Punto de corte óptimo del antígeno carbohidrato 125 para la identificación de pacientes con bajo riesgo tras un ingreso por insuficiencia cardiaca aguda / Optimal carbohydrate antigen 125 cutpoint for identifying low-risk patients after admission for acute heart failure

Introducción y objetivos: El antígeno carbohidrato 125 (CA125) se ha mostrado útil para la estratificación del riesgo de los pacientes ingresados por insuficiencia cardiaca aguda (ICA). Se intenta determinar un punto de corte para identificar a los pacientes con bajo riesgo de muerte y muerte/reingreso por insuficiencia cardiaca 1 mes tras el ingreso por ICA. Métodos: La cohorte de derivación incluyó a 3.231 pacientes con ICA consecutivos. Se identificaron valores de corte de CA125 con un valor predictivo negativo (VPN) del 90% y una sensibilidad de hasta el 85%. La idoneidad de estos puntos de corte y el riesgo de muerte/reingreso al mes se evaluaron mediante el método de Royston-Parmar. Se seleccionó el mejor punto de corte y se validó en una cohorte del BIOSTAT-CHF (n=1.583). Resultados: En la cohorte de derivación, la mediana [intervalo intercuartílico] de CA125 fue 57 [25,3-157] U/ml. El punto de corte óptimo fue <23 U/ml (el 21,5% de los pacientes), con VPN de muerte y del objetivo compuesto del 99,3 y el 94,1% respectivamente. En los análisis multivariables, el CA125 <23 U/ml se asoció con un menores riesgos de muerte (HR=0,20; IC95%, 0,08-0,50; p <0,001) y del objetivo combinado (HR=0,63; IC95%, 950,45-0,90; p=0,009). Su capacidad para discriminar a los pacientes con riesgo bajo a 1 mes se confirmó en la cohorte de validación (VPN de muerte y del objetivo compuesto, el 98,6 y el 96,6%). La capacidad predictiva seguía siendo significativa a los 6 meses de seguimiento. Conclusiones: En pacientes ingresados por ICA, el CA125 <23 U/ml identificó un subgrupo de pacientes con bajo riesgo de eventos clínicos adversos a corto plazo que pueden no requerir un seguimiento estrecho (AU)

Introduction and objectives: Carbohydrate antigen 125 (CA125) has been shown to be useful for risk stratification in patients admitted with acute heart failure (AHF). We sought to determine a CA125 cutpoint for identifying patients at low risk of 1-month death or the composite of death/HF readmission following admission for AHF. Methods: The derivation cohort included 3231 consecutive patients with AHF. CA125 cutoff values with 90% negative predictive value (NPV) and sensitivity up to 85% were identified. The adequacy of these cutpoints and the risk of 1-month death/HF readmission was then tested using the Royston-Parmar method. The best cutpoint was selected and externally validated in a cohort of patients hospitalized from BIOSTAT-CHF (n=1583). Results: In the derivation cohort, the median [IQR] CA125 was 57 [25.3-157] U/mL. The optimal cutoff value was <23 U/mL (21.5% of patients), with NPVs of 99.3% and 94.1% for death and the composite endpoint, respectively. On multivariate survival analyses, CA125 <23 U/mL was independently associated with a lower risk of death (HR, 0.20; 95%CI, 0.08-0.50; P <.001), and the combined endpoint (HR, 0.63; 95%CI, 950.45-0.90; P=.009). The ability of this cutpoint to discriminate patients at a low 1-month risk was confirmed in the validation cohort (NPVs of 98.6% and 96.6% for death and the composite endpoint). The predicted ability of this cutoff remained significant at 6 months of follow-up. Conclusions: In patients admitted with AHF, CA125 <23 U/mL identified a subgroup at low risk of short-term adverse events, a population that may not require intense postdischarge monitoring (AU)

Insuficiencia cardiaca en el seno de un síndrome coronario agudo como predictor de infarto a largo plazo / Acute coronary syndrome complicated by heart failure as predictor of long-term infarction

Antecedentes. La insuficiencia cardiaca (Killip>I) en pacientes con síndrome coronario agudo (SCA) es un reconocido factor de riesgo para mortalidad; sin embargo, su relación con la aparición de nuevos episodios isquémicos agudos no ha sido bien establecida. Objetivo. El objetivo del presente trabajo fue evaluar la asociación entre Killip>I al ingreso y la aparición de infarto agudo de miocardio (IAM) tras el alta hospitalaria por SCA. Pacientes y métodos. Se estudió de forma prospectiva y consecutiva 972 y 426 supervivientes a un SCA sin elevación del segmento ST (SCASEST) e IAM con elevación del segmento ST (IAMCEST) respectivamente. Se determinó la presencia de Killip>I en el momento del ingreso junto con variables pronósticas clásicas. La asociación entre Killip>I e IAM se determinó mediante regresión de Cox adaptada para episodios competitivos. Resultados. Durante una mediana de seguimiento de 3 años, 135 (13,9%) y 53 (12,4%) pacientes con SCASEST y IAMCEST presentaron un IAM. Los pacientes con SCASEST y IAMCEST con Killip>I (15,6 y 21,3% respectivamente) presentaron más frecuentemente IAM (28,3 vs 6,3 y 10,6 vs 3,3 por 100 pacientes-año seguimiento, p<0 001 respectivamente el análisis multivariante ajustado por factores de riesgo y controlado episodios competitivos muerte revascularización confirmó que scasest iamcest killip I mostraron un incremento en el riesgo de IAM (HR=1,76; IC 95%: 1,15-2,68; p<0 009 y hr="1,90;" ic 95 : 1 07-3 36 p="0,029" respectivamente. Conclusiones. En pacientes con SCASEST y IAMCEST, la presencia de Killip>I al ingreso se asocia de manera independiente con mayor riego de IAM en el seguimiento(AU)

Background. Heart failure (Killip>I) in patients with acute coronary syndrome (ACS) is a recognized risk factor for death. However, its relationship with the risk of new acute ischemic events has not been well established. Objective. The aim of this study has been to evaluate the association between Killip>I on admission and the risk of a new acute myocardial infarction (AMI) during follow-up due to ACS. Patients and methods. A total of 972 and 426 survivors of an ACS with non-ST segment evaluation (Non-STE-ACS) and AMI with ST segment elevation (STEMI) were studied prospectively and consecutively. The presence of Killip>I was determined on admission together with the classical prognostic variables. The relationship between Killip>I and subsequent post-discharge AMI was established with the Cox regression adapted for competitive events. Results. During a median follow-up of 3 years, 135 (13.9%) and 53 (12.4%) patients with Non-STE-ACS and STEMI presented a new AMI. Patients with Non-STE-ACS and STEMI with Killip>I (15.6% and 21.3% respectively) showed a higher incidence of AMI (28.3 vs 6.3 and 10.6 vs 3.3 per 100 patients-years of follow-up, p<0 001 respectively in the multivariate analysis adjusted for traditional risk factors and controlled competitive events death revascularization confirmed that killip I subjects with Non-STE-ACS and STEMI showed a significantly higher risk of AMI (HR: 1.76; CI 95%: 1.15-2.68; p=0.009 and HR: 1.90; 95% CI: 1.07-3.36; p=0.029 respectively). Conclusions. In patients with Non-STE-ACS and STEMI, the presence of Killip>I on admission is independently associated to an increased risk of long-term AMI(AU)

Relación entre el volumen espiratorio máximo en un segundo, el índice BODE y la calidad de vida percibida por el paciente de enfermedad pulmonar obstructiva crónica / Relation between maximum expiratory volume in one section, BODE index and quality of life perceived by the chronic obstructive pulmonary disease patient

Objetivo: Evaluar la correlación existente entre la calidad de vida percibida por los pacientes y dos parámetros objetivos de gravedad: a) la gravedad de la obstrucción por el volumen espiratorio máximo en el primer segundo (FEV1), y b) el índice BODE (Body Mass Index, Airflow Obstruction, Dyspnea and Exercice Capacity). Material y métodos: Estudio observacional descriptivo de corte transversal, realizado en 40 pacientes diagnosticados de la enfermedad pulmonar obstructiva crónica (EPOC) y clasificados según la escala GOLD (Global initiative for chronic obstructive lung disease) en moderados o graves, a los que se entrevistó mediante el cuestionario respiratorio de St. George (SGRQ). Se calculó el índice BODE, previa medición de los parámetros que lo componen. También se recogieron datos antropométricos y demográficos de los pacientes. Resultados: De los 40 pacientes del estudio, 38 eran varones (95%), con una edad media ± desviación estándar (DE) de 76,15 ± 5,82 años. Las medias ± DE obtenidas en referencia a la variable subjetiva del cuestionario SGRQ fueron de 33,58 ± 18,14. En referencia a los datos conseguidos de las variables objetivas, obtuvimos del FEV1 una media ± DE de 49,05 ± 15,731, y del índice BODE de 2,33 ± 1,8 y de sus parámetros integrantes: test de los 6 minutos, 440 ± 87,9; escala Medical Research Council, 1,4 ± 0,6; índice de masa corporal, 28,16 ± 4,4. Según los valores obtenidos observamos la existencia de correlación entre SGRQ y el índice BODE, al igual que entre la actividad, como subescala de la SGRQ y el índice BODE. Conclusiones: El resultado del índice BODE se correlaciona débilmente con los resultados de la SGRQ de forma conjunta, por lo que un elevado índice BODE afecta negativamente a la calidad de vida de los pacientes con EPOC moderados o graves (AU)

Objective: To measure the correlation between perceived quality of life and two objective severity parameters: forced expiratory volume in one second (FEV1) and body mass, airflow obstruction, dyspnea and exercise capacity (BODE) index. Material and methods: Observational descriptive cross-sectional study involving 40 Chronic Obstruction Pulmonary Disease (COPD) patients. They were classified using the Global Initiative for Chronic Obstructive Lung Disease (GOLD) classification system into moderate or severe. The Saint George Respiratory Questionnaire (SGRQ) was carried out by interview and the BODE value was analyzed after measurement of the parameters included in it. Anthropometry and demography data were also collected. Results: A study including 40 patients, 38 of them men 38 (95%), with mean age 76.15 ± 5.82 was performed. The means obtained for the subjective variable of the SGRQ was 33.58 ± 18.14. Regarding the data obtained for the objective variables, the FEV1 had a mean of 49.05 ± 15.731, and the BODE index showed 2.33 ± 1.8. The parameters making it up were: 6-minute exercise test 440 ± 87.9, mean MRC score: 1.4 ± 0.6, and body mass index (BMI) 28.16 ± 4.4. According to the values obtained, we observed the existence of a correlation between SGRO and the BODE index and between the activity, and subscale of the SGRO and BODE index. Conclusions: The BODE index are weakly correlative with the results of the SGRO combined. High index BODE negatively affects the perceived quality of life of moderate/severe COPD patients (AU)

[Acute coronary syndrome complicated by heart failure as predictor of long-term infarction]. / Insuficiencia cardiaca en el seno de un síndrome coronario agudo como predictor de infarto a largo plazo.

BACKGROUND: Heart failure (Killip>I) in patients with acute coronary syndrome (ACS) is a recognized risk factor for death. However, its relationship with the risk of new acute ischemic events has not been well established. OBJECTIVE: The aim of this study has been to evaluate the association between Killip>I on admission and the risk of a new acute myocardial infarction (AMI) during follow-up due to ACS. PATIENTS AND METHODS: A total of 972 and 426 survivors of an ACS with non-ST segment evaluation (Non-STE-ACS) and AMI with ST segment elevation (STEMI) were studied prospectively and consecutively. The presence of Killip>I was determined on admission together with the classical prognostic variables. The relationship between Killip>I and subsequent post-discharge AMI was established with the Cox regression adapted for competitive events. RESULTS: During a median follow-up of 3 years, 135 (13.9%) and 53 (12.4%) patients with Non-STE-ACS and STEMI presented a new AMI. Patients with Non-STE-ACS and STEMI with Killip>I (15.6% and 21.3% respectively) showed a higher incidence of AMI (28.3 vs 6.3 and 10.6 vs 3.3 per 100 patients-years of follow-up, p<0.001, respectively). In the multivariate analysis, adjusted for traditional risk factors and controlled for competitive events (death and revascularization), confirmed that Killip>I subjects with Non-STE-ACS and STEMI showed a significantly higher risk of AMI (HR: 1.76; CI 95%: 1.15-2.68; p=0.009 and HR: 1.90; 95% CI: 1.07-3.36; p=0.029 respectively). CONCLUSIONS: In patients with Non-STE-ACS and STEMI, the presence of Killip>I on admission is independently associated to an increased risk of long-term AMI.

Microvascular perfusion 1 week and 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging.

OBJECTIVE: To characterise the evolution of myocardial perfusion during the first 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging (CMR) and determine its significance. DESIGN: Prospective cohort design. SETTING: Single-centre study in a teaching hospital in Spain. PATIENTS: 40 patients with a first ST-elevation myocardial infarction, single-vessel disease and thrombolysis in myocardial infarction (TIMI) grade 3 flow (stent in 33 patients) underwent rest and low-dose dobutamine CMR 7 (SD 1) and 184 (SD 11) days after infarction. Microvascular perfusion was assessed at rest by visual assessment and quantitative analysis of first-pass perfusion CMR. Of the 640 segments, 290 segments subtended by the infarct-related artery (IRA) were focused on. RESULTS: Both 1 week and 6 months after infarction, segments with normal perfusion showed more wall thickening, contractile reserve and wall thickness, and less transmural necrosis, p <0.05 in all cases. Of 76 hypoperfused segments at the first week, 47 (62%) normalised perfusion at the sixth month. However, 42 segments (14% of the whole group) showed chronic abnormal perfusion; these segments showed worse CMR indices in the late phase (p<0.05 in all cases). CONCLUSIONS: In patients with an open IRA, more than half of the segments with abnormal perfusion at the first week are normally perfused after six months. First-pass perfusion CMR shows that in a small percentage of segments, abnormal perfusion may become a chronic phenomenon-these areas have a more severe deterioration of systolic function, wall thickness, contractile reserve and the transmural extent of necrosis.

Calcium inhibits colon carcinogenesis in an experimental model in the rat.

Different dietary factors can affect colorectal cancer incidence. However, the effect of increased levels of dietary calcium on neoplasms is unclear. The present study was designed to examine the effect of a low calcium supplement on experimental colon carcinogenesis induced by parenteral administration of dimethylhydrazine (DMH). One hundred and twenty 10-week-old Sprague-Dawley rats were divided into five groups of equal sex distribution. The 10 rats in group A (control group) received no treatment; the 30 rats in group B (DMH group) were injected subcutaneously with 18 weekly doses of 21 mg/kg DMH; the 20 rats in group C (EDTA control group) received EDTA solution only; the 30 rats in group D (calcium group) received calcium at 3.2 g/l by adding calcium lactate to the drinking water from the start until the conclusion of the experiment; and the 30 rats in group E (DMH + calcium group) received oral calcium supplements at the same dose as the rats in group D (calcium group) and the same DMH injections as the rats in group B (DMH group). The rats were sacrificed at 25-34 weeks. In group E, we observed a significant diminution in the number of tumours (P = 0.01); an increase in the number of tumour-free animals (P = 0.006); a change in tumour location towards the distal colon (P < 0.025); more adenomas (P = 0.02); and a diminution of adenocarcinomas and mucinous carcinomas, although this was not significant. We conclude that a low dietary calcium supplement in rats inhibits colon cancer carcinogenesis induced by DMH, and changes tumour location towards the distal colon.