Identification of the culprit artery in inferior myocardial infarction through the 12-lead ECG.

BACKGROUND: Identification of the culprit artery can be helpful in the management of inferior infarction with ST-segment elevation myocardial infarction. Some studies suggest that previously published algorithms intended to help identify the infarct-related artery are suboptimal. Our aim is to develop a better method to localise the culprit artery on the basis of the 12-lead ECG. PATIENTS AND METHODS: We analysed the ECG and coronary angiograms of two different cohorts of patients with inferior ST-segment elevation myocardial infarction. Patients from the first cohort were labelled the derivative cohort (group A), whereas patients in the second cohort were labelled the validation cohort (group B). ST-segment elevation was measured in each lead, and a multiple logistic regression analysis was carried out to determine the best equation to predict the culprit artery. A derived algorithm was then applied to the validation cohort. Next, our algorithm was applied to the total cohort of both groups and compared with four different previously published algorithms. We analysed differences in sensitivity, specificity and area under the curve (AUC). RESULTS: We included 252 patients in the derivative group and 90 in the validation group. The multiple models analysis concluded that the best model should include five leads. This model was validated by internal bootstrapping with 1000 repetitions in group A and externally in group B. The resultant algorithm was as follows: (ST-elevation in III + aVF + V3) - (ST-elevation in II + V6) less than 0.75 mm means that the culprit artery is the left circumflex artery (Cx). If the result is at least 0.75, the culprit artery is the right coronary artery. The total group of both cohorts comprised 342 patients, aged 61.2 ± 12.4 years, of whom 19.6% were female and 80.4% were male. The Cx was the culprit artery in 67 (19.6%) patients. Our algorithm had a sensitivity of 72.3, a specificity of 80.9 and an AUC of 0.766. The AUC value was better compared with the other algorithms. CONCLUSION: The best algorithm to localise the culprit artery includes ST-elevation in leads II and V6 related to Cx, and ST-elevation in leads III, aVF and V3 related to right coronary artery. Our algorithm has been validated internally and externally, and works better than other previously published algorithms.

Elevation of ST-segment in aVR is predictive of cardiogenic shock but not of multivessel disease in inferior myocardial infarction.

INTRODUCTION: Some studies suggest that ST elevation in aVR (aVR-STE) can predict the presence of left main or multivessel disease (MVD) and relates to prognosis. Our purpose was to analyze the relationship of aVR-STE to MVD disease or cardiogenic shock (CS) in patients with inferior myocardial infarction (inferior STEMI). METHODS: We analyzed two cohorts of consecutive patients admitted for inferior STEMI in the Coronary Unit of two university hospitals. ST elevation and ST depression in each derivation were compared between patients with and without MVD and with and without CS. RESULTS: We included 342 patients-19.6% women and 80.4% men-with a median age of 60 (52, 70); 18 patients (5.2%) had MVD, and 25 (7.3%) patients presented CS. There was no relationship between ST elevation or ST depression in either derivation and MVD. In contrast, CS was associated with aVR-STE, ST-segment depression in lead aVL, and the sum of ST-segment depression. aVR-STE of 0.25 mm had a sensitivity of 24.0% and a specificity of 95.9% for CS. After multivariate analysis including clinical variables, aVR-STE was independently associated with CS. CONCLUSIONS: In patients with inferior STEMI, ST-segment analysis was not useful in predicting multivessel disease. aVR-STE was an independent predictor of CS, with high specificity but low sensitivity.

Localization of the culprit artery in inferior myocardial infarction: Influence of the point of measurement of ST segment.

BACKGROUND: There are several approaches widely used in the localization of the responsible artery in inferior myocardial infarction. However, the existing papers show differences in the point where the ST segment is measured. The purpose of our investigation is to analyse the influence of the point at which elevation of the ST segment is measured on the results of these algorithms. METHODS: We analysed the 12­lead electrocardiograms of 90 consecutive patients with inferior myocardial infarction. The ST segment elevation or depression was measured at the J-point and at 80 ms, and three algorithms were applied to predict the culprit artery with both measurements. Sensitivity, specificity, the area under the curve, and the kappa index of agreement were analysed to compare each algorithm at the J-point and at 80 ms. RESULTS: The area under the curve was better at the J-point than at 80 ms in two algorithms (0.696 vs. 0.635, p < 0.043, and 0.754 vs. 0.661, p < 0.045) and did not change in one. Agreement between the J-point and 80 ms was suboptimal in all three algorithms (0.71, 0.65, and 0.58). CONCLUSIONS: The result of different algorithms to detect the culprit artery in inferior STEMI patients can change significantly depending on the point where ST elevation or depression is measured.

Síndrome coronario agudo en nonagenarios: evolución clínica y validación de las principales escalas de riesgo / Acute coronary syndrome in nonagenarians: clinical evolution and validation of the main risk scores

Introducción. Existen escalas de riesgo que estiman adecuadamente la probabilidad de muerte en la fase aguda y el seguimiento de los pacientes con síndrome coronario agudo (SCA) como el GRACE, TIMI y ZWOLLE. El objetivo de nuestro estudio, además de determinar el pronóstico, fue valorar la validez de estas escalas en los nonagenarios ingresados en la unidad coronaria de nuestro centro. Material y métodos . Análisis de todos los nonagenarios con SCA ingresados entre abril de 2003 y 2011 en una unidad coronaria. El estado vital se determinó a los 14, 30 días y 6 meses del episodio agudo y en el momento del seguimiento. Evaluamos dichas puntuaciones por medio del área bajo la curva ROC (ABC). Resultados . Se incluyeron 45 pacientes con SCA, 26 (57,8%) con elevación del ST y 19 (42,2%) sin elevación. El ABC para GRACE en mortalidad intrahospitalaria fue excelente: 0,91 (IC 95%: 0,82-1; p < 0,001). El GRACE para el episodio combinado de mortalidad o reinfarto intrahospitalario fue 0,83 (IC 95%: 0,66-1; p < 0,01). El ABC del GRACE respecto a la mortalidad a los 6 meses fue 0,34 (IC 95%: 0,09-0,58; p = 0,45), y para el objetivo combinado de mortalidad o reinfarto 0,51 (IC 95%: 0,26-0,77; p = 0,95). El ABC para la escalas TIMI y ZWOLLE no alcanzó significación estadística. Conclusiones. Parece útil aplicar el instrumento GRACE para estimar el riesgo y la supervivencia de nonagenarios en la fase aguda de un SCA. Estos datos nos podrían ayudar para tomar las decisiones terapéuticas más adecuadas, invasivas o conservadoras (AU)

Introduction: Several risk scores regarding the probability of death/complications in the acute setting and during the follow-up of patients admitted with acute coronary syndromes (ACS) have been published, such as the GRACE, TIMI and ZWOLLE risk score. Our objective was to assess the prognosis of nonagenarians admitted to a coronary care unit with an ACS, as well as the usefulness of each of these scores. Material and methods: A retrospective analysis was performed on nonagenarians with an ACS admitted between 2003 and 2011. Vital status was determined at 14, 30 days, and 6 months after the ACS, and later during the follow-up. The risk scores were evaluated by area under the curve ROC (AUC). Results: A total of 45 patients with an ACS, 26 (57.8%) with ST-segment elevation and 19 (42.2%) with non-ST elevation. The GRACE- AUC for in-hospital mortality was excellent, 0.91, (95% CI: 0.82-1; P<.001), and for the combined event (in-hospital mortality and re-infarction) was 0.83 (95% CI: 0.66-1.0; P<.01). However, the GRACE-AUC at 6 months for mortality was 0.34 (95% CI: 0.09-0.58; P=.45), and for the combined event it was 0.51 (95% CI: 0.26-0.77; P=.95). The TIMI-AUC and ZWOLLE-AUC did not reach statistical significance. Conclusions: It is useful calculate the GRACE risk score in order to estimate risk and survival in the acute phase of ACS in nonagenarians. This can help appropriate in making invasive or conservative treatment decisions (AU)

[Acute coronary syndrome in nonagenarians: clinical evolution and validation of the main risk scores]. / Síndrome coronario agudo en nonagenarios: evolución clínica y validación de las principales escalas de riesgo.

INTRODUCTION: Several risk scores regarding the probability of death/complications in the acute setting and during the follow-up of patients admitted with acute coronary syndromes (ACS) have been published, such as the GRACE, TIMI and ZWOLLE risk score. Our objective was to assess the prognosis of nonagenarians admitted to a coronary care unit with an ACS, as well as the usefulness of each of these scores. MATERIAL AND METHODS: A retrospective analysis was performed on nonagenarians with an ACS admitted between 2003 and 2011. Vital status was determined at 14, 30 days, and 6 months after the ACS, and later during the follow-up. The risk scores were evaluated by area under the curve ROC (AUC). RESULTS: A total of 45 patients with an ACS, 26 (57.8%) with ST-segment elevation and 19 (42.2%) with non-ST elevation. The GRACE- AUC for in-hospital mortality was excellent, 0.91, (95% CI: 0.82-1; P<.001), and for the combined event (in-hospital mortality and re-infarction) was 0.83 (95% CI: 0.66-1.0; P<.01). However, the GRACE-AUC at 6 months for mortality was 0.34 (95% CI: 0.09-0.58; P=.45), and for the combined event it was 0.51 (95% CI: 0.26-0.77; P=.95). The TIMI-AUC and ZWOLLE-AUC did not reach statistical significance. CONCLUSIONS: It is useful calculate the GRACE risk score in order to estimate risk and survival in the acute phase of ACS in nonagenarians. This can help appropriate in making invasive or conservative treatment decisions.

Effect of early metoprolol on infarct size in ST-segment-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention: the Effect of Metoprolol in Cardioprotection During an Acute Myocardial Infarction (METOCARD-CNIC) trial.

BACKGROUND: The effect of ß-blockers on infarct size when used in conjunction with primary percutaneous coronary intervention is unknown. We hypothesize that metoprolol reduces infarct size when administered early (intravenously before reperfusion). METHODS AND RESULTS: Patients with Killip class II or less anterior ST-segment-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention within 6 hours of symptoms onset were randomized to receive intravenous metoprolol (n=131) or not (control, n=139) before reperfusion. All patients without contraindications received oral metoprolol within 24 hours. The predefined primary end point was infarct size on magnetic resonance imaging performed 5 to 7 days after STEMI. Magnetic resonance imaging was performed in 220 patients (81%). Mean ± SD infarct size by magnetic resonance imaging was smaller after intravenous metoprolol compared with control (25.6 ± 15.3 versus 32.0 ± 22.2 g; adjusted difference, -6.52; 95% confidence interval, -11.39 to -1.78; P=0.012). In patients with pre-percutaneous coronary intervention Thrombolysis in Myocardial Infarction grade 0 to 1 flow, the adjusted treatment difference in infarct size was -8.13 (95% confidence interval, -13.10 to -3.16; P=0.0024). Infarct size estimated by peak and area under the curve creatine kinase release was measured in all study populations and was significantly reduced by intravenous metoprolol. Left ventricular ejection fraction was higher in the intravenous metoprolol group (adjusted difference, 2.67%; 95% confidence interval, 0.09-5.21; P=0.045). The composite of death, malignant ventricular arrhythmia, cardiogenic shock, atrioventricular block, and reinfarction at 24 hours in the intravenous metoprolol and control groups was 7.1% and 12.3%, respectively (P=0.21). CONCLUSIONS: In patients with anterior Killip class II or less ST-segment-elevation myocardial infarction undergoing primary percutaneous coronary intervention, early intravenous metoprolol before reperfusion reduced infarct size and increased left ventricular ejection fraction with no excess of adverse events during the first 24 hours after STEMI. CLINICAL TRIAL REGISTRATION URL: http://www.clinicaltrials.gov. Unique identifier: NCT01311700. EUDRACT number: 2010-019939-35.

Síndrome de tako-tsubo e insuficiencia cardiaca: seguimiento a largo plazo / Tako-tsubo syndrome and heart failure: long-term follow-up

Introducción y objetivos. El síndrome de tako-tsubo induce un grado variable de disfunción ventricular izquierda transitoria. Nuestro objetivo es determinar su pronóstico a corto y largo plazo y valorar la incidencia de insuficiencia cardiaca en este ámbito, los factores de riesgo relacionados con su desarrollo y su influencia en la evolución posterior en nuestro medio. Métodos. Se recogieron prospectivamente las características clínicas y los eventos durante el ingreso hospitalario y durante el seguimiento de 100 pacientes con síndrome de tako-tsubo. Se llevó a cabo un análisis estratificado en relación con el desarrollo de insuficiencia cardiaca (Killip ≥ II) durante el ingreso índice. Resultados. El 89% eran mujeres (media de edad, 68 años); 70 pacientes cursaban sin insuficiencia cardiaca; 15 estaban en Killip II; 5; en Killip III, y 10, en Killip IV. Los factores de riesgo cardiovascular -diabetes incluida- eran frecuentes, pero más en el grupo con insuficiencia cardiaca. La fracción de eyección del ventrículo izquierdo era inferior en aquellos con insuficiencia cardiaca al ingreso (el 51 frente al 42%; p<0,01). No se detectaron diferencias en cuanto a los tratamientos previos al ingreso ni en los biomarcadores de necrosis. Durante una mediana de seguimiento de 1.380 días, se observaron más complicaciones intrahospitalarias y en la cohorte con insuficiencia cardiaca tanto para la variable combinada como para muerte. Conclusiones. En el síndrome de tako-tsubo, la insuficiencia cardiaca es frecuente; se observa sobre todo en pacientes con más comorbilidades y peores clases funcionales previas y se asocia a más eventos adversos, tanto durante el ingreso como en el seguimiento a largo plazo. El pronóstico a largo plazo es generalmente bueno (AU)

Introduction and objectives. Tako-tsubo syndrome produces a variable degree of transient left ventricular dysfunction. Our objective was to determine the short- and long-term prognosis of this syndrome, the incidence of and risk factors for the development of heart failure, and the influence on heart failure on the long-term outcome in our patient population. Methods. We prospectively recorded the clinical features and events during the hospital stay and follow-up of 100 patients with tako-tsubo syndrome. The risk factors for heart failure during hospital stay, considered as Killip class≥II, were assessed. Results. Most of the patients were women (89%), with a mean age of 68 years. The distribution according to Killip class was: Killip I, 70 patients; Killip II, 15; Killip III, 5; and Killip IV, 10. Cardiovascular risk factors, including diabetes, were common in the overall group, but were more so in the heart failure cohort. The left ventricular ejection fraction was lower in the heart failure group (51% vs 42%; P<.01). There were no differences in preadmission medications or biomarkers of necrosis. Over a median follow-up of 1380 days, the incidence of events reported during the hospital stay and long-term follow-up, both for death and the combined endpoints, was higher in the heart failure cohort. Conclusions. Although the prognosis in tako-tsubo syndrome is usually good, heart failure occurs quite frequently, mainly in patients with a greater number of comorbidities and poorer previous functional class. Moreover, heart failure is associated with a higher number of early and late adverse events. The overall long-term prognosis is good (AU)

Study design for the "effect of METOprolol in CARDioproteCtioN during an acute myocardial InfarCtion" (METOCARD-CNIC): a randomized, controlled parallel-group, observer-blinded clinical trial of early pre-reperfusion metoprolol administration in ST-segment elevation myocardial infarction.

BACKGROUND: Infarct size predicts post-infarction mortality. Oral ß-blockade within 24 hours of a ST-segment elevation acute myocardial infarction (STEMI) is a class-IA indication, however early intravenous (IV) ß-blockers initiation is not encouraged. In recent magnetic resonance imaging (MRI)-based experimental studies, the ß(1)-blocker metoprolol has been shown to reduce infarct size only when administered before coronary reperfusion. To date, there is not a single trial comparing the pre- vs. post-reperfusion ß-blocker initiation in STEMI. OBJECTIVE: The METOCARD-CNIC trial is testing whether the early initiation of IV metoprolol before primary percutaneous coronary intervention (pPCI) could reduce infarct size and improve outcomes when compared to oral post-pPCI metoprolol initiation. DESIGN: The METOCARD-CNIC trial is a randomized parallel-group single-blind (to outcome evaluators) clinical effectiveness trial conducted in 5 Counties across Spain that will enroll 220 participants. Eligible are 18- to 80-year-old patients with anterior STEMI revascularized by pPCI ≤6 hours from symptom onset. Exclusion criteria are Killip-class ≥III, atrioventricular block or active treatment with ß-blockers/bronchodilators. Primary end point is infarct size evaluated by MRI 5 to 7 days post-STEMI. Prespecified major secondary end points are salvage-index, left ventricular ejection fraction recovery (day 5-7 to 6 months), the composite of (death/malignant ventricular arrhythmias/reinfarction/admission due to heart failure), and myocardial perfusion. CONCLUSIONS: The METOCARD-CNIC trial is testing the hypothesis that the early initiation of IV metoprolol pre-reperfusion reduces infarct size in comparison to initiation of oral metoprolol post-reperfusion. Given the implications of infarct size reduction in STEMI, if positive, this trial might evidence that a refined use of an approved inexpensive drug can improve outcomes of patients with STEMI.

Tako-tsubo syndrome and heart failure: long-term follow-up.

INTRODUCTION AND OBJECTIVES: Tako-tsubo syndrome produces a variable degree of transient left ventricular dysfunction. Our objective was to determine the short- and long-term prognosis of this syndrome, the incidence of and risk factors for the development of heart failure, and the influence on heart failure on the long-term outcome in our patient population. METHODS: We prospectively recorded the clinical features and events during the hospital stay and follow-up of 100 patients with tako-tsubo syndrome. The risk factors for heart failure during hospital stay, considered as Killip class≥II, were assessed. RESULTS: Most of the patients were women (89%), with a mean age of 68 years. The distribution according to Killip class was: Killip I, 70 patients; Killip II, 15; Killip III, 5; and Killip IV, 10. Cardiovascular risk factors, including diabetes, were common in the overall group, but were more so in the heart failure cohort. The left ventricular ejection fraction was lower in the heart failure group (51% vs 42%; P<.01). There were no differences in preadmission medications or biomarkers of necrosis. Over a median follow-up of 1380 days, the incidence of events reported during the hospital stay and long-term follow-up, both for death and the combined endpoints, was higher in the heart failure cohort. CONCLUSIONS: Although the prognosis in tako-tsubo syndrome is usually good, heart failure occurs quite frequently, mainly in patients with a greater number of comorbidities and poorer previous functional class. Moreover, heart failure is associated with a higher number of early and late adverse events. The overall long-term prognosis is good. Full English text available from:www.revespcardiol.org.

Circadian variations of infarct size in acute myocardial infarction.

BACKGROUND: The circadian clock influences a number of cardiovascular (patho)physiological processes including the incidence of acute myocardial infarction. A circadian variation in infarct size has recently been shown in rodents, but there is no clinical evidence of this finding. OBJECTIVE: To determine the impact of time-of-day onset of ST segment elevation myocardial infarction (STEMI) on infarct size. METHODS: A retrospective single-centre analysis of 811 patients with STEMI admitted between 2003 and 2009 was performed. Infarct size was estimated by peak enzyme release. The relationship between peak enzyme concentrations and time-of-day were characterised using multivariate regression splines. Time of STEMI onset was divided into four 6-hour periods in phase with circadian rhythms. RESULTS: Model comparisons based on likelihood ratio tests showed a circadian variation in infarct size across time-of-day as evaluated by peak creatine kinase (CK) and troponin-I (TnI) concentrations (p=0.015 and p=0.012, respectively). CK and TnI curves described similar patterns across time, with a global maximum in the 6:00-noon period and a local minimum in the noon-18:00 period. Infarct size was largest in patients with STEMI onset in the dark-to-light transition period (6:00-noon), with an increase in peak CK and TnI concentrations of 18.3% (p=0.031) and 24.6% (p=0.033), respectively, compared with onset of STEMI in the 18:00-midnight period. Patients with anterior wall STEMI also had significantly larger infarcts than those with STEMI in other locations. CONCLUSIONS: Significant circadian oscillations in infarct size were found in patients according to time-of-day of STEMI onset. The infarct size was found to be significantly larger with STEMI onset in the dark-to-light transition period (6:00-noon). If confirmed, these results may have a significant impact on the interpretation of clinical trials of cardioprotective strategies in STEMI.

Propiedades de los diferentes inhibidores de la glucoproteína IIb/IIIa: ¿se puede aceptar el efecto de clase? / Properties of different glycoprotein-IIB/IIIA inhibitors: do these drugs have a class effect?

Los tres agentes inhibidores de la glucoproteína IIb/IIIa actualmente en uso clínico, abciximab, eptifibatida y tirofibán, comparten como diana terapéutica el bloqueo de la vía final común de la agregación plaquetaria, pero difieren significativamente en su estructura química, en la forma de bloquear la integrina α2bβ3 plaquetaria y en la especificidad por el receptor. Como consecuencia de ello, el patrón de inhibición de cada uno de estos fármacos en la funcionalidad plaquetaria varía y la equivalencia de beneficio clínico para una misma indicación es cuestionable. Hoy por hoy, no se dispone de ensayos clínicos de equivalencia que nos permitan aceptar o excluir un efecto de clase para los inhibidores de la glucoproteína IIb/IIIa en una determinada indicación clínica. Los resultados de los metaanálisis realizados en las diversas indicaciones clínicas tampoco han sido concluyentes, ya que no siempre muestran beneficios clínicos similares en magnitud y dirección para cada uno de los inhibidores de la glucoproteína IIb/IIIa. Por lo tanto, no podemos recomendar el intercambio o sustitución de un inhibidor por otro más allá de la indicación particular para la que se lo haya estudiado y aprobado (AU)

The three glycoprotein-IIb/IIIa inhibitors currently in clinical use, abciximab, eptifibatide and tirofiban, all share the same therapeutic target, namely blockade of the final common pathway of platelet aggregation. However, they differ significantly in chemical structure, in the way in which they block platelet integrin α2bβ3, and in specificity for the receptor. Consequently, each drug inhibits platelet function in a different way and it is unclear whether they offer equivalent clinical benefits for the same indication. To date, there have been no clinical trials on the equivalence of these drugs that would enable us to conclude that glycoprotein-IIb/IIIa inhibitors either do or do not exhibit a class effect for any particular clinical indication. Moreover, the findings of meta-analyses carried out for various indications have been inconclusive because the magnitude and direction of the clinical benefits associated with different glycoprotein-IIb/IIIa inhibitors have often diverged. Therefore, the exchange or substitution of one glycoprotein-IIb/IIIa inhibitor for another cannot be recommended beyond the specific indication for which the drug has been investigated and approved (AU)

Calcified right ventricular thrombus and antiphospholipid syndrome.

Antiphospholipid syndrome has been associated with venous and arterial thrombotic events but intracardiac thrombosis is rare. We describe a case about a 30-year-old woman, admitted with a 6-month history of arthralgia, fatigue, and intermittent fever. Subsequent investigation revealed the presence of a large and calcified mass in the right ventricular outflow tract attached to the subvalvular tricuspid apparatus. Cardiac surgery was performed and histological examination demonstrated it to be composed entirely of calcified thrombus. Screening laboratory evaluation for hypercoagulable states confirmed the diagnosis of antiphospholipid syndrome.

[Creatinine clearance and contrast nephropathy in patients with normal creatinine levels]. / Aclaramiento de creatinina y nefropatía por contraste en pacientes con creatinina normal.

The main risk factor for contrast nephropathy is the presence of poor renal function. Plasma creatinine level is not a reliable measure of renal function as its value could lie within the normal range despite the presence of significant nephropathy. The purpose of this study was to evaluate the creatinine clearance rate as a predictor of contrast nephropathy in patients with a normal plasma creatinine level. The study included 273 consecutive patients with non-ST elevation acute coronary syndrome (NSTEACS) and a normal plasma creatinine level at admission who underwent coronary angiography. Patients who developed contrast nephropathy had a lower creatinine clearance rate at admission (66.3 mL/min vs. 83.4 mL/min; P<.001). A creatinine clearance rate < 80 mL/min had a sensitivity of 81% for predicting contrast nephropathy. Creatinine clearance should be measured routinely in patients with NSTEACS who are scheduled for coronary angiography.

Aclaramiento de creatinina y nefropatía por contraste en pacientes con creatinina normal / Creatinine clearance and contrast nephropathy in patients with normal creatinine levels

El principal factor de riesgo de nefropatía por contraste (NC) es la presencia de una función renal deteriorada. La creatinina plasmática (Cp) es una medida poco exacta de la función renal y puede ser normal en presencia de nefropatía significativa. El objetivo del estudio es evaluar el valor del aclaramiento de creatinina (ACr) como predictor de NC en pacientes con Cp normal. Se incluyó a 273 pacientes consecutivos con síndrome coronario agudo sin elevación del segmento ST (SCASEST), con Cp normal en el momento ingreso y en los que se realizó una coronariografía. El ACr fue significativamente menor en el grupo de pacientes que presentaron NC (66,3 frente a 83,4 ml/min: p < 0,001). Un ACr < 80 ml/min presentó una sensibilidad de 81% para predecir el desarrollo de NC. El ACr se debería obtener de manera sistemática en pacientes con SCASEST (AU)

The main risk factor for contrast nephropathy is the presence of poor renal function. Plasma creatinine level is not a reliable measure of renal function as its value could lie within the normal range despite the presence of significant nephropathy. The purpose of this study was to evaluate the creatinine clearance rate as a predictor of contrast nephropathy in patients with a normal plasma creatinine level. The study included 273 consecutive patients with non-ST elevation acute coronary syndrome (NSTEACS) and a normal plasma creatinine level at admission who underwent coronary angiography. Patients who developed contrast nephropathy had a lower creatinine clearance rate at admission (66.3 mL/min vs. 83.4 mL/min; P<.001). A creatinine clearance rate < 80 mL/min had a sensitivity of 81% for predicting contrast nephropathy. Creatinine clearance should be measured routinely in patients with NSTEACS who are scheduled for coronary angiography (AU)