days, and cooling to a lower target temperature may influence on a late neurological recovery. Therefore, withdrawal of life supporting treatment should be delayed to more than 5 days in patients cooled to 33°C or less. Time to advanced CPR was found to be a predictor of early awakening.

Reasons for initiation of proton pump inhibitor therapy for hospitalised patients and its impact on outpatient prescription in primary care.

BACKGROUND: Proton-pump-inhibitors are often prescribed unnecessarily in hospitals, which in turn induces their prescriptions after discharge. OBJECTIVE: To evaluate patients starting treatment with proton-pump-inhibitors during hospitalisation and proportion of inappropriate prescriptions. Patient risk factors and whether initiation in hospital induced their continuation in ambulatory care were also analyzed. METHODS: An observational, cross-sectional study in a tertiary hospital (1350 beds) was carried out on the first Tuesday in February 2015. Pharmacists screened admitted patients treated with proton-pump-inhibitors using an electronic prescription program (FarmaTools®-5.0). They also checked patients' home medications before admission by accessing a primary care program (Horus®). Authorized indications according to Spanish-Medicines-Agency and those recommended in Spanish-Clinical-Practice-Guidelines were considered appropriate. Hospital-medical-records were checked to know whether proton-pump-inhibitors were prescribed at discharge. RESULTS: Three hundred seventy nine patients were analysed. Two hundred ninety four of them were prescribed proton-pump-inhibitors (77.6%). Treatment was initiated during admission for 143 patients (48.6%, 95% CI: 42.8-54.5). Of them, 91 (63.6%, 95% CI: 55.2-71.5) were inappropriate, mainly due to its inclusion unnecessarily in protocols associated with surgeries or diseases (56 cases of 91, 61.5%). Additional inappropriate indications were surgical stress ulcer prophylaxis for surgeries without bleeding risks (19.8%) and polypharmacy without drugs that increase the risk of bleeding (18.7%). Of 232 discharge reports assessed, in 153 (65.9%, 95% CI: 59.5-72), proton-pump-inhibitor continuation was recommended, of them, 51 (33.3%) were initiated at admission. CONCLUSION: In hospitalized patients there is a high prevalence of prescription of proton-pump-inhibitors unnecessarily. The superfluous use is often associated with the prescription of treatment protocols. Those treatments started in the hospital generally did not contribute to over-use existing primary care, most of them were removed at discharge.

Reasons for initiation of proton pump inhibitor therapy for hospitalised patients and its impact on outpatient prescription in primary care

BACKGROUND: Proton-pump-inhibitors are often prescribed unnecessarily in hospitals, which in turn induces their prescriptions after discharge. OBJECTIVE: To evaluate patients starting treatment with proton-pump-inhibitors during hospitalisation and proportion of inappropriate prescriptions. Patient risk factors and whether initiation in hospital induced their continuation in ambulatory care were also analyzed. METHODS: An observational, cross-sectional study in a tertiary hospital (1350 beds) was carried out on the first Tuesday in February 2015. Pharmacists screened admitted patients treated with proton-pump-inhibitors using an electronic prescription program (FarmaTools®-5.0). They also checked patients' home medications before admission by accessing a primary care program (Horus®). Authorized indications according to Spanish-Medicines-Agency and those recommended in Spanish-Clinical-Practice- Guidelines were considered appropriate. Hospital-medical-records were checked to know whether proton-pump-inhibitors were prescribed at discharge. RESULTS: Three hundred seventy nine patients were analysed. Two hundred ninety four of them were prescribed proton-pumpinhibitors (77.6%). Treatment was initiated during admission for 143 patients (48.6%, 95% CI: 42.8-54.5). Of them, 91 (63.6%, 95% CI: 55.2-71.5) were inappropriate, mainly due to its inclusion unnecessarily in protocols associated with surgeries or diseases (56 cases of 91, 61.5%). Additional inappropriate indications were surgical stress ulcer prophylaxis for surgeries without bleeding risks (19.8%) and polypharmacy without drugs that increase the risk of bleeding (18.7%). Of 232 discharge reports assessed, in 153 (65.9%, 95% CI: 59.5-72), proton-pump-inhibitor continuation was recommended, of them, 51 (33.3%) were initiated at admission. CONCLUSION: In hospitalized patients there is a high prevalence of prescription of proton-pump-inhibitors unnecessarily. The superfluous use is often associated with the prescription of treatment protocols. Those treatments started in the hospital generally did not contribute to over-use existing primary care, most of them were removed at discharge

Electrocardiographic changes during induced therapeutic hypothermia in comatose survivors after cardiac arrest.

AIM: To assess the safety of therapeutic hypothermia (TH) concerning arrhythmias we analyzed serial electrocardiograms (ECG) during TH. METHODS: All patients recovered from a cardiac arrest with Glasgow < 9 at admission were treated with induced mild TH to 32-34 °C. TH was obtained with cool fluid infusion or a specific intravascular device. Twelve-lead ECG before, during, and after TH, as well as ECG telemetry data was recorded in all patients. From a total of 54 patients admitted with cardiac arrest during the study period, 47 patients had the 3 ECG and telemetry data available. ECG analysis was blinded and performed with manual caliper by two independent cardiologists from blinded copies of original ECG, recorded at 25 mm/s and 10 mm/mV. Coronary care unit staff analyzed ECG telemetry for rhythm disturbances. Variables measured in ECG were rhythm, RR, PR, QT and corrected QT (QTc by Bazett formula, measured in lead v2) intervals, QRS duration, presence of Osborn's J wave and U wave, as well as ST segment displacement and T wave amplitude in leads II, v2 and v5. RESULTS: Heart rate went down an average of 19 bpm during hypothermia and increased again 16 bpm with rewarming (P < 0.0005, both). There was a non-significant prolongation of the PR interval during TH and a significant decrease with rewarming (P = 0.041). QRS duration significantly prolonged (P = 0.041) with TH and shortened back (P < 0.005) with rewarming. QTc interval presented a mean prolongation of 58 ms (P < 0.005) during TH and a significant shortening with rewarming of 22.2 ms (P = 0.017). Osborn or J wave was found in 21.3% of the patients. New arrhythmias occurred in 38.3% of the patients. Most frequent arrhythmia was non-sustained ventricular tachycardia (19.1%), followed by severe bradycardia or paced rhythm (10.6%), accelerated nodal rhythm (8.5%) and atrial fibrillation (6.4%). No life threatening arrhythmias (sustained ventricular tachycardia, polymorphic ventricular tachycardia or ventricular fibrillation) occurred during TH. CONCLUSION: A 38.3% of patients had cardiac arrhythmias during TH but without life-threatening arrhythmias. A concern may rise when inducing TH to patients with long QT syndrome.

Spectral analysis-based risk score enables early prediction of mortality and cerebral performance in patients undergoing therapeutic hypothermia for ventricular fibrillation and comatose status.

BACKGROUND: Early prognosis in comatose survivors after cardiac arrest due to ventricular fibrillation (VF) is unreliable, especially in patients undergoing mild hypothermia. We aimed at developing a reliable risk-score to enable early prediction of cerebral performance and survival. METHODS: Sixty-one out of 239 consecutive patients undergoing mild hypothermia after cardiac arrest, with eventual return of spontaneous circulation (ROSC), and comatose status on admission fulfilled the inclusion criteria. Background clinical variables, VF time and frequency domain fundamental variables were considered. The primary and secondary outcomes were a favorable neurological performance (FNP) during hospitalization and survival to hospital discharge, respectively. The predictive model was developed in a retrospective cohort (n = 32; September 2006-September 2011, 48.5 ± 10.5 months of follow-up) and further validated in a prospective cohort (n = 29; October 2011-July 2013, 5 ± 1.8 months of follow-up). RESULTS: FNP was present in 16 (50.0%) and 21 patients (72.4%) in the retrospective and prospective cohorts, respectively. Seventeen (53.1%) and 21 patients (72.4%), respectively, survived to hospital discharge. Both outcomes were significantly associated (p < 0.001). Retrospective multivariate analysis provided a prediction model (sensitivity = 0.94, specificity = 1) that included spectral dominant frequency, derived power density and peak ratios between high and low frequency bands, and the number of shocks delivered before ROSC. Validation on the prospective cohort showed sensitivity = 0.88 and specificity = 0.91. A model-derived risk-score properly predicted 93% of FNP. Testing the model on follow-up showed a c-statistic ≥ 0.89. CONCLUSIONS: A spectral analysis-based model reliably correlates time-dependent VF spectral changes with acute cerebral injury in comatose survivors undergoing mild hypothermia after cardiac arrest.

Prolongación del intervalo QT inducido por fármacos: ¿conocemos sus riesgos? / Drug-induced QT interval prolongation: Do we know the risks?

La muerte súbita cardiaca es una causa importante de mortalidad en los países desarrollados. La mayoría de ellas derivan de arritmias ventriculares agudas que, en algunas ocasiones, se producen como consecuencia de la prolongación del intervalo QT. Un importante factor de riesgo para esta alteración es el uso de fármacos que prolongan este intervalo. De hecho, en los últimos años, uno de los motivos más frecuentes de retirada del mercado de medicamentos o de restricciones de uso ha sido la prolongación del intervalo QT, e implica tanto fármacos cardiovasculares como no cardiovasculares. Dada la gravedad que puede conllevar la aparición de un suceso por esta causa, es importante que los clínicos conozcan los riegos del uso de estos fármacos en determinados pacientes. En esta revisión analizamos los fármacos que prolongan el intervalo QT, los factores de riesgo que pueden influir y las combinaciones de fármacos que pueden agravar esta situación (AU)

Sudden cardiac death is an important cause of mortality in developed countries, most of them being consequence of acute ventricular arrhythmias. These arrhythmias, in some cases, owe to QT interval prolongation. A major risk factor for this condition is the use of drugs that prolong the QT interval. In fact, in recent years, one of the most common reasons for drug withdrawal or usage restrictions has been drug induced QT interval prolongation that involves both cardiovascular and non-cardiovascular drugs. Taking into account the severity that the occurrence of such an event may have, it is important for clinicians to know the risks of these drugs in certain patients. In this review we analyze the drugs that prolong the QT interval, the risk factors that can enhance QT prolongation and the drug interactions that can increase these risks (AU)

[Drug-induced QT interval prolongation: do we know the risks?]. / Prolongación del intervalo QT inducido por fármacos: ¿conocemos sus riesgos?

Sudden cardiac death is an important cause of mortality in developed countries, most of them being consequence of acute ventricular arrhythmias. These arrhythmias, in some cases, owe to QT interval prolongation. A major risk factor for this condition is the use of drugs that prolong the QT interval. In fact, in recent years, one of the most common reasons for drug withdrawal or usage restrictions has been drug induced QT interval prolongation that involves both cardiovascular and non-cardiovascular drugs. Taking into account the severity that the occurrence of such an event may have, it is important for clinicians to know the risks of these drugs in certain patients. In this review we analyze the drugs that prolong the QT interval, the risk factors that can enhance QT prolongation and the drug interactions that can increase these risks.

Computerized physician order entry in the cardiac intensive care unit: effects on prescription errors and workflow conditions.

PURPOSES: To evaluate the effects of a computerized physician order entry (CPOE) system in the cardiac intensive care unit by detecting prescription errors (PEs) and also to assess the impact on working conditions. METHODS: A longitudinal, prospective, before-after study was conducted during the periods before and after the implementation of the CPOE system. Clinical pharmacists were responsible for the registration, description and classification of PEs, and their causes and severity, according to an international taxonomy. Professionals were also surveyed for their opinion, concerns, and level of satisfaction. RESULTS: A total of 470 treatment orders containing 5729 prescriptions were evaluated. The CPOE resulted in a marked reduction in the number of PEs: error rate was 44.8% (819 errors among 1829 prescriptions) with handwritten orders and 0.8% (16 among 2094 prescriptions) at the final electronic phase (P < .001). Lapses were the main cause of error in both prescription methods. Most errors did not reach the patients. Errors related with the computerized system were scarce. Most users were satisfied with many aspects of this technology, although a higher workload was reported. CONCLUSIONS: Computerized physician order entry in the cardiac intensive care unit proved to be a safe and effective strategy in reducing PEs and was globally well received by professionals.

Atrial arrhythmias in obstructive sleep apnea: underlying mechanisms and implications in the clinical setting.

Obstructive sleep apnea (OSA) is a common disorder characterized by repetitive interruption of ventilation during sleep caused by recurrent upper airway collapse, which leads to intermittent hypoxia. The disorder is commonly undiagnosed despite its relationship with substantial cardiovascular morbidity and mortality. Moreover, the effects of the disorder appear to be particularly dangerous in young subjects. In the last decade, substantial clinical evidence has identified OSA as independent risk factor for both bradyarrhythmias and tachyarrhythmias. To date the mechanisms leading to such arrhythmias have not been completely understood. However, recent data from animal models and new molecular analyses have increased our knowledge of the field, which might lead to future improvement in current therapeutic strategies mainly based on continuous positive airway pressure. This paper aims at providing readers a brief and specific revision of current knowledge about the mechanisms underlying atrial arrhythmias in OSA and their clinical and therapeutic implications.

Potential medication errors associated with computer prescriber order entry.

INTRODUCTION: To assess the frequency of medication errors (ME) induced or enhanced by computerized physician order entry (CPOE). Error type, drug classes involved, specialty, patient outcome and system failures were also evaluated. METHODS: Observational quantitative study in a large tertiary care medical center over March 2012 3 years after CPOE implementation. Pharmacists detected ME associated with CPOE (those that wouldn't have occurred if the clinician had prescribed manually) and unassociated in pharmacological treatments in inpatients of 13 specialties (421 beds). Main outcome measured were ME associated and unassociated with CPOE. RESULTS: We found 714 ME with 85.857 drug prescriptions (a 0.8 % error rate, 95 % CI 0.6-0.7). Percentage of error associated with CPOE was 77.7 %. The main types of error related to CPOE were wrong medication selection (20.9 %) and improper data placement (20.3 %). Failures with medications prescribed in primary care, unavailable in the hospital pharmacy, were involved in 21.6 % of all ME. Errors involving surgical specialties were double those involving medical specialties (1.2 vs. 0.6 %). Most ME associated with CPOE were potential errors (90 %). During the study system failures occurred four times. CONCLUSIONS: The use of CPOE minimises the occurrence of medication errors, however, they still occur. Most errors are associated with the CPOE technology. We therefore face a new challenge in the prevention of ME that require a change in strategy for patient safety. Continued training of prescribers, standardization of the electronic prescription programs and integration between computer applications in hospitals and with primary care should be a priority.

CPAP effect on recurrent episodes in patients with sleep apnea and myocardial infarction.

BACKGROUND: Obstructive sleep apnea (OSA) is linked to increased cardiovascular risk, but the association between OSA and myocardial infarction (MI) remains controversial. Our objectives were to compare the frequency of OSA in patients with acute MI and in a population-based sample of control subjects, and to evaluate the impact of CPAP on recurrent MI and coronary revascularization. METHODS: Case-control study with a 6-year follow-up of the case cohort. 192 acute MI patients and 96 matched control subjects without coronary artery disease (CAD) (ratio 2:1). After overnight polysomnography, CPAP was recommended if apnea-hypopnea index (AHI) ≥ 5, and a mean daily use >3.5h/day was considered necessary to maintain the treatment. Lipids, fasting glucose, blood pressure, spirometry, comorbidity and current treatment were also registered. End-points were recurrent MI or need of revascularization. RESULTS: OSA was an independent predictor of MI, with odds ratio 4.9 (95% confidence interval [CI] 2.9-8.3, p=0.017). 63 MI patients without OSA, 52 untreated patients with OSA and 71 OSA patients treated with CPAP were included in the follow-up study. After adjustment for confounding factors, treated OSA patients had a lower risk of recurrent MI (adjusted hazard ratio 0.16 [95%CI 0.03-0.76, p=0.021]) and revascularization (adjusted hazard ratio 0.15 [95%CI 0.03-0.79, p=0.025]) than untreated OSA patients, and similar to non-OSA patients. CONCLUSION: Mild-severe OSA is an independent risk factor for MI. Risk of recurrent MI and revascularization was lower in OSA patients who tolerated CPAP.