ABSTRACT
Background and Objectives: Available studies confirm myocardial injury and its association with mortality in patients with COVID-19, but few data have been reported from echocardiographic studies. The aim of this study was to identify subclinical left ventricular dysfunction by global longitudinal strain (GLS) and its evolution in the short term in hospitalized patients with COVID-19. Materials and Methods: Thirty-one consecutive noncritical patients admitted for COVID-19 were included. Information on demographics, laboratory results, comorbidities, and medications was collected. Transthoracic echocardiograms were performed using a Philips Affinity 50, at the acute stage and at a 30-day follow-up. Automated left ventricular GLS was measured using a Philips Qlab 13.0. A GLS of <-15.9% was defined as abnormal. Results: The mean age was 65 ± 15.2 years, and 61.3% of patients were male. Nine patients (29%) had elevated levels of high-sensitivity troponin I. Left ventricular ejection fraction was preserved in all; however, 11 of them (35.5%) showed reduced GLS. These patients had higher troponin levels (median, 23.7 vs. 3.2 ng/L; p < 0.05) and NT-proBNP (median, 753 vs. 81 pg/mL; p < 0.05). The multivariate analysis revealed that myocardial injury, defined as increased troponin, was significantly associated with GLS values (coefficient B; p < 0.05). Follow-up at 30 days showed an improvement in GLS values in patients with subclinical left ventricular dysfunction (-16.4 ± 2.07% vs. -13.2 ± 2.40%; p < 0.01), without changes in the normal GLS group. Conclusions: Subclinical left ventricular dysfunction is common in noncritical hospitalized patients with COVID-19 (one in every three patients), even with preserved left ventricular ejection fraction. This impairment tends to be reversible on clinical recovery.
Subject(s)
COVID-19 , Ventricular Dysfunction, Left , Humans , Male , Middle Aged , Aged , Aged, 80 and over , Female , Ventricular Function, Left , Stroke Volume , Follow-Up Studies , COVID-19/complications , Ventricular Dysfunction, Left/diagnostic imaging , Echocardiography/methods , TroponinABSTRACT
La medición del filtrado glomerular es el mejor índice de valoración de la función renal. La creatinina sérica es el marcador de filtrado glomerular más utilizado, a pesar de estar sometido a diferentes fuentes de variabilidad. La cistatina C es una proteína de bajo peso molecular propuesta como marcador de función renal más sensible que la creatinina al detectar de forma precoz alteraciones en la función renal. La medida de cistatina C en suero en determinados grupos de pacientes como ancianos, niños o diabéticos parece aportar mayor información que la creatinina. Sin embargo, presenta alteraciones en su concentración sérica por factores diferentes al filtrado glomerular. Actualmente no hay evidencia científica suficiente que justifique el cambio de las ecuaciones de estimación del filtrado glomerular basadas en la concentración sérica de creatinina por la medida de la concentración sérica de cistatina C en la evaluación de la función (AU)
Glomerular filtration is the best index for assessing renal function. Despite being subjected to several sources of variability, serum creatinine is the most common glomerular filtration marker in use. Cystatin C is a low molecular weight protein which is more sensitive than creatinine, particularly for the identification of initial small decreases in renal function. The use of cystatin C in certain groups of patients such as elderly, children or diabetics appears to provide more information than creatinine. However, serum cystatin C can be influenced by non-renal factors. Currently, there is not enough scientific evidence to recommend the use of cystatin C to assess renal function instead of creatinine and creatinine equations (AU)
Subject(s)
Humans , Male , Female , Cystatins , Cystatins/isolation & purification , Plasma/cytology , Plasma/physiology , Immunoassay/methods , Glomerular Filtration Rate , Glomerular Filtration Rate/physiologyABSTRACT
La cardiopatía isquémica supone el 1,3% de los casos de atención en un servicio de urgencias hospitalario en España. El manejo del paciente es complejo por el riesgo de producir una alta médica incorrecta, el beneficio de instaurar una revascularización rápida y el gasto excesivo por admisiones injustificadas. La última década ha permitido un importante avance en el desarrollo de nuevos marcadores cardíacos. Tradicionalmente los marcadores del síndrome coronario agudo han sido indicadores de necrosis cardíaca. Esta función se ha ampliado actualmente. Aún hay muchas limitaciones en la medición de estos marcadores, como la falta de un procedimiento estandarizado o materiales de referencia certificados. Además de las troponinas cardíacas y el electrocardiograma, medir la albúmina modificada por isquemia puede ayudar a excluir un síndrome coronario agudo en pacientes con baja probabilidad de isquemia miocárdica. La proteína fijadora de ácidos grasos-H es un marcador de necrosis útil en el diagnóstico precoz del infarto agudo de miocardio. En el pronóstico del síndrome coronario agudo, la proteína C reactiva, los péptidos natriuréticos y la mieloperoxidasa complementan el valor pronóstico de la troponina. El ligando soluble CD40 permite la clasificación e individualización del tratamiento del síndrome coronario agudo. Actualmente no hay suficiente evidencia para que ningún nuevo marcador sustituya a los que recomiendan las sociedades científicas ni se dispone de procedimientos de medición rápidos para algunos de ellos. Deben establecerse paneles utilizando la evidencia científica disponible y tomando como objetivo su contribución a una mejor evolución del paciente(AU)
Myocardical ischemia involves 1.3% of the patients attending emergency departments in Spain. The management of these patients is complex, due to the risk of an incorrect discharge diagnosis, the benefit of rapid revascularization and the excessive cost due to unnecessary admissions. There has been a significant improvement in the development of new cardiac biomarkers over the last ten years. Biomarkers traditionally used for identifying acute coronary syndrome were indicators of myocardial necrosis. This role has currently been expanded. There are still some limitations in the measurement of these biomarkers, due to lack of standardised assays or certified calibrators. Ischemia-modified albumin in conjunction with cardiac troponin and electrocardiogram, can help to rule out an acute coronary syndrome in patients with a low probability of having myocardical ischemia. Heart-type fatty acid-binding protein is a strong necrosis biomarker in the early diagnosis of acute myocardical infarction. C-reactive protein, natriuretic peptides and myeloperoxidase have been shown to complement cardiac troponin in the prognosis of acute coronary syndrome. Soluble CD40 ligand enables the identification of a subgroup of patients who will benefit from a treatment in acute coronary syndrome. There is currently not enough evidence to replace new biomarkers with any of these already been recommended by the scientific societies. Also, the assays of some of them are not sufficiently rapid. A multimarker strategy must be created to take into account the existing scientific-based evidence, with the aim of improving outcomes in patients(AU)
