ABSTRACT
BACKGROUND: Coronavirus disease COVID-19 produces a predominantly pulmonary affection, being cardiac involvement an important component of the multiorganic dysfunction. At the moment there are few reports about the behavior of echocardiographic images in the patients who have the severe forms of the disease. OBJECTIVE: Identify the echocardiographic prognostic markers for death within 60 days in patients hospitalized in intensive care. METHODS: A single-center prospective cohort was made with patients hospitalized in intensive care for COVID-19 confirmed via polymerase chain reaction who got an echocardiogram between May and October 2020. A Cox multivariate model was plotted reporting the HR and confidence intervals with their respective p values for clinical and echocardiographic variables. RESULTS: Out of the 326 patients included, 153 patients got an echocardiogram performed on average 6.8 days after admission. The average age was 60.7, 47 patients (30.7%) were females and 67 (44.7%) registered positive troponin. 91 patients (59.5%) died. The univariate analysis identified TAPSE, LVEF, pulmonary artery systolic pressure, acute cor pulmonale, right ventricle diastolic dysfunction, and right ventricular dilatation as variables associated with mortality. The multivariate model identified that the acute cor pulmonale with HR= 4.05 (CI 95% 1.09 - 15.02, p 0.037), the right ventricular dilatation with HR= 3.33 (CI 95% 1.29 - 8.61, p 0.013), and LVEF with HR= 0.94 (CI 95% 0.89 - 0.99, p 0.020) were associated with mortality within 60 days. CONCLUSIONS: In patients hospitalized in the intensive care unit for COVID-19, the LVEF, acute cor pulmonale and right ventricular dilatation are prognostic echocardiographic markers associated with death within 60 days.
Subject(s)
COVID-19 , Ventricular Dysfunction, Right , Critical Care , Echocardiography , Female , Humans , Prospective Studies , Ventricular Dysfunction, Right/complicationsABSTRACT
Congenital heart disease occurs in about 0,8% of all newborns. Many cardiac malformations occur among relatives and have a polymorphic presentation. The origin of most congenital heart disease is thought to be multifactorial, implying both anomalous expression of genes and the influence of epigenetic factors. However, in a small number of cases, the origin of congenital heart disease has been directly related to chromosomal anomalies or to defects in a single gene. Curiously, defects in a single gene can explain a polymorphic presentation if the anomalous gene controls a basic embryonic process that affects different organs in time and space. Some of these genes appear to control the establishment of laterality. The establishment of the left-right asymmetry starts at the Hensen node. Here, the initial embryonic symmetry is broken by cascades of gene activation that confer specific properties on the left and right sides of the embryo. Although there are variations between species, some basic patterns of gene expression (Nodal, Pitx2) appear to be maintained along the phylogenetic scale. Anomalous expression of these genes induces the heterotaxia syndrome, which usually courses with congenital heart disease. The development of heart malformations is illustrated with the mouse mutant iv/iv, which is a model for the heterotaxia syndrome and the associated congenital heart disease.
Subject(s)
Heart Defects, Congenital/pathology , Animals , Chromosome Aberrations , Disease Models, Animal , Heart Defects, Congenital/genetics , HumansABSTRACT
Las malformaciones cardíacas ocurren en aproximadamente el 0,8 por ciento de todos los nacidos vivos. Muchas de estas malformaciones se presentan en grupos familiares y muestran un tremendo polimorfismo. El origen de la mayor parte de las malformaciones cardíacas se desconoce, estableciéndose lo que se ha llamado un origen multifactorial. Aunque este término implica la expresión anómala de genes y la intervención de factores epigenéticos, el desarrollo de las malformaciones cardíacas se asocia en algunos casos a anomalías cromosómicas o a defectos de un único gen. Curiosamente, defectos de un único gen pueden explicar gran parte de las presentaciones polimórficas si este gen controla procesos embrionarios básicos que afectan, en tiempo y espacio diferentes, a distintos órganos. Algunos de estos genes parecen estar implicados en el establecimiento de la lateralidad embrionaria. El establecimiento izquierda-derecha del eje embrionario comienza en el nódulo de Hensen donde se rompe la simetría inicial y se inducen cascadas de expresión génica que confieren a cada lado del embrión propiedades específicas. Aunque los desencadenantes de la ruptura inicial de la simetría varían entre las diferentes especies, existen patrones de expresión génica (Nodal, Pitx2) conservados a lo largo de la escala filogenética. La expresión anormal de estos genes induce la aparición del síndrome de heterotaxia, que se acompaña de malformaciones cardíacas. El desarrollo de estas malformaciones se ilustra con la mutante de ratón iv/iv, que constituye un modelo del síndrome de heterotaxia y las malformaciones cardíacas asociadas (AU)
