Association of hemostasis and inflammation biomarkers with outcomes in acute coronary syndromes.

Plaque rupture triggers a prothrombotic response that is counterbalanced by a fibrinolytic response. d -dimer serves as a marker of both processes. Inflammatory mediators are also released, evidenced with the rise of high-sensitive C reactive protein (hsCRP). Current evidence with these biomarkers has shown conflicting results. Determine an association between d -dimer and hsCRP within hospital and 1-year mortality in patients with acute coronary syndromes. In total, 127 patients were included. In-hospital mortality was 5.7%, and 1-year all-cause and cardiovascular mortality were 14.6 and 9.7%, respectively. The median of admission d -dimer for patients who died during hospital stay was higher than those who survived [4.59 (interquartile ranges (IQR) 1.94-6.05 µg/ml fibrinogen equivalent units (FEU)) vs. 0.56 (IQR 0.31-1.12 µg/ml FEU), P  = 0.001]. At 1-year follow-up, the median of admission d -dimer for patients who died was significantly higher than those who survived: 1.55 (IQR 0.91-5.08 µg/ml FEU) vs. 0.53 (IQR 0.29-0.90 µg/ml FEU), P  < 0.001. Positive d -dimer vs. negative d -dimer at admission analysis evidenced that almost 25% of the positive patients were dead at 1-year follow-up (22.4 vs. 2.4% negative d -dimer, P  = 0.011). Multivariate logistic regression analysis showed that d -dimer has an independent association with 1-year mortality [odds ratio 1.06 (95% confidence interval 1.02-1.10), P  = 0.006]. Positive significative correlations between d -dimer and hsCRP levels ( R  = 0.56, P  < 0.001) were found. High levels of admission d -dimer were strongly associated with in-hospital and 1-year mortality. Significant correlations with hsCRP could explain the inflammatory nature that led to poorer outcomes. d -dimer could be useful in risk stratification in acute coronary syndromes; however, a specific threshold should be defined for this type of patient.

Neurohumoral response and stress hyperglycemia in myocardial infarction.

Background: Hyperglycemia is associated with an increased risk for death in acute coronary syndromes. This could be related to underlying glucose metabolism abnormalities or be caused by a counter-regulatory stress response. However, there is a paucity of data on the relationship between stress hormones, hyperglycemia, and clinical outcomes in myocardial infarction. Methods: Single-center, prospective, observational study. Patients admitted to the coronary care unit with a diagnosis of myocardial infarction were included. On admission, blood samples were obtained to measure serum glucose, cortisol, and catecholamines. A second sample was obtained at 8 AM after 48 h from admission. Results: There was a mild and positive correlation between serum cortisol and glucose (Spearman's rho = 0.24, p = 0.005), and no significant correlation was found between glucose and catecholamines. A similar correlation between cortisol and glucose among diabetics and non-diabetics was observed. Significantly higher serum cortisol and glucose levels were present in patients who developed heart failure or died during hospitalization. The association between glycemia and mortality lost significance in multivariate analysis, with a significant interaction term with cortisol (p = 0.003). Conclusion: Cortisol is a key responsible for stress hyperglycemia, and its deleterious effects on the cardiovascular system could be the cause for worst outcomes associated with hyperglycemia in ACS. Further research is warranted to ascertain this relationship and to investigate potential therapeutic targets.

Analysis of The Left Atrial Function Using Two-Dimensional Strain in Patients with Recent Diagnosis of Hereditary Hemochromatosis.

Hereditary Hemochromatosis (HH) is a genetic condition associated with a systemic iron overload. Heart failure is an important cause of mortality. It has been demonstrated early stages of systolic and diastolic left ventricular dysfunction in previous studies. The aim of the study is to compare the left atrial (LA) function between asymptomatic HH patients and a control group using 2D speckle tracking. Prospective study. LA strain, LA strain rate and LA volumetric parameters during the reservoir, conduit and contraction phases were studied. The LA Stiffness Index was calculated by the ratio between E/e and LA reservoir strain. 30 patients with HH (90% males, 47 ± 18 years old) and 30 healthy controls (85% males, 45 ± 13 years old) were included. LA volume was similar in both groups. No differences were observed in LA ejection fraction (EF), LA passive EF and LA active ejection fraction between both groups. On the contrary, the HH group had lower LA strain during the reservoir (31.5 ± 6.5% vs 38.3 ± 7.9%; P=0.002), and conduit phases (-18 ± 7% vs -23.3 ± 6.4%; P=0.01) and lower LA conduit strain rate (-1.7 ± 0.7 seg-1 vs -2.1 ± 0.5 seg-1; P=0.02) than controls. The LA stiffness index was significantly higher in the HH group (0.25 ± 0.9 vs 0.19 ± 0.6; P=0.01) Early abnormalities in the LA function could be detected by using 2D speckle tracking study despite no evidence of changes in atrial size or volumetric parameters.

Cortisol-Mediated Stress Response and Mortality in Acute Coronary Syndrome.

Acute coronary syndrome is a frequent cause of morbidity and mortality, and a known stress response trigger. We aim to investigate the association between cortisol, as a primary stress hormone, and prognosis/mortality in this scenario. Single-center, prospective, observational, and analytical study in patients admitted for acute coronary syndrome. Clinical characteristics and prognosis markers were registered, along with serum cortisol levels on admission and in-hospital mortality. Cortisol levels were higher in patients with a depressed ST segment (18.22 ± 13.38 µg/dL), compared to those with an isoelectric ST segment (12.66 ± 10.47 µg/dL), and highest in patients with an elevated ST segment (22.61 ± 14.45 µg/dL), with P< 0.001. Also, cortisol was significantly increased in patients with elevated troponin I values (18.90 ± 14.19 µg/dL vs 11.87 ± 8.21 µg/dL, P< 0.001). Patients with Killip-Kimball class I or II had a lower mean serum cortisol (14.66 ± 10.82 µg/dL) than those with class III or IV (41.34 ± 15.57 µg/dL), P< 0.001. Finally, we found that patients who died during hospitalization had higher cortisol on admission: 36.39 ± 17.85 µg/dL vs 15.26 ± 11.59 µg/dL, P= 0.003. Cortisol was directly related to the electrocardiographic presentation of ACS and with the maximum troponin I value. This indicates that serum cortisol levels parallel the extension of ischemia and myocardial injury, and in this way affect the clinical prognosis, evidenced by the Killip-Kimball class and the increase in mortality.

[MINOCA, infarction with normal coronaries. The fall of the paradigm ?] / MINOCA, infarto con coronarias normales ¿ la caída del paradigma ?

Myocardial infarction is the leading cause of death in the world, being the coronary atherosclerotic obstruction the main finding. Although 6% of all the patients had no significant coronary arteries disease on coronary angiography, defined by lumen vascular obstruction greater than 50%. This type of cases was defined by the term MINOCA (myocardial infarction with non-obstructive coronary arteries). They are usually young women, with cardiovascular risk factors, high cardiac biomarkers with non-ST elevation in the electrocardiogram. The main etiologies are myocarditis, Takotsubo syndrome and subendocardial myocardial infarction. We present the case of a 65 years-old woman with history of hypertension and complete left bundle branch block, who was admitted to the emergency department with typical chest pain, complete left bundle branch block in the electrocardiogram, with negative Sgarbossa criteria and positive cardiac biomarkers. The echocardiography evidenced inferolateral regional wall motion abnormalities, and the coronary angiography a single non-significative lesion (40%) in the proximal segment of the circumflex artery. Cardiac magnetic resonance evidenced subendocardial late adolinium enhancement in inferolateral medial with latero-apical extension segments consistent with circumflex artery-related infarction. This case illustrates an example of MINOCA secondary to myocardial infarction with posterior spontaneous thrombolysis, in which the clinical presentation was typical, however the coronary angiography showed non obstructive lesions. Therefore, another complementary imaging methods were needed such as the cardiac magnetic resonance.

El infarto agudo de miocardio es la principal causa de muerte en el mundo, siendo la obstrucción coronaria aterosclerótica el hallazgo más frecuente. Sin embargo, el 6% de los pacientes no presenta lesiones angiográficamente significativas, definidas por obstrucción de la luz vascular mayor al 50%. Estos casos se han definido bajo el término MINOCA (myocardial infarction with non-obstructive coronary arteries). Suelen ocurrir en mujeres jóvenes, con factores de riesgo cardiovascular, elevación de biomarcadores cardíacos e infradesnivel del segmento ST en el electrocardiograma. Las principales etiologías son la miocarditis, el síndrome de Takotsubo y el infarto subendocárdico. Presentamos el caso de una mujer de 65 años con antecedentes de hipertensión arterial y bloqueo completo de rama izquierda previo, que ingresó con ángor, imagen de bloqueo completo de rama izquierda en el electrocardiograma con criterios de Sgarbossa negativos y biomarcadores cardíacos positivos. En el ecocardiograma evidenció trastorno en la motilidad de la pared inferolateral y en la coronariografía solo una lesión no significativa (40%) en segmento proximal de la arteria circunfleja. La cardiorresonancia, en la secuencia de realce tardío de gadolinio, mostró retención de contraste subendocárdico a nivel de los segmentos inferolateral medial con extensión lateroapical compatible con infarto correspondiente a territorio de arteria circunfleja. Este caso ilustra un ejemplo de MINOCA secundario a infarto subendocárdico con trombólisis espontánea, en el que la presentación clínica fue típica, sin embargo en la coronariografía no se observaron lesiones significativas, por lo que fue necesario complementar con otro método de imágenes: la cardiorresonancia.

Estado inflamatorio en el infarto agudo de miocardio, su impacto en el remodelado ventricular y nuevas dianas terapéuticas / Inflammation in acute myocardial infarction, impact on ventricular remodeling, and new therapeutic targets

RESUMEN La cardiopatía isquémica es la causa más frecuente de insuficiencia cardíaca, con una alta incidencia de esta a pesar de la revascularización precoz y la modulación neurohormonal. En el contexto del infarto agudo de miocardio los cardiomiocitos necrosados inducen la activación del sistema inmune innato, con aumento de la concentración de células inflamatorias que ayudan a eliminar las células muertas, e iniciar una respuesta correctiva que permite la formación adecuada de tejido cicatrizal.La prolongación o expansión de la respuesta inflamatoria posterior al infarto contribuye al remodelado adverso ventricular y al desarrollo de insuficiencia cardíaca.Entender los mecanismos inflamatorios que se desarrollan producto del infarto, y su impacto en el remodelado adverso que aumenta el número de eventos cardiovasculares mayores, permite comprender a la inflamación como un objetivo terapéutico.

ABSTRACT Ischemic heart disease is the most common cause of heart failure, with a high incidence of heart failure despite early revascularization and neurohormonal modulation.In the acute myocardial infarction setting, necrotized cardiomyocytes induce activation of the innate immune system, increasing the levels of inflammatory cells to help remove dead cells and initiate a corrective response, which allows for proper scar tissue formation.A prolonged or expanded inflammatory response after infarction contributes to adverse ventricular remodeling and development of heart failure.Understanding the inflammatory mechanisms that emerge as a result of myocardial infarction and their impact on adverse remodeling that leads to an increased.

Frailty is independently associated with 1-year mortality after hospitalization for acute heart failure.

INTRODUCTION: Frailty is a complex condition that results from the loss of physiological reserve across multiple systems. Its presence should be considered in the aging heart failure population, since it is an important predictor of death and institutionalization in the elderly. METHODS AND RESULTS: In a prospective, observational and analytical single-center study of 100 elderly patients hospitalized for acute heart failure, we assessed the characteristics associated with an increased hospital and 1-year mortality. Frailty was evaluated with the Clinical Frailty Scale, and there was a significant association between its presence and 1-year mortality (RR = 2.03; 95% CI = 1.18-3.48; p = 0.014), although not with in-hospital mortality. After adjusting for probable confounders, it remained independently associated with 1-year mortality. CONCLUSION: Frailty can be assessed with a simple bed-side scale and provides significant prognostic information in acute heart failure patients.

Laboratorio de Insuficiencia Cardíaca: experiencia en un hospital universitario / Heart failure laboratory: experience in an university hospital

Introducción: La mayor parte del manejo del paciente con insuficiencia cardíaca (IC) se logra de manera ambulatoria. La adhesión a los estándares de tratamiento recomendados y el acceso al sistema de salud determinan su evolución. Se describe nuestra experiencia en pacientes con IC ambulatoria en un Hospital Universitario. Material y métodos: Se incluyeron pacientes derivados para interconsulta al Laboratorio de IC entre los meses de enero de 2021 y octubre de 2022. Se realizó una intervención estructurada, que incluyó visitas presenciales y seguimiento por email y/o telefónico y asesoramiento nutricional. Resultados: Se incluyeron 98 pacientes. La media de edad fue 64,05 años. El promedio total de FEVI fue 36,26%. Se observó asociación significativa entre los mayores de 60 años (n=65; 66,33%) y dislipemia, hipertensión arterial, enfermedad oncológica y enfermedad coronaria, en comparación con los individuos más jóvenes. La FEVI baja se correlacionó con los portadores de enfermedad coronaria y oncológica. En ellos se observó mayor utilización de betabloqueantes, ARNI, iSGLT2 y ácido acetil salicílico. El sexo masculino, la FEVI disminuida y la edad, fueron predictores de peor pronóstico. Conclusión: La utilización del tratamiento farmacológico en la IC depende de múltiples factores. A pesar de ello, se observó una distribución de la terapéutica instaurada acorde a la recomendación de guía y registros nacionales e internaciones de pacientes con IC

Introduction: Most of the management of the patient with heart failure (HF) is accomplished on an outpatient basis. Adherence to the recommended treatment standards and access to the health system determine their evolution. We describe our experience in patients with ambulatory HF in a University Hospital. Material and methods: Patients referred for interconsultation to the HF Laboratory between the months of January 2021 and October 2022 were included. A structured intervention was carried out, which included face-to-face visits and follow-up by email and/or telephone and nutritional advice. Results: 98 patients were included. Mean age was 64.05 years. Total mean LVEF was 36.26%. A significant association was observed between those over 60 years of age (n=65; 66.33%) and dyslipidemia, arterial hypertension, oncological disease, and coronary disease, compared to younger individuals. The low LVEF was correlated with coronary and oncological disease. In them was observed greater use of beta-blockers, ARNI, iSGLT2 and acetylsalicylic acid. Male sex, decreased LVEF and age were predictors of worse prognosis. Conclusion: The use of pharmacological treatment in HF depends on multiple factors. Despite this, a distribution of the established therapy according to the guideline recommendation and national registries and hospitalizations of patients with HF was observed.

Neuroendocrine System Regulatory Mechanisms: Acute Coronary Syndrome and Stress Hyperglycaemia.

Neurohormonal systems are activated in the early phase of acute coronary syndromes to preserve circulatory homeostasis, but prolonged action of these stress hormones might be deleterious. Cortisol reaches its peak at 8 hours after the onset of symptoms, and individuals who have continued elevated levels present a worse prognosis. Catecholamines reach 100-1,000-fold their normal plasma concentration within 30 minutes of ischaemia, therefore inducing the propagation of myocardial damage. Stress hyperglycaemia induces inflammation and endothelial dysfunction, and also has procoagulant and prothrombotic effects. Patients with hyperglycaemia and no diabetes elevated in-hospital and 12-month mortality rates. Hyperglycaemia in patients without diabetes has been shown to be an appropriate independent mortality prognostic factor in this type of patient.

Valoración de la reserva contráctil y cronotrópica en estudios de eco estrés negativos para isquemia miocárdica / Contractile and chronotropic reserve assessment in stress echocardiography studies negative for myocardial ischemia

RESUMEN Introducción: Si bien el principal objetivo del ecocardiograma estrés (EE) es analizar los cambios en la motilidad parietal, el análisis de otras variables como la reserva contráctil (RCon) por el método de elastancia y la reserva cronotrópica (RCro) permiten agregar valor pronóstico al estudio. No obstante, las mismas no suelen analizarse ni informarse en la mayoría de los estudios de EE en nuestro medio. Objetivos: Comparar las características clínicas y ecocardiográficas de pacientes a quienes se les realizó un EE con ejercicio negativo para isquemia miocárdica de acuerdo con la presencia o no de RCon y RCro. Material y métodos: Estudio retrospectivo realizado sobre 73 pacientes con EE con ejercicio, sin isquemia. De acuerdo con la presencia o ausencia de RCon y RCro se los dividió en tres grupos. Grupo 1: presencia de ambas reservas; grupo 2: presencia de solo una reserva y grupo 3: ausencia de ambas reservas. La RCon se determinó mediante el cociente entre la tensión arterial sistólica y el volumen de fin de sístole tanto en reposo como en estrés (Valor normal: > 2) y la RCro se definió como el aumento mayor al 80% de la frecuencia cardíaca basal. Resultados: Se incluyeron 73 pacientes (64% varones, edad 63 ± 12 años). En el Grupo 1 se incluyeron 23 pacientes (62% varones, 59,8 ± 12,5 años), en el grupo 2, 29 pacientes (65% varones, 60,7 ± 13 años) y en el grupo 3, 21 pacientes (65% varones, 68,8 ± 7,8 años). Los pacientes sin ninguna reserva fueron más añosos y presentaron una tendencia a mayor prevalencia de los factores de riesgo tradicionales, más antecedentes de IAM y mayor uso de betabloqueantes. Desde el punto de vista ecocardiográfico, este mismo grupo presentó menores valores de fracción de eyección ventricular izquierda (FEVI) y strain longitudinal global (SLG) tanto en reposo como en esfuerzo, mayor masa ventricular, y en la ergometría menor cantidad de minutos de ejercicio realizado. Se realizó una regresión logística binaria con aquellas variables asociadas a la ausencia de RCon y RCro. La edad (OR 1,12, IC95% 1,02-1,22; p = 0,01) y el valor de SLG en reposo (OR 0,68, IC95% 0,51-0,90; p= 0,008) fueron las variables asociadas en forma independiente a la ausencia de ambas reservas. En una curva ROC, un valor de SLG de -18% fue el mejor punto de corte (área bajo la curva 0,72; IC 95% 0,57-0,87). Conclusiones: Los pacientes con EE negativo para isquemia miocárdica, y que además presentan ausencia de RCon y RCro tienen un perfil de riesgo más elevado. Esto podría estar asociado a mayor riesgo de eventos cardiovasculares durante el seguimiento.

ABSTRACT Background: While the primary objective of the stress echocardiography (stress echo) is to assess wall motion abnormalities, evaluation of other variables, such as contractile reserve (CR) via elastance, and chronotropic reserve (ChR), may add prognostic value to the study. However, these are unusually evaluated or reported in most stress echo studies in our field. Objectives: To compare clinical and echocardiographic characteristics in patients undergoing an exercise stress echo with negative results for myocardial ischemia based on the presence or absence of CR and ChR. Methods: A rRetrospective study in 73 patients, with exercise stress echo and no ischemia. Patients were divided into three groups, based on the presence or absence of CR and ChR. Group 1: presence of both; Group 2: presence of either of the two, and Group 3: absence of both. The CR was established using as the systolic blood pressure and end-systolic volume ratio, both at rest and under stress (normal value: >2), and the ChR was defined as a more than 80% increase in baseline heart rate. Results: The study enrolled 73 patients (64% males, aged 63±12 years). Group 1 included 23 patients (62% males, agedaged 59.8±12.5 years); Group 2 included 29 patients (65% males, aged 60.7±13 years), and Group 3 included 21 patients (65% males, aged 68.8±7.8 years). Patients with no reserve were older and showed a tendency to higher prevalence of traditional risk factors, a longer history of AMI and increased use of beta blockers. In the Echocardiographicallyechocardiographic study, his group had lower values of left ventricular ejection fraction (LVEF) and global longitudinal strain (GLS) both at rest and under stress, a larger ventricular mass, and less minutes of exercise according toin the exercise stress test. A binary logistic regression was performed using variables associated with the absence of CR and ChR. Age (OR 1.12, 95% CI 1.02-1.22; p=0.01) and GLS at rest (OR 0.68, 95% CI 0.51-0.90; p=0.008) were variables independently associated with the absence of both reserves. On a ROC curve, a GLS of -18% was the best cutoff point (area under the curve 0.72). Conclusion: Patients with a stress echo negative for myocardial ischemia and absence of CR and ChR have a higher risk profile. This could be associated with a higher risk of cardiovascular events during the follow-up.