RESUMEN
Congenital fistula between the first diagonal branch of the coronary artery and left ventricle with a giant coronary artery aneurysm is extremely rare. We present the case of a 50-year-old asymptomatic male patient with such a condition that was diagnosed by transthoracic echocardiography, coronary computed tomography angiography, and coronary angiography. The patient was treated by surgical fistula closure under cardiopulmonary bypass. The postoperative coronary computed tomography angiography showed the patient got a complete cure, and the patient remains asymptomatic after 5-year follow up.
Asunto(s)
Aneurisma Coronario , Fístula , Masculino , Humanos , Persona de Mediana Edad , Ventrículos Cardíacos/cirugía , Vasos Coronarios/cirugía , Estudios de Seguimiento , Aneurisma Coronario/diagnóstico , Fístula/complicaciones , Fístula/cirugía , Angiografía CoronariaRESUMEN
Macrophages are crucial immune cells that play essential roles in the healing of myocardial infarction (MI), undergoing continuous polarization throughout this process. C-C motif chemokine 2 (CCL2) is a chemokine that regulates inflammatory responses during MI. However, the extent to which CCL2 influences macrophage polarization and MI healing remains incompletely understood. In this study, we investigate the role of CCL2 in macrophage polarization and MI healing. Our findings reveal that CCL2 is differentially expressed in lipopolysaccharide (LPS)-induced M1 and interleukin (IL)-4-induced M2 RAW264.7 macrophages. Knockdown of CCL2 attenuates TNF-α secretion stimulated by LPS, while overexpression of CCL2 mitigates IL-10 production triggered by IL-4 in these macrophages. Moreover, CCL2 deficiency disrupts LPS-induced M1 polarization, whereas CCL2 overexpression reduces M2 polarization of RAW264.7 macrophages induced by IL-4. Further exploration indicates that the promotion of M1 polarization by CCL2 is significantly impaired by inhibition of the p38-mediated MAPK pathway and NF-κB pathway. In a MI mouse model, CCL2 knockdown remarkably reduces infarct size, collagen synthesis, and the expression of cardiac fibrosis and hypertrophy markers. The activity of the p38-mediated MAPK pathway and NF-κB pathway is downregulated by CCL2 knockdown as well. Additionally, the number of total macrophages and M1 macrophages in the infarct decreases, while the number of M2 macrophages increases upon CCL2 deficiency. In conclusion, these results suggest that CCL2 is a key regulator of macrophage polarization, controlling MI healing in vivo.
Asunto(s)
Interleucina-4 , Infarto del Miocardio , Animales , Ratones , Interleucina-4/metabolismo , Lipopolisacáridos/farmacología , Macrófagos/metabolismo , Infarto del Miocardio/genética , Infarto del Miocardio/metabolismo , FN-kappa B/metabolismoRESUMEN
Uncontrollable bleeding is a major problem in surgical procedures and after major trauma. Existing hemostatic agents poorly control hemorrhaging from traumatic arterial and cardiac wounds because of their weak adhesion to wet and mobile tissues. Here we design a photo-reactive adhesive that mimics the extracellular matrix (ECM) composition. This biomacromolecule-based matrix hydrogel can undergo rapid gelling and fixation to adhere and seal bleeding arteries and cardiac walls after UV light irradiation. These repairs can withstand up to 290 mm Hg blood pressure, significantly higher than blood pressures in most clinical settings (systolic BP 60-160 mm Hg). Most importantly, the hydrogel can stop high-pressure bleeding from pig carotid arteries with 4~ 5 mm-long incision wounds and from pig hearts with 6 mm diameter cardiac penetration holes. Treated pigs survived after hemostatic treatments with this hydrogel, which is well-tolerated and appears to offer significant clinical advantage as a traumatic wound sealant.