RESUMEN
Left ventricular (LV) longitudinal function is mechanically coupled to the elasticity of the ascending aorta (AA). The pathophysiologic link between a stiff AA and reduced longitudinal strain and the subsequent deterioration in longitudinal LV systolic function is likely relevant in heart failure with preserved ejection fraction (HFpEF). The proposed therapeutic effect of freeing the LV apex and allowing for LV inverse longitudinal shortening was studied in silico utilizing the Living Left Heart Human Model (Dassault Systémes Simulia Corporation). LV function was evaluated in a model with (A) an elastic AA, (B) a stiff AA, and (C) a stiff AA with a free LV apex. The cardiac model simulation demonstrated that freeing the apex caused inverse LV longitudinal shortening that could abolish the deleterious mechanical effect of a stiff AA on LV function. A stiff AA and impairment of the LV longitudinal strain are common in patients with HFpEF. The hypothesis-generating model strongly suggests that freeing the apex and inverse longitudinal shortening may improve LV function in HFpEF patients with a stiff AA.
RESUMEN
During systole, longitudinal shortening of the left ventricle (LV) displaces the aortic root toward the apex of the heart and stretches the ascending aorta (AA). An in silico study (Living Left Heart Human Model, Dassault Systèmes Simulia Corporation) demonstrated that stiffening of the AA affects myocardial stress and LV strain patterns. With AA stiffening, myofiber stress increased overall in the LV, with particularly high-stress areas at the septum. The most pronounced reduction in strain was noted along the septal longitudinal region. The pressure-volume loops showed that AA stiffening caused a deterioration in LV function, with increased end-systolic volume, reduced systolic LV pressure, decreased stroke volume and effective stroke work, but elevated end-diastolic pressure. An increase in myofiber contractility indicated that stroke volume and effective stroke work could be recovered, with an increase in LV end-systolic pressure and a decrease in end-diastolic pressure. Longitudinal and radial strains remained reduced, but circumferential strains increased over baseline, compensating for lost longitudinal LV function. Myofiber stress increased overall, with the most dramatic increase in the septal region and the LV apex. We demonstrate a direct mechanical pathophysiologic link between stiff AA and reduced longitudinal left ventricular strain which are common in patients with HFpEF.
RESUMEN
INTRODUCTION: Most patients on extracorporeal membrane oxygenation (ECMO) decease during therapy on the system. However, the actual causes of death have not been studied sufficiently. This study analyses the etiology, prevalence, and risk factors for the outcome variable death during ongoing ECMO for all patients and divided according to venoarterial (VA) or venovenous (VV) support. METHODS: We retrospectively analysed all patients receiving ECMO support at our institution between March 2006 to January 2021. Only the patients deceased during ongoing support were included. RESULTS: 2016 patients were placed on VA (n = 1168; 58%) or VV (n = 848; 42%) ECMO; 759 patients (37.7%) deceased on support. The causes of death differed between the support types: VA ECMO patients mostly died from cerebral ischemia (34%), low-cardiac output (LCO; 24.1%) and multi-organ failure (MOF; 21.6%), whereas in VV ECMO cases, refractory respiratory failure (28.2%), and sepsis (20.4%) dominated. Multivariate regression analysis revealed cardiopulmonary resuscitation (CPR) and acidosis prior to ECMO as risk factors for dying on VA ECMO, while high inotropic doses pre-ECMO, a high fraction of inspired oxygen on day 1, elevated lactate dehydrogenase, and international normalized ratio levels lead to an unfavourable outcome in VV ECMO patients. CONCLUSION: Even in highly experienced centers, ECMO mortality remains high and occurs mainly on support or 24 h after its termination. The causes of death differ between VV and VA ECMO, depending on the underlying diseases responsible for the need of extracorporeal support.
RESUMEN
OBJECTIVES: Both postoperative and spontaneous chylothorax remain therapeutic challenges without recommendations for a standardized treatment approach. Regardless of its aetiology, patients with chylothorax experience prolonged hospitalization and suffer from the associated complications or the invasive therapy administered. METHODS: We conducted a retrospective, observational review of adult patients with chylothorax treated between January 2010 and September 2019. The primary end point was successful management with sustained cessation and/or controlled chylous output. Therapy duration, inpatient stay and the incidence of complications were evaluated as secondary end points. RESULTS: Of the 36 patients included (22 men; median age 63 years), 24 patients (67%) suffered from a postoperative accumulation of chylous fluid in the pleural space; in the remaining 12 (33%) patients, chylothoraces occurred spontaneously. Initial conservative treatment was successful in 42% (n = 15); in the other 20 cases (56%) additional invasive therapeutic strategies were followed. A complicated course requiring more than 1 treatment was seen in 54% (n = 13) of the postoperative and in 58% (n = 7) of the spontaneous cases. The median length of hospitalization was significantly longer in the postoperative group (37.5 vs 15.5 days; P = 0.016). Serious complications were observed only in the postoperative group (P = 0.28). There were no in-hospital deaths. CONCLUSIONS: Basic treatment of both postoperative and spontaneous chylothorax should include dietary measures in all patients. Additional sclerosing radiotherapy and interventional or surgical therapy are often necessary. The choice of therapeutic approach should be indicated, depending on the aetiology and development of the chylothorax. Early, multimodal treatment is recommended.
Asunto(s)
Quilotórax , Adulto , Quilotórax/etiología , Quilotórax/terapia , Terapia Combinada , Humanos , Masculino , Persona de Mediana Edad , Complicaciones Posoperatorias/etiología , Complicaciones Posoperatorias/terapia , Periodo Posoperatorio , Estudios RetrospectivosRESUMEN
Lymphatic malformations are benign focal proliferations of lymphatic vessels with a congenital origin. We present a case of an 18-year-old patient with post-traumatic chylopericardium and recurrent left-sided chylothorax, who was unresponsive to a variety of therapeutic measures until he was diagnosed with a complicated thoracic lymphatic malformation.